this chapter covers several aspects of carbohydrate digestion. first it goes over some basics about carbohydrates and digestion in general, then talks about the specific enzymes at work in the brush border of the small intestine, then a brief section about lactose intolerance, and finally, a section about the transport of glucose from the intestine into the blood.
the normal american diet is made of 40-50% carbohydrates, and of this, 50-60% is made of the starch molecules (10,000 to 1 million glucosyl units long) amylose and amylopectin. amylose consists of glucose molecules bonded with alpha 1-4 bonds, while amylopectin is the same, but with alpha 1-6 bonds (and therefore branches) as well. digestion of these starches begins in the mouth with alpha amylase, which is an example of an endoglucosidase-- an enzyme which cleaves alpha 1-4 bonds at random intervals. this initial digestion leaves chunks of polysaccharides called alpha-dextrins. stomach acid deactivates the amylase, and carbohydrate digestion continues in the small intestine.
in the small intestine, carbohydrate digestion takes place mainly on the "brush border" of the intestinal mucosa, which have enzymes that are embedded in the intestinal membrane that poke into the intestinal lumen. the four major "glucosidases" are glucoamylase, trehalase, beta-glucosidase, and sucrase-isomaltase. each of these enzymes has a specific structure and catalytic sites that are specific to certain types of carbohydrates. glucoamylase breaks down alpha 1-4 bonds from the non reducing end ("tail end") of the sugar, until isomaltase remains-- isomaltase is basically just two sugar units branched together in an alpha 1-6 bond. the action of glucoamylase on polysaccharides seems similar to the action of glycogen phosphorylase in the breakdown of glycogen in that both are removing glucose residues one at a time from the tail end, and both can not remove the last glucose unit (or in glucose phosphorylase's case, the last 4).
sucrase-isomaltase is another brush border glucosidase with two catalytic sites. one is specific to isomaltose and maltose (and thus can break down the isomaltose from glucoamylase's activity) and one is specific to sucrose and maltose. beta glucosidase also has two catalytic sites. one is specific to breaking the beta 1-4 bond between glucose and galactose in lactose, and the other is specific to cleaving beta 1-4 bonds in glycolipids. the last glucosidase in the brush border is trehalase, which has only one catalytic site which is specific to trehalose, a sugar found only in some insects, mushrooms, and algae. these four enzymes work in tandem to break down the different types of carbohydrates that are dumped into the duodenum. the relative concentration of these enzymes change depending on the location in the gut. for example, pancreatic alpha amylase is secreted mainly in the duodenum, sucrase-maltase and beta-glucosidase is mainly in the jejunum, and glucoamylases is most common in the ileum.
a couple other notes about carbohydrate digestion. lactose intolerance occurs with either a lactase deficiency or intestinal damage. most adults only have 10% of the lactase activity that they had as children. lactose intolerance can ultimately lead to malabsorption of nutrients: lactose is undigested in the gut, and is instead metabolized by the bacterial flora in the colon, producing gases and lactic acid. the lactic acid can increase the intestinal lumen's osmolarity and cause water to distend the abdomen, which increases peristalsis and potentially causes diarrhea and malabsorption of other nutrients.
the last section of the chapter focused on the membrane channels that transport glucose across the intestinal lining into the blood. there are two types of such transport proteins, regular facilitated glucose channels and Na+ facilitated channels. Na+ facilitated channels use an ATPase Na+/K+ pump to establish a low concentration of Na+ inside the intestinal cell. the concentration gradient that is formed from the higher Na+ concentration in the intestinal lumen is then coupled with glucose transport in these membrane proteins. facilitative glucose transporters (also called "GLUT" transporters) do not require ATP and simply allow glucose to flow down its concentration gradient from the intestinal lumen, into the epithelium, and out into the serosa side ("blood side").
a few interesting notes relating to these glucose transporting membrane proteins. the liver's GLUT transporters have a higher than usual Km (the concentration at which the substrate is half-saturated with enzyme-- generally representing the enzyme's affinity for substrate and in this case the GLUT for glucose) for glucose, because it will only accept glucose into its cells (to be converted into glycogen for storage) when the blood glucose concentration is very high, like after a high carb meal. also, in muscle and fat cells, insulin stimulates glucose absorption by means of recruiting intracellular vesicles of glucose transport proteins to the cell membrane, where they can facilitate glucose transport into the cell.
questions
1. what percentage of a normal american diet consists of carbohydrates?
2. what percentage of the carbohydrate calories consists of amylose and amylopectin?
3. how many glucosyl units do amylose and amylopectin have?
4. what types of bonds do amylose and amylopectin have?
5. what are the major natural sweeteners found in fruit, honey, and vegetables?
6. what is the major dietary carb found from animal sources?
7. how much liquid do the salivary glands secrete per day?
8. what is an "endoglucosidase" and what is an example of one?
9. what is salivary amylase inactivated by?
10. how much digestive enzyme is secreted by the pancreas per day?
11. what are in the pancreatic secretions?
12. what are oligosaccharides?
13. what are the glucosidases found in the brush border of the small intestine?
14. describe the digestion of lactose and sucrose in the small intestine.
15. describe the structure and activity of glucoamylase?
16. what are alpha-dextrins vs. limit-dextrins?
17. describe the structure and activity of the sucrase-isomaltase complex.
18. what percentage of maltase activity can be attributed to the sucrose-isomaltose complex?
19. describe the structure and activity of trehalase.
20. describe the structure and activity of the beta-glucosidase complex
21. pancreatic alpha-amylase activity is highest in...
22. sucrase-isomaltase activity is highest in...
23. beta-glucosidase activity is highest in...
24. glucoamylase activity is highest in...
25. what type of carbohydrates enter the colon?
26. what are the fatty acids that result from bacterial starch digestion in the colon?
27. what are the gases that result from bacterial starch digestion in the colon?
28. lactose intolerance can be caused by...
29. what are normal lactase levels of an adult as compared to a child?
30. what happens when lactose is ingested by a lactose intolerant person?
31. what does the glycemic index represent?
32. which sugars have the highest glycemic index?
33. what are the two types of glucose transport proteins?
34. describe the mechanism of the Na+ dependent glucose transporter.
35. what are facilitative glucose transporters?
36. compare the digestion of glucose with that of galactose and fructose.
37. in body tissues, why is glucose transport across membranes not the rate limiting step of glucose metabolism?
38. how does the high Km of glucose transport proteins in the liver relate to the liver's blood glucose regulation?
39. how is insulin related to glucose transport proteins in the liver?
answers
1. 40-45%
2. 50-60%
3. 10,000 to 1 million
4. amylose has alpha 1-4 bonds between glucosyl residues. amylopectin has alpha 1-4 bonds between glucosyl units as well as alpha 1-6 bonds between branches.
5. fructose, sucrose, glucose.
6. lactose, which is made of glucose and galactose.
7. ~1 liter a day
8. an enzyme that breaks internal alpha 1-4 bonds in a polysaccharide at random intervals, such as amylase.
9. acidity of the stomach
10. ~1.5 liters a day
11. trypsinogen, chymotrypsinogen, carboxypeptidase (for digestion of proteins), alpha-amylase (for carbohydrates), lipase (fat), and bicarbonate (neutralizing gastric acidity)
12. 4-9 glucosyl units long, contain one or more alpha-1,6 branches.
13. beta-glucoamylase, sucrase-isomaltase, beta-glycosidase, trehalase.
14. converted to monosaccharides by glucosidases attached to the brush border lining.
15. it has two domains that have different substrate specificity, and acts as an exoglucosidase by breaking alpha 1-4 bonds on the non reducing ("tail end") of the saccharides, releasing glucose units until only isomaltose remains.
16. alpha dextrins are the pieces of polysaccharides that result from salivary alpha-amylase's endoglucosidase activity. limit dextrins are oligosaccharides that have been formed from the further breakdown of polysaccharides by pancreatic alpha-amylase.
17. made of two subunits: sucrose-maltose subunit cleaves alpha 1-4 bonds in sucrose, maltose. isomaltose-maltose unit cleaves alpha 1-6 bonds in isomaltose, and also breaks down maltose.
18. 80%
19. trehalose is a smaller dissaccharidase that only has one catalytic site with specificity for trehalose, which is a relatively rare source of carbohydrate found in some insects, algae, and mushrooms.
20. has two catalytic sites: glucosyl-ceramidase site, which cleaves beta bonds in glycolipids, and lactase site, which breaks beta 1-4 bonds between glucose and galactose in lactose.
21. duodenum
22. jejunum
23. jejunum
24. ileum
25. any undigested starches: starches high in amylose, poorly hydrated starches (like in dried beans), dietary fiber.
26. acetic acid, propionic acid, butyric acid. 2,3,4 carbon.
27. hydrogen gas, CO2, methane
28. low lactase levels or intestinal injury
29. 10% of the level of a child
30. lactose is undigested by the lactase in the small intestine and is therefore metabolized by the colonic bacteria, which produces lactic acid, methane, and H2. the increased lactic acid increases osmolarity of the intestinal lumen, causing more water to be dumped into the lumen, causing excess peristalsis, causing malabsorption of other nutrients.
31. how quickly blood glucose levels rise after consumption of a food.
32. glucose and maltose.
33. sodium dependent glucose transporters and facilitative glucose transporters
34. a Na+ / K+ ATPase pump pumps Na+ out of the intestinal epithelium cells so that there is a low Na+ concentration within. the Na+ dependent transporter channels then use the resulting Na+ concentration gradient to power movement of glucose within the cell.
35. these are glucose channels that exist on both the luminal and serosal side of the intestinal epithelium that allow glucose to move down its concentration gradient without expenditure of energy.
36. galactose passes through the intestinal membrane in a similar way to glucose- via both Na+ facilitated channels and facilitative glucose transporters. fructose passes through by facilitated diffusion only.
37. because the transport proteins have a high affinity for glucose (a low Km) or are present in high numbers.
38. the liver will only transport glucose into its cells (and therefore convert glucose to glycogen for storage) when the blood glucose level is high, such as right after a high carb meal.
39. binding of insulin recruits GLUT proteins from intracellular vescicles onto the membrane.
Showing posts with label nd1 fall finals. Show all posts
Showing posts with label nd1 fall finals. Show all posts
Tuesday, December 9, 2008
ms anatomy: embryology of limbs
this lecture covered some basic ideas about the formation of limbs in an embryo. it covered: the structural development of limbs from somites, the formation of bones, formation of blood vessels, and some structural abnormalities.
somites are described as "paraxial mesodermal segments" that ultimately differentiate into three parts: sclerotome, which forms the spine and ribs, dermatome, which forms the dermal layer of the skin, and myotome, which forms the muscles of the back and limbs. the limb "bud" starts growing off of the lateral plate mesoderm, with migrating somatic cells contributing to its development as well. it grows outward, developing along the proximal-distal axis via FGF, spearheaded by the apical ectodermal ridge. the "zone of polarization activation" is what develops patterns in the caudal-cranial axis (such as the different sizes and shapes of the 5 fingers) via Shh. these two mechanisms feed off of each other in a positive feedback loop, where Shh from the ZPA promotes the FGF in the AER and vice versa, through intermediates called formin, gremlin, and bone morphogenetic protein.
the process of endochondrial ossification is then described briefly: mesenchymal cells condense and form "pre-cartilaginous aggregates". cartilage producing cells (chondroblasts) secrete BMP to promote growth and Ihh to promote BMP, another positive feedback mechanism. chondroblasts then secrete hyaline cartilage, and become chondroblasts that reside in empty pools called lacunae. hydroxyapetite, an inorganic calcium phosphate crystal, is then secreted and eventually kills off the chondrocytes via apoptosis. osteoblasts then secrete bone matrix and bone is formed. bone remodeling occurs through the balance of osteoblast (bone forming cells, formed from mesenchymally derived osteoprogenitor cells) and osteoclast (bone destroying cells, derived from fused mononuclear hemopoetic progenitor cells) activity on opposite ends of a surface of bone.
some facts about blood vessel development: angioblasts form vascular plexuses which form the aorta and cardinal veins. central artery distributes blood to marginal sinus, which becomes the basilic and cephalic veins. central artery becomes brachial and interossei arteries.
finally, some abnormalities of limb development: amelia is absence of limbs. meromelia is absence of limb segments. phocomelia is absence of proximal limb segments but normal distal segments. polydactylyl is extra digits. syndactylyl is webbed digits.
questions
1. what are somites made from and what induces them?
2. somites divide into...
3. what does the sclerotome become?
4. what does the dermatome become?
5. what does the myotome become?
6. describe the production of cartilage producing cells.
7. what do Wnt genes do?
8. where do the limb buds originate?
9. limb develops from both...
10. what is skeletal muscle formed from?
11. what is dermis formed from?
12. what is the epidermis formed from?
13. what are sensory neurons formed from?
14. what is the AER and what does it do?
15. what is the ZPA and what does it do?
16. what does the myotome form in the limbs?
17. describe the interaction between the AER and ZPA.
18. what are the signaling factors between the AER and ZPA?
19. describe the process of endochondral ossification.
20. what do cartilaginous cells secrete?
21. what is mineralization triggered by?
22. what are osteoblasts derived from?
23. epiphyseal plates expand...
24. achondroplasia is...
25. bone remodeled by...
26. osteoblasts are derived from...
27. osteoclasts are derived from...
28. osteoclasts are activated by...
29. amelia...
30. meromelia...
31. phocomelia...
32. polydactyly...
33. syndactyly...
34. angioblasts form...
35. central artery distributes...
36. marginal sinus becomes...
37. central artery becomes...
answers
1. made from paraxial mesoderm segments, induced by hox genes.
2. sclerotome, dermatome, myotome.
3. vertebrae and ribs
4. dermis
5. muscles of back and limbs
6. Shh from notochord and neural tube induce Pax (1,9) genes, which converted somitic cells into chondroblasts.
7. influence the conversion of dorsal somitic cells into dermatome and myotome.
8. lateral plate mesoderm.
9. local limb bud tissue, as well as migrating tissue from somites.
10. migrating mesoderm cells from myotome differentiate into muscle (following tendons during migration)
11. dermatomal cells
12. ectoderm
13. neural crest cells.
14. apical ectodermal ridge, forms bones along the proximal-distal axis via FGF.
15. forms bones along the cranial-caudal axis via Shh.
16. dorsal-ventral compartment muscles via Wnt.
17. the two centers have a positive feedback system where FGF from the AER maintains Shh expression at the ZPA and Shh in turn activates FGF in AER.
18. formin, gremlin, bone morphogenetic protein (BMP)
19. mesenchymal cells in center of limb condense into "pre-cartilaginous aggregates". chondroblasts form hyaline cartilage matrix. chondroblasts enlarge and form lacunae. hydroxyapetite deposits on partitions between lacunae. cartilage cells die by apoptosis. capillaries vascularize calcified cartilage. osteoblasts deposit bone matrix which replaces cartilage.
20. BMP to promote growth and Ihh to promote production of BMP
21. local secretion of alkaline phosphatase.
22. mesenchymally derived osteoprogenitor cells.
23. with growth hormone
24. premature ossification of epiphyseal plates
25. selective deposition and resorption of bone from opposing surfaces, depending on relative activity of osteoblasts and osteoclasts.
26. osteoprogenitor cells
27. "fused mononuclear hemopoietic progenitor cells"
28. cytokine signaling.
29. absence of limbs
30. absence of limb segments
31. absence of proximal end of limb with normal distal end
32. extra digits
33. webbed digits
34. vascular plexus with aorta and cardinal veins
35. blood through capillaries into marginal sinus
36. cephalic and basilic veins
37. brachial and interosseus arteries
somites are described as "paraxial mesodermal segments" that ultimately differentiate into three parts: sclerotome, which forms the spine and ribs, dermatome, which forms the dermal layer of the skin, and myotome, which forms the muscles of the back and limbs. the limb "bud" starts growing off of the lateral plate mesoderm, with migrating somatic cells contributing to its development as well. it grows outward, developing along the proximal-distal axis via FGF, spearheaded by the apical ectodermal ridge. the "zone of polarization activation" is what develops patterns in the caudal-cranial axis (such as the different sizes and shapes of the 5 fingers) via Shh. these two mechanisms feed off of each other in a positive feedback loop, where Shh from the ZPA promotes the FGF in the AER and vice versa, through intermediates called formin, gremlin, and bone morphogenetic protein.
the process of endochondrial ossification is then described briefly: mesenchymal cells condense and form "pre-cartilaginous aggregates". cartilage producing cells (chondroblasts) secrete BMP to promote growth and Ihh to promote BMP, another positive feedback mechanism. chondroblasts then secrete hyaline cartilage, and become chondroblasts that reside in empty pools called lacunae. hydroxyapetite, an inorganic calcium phosphate crystal, is then secreted and eventually kills off the chondrocytes via apoptosis. osteoblasts then secrete bone matrix and bone is formed. bone remodeling occurs through the balance of osteoblast (bone forming cells, formed from mesenchymally derived osteoprogenitor cells) and osteoclast (bone destroying cells, derived from fused mononuclear hemopoetic progenitor cells) activity on opposite ends of a surface of bone.
some facts about blood vessel development: angioblasts form vascular plexuses which form the aorta and cardinal veins. central artery distributes blood to marginal sinus, which becomes the basilic and cephalic veins. central artery becomes brachial and interossei arteries.
finally, some abnormalities of limb development: amelia is absence of limbs. meromelia is absence of limb segments. phocomelia is absence of proximal limb segments but normal distal segments. polydactylyl is extra digits. syndactylyl is webbed digits.
questions
1. what are somites made from and what induces them?
2. somites divide into...
3. what does the sclerotome become?
4. what does the dermatome become?
5. what does the myotome become?
6. describe the production of cartilage producing cells.
7. what do Wnt genes do?
8. where do the limb buds originate?
9. limb develops from both...
10. what is skeletal muscle formed from?
11. what is dermis formed from?
12. what is the epidermis formed from?
13. what are sensory neurons formed from?
14. what is the AER and what does it do?
15. what is the ZPA and what does it do?
16. what does the myotome form in the limbs?
17. describe the interaction between the AER and ZPA.
18. what are the signaling factors between the AER and ZPA?
19. describe the process of endochondral ossification.
20. what do cartilaginous cells secrete?
21. what is mineralization triggered by?
22. what are osteoblasts derived from?
23. epiphyseal plates expand...
24. achondroplasia is...
25. bone remodeled by...
26. osteoblasts are derived from...
27. osteoclasts are derived from...
28. osteoclasts are activated by...
29. amelia...
30. meromelia...
31. phocomelia...
32. polydactyly...
33. syndactyly...
34. angioblasts form...
35. central artery distributes...
36. marginal sinus becomes...
37. central artery becomes...
answers
1. made from paraxial mesoderm segments, induced by hox genes.
2. sclerotome, dermatome, myotome.
3. vertebrae and ribs
4. dermis
5. muscles of back and limbs
6. Shh from notochord and neural tube induce Pax (1,9) genes, which converted somitic cells into chondroblasts.
7. influence the conversion of dorsal somitic cells into dermatome and myotome.
8. lateral plate mesoderm.
9. local limb bud tissue, as well as migrating tissue from somites.
10. migrating mesoderm cells from myotome differentiate into muscle (following tendons during migration)
11. dermatomal cells
12. ectoderm
13. neural crest cells.
14. apical ectodermal ridge, forms bones along the proximal-distal axis via FGF.
15. forms bones along the cranial-caudal axis via Shh.
16. dorsal-ventral compartment muscles via Wnt.
17. the two centers have a positive feedback system where FGF from the AER maintains Shh expression at the ZPA and Shh in turn activates FGF in AER.
18. formin, gremlin, bone morphogenetic protein (BMP)
19. mesenchymal cells in center of limb condense into "pre-cartilaginous aggregates". chondroblasts form hyaline cartilage matrix. chondroblasts enlarge and form lacunae. hydroxyapetite deposits on partitions between lacunae. cartilage cells die by apoptosis. capillaries vascularize calcified cartilage. osteoblasts deposit bone matrix which replaces cartilage.
20. BMP to promote growth and Ihh to promote production of BMP
21. local secretion of alkaline phosphatase.
22. mesenchymally derived osteoprogenitor cells.
23. with growth hormone
24. premature ossification of epiphyseal plates
25. selective deposition and resorption of bone from opposing surfaces, depending on relative activity of osteoblasts and osteoclasts.
26. osteoprogenitor cells
27. "fused mononuclear hemopoietic progenitor cells"
28. cytokine signaling.
29. absence of limbs
30. absence of limb segments
31. absence of proximal end of limb with normal distal end
32. extra digits
33. webbed digits
34. vascular plexus with aorta and cardinal veins
35. blood through capillaries into marginal sinus
36. cephalic and basilic veins
37. brachial and interosseus arteries
Sunday, December 7, 2008
biochem: mark's medical biochem chapter 29- fructose, galactose, pentose pathway
this chapter looked at the metabolic pathways for two other common dietary carbohydrates, fructose and galactose, as well as the pentose pathway, which produces NADPH and ribose 5-phosphate (used in nucleotide synthesis). fructose and galactose metabolism are similar in that they are basically phosphorylated and then converted into intermediates of the glycolytic pathway.
fructose metabolism:
1. fructose is phosphorylated to fructose 1-phosphate via fructokinase
2. fructose 1-phosphate is cleaved to DHAP and glyceraldehyde via aldolase B
3. glyceraldehyde phosphorylated to G3P via triose kinase
4. G3P and DHAP can be used in the glycolytic pathway
galactose metabolism:
1. galactose is phosphorylated to galactose 1-phosphate via galactokinase
2. galactose 1-phosphate plus UDP-glucose yields glucose 1-phosphate plus UDP-galactose
3. glucose 1-phosphate is converted to glucose 6-phosphate, which can be used in the glycolytic pathway.
production of fructose from glucose was also looked at in the "polyol" pathway:
1. glucose is reduced to sorbitol (polyol) via aldolase reductase, using NADPH as the reducing equivalents.
2. sorbitol is oxidized to fructose via sorbital dehydrogenase, producing NADH.
this conversion of glucose to fructose is used mainly in the seminiferous tubules, where spermatozoans use fructose instead of glucose in order to maintain the integrity of their plasma membrane (apparently glucose causes "acrosomal damage")
the pentose pathway is introduced as an alternate use of glucose 6-phosphate: instead of oxidizing for ATP, glucose 6-phosphate can taken through the pentose pathway to create NADPH (provides reducing equivalents, aids in catabolic reactions and helps protect against reactive oxygen species) and ribose 5-phosphate (used in nucleotide synthesis). the pentose pathway has two parts, an oxidative and non oxidative pathway. the oxidative pathway takes glucose 6-phosphate and creates 2 NADPH and ribulose 5-phosphate:
1. glucose 6-phosphate is oxidized to 6-phosphoglucanolactone via glucose 6 phosphate dehydrogenase, producing NADPH
2. 6-phosphoglucanolactone is hydrolyzed to 6-phosphoglucanolactate via glucanolactase
3. 6-phosphoglucanolactate undergoes oxidative decarboxylation to ribulose 5-phosphate, releasing CO2 and producing another NADPH
the non-oxidative portion of the pentose pathway takes three molecules of 5-ribulose phosphate, the product of the oxidative portion, and rearranges the molecules using transferases to eventually form 2 molecules of fructose 6-phosphate and 1 molecule of G3P. the reactions are as follows:
1. out of 3 molecules of 5-ribulose phosphate, 2 are converted to xylulose 5-phosphate via epimerases
2. the 3rd molecule of 5-ribulose phosphate is converted to ribose 5-phosphate (which can be used for nucleotide synthesis if necessary)
3. xylulose 5-P and ribose 5-P are rearranged to G3P and sedoheptulose 7-P via transketolase
4. sedoheptulose 7-P and G3P are rearranged to fructose 6-P and erythrose 4-P via transaldolase
5. erythrose 4-P and xylulose 5-P are rearranged to fructose 6-P and G3P
thus, 3 molecules of ribulose 5-phosphate are converted to 2 molecules of fructose 6-phosphate and one molecule of G3P.
we then look at how the pentose pathway can be used to accommodate and balance cellular needs for ATP, ribose 5-phosphate, and NADPH. several scenarios are considered-- when only NADPH is needed, only the oxidative portion of the pathway is activated, producing two molecules of NADPH per glucose molecule, and the nonoxidative pathway converts ribulose 5-phosphate to glucose 6-phosphate (presumably by isomerization of fructose 6-phosphate) which is then put back into the oxidative portion to create even more NADPH. when NADPH and ribose 5-phosphate are both needed, the oxidative pathway is activated to produce NADPH, and ribose 5-phosphate is produced from the non-oxidative pathway via isomerase. when only ribose 5-phosphate is needed, this implies that NADPH levels are relatively high-- which actually inhibits the first enzyme in the oxidative pathway. thus the oxidative pathway is inhibited, but the nonoxidative pathway produces ribose 5-phosphate from ribulose 5-phosphate. finally, in the case when NADPH and pyruvate are needed, both the oxidative and non oxidative portions are stimulated.
questions
1. describe the mechanism for the metabolism of fructose.
2. where does metabolism of fructose occur?
3. describe the mechanism for the polyol pathway.
4. where is the polyol pathway mainly used and why?
5. what is the galactose metabolism pathway?
6. what does the pentose pathway produce and why are the products useful?
7. why is NADP+ used instead of NAD+?
8. describe the mechanism for the oxidative branch of the pentose pathway.
9. describe the mechanism for the non-oxidative branch of the pentose pathway.
10. describe how the glycolytic intermediates can be used to produce ribose 5-phosphate for nucleotide synthesis.
11. what are some uses of NADPH in the body?
12. the entry of glucose 6-phosphate into the pentose phosphate pathway is regulated by...
describe how the pentose phosphate pathway is used to respond to cellular needs for:
13. NADPH
14. NADPH and ribose 5-phosphate
15. ribose 5-P only
16. NADPH and pyruvate
answers
1. fructose is phosphorylated by fructokinase to fructose 1-phosphate. fructose 1-phosphate is cleaved by aldosase B into DHAP and glyceraldehyde. glyceraldehyde is phosphorylated by triose kinase into G3P. G3P can then be converted to 1,3 bisphosphoglycerate in the glycolytic pathway or combined with DHAP to form fructose 1,6 bisphosphate in the gluconeogenic / glycolytic pathway.
2. mainly in the liver, but also in the mucosa of the small intestine.
3. glucose is reduced to sorbitol (polyol) by aldolase reductase, forming NADPH. sorbitol is oxidized to fructose via sorbitol dehydrogenase.
4. glucose conversion into fructose is mainly used in the seminal vescicles, which store the spermatozoans. spermatozoans use fructose rather than glucose to avoid plasma membrane damage while in the male reproductive system.
5. galactose is phosphorylate by galactokinase to galactose 1-phosphate. galactose 1-phosphate is converted to glucose 1-phosphate via galactose 1-phosphate uridylyltransferase. glucose 1-phosphate is then isomerized to glucose 6 phosphate for use in other metabolic pathways.
6. an alternative pathway to the first few steps of glycolysis that produces ribose 5-phosphate, which is used in nucleotide synthesis, and NADPH, which is used in reductive detoxification.
7. NADPH is used in reactions that have need for reducing equivalents because the ratio of NADPH to NADP+ is much higher than that of NADH to NAD (because NADH is immediately used in the electron transport chain)
8. glucose 6-phosphate is oxidized to 6-phosphogluconolactone via glucose 6-phosphate dehydrogenase (producing NADPH). 6-phosphogluconolactone is hydrolyzed to 6-phosphogluconolactate via gluconolactase. 6-phosphate gluconolactate undergoes oxidative decarboxylation to ribulose 5 phosphate, releasing CO2 and forming NADPH.
9. 3 molecules of ribulose 5-phosphate are converted via isomerases, epimerases, transketolases, and transaldolases into two molecules of fructose 6-phosphate and one molecule of G3P, which can be used in glycolysis.
10. ribose 5-phosphate can be synthesized using the non-oxidative portion of the pentose pathway because the reactions are reversible. 2 molecules of fructose 6-phosphate and 1 molecule of G3P can ultimately produce 3 molecules of ribose 5-phosphate.
11. NADPH is mainly produced from the oxidative portion of the pentose pathway and is used to provide reducing equivalents and is involved in protecting the body against reactive oxygen species. it is also involved in anabolic processes such as cholesterol synthesis, fatty acid synthesis and chain elongation.
12. the concentration of NADPH in the cell. high NADPH inhibits glucose 6-phosphate dehydrogenase.
13. the oxidative portion of the pentose phosphate pathway is utilized to produced 2 moles of NADPH per molecule of glucose. the non oxidative portion of the pentose pathway is used to convert ribulose 5-phosphate back to glucose 6-phosphate, where it can be used to generated more NADPH.
14. the oxidative portion creates NADPH and ribulose 5-phosphate. isomerases convert ribulose 5 phosphate into ribose 5-phosphate.
15. high levels of NADPH will inhibit the oxidative portion; just the non-oxidative portion will create ribose 5-phosphate from fructose 6-phosphate and G3P.
16. the oxidative portion will create NADPH and the nonoxidative will create fructose 6-phosphate and G3P, which can be used in glycolysis to produce pyruvate.
fructose metabolism:
1. fructose is phosphorylated to fructose 1-phosphate via fructokinase
2. fructose 1-phosphate is cleaved to DHAP and glyceraldehyde via aldolase B
3. glyceraldehyde phosphorylated to G3P via triose kinase
4. G3P and DHAP can be used in the glycolytic pathway
galactose metabolism:
1. galactose is phosphorylated to galactose 1-phosphate via galactokinase
2. galactose 1-phosphate plus UDP-glucose yields glucose 1-phosphate plus UDP-galactose
3. glucose 1-phosphate is converted to glucose 6-phosphate, which can be used in the glycolytic pathway.
production of fructose from glucose was also looked at in the "polyol" pathway:
1. glucose is reduced to sorbitol (polyol) via aldolase reductase, using NADPH as the reducing equivalents.
2. sorbitol is oxidized to fructose via sorbital dehydrogenase, producing NADH.
this conversion of glucose to fructose is used mainly in the seminiferous tubules, where spermatozoans use fructose instead of glucose in order to maintain the integrity of their plasma membrane (apparently glucose causes "acrosomal damage")
the pentose pathway is introduced as an alternate use of glucose 6-phosphate: instead of oxidizing for ATP, glucose 6-phosphate can taken through the pentose pathway to create NADPH (provides reducing equivalents, aids in catabolic reactions and helps protect against reactive oxygen species) and ribose 5-phosphate (used in nucleotide synthesis). the pentose pathway has two parts, an oxidative and non oxidative pathway. the oxidative pathway takes glucose 6-phosphate and creates 2 NADPH and ribulose 5-phosphate:
1. glucose 6-phosphate is oxidized to 6-phosphoglucanolactone via glucose 6 phosphate dehydrogenase, producing NADPH
2. 6-phosphoglucanolactone is hydrolyzed to 6-phosphoglucanolactate via glucanolactase
3. 6-phosphoglucanolactate undergoes oxidative decarboxylation to ribulose 5-phosphate, releasing CO2 and producing another NADPH
the non-oxidative portion of the pentose pathway takes three molecules of 5-ribulose phosphate, the product of the oxidative portion, and rearranges the molecules using transferases to eventually form 2 molecules of fructose 6-phosphate and 1 molecule of G3P. the reactions are as follows:
1. out of 3 molecules of 5-ribulose phosphate, 2 are converted to xylulose 5-phosphate via epimerases
2. the 3rd molecule of 5-ribulose phosphate is converted to ribose 5-phosphate (which can be used for nucleotide synthesis if necessary)
3. xylulose 5-P and ribose 5-P are rearranged to G3P and sedoheptulose 7-P via transketolase
4. sedoheptulose 7-P and G3P are rearranged to fructose 6-P and erythrose 4-P via transaldolase
5. erythrose 4-P and xylulose 5-P are rearranged to fructose 6-P and G3P
thus, 3 molecules of ribulose 5-phosphate are converted to 2 molecules of fructose 6-phosphate and one molecule of G3P.
we then look at how the pentose pathway can be used to accommodate and balance cellular needs for ATP, ribose 5-phosphate, and NADPH. several scenarios are considered-- when only NADPH is needed, only the oxidative portion of the pathway is activated, producing two molecules of NADPH per glucose molecule, and the nonoxidative pathway converts ribulose 5-phosphate to glucose 6-phosphate (presumably by isomerization of fructose 6-phosphate) which is then put back into the oxidative portion to create even more NADPH. when NADPH and ribose 5-phosphate are both needed, the oxidative pathway is activated to produce NADPH, and ribose 5-phosphate is produced from the non-oxidative pathway via isomerase. when only ribose 5-phosphate is needed, this implies that NADPH levels are relatively high-- which actually inhibits the first enzyme in the oxidative pathway. thus the oxidative pathway is inhibited, but the nonoxidative pathway produces ribose 5-phosphate from ribulose 5-phosphate. finally, in the case when NADPH and pyruvate are needed, both the oxidative and non oxidative portions are stimulated.
questions
1. describe the mechanism for the metabolism of fructose.
2. where does metabolism of fructose occur?
3. describe the mechanism for the polyol pathway.
4. where is the polyol pathway mainly used and why?
5. what is the galactose metabolism pathway?
6. what does the pentose pathway produce and why are the products useful?
7. why is NADP+ used instead of NAD+?
8. describe the mechanism for the oxidative branch of the pentose pathway.
9. describe the mechanism for the non-oxidative branch of the pentose pathway.
10. describe how the glycolytic intermediates can be used to produce ribose 5-phosphate for nucleotide synthesis.
11. what are some uses of NADPH in the body?
12. the entry of glucose 6-phosphate into the pentose phosphate pathway is regulated by...
describe how the pentose phosphate pathway is used to respond to cellular needs for:
13. NADPH
14. NADPH and ribose 5-phosphate
15. ribose 5-P only
16. NADPH and pyruvate
answers
1. fructose is phosphorylated by fructokinase to fructose 1-phosphate. fructose 1-phosphate is cleaved by aldosase B into DHAP and glyceraldehyde. glyceraldehyde is phosphorylated by triose kinase into G3P. G3P can then be converted to 1,3 bisphosphoglycerate in the glycolytic pathway or combined with DHAP to form fructose 1,6 bisphosphate in the gluconeogenic / glycolytic pathway.
2. mainly in the liver, but also in the mucosa of the small intestine.
3. glucose is reduced to sorbitol (polyol) by aldolase reductase, forming NADPH. sorbitol is oxidized to fructose via sorbitol dehydrogenase.
4. glucose conversion into fructose is mainly used in the seminal vescicles, which store the spermatozoans. spermatozoans use fructose rather than glucose to avoid plasma membrane damage while in the male reproductive system.
5. galactose is phosphorylate by galactokinase to galactose 1-phosphate. galactose 1-phosphate is converted to glucose 1-phosphate via galactose 1-phosphate uridylyltransferase. glucose 1-phosphate is then isomerized to glucose 6 phosphate for use in other metabolic pathways.
6. an alternative pathway to the first few steps of glycolysis that produces ribose 5-phosphate, which is used in nucleotide synthesis, and NADPH, which is used in reductive detoxification.
7. NADPH is used in reactions that have need for reducing equivalents because the ratio of NADPH to NADP+ is much higher than that of NADH to NAD (because NADH is immediately used in the electron transport chain)
8. glucose 6-phosphate is oxidized to 6-phosphogluconolactone via glucose 6-phosphate dehydrogenase (producing NADPH). 6-phosphogluconolactone is hydrolyzed to 6-phosphogluconolactate via gluconolactase. 6-phosphate gluconolactate undergoes oxidative decarboxylation to ribulose 5 phosphate, releasing CO2 and forming NADPH.
9. 3 molecules of ribulose 5-phosphate are converted via isomerases, epimerases, transketolases, and transaldolases into two molecules of fructose 6-phosphate and one molecule of G3P, which can be used in glycolysis.
10. ribose 5-phosphate can be synthesized using the non-oxidative portion of the pentose pathway because the reactions are reversible. 2 molecules of fructose 6-phosphate and 1 molecule of G3P can ultimately produce 3 molecules of ribose 5-phosphate.
11. NADPH is mainly produced from the oxidative portion of the pentose pathway and is used to provide reducing equivalents and is involved in protecting the body against reactive oxygen species. it is also involved in anabolic processes such as cholesterol synthesis, fatty acid synthesis and chain elongation.
12. the concentration of NADPH in the cell. high NADPH inhibits glucose 6-phosphate dehydrogenase.
13. the oxidative portion of the pentose phosphate pathway is utilized to produced 2 moles of NADPH per molecule of glucose. the non oxidative portion of the pentose pathway is used to convert ribulose 5-phosphate back to glucose 6-phosphate, where it can be used to generated more NADPH.
14. the oxidative portion creates NADPH and ribulose 5-phosphate. isomerases convert ribulose 5 phosphate into ribose 5-phosphate.
15. high levels of NADPH will inhibit the oxidative portion; just the non-oxidative portion will create ribose 5-phosphate from fructose 6-phosphate and G3P.
16. the oxidative portion will create NADPH and the nonoxidative will create fructose 6-phosphate and G3P, which can be used in glycolysis to produce pyruvate.
organ systems: control of respiration
this is the last unit in dr. kaminski's guest lecture on respiration and talks about the control and regulation of respiration. it focuses on the "respiratory group", which is an area in the upper medulla and contains four different groupings of neurons: the dorsal respiratory group, the ventral respiratory group, the pneumotaxic center, and the chemisensitive area. the dorsal group contains motor neurons which innervate the muscles involved in inspiration ("inspiratory neurons") as well as afferent sensory neurons. most of the impetus for inspiration comes from the dorsal respiratory group. during normal restful breathing, these neurons fire to stimulate the inspiratory muscles, and expiration occurs due to relaxation of the muscles and elastic recoil of the ribcage. in vigorous, more ribcage based breathing, the ventral respiratory center gets stimulated as well, which has inspiratory as well as expiratory neurons-- this causes both the inspiratory muscles to be activated during inspiration (external intercostals, SCM, scalenes, etc) as well as the expiratory muscles during expiration (rectus abdominis and internal intercostals).
we then look at the different factors that can affect this rhythm. the pneumotaxic center inhibits the neurons of the dorsal and ventral respiratory center, specifically causing the amplitude of the "inspiratory ramp signal" to decrease. this causes more shallow, rapid breathing. the central chemoreceptor (of the "chemosensitive area") detects levels of H+ in the cerebrospinal fluid-- H+ in the CSF is directly representative of CO2 levels because the only H+ that is beyond the blood brain barrier is that which is produced from the dissociation of carbonic acid, which is formed from CO2. if H+ levels rise, the chemosensitive area stimulates the dorsal inspiratory neurons to increase the ramp signal. peripheral chemoreceptors are a secondary chemical feedback system and are located near the aorta and carotid artery and measure O2 levels -- if PO2 falls below 100mmHg, they also activate the dorsal respiratory group.
a couple other ways in which ventilation can be regulated: via stretch receptors in the lungs, which inhibit the dorsal inspiratory neurons if the pressure from inspiration becomes too great-- this is called the hering breuer reflex. conscious control of breathing from higher brain centers can bypass the respiratory group completely and innervate the thoracic muscles directly.
questions
1. where is the "neurogenesis" of the respiratory drive?
2. what is the "respiratory control center" and where is it located?
3. what are the different neuronal groupings of the respiratory control center?
4. describe the dorsal respiratory group.
5. describe the ventral respiratory group.
6. describe the pneumotaxic center.
7. describe the chemosensitive area.
8. within the respiratory control center, where does the main respiratory drive come from?
9. describe how the inspiratory neurons control breathing.
10. describe the effect of the pneumotaxic center on the depth of breathing.
11. describe what happens in the respiratory center during vigorous breathing.
12. what are the three factors that can modify the ventilation cycle?
13. describe how the higher brain centers modify the ventilation cycle.
14. what is the hering breuer reflex?
15. where is the central chemoreceptor and what does it measure?
16. why does the central chemoreceptor measure H+ levels?
17. what does the central chemoreceptor stimulate?
18. describe the peripheral chemoreceptors.
answers
1. the medullary centers
2. a set of neuronal groupings that are found in the upper medulla and pons.
3. dorsal respiratory group, ventral respiratory group, pneumotaxic center, chemosensitive area.
4. contains inspiratory neurons and afferent sensory neurons.
5. contains both inspiratory and expiratory neurons.
6. inhibits the inspiratory neurons of the respiratory groups.
7. wired into the dorsal inspiratory neurons, has neurons that are sensitive to the chemistry of CSF.
8. inspiratory neurons of the dorsal respiratory group.
9. inspiratory neurons have a rhythm in the form of a "ramp signal" that signals the diaphragm. the faster the inspiratory neurons fire, the more the diaphragm is stimulated to contract via the phrenic nerve.
10. the pneumotaxic center inhibits inspiratory neurons and thus greater pneumotaxic activity facilitates shallow, rapid breathing.
11. during vigorous breathing, the ventral inspiratory and expiratory neurons get activated and both the inspiratory and expiratory muscles get activated.
12. voluntary override by higher centers of the brain, physical input from stretch receptors in the lung, evaluation of blood chemistry.
13. corticospinal and corticobulbar tracts connect directly to lower motor neurons of thoracic musculature, bypassing the respiratory control center.
14. when stretch receptors in the lung are activated by inspiration and inhibit the inspiratory neurons of the dorsal respiratory group.
15. in the "chemosensitive area" on the ventral surface of the medulla.
16. H+ is representative of CO2 levels since CO2 converts into carbonic acid, which dissociates into H+ and bicarbonate. furthermore, H+ does not cross the blood brain barrier, so it is directly representative of CO2.
17. the dorsal respiratory group.
18. the peripheral chemoreceptors are the aortic and carotid bodies, which sense O2 levels and begin firing if O2 levels fall below 100mmHg, stimulating the dorsal respiratory group.
we then look at the different factors that can affect this rhythm. the pneumotaxic center inhibits the neurons of the dorsal and ventral respiratory center, specifically causing the amplitude of the "inspiratory ramp signal" to decrease. this causes more shallow, rapid breathing. the central chemoreceptor (of the "chemosensitive area") detects levels of H+ in the cerebrospinal fluid-- H+ in the CSF is directly representative of CO2 levels because the only H+ that is beyond the blood brain barrier is that which is produced from the dissociation of carbonic acid, which is formed from CO2. if H+ levels rise, the chemosensitive area stimulates the dorsal inspiratory neurons to increase the ramp signal. peripheral chemoreceptors are a secondary chemical feedback system and are located near the aorta and carotid artery and measure O2 levels -- if PO2 falls below 100mmHg, they also activate the dorsal respiratory group.
a couple other ways in which ventilation can be regulated: via stretch receptors in the lungs, which inhibit the dorsal inspiratory neurons if the pressure from inspiration becomes too great-- this is called the hering breuer reflex. conscious control of breathing from higher brain centers can bypass the respiratory group completely and innervate the thoracic muscles directly.
questions
1. where is the "neurogenesis" of the respiratory drive?
2. what is the "respiratory control center" and where is it located?
3. what are the different neuronal groupings of the respiratory control center?
4. describe the dorsal respiratory group.
5. describe the ventral respiratory group.
6. describe the pneumotaxic center.
7. describe the chemosensitive area.
8. within the respiratory control center, where does the main respiratory drive come from?
9. describe how the inspiratory neurons control breathing.
10. describe the effect of the pneumotaxic center on the depth of breathing.
11. describe what happens in the respiratory center during vigorous breathing.
12. what are the three factors that can modify the ventilation cycle?
13. describe how the higher brain centers modify the ventilation cycle.
14. what is the hering breuer reflex?
15. where is the central chemoreceptor and what does it measure?
16. why does the central chemoreceptor measure H+ levels?
17. what does the central chemoreceptor stimulate?
18. describe the peripheral chemoreceptors.
answers
1. the medullary centers
2. a set of neuronal groupings that are found in the upper medulla and pons.
3. dorsal respiratory group, ventral respiratory group, pneumotaxic center, chemosensitive area.
4. contains inspiratory neurons and afferent sensory neurons.
5. contains both inspiratory and expiratory neurons.
6. inhibits the inspiratory neurons of the respiratory groups.
7. wired into the dorsal inspiratory neurons, has neurons that are sensitive to the chemistry of CSF.
8. inspiratory neurons of the dorsal respiratory group.
9. inspiratory neurons have a rhythm in the form of a "ramp signal" that signals the diaphragm. the faster the inspiratory neurons fire, the more the diaphragm is stimulated to contract via the phrenic nerve.
10. the pneumotaxic center inhibits inspiratory neurons and thus greater pneumotaxic activity facilitates shallow, rapid breathing.
11. during vigorous breathing, the ventral inspiratory and expiratory neurons get activated and both the inspiratory and expiratory muscles get activated.
12. voluntary override by higher centers of the brain, physical input from stretch receptors in the lung, evaluation of blood chemistry.
13. corticospinal and corticobulbar tracts connect directly to lower motor neurons of thoracic musculature, bypassing the respiratory control center.
14. when stretch receptors in the lung are activated by inspiration and inhibit the inspiratory neurons of the dorsal respiratory group.
15. in the "chemosensitive area" on the ventral surface of the medulla.
16. H+ is representative of CO2 levels since CO2 converts into carbonic acid, which dissociates into H+ and bicarbonate. furthermore, H+ does not cross the blood brain barrier, so it is directly representative of CO2.
17. the dorsal respiratory group.
18. the peripheral chemoreceptors are the aortic and carotid bodies, which sense O2 levels and begin firing if O2 levels fall below 100mmHg, stimulating the dorsal respiratory group.
biochem: mark's medical biochem chapter 28- glycogen
this chapter is about the synthesis and breakdown of glycogen in the liver and skeletal muscles. glycogen is a huge branched molecule which serves as a storage form for glucose. its role in the liver is to aid in regulating blood sugar levels by degradation of glycogen into free glucose, which can be used to replenish flagging blood glucose levels. in skeletal muscle, glycogen is broken down expressly for the purpose of supplying glucose 6-phosphate for anaerobic glycolysis when ATP demand is high.
glycogen itself is a large, highly branched polysaccharide made of repeating glucosyl units with alpha 1-4 bonds (elongating a given branch) and alpha 1-6 bonds (creating a new branch point). glycogen's synthesis mechanism is as follows:
1. glucose is phosphorylated to glucose 6-phosphate via glucokinase.
2. glucose 6-phosphate is isomerized to glucose 1-phosphate via phosphoglucomutase.
3. glucose 1-phosphate is activated by UTP into UDP glucose.
4. UDP glucose units are repeatedly added to a glycogen primer via glycogen synthase.
5. when a given branch is ~11 units (or "residues") long, a 6-8 residue piece is transferred via a transferase to another glucosyl unit with a alpha 1-6 bond, creating new branches.
glycogen breakdown is not the reverse of the synthesis pathway:
1. glycogen residues are phosphorylated by glycogen phosphorylase, forming molecules of glucose 1-phosphate (which can be isomerized to glucose 6-phosphate for use in glycolysis, etc)
2. when any given branch is shortened to 4 residues long, the glycogen phosphorylase can not remove any more due to steric hindrance.
3. the "debrancher" enzyme then transfers the last 3 residues to another branch, where they can be acted on by glycogen phosphorylase.
4. the last residue is hydrolyzed by alpha 1,6 glucosidase into a glucose molecule.
the regulation of glycogen synthesis and degradation is somewhat involved and is different in the liver and muscle due to the different uses of glycogen as mentioned above. in the liver, the primary factor that regulates glycogen synthesis/breakdown activity is the glucagon/insulin ratio in the blood, which reflects the liver's need to maintain blood sugar levels. in skeletal muscle the primary factor that regulates glycogen synthesis/degradation is AMP levels, which indicate relative ATP usage -- reflecting skeletal muscle's use of glycogen as a direct backup energy source for contraction. during times of stress, epinephrine is released and stimulates glycogen degradation in both liver and skeletal muscle.
the stimulation of glycogen synthesis by rising glucagon, AMP levels, or epinephrine levels occurs via an enzymatic cascade which begins with the synthesis of cAMP via adenylate cyclate. cAMP then activates protein kinase A, which phosphorylates two enzymes, glycogen synthase and phosphorylase kinase. glycogen synthase, which (as described above) synthesizes glycogen from glucose 6-phosphate, is inactivated by this phosphorylation whereas phosphorylase kinase, which begins the degradation pathway, is activated by the phosphorylation. thus, activated protein kinase A's net effect is to simultaneously shut down the synthesis of new glycogen as well as initiate glycogen breakdown. in the breakdown pathway: phosphorylase kinase activates glycogen phosphorylase, which then removes glycosyl residues from glycogen as described above.
protein kinase A's counterparts are the "protein phosphorylases" that removes the phosphates from glycogen synthase (thereby activating synthesis) and phosphorylase kinase (thereby deactivating breakdown). this stimulation of synthesis of glycogen can happen after a high carbohydrate meal, when glucose levels are high and need to be converted into glycogen for storage and lowering blood glucose levels. during a high carb meal, glucagon levels fall, and insulin levels rise -- it is thought that compared to glucagon, the level of insulin is more actively involved in the regulation of glycogen synthesis and breakdown although the exact mechanisms are not well understood. however, higher insulin levels are known to activate these protein phosphorylases, which inhibit the breakdown pathway and stimulate the synthesis pathway.
questions
1. what is the structure of glycogen?
2. describe the usage of glycogen in skeletal muscle vs. in the liver.
3. describe the synthesis pathway of glycogen.
4. what are the two enzymes involved in the breakdown of glycogen?
5. what are the two functions of the "debrancher" enzyme?
6. describe the mechanism for the breakdown of glycogen.
7. describe the three factors that regulate glycogen synthesis and breakdown in the liver.
8. describe the three factors that regulate glycogen synthesis and breakdown in skeletal muscle.
9. compare glycogenolysis and gluconeogenesis as means of replenishing blood glucose levels.
10. describe the role of phosphorylation states in the regulation of glycogen synthesis / regulation in the liver.
11. what is synergistic phosphorylation and how does it relate to glycogen degradation?
12. what is hepatic PP-1 and what does it do?
13. why is insulin considered the primary hormone that regulates glycogen synthesis / breakdown?
14. describe how glucose levels affect glycogen synthesis / breakdown.
15. describe epinephrine's actions on beta-receptors in the liver.
16. describe epinephrine's actions on alpha-receptors in the liver.
17. why is glucose 6-phosphate produced from glycogenolysis in skeletal muscle "committed" to the glycolytic pathway?
18. how does glucagon affect the regulation of skeletal muscle glycogen synthesis/degradation?
19. how does AMP affect the regulation of skeletal muscle glycogen synthesis/degradation?
20. contrast the intracellular Ca2+ production in the liver and skeletal muscle.
answers
1. glucosyl units linked by alpha 1-4 glycosidic bonds with alpha 1,6 branches every 8-10 residues.
2. in skeletal muscle, when ATP demands are high or when glucose 6-phosphate is used up by anaerobic glycolysis, glucose 6-phosphate can be replenished via glycogen breakdown in order to ultimately enter the glycolytic pathway. in the liver, glycogen breakdown produces glucose 6-phosphate, which is then converted to via glucose 6-phosphatase to glucose, which is then released into the blood.
3. glucose is converted to glucose 6-phosphate by hexokinases (or glucokinases in the liver). glucose 6-phosphate is converted to glucose 1-phosphate by phosphoglucomutase. glucose 1-phosphate is activated by UTP and converted to UDP-glucose, which can then be attached via glycogen synthase to a glycogen primer. when the chain of glycosyl is 11 residues long, amylotransferase transfers the chain back onto another glycogen branch in an alpha 1-4 bond-- this process happens repeatedly and creates a highly branched structure.
4. glycogen phosphorylase and the "debrancher enzyme"
5. it acts as a transferase and an alpha 1-6 glucosidase.
6. glycogen phosphorylase continually removes glucosyl residues by phosphorylating the terminal glycosidic bond, creating glucose 1-phosphate. however, due to steric hindrance, it can not free glucosyl residues that are closer than 4 units away from a branch point. the transferase portion of the debrancher enzyme transfers the end three residues onto another chain, where it can be acted on by the glycogen phosphorylase enzyme. the alpha-1,6 glucosidase portion of the debrancher enzyme then hydrolyzes the final glucosyl residue on the branch to glucose.
7. the liver's glycogenolytic activity is regulated by glucagon, insulin, and epinephrine levels: when fasting, glucagon is high and insulin is low, which stimulates glycogenolysis and inhibits glycogen synthesis. during a high carbohydrate meal, insulin levels are high and glucagon levels are low -- stimulating glycogen synthesis and inhibiting glycogen breakdown. during exercise, epinephrine stimulates glycogen breakdown and inhibits glycogen synthesis as well.
8. epinephrine, AMP, and Ca2+. higher levels of all three molecules signal the need for greater energy production, which stimulates glycogen degradation and inhibits glycogen synthesis.
9. while both are employed by the liver to replenish blood glucose levels, glycogenolysis is both faster and supplies more glucose.
10. glucagon and insulin regulate glycogen synthesis / breakdown via a mechanism involving phosphorylating the glycogen synthase and glycogen phosphorylase enzymes between inactive and active states. for example, during fasting, high glucagon stimulates phosphorylation of glycogen phosphorylase to the active form, beginning glycogen degradation, while also phosphorylating glycogen synthase to an inactive form, inhibiting glycogen synthesis.
11. the phosphorylation of glycogen synthase into the inactive form is much more complex than that of glycogen phosphorylase into the active form, in that it has up to 10 different phosphorylation sites. "synergistic phosphorylation" is the process by which glycogen synthase is inactivated, where phosphorylation of one site (by protein kinase A) changes the conformation of the enzyme and facilitates phosphorylation at the remaining sites. (analogous to oxygen binding to hemoglobin)
12. hepatic PP-1 is a protein phosphatase that works in opposition to the protein kinase A in that it removes the phosphates from phosphorylase kinase and glycogen phosphorylase (thereby inhibiting glycogen breakdown), and glycogen synthase (thereby stimulates glycogen synthesis).
13. because its levels change to a greater degree in response to changing blood sugar levels than glucagon.
14. high glucose levels inhibit glycogen breakdown almost immediately (faster than the effect of glucagon's cAMP and protein kinase A pathway, which takes 10-15 minutes). glucose stimulates protein phosphatases to remove the phosphates from glycogen synthase b and phosphorylase a, the net effect being inhibition of glycogen degradation.
15. when epinephrine binds to beta receptors in the liver, it stimulates adenylate cyclase to produce cAMP and activate protein kinase A in a similar fashion as glucagon.
16. when epinephrine binds to alpha receptors, it activates the PIP-Ca2+ signal transduction system which increases intracellular levels of Ca2+.
17. because skeletal muscle has no glucose 6-phosphatase to facilitate the conversion to glucose.
18. glucagon has no effect on skeletal muscle regulation of glycogen synthesis/degradation and therefore glycogen levels in skeletal muscle do not vary much depending on food intake.
19. AMP represents the usage of ATP and activates the muscle isozyme of glycogen phosphorylase.
glycogen itself is a large, highly branched polysaccharide made of repeating glucosyl units with alpha 1-4 bonds (elongating a given branch) and alpha 1-6 bonds (creating a new branch point). glycogen's synthesis mechanism is as follows:
1. glucose is phosphorylated to glucose 6-phosphate via glucokinase.
2. glucose 6-phosphate is isomerized to glucose 1-phosphate via phosphoglucomutase.
3. glucose 1-phosphate is activated by UTP into UDP glucose.
4. UDP glucose units are repeatedly added to a glycogen primer via glycogen synthase.
5. when a given branch is ~11 units (or "residues") long, a 6-8 residue piece is transferred via a transferase to another glucosyl unit with a alpha 1-6 bond, creating new branches.
glycogen breakdown is not the reverse of the synthesis pathway:
1. glycogen residues are phosphorylated by glycogen phosphorylase, forming molecules of glucose 1-phosphate (which can be isomerized to glucose 6-phosphate for use in glycolysis, etc)
2. when any given branch is shortened to 4 residues long, the glycogen phosphorylase can not remove any more due to steric hindrance.
3. the "debrancher" enzyme then transfers the last 3 residues to another branch, where they can be acted on by glycogen phosphorylase.
4. the last residue is hydrolyzed by alpha 1,6 glucosidase into a glucose molecule.
the regulation of glycogen synthesis and degradation is somewhat involved and is different in the liver and muscle due to the different uses of glycogen as mentioned above. in the liver, the primary factor that regulates glycogen synthesis/breakdown activity is the glucagon/insulin ratio in the blood, which reflects the liver's need to maintain blood sugar levels. in skeletal muscle the primary factor that regulates glycogen synthesis/degradation is AMP levels, which indicate relative ATP usage -- reflecting skeletal muscle's use of glycogen as a direct backup energy source for contraction. during times of stress, epinephrine is released and stimulates glycogen degradation in both liver and skeletal muscle.
the stimulation of glycogen synthesis by rising glucagon, AMP levels, or epinephrine levels occurs via an enzymatic cascade which begins with the synthesis of cAMP via adenylate cyclate. cAMP then activates protein kinase A, which phosphorylates two enzymes, glycogen synthase and phosphorylase kinase. glycogen synthase, which (as described above) synthesizes glycogen from glucose 6-phosphate, is inactivated by this phosphorylation whereas phosphorylase kinase, which begins the degradation pathway, is activated by the phosphorylation. thus, activated protein kinase A's net effect is to simultaneously shut down the synthesis of new glycogen as well as initiate glycogen breakdown. in the breakdown pathway: phosphorylase kinase activates glycogen phosphorylase, which then removes glycosyl residues from glycogen as described above.
protein kinase A's counterparts are the "protein phosphorylases" that removes the phosphates from glycogen synthase (thereby activating synthesis) and phosphorylase kinase (thereby deactivating breakdown). this stimulation of synthesis of glycogen can happen after a high carbohydrate meal, when glucose levels are high and need to be converted into glycogen for storage and lowering blood glucose levels. during a high carb meal, glucagon levels fall, and insulin levels rise -- it is thought that compared to glucagon, the level of insulin is more actively involved in the regulation of glycogen synthesis and breakdown although the exact mechanisms are not well understood. however, higher insulin levels are known to activate these protein phosphorylases, which inhibit the breakdown pathway and stimulate the synthesis pathway.
questions
1. what is the structure of glycogen?
2. describe the usage of glycogen in skeletal muscle vs. in the liver.
3. describe the synthesis pathway of glycogen.
4. what are the two enzymes involved in the breakdown of glycogen?
5. what are the two functions of the "debrancher" enzyme?
6. describe the mechanism for the breakdown of glycogen.
7. describe the three factors that regulate glycogen synthesis and breakdown in the liver.
8. describe the three factors that regulate glycogen synthesis and breakdown in skeletal muscle.
9. compare glycogenolysis and gluconeogenesis as means of replenishing blood glucose levels.
10. describe the role of phosphorylation states in the regulation of glycogen synthesis / regulation in the liver.
11. what is synergistic phosphorylation and how does it relate to glycogen degradation?
12. what is hepatic PP-1 and what does it do?
13. why is insulin considered the primary hormone that regulates glycogen synthesis / breakdown?
14. describe how glucose levels affect glycogen synthesis / breakdown.
15. describe epinephrine's actions on beta-receptors in the liver.
16. describe epinephrine's actions on alpha-receptors in the liver.
17. why is glucose 6-phosphate produced from glycogenolysis in skeletal muscle "committed" to the glycolytic pathway?
18. how does glucagon affect the regulation of skeletal muscle glycogen synthesis/degradation?
19. how does AMP affect the regulation of skeletal muscle glycogen synthesis/degradation?
20. contrast the intracellular Ca2+ production in the liver and skeletal muscle.
answers
1. glucosyl units linked by alpha 1-4 glycosidic bonds with alpha 1,6 branches every 8-10 residues.
2. in skeletal muscle, when ATP demands are high or when glucose 6-phosphate is used up by anaerobic glycolysis, glucose 6-phosphate can be replenished via glycogen breakdown in order to ultimately enter the glycolytic pathway. in the liver, glycogen breakdown produces glucose 6-phosphate, which is then converted to via glucose 6-phosphatase to glucose, which is then released into the blood.
3. glucose is converted to glucose 6-phosphate by hexokinases (or glucokinases in the liver). glucose 6-phosphate is converted to glucose 1-phosphate by phosphoglucomutase. glucose 1-phosphate is activated by UTP and converted to UDP-glucose, which can then be attached via glycogen synthase to a glycogen primer. when the chain of glycosyl is 11 residues long, amylotransferase transfers the chain back onto another glycogen branch in an alpha 1-4 bond-- this process happens repeatedly and creates a highly branched structure.
4. glycogen phosphorylase and the "debrancher enzyme"
5. it acts as a transferase and an alpha 1-6 glucosidase.
6. glycogen phosphorylase continually removes glucosyl residues by phosphorylating the terminal glycosidic bond, creating glucose 1-phosphate. however, due to steric hindrance, it can not free glucosyl residues that are closer than 4 units away from a branch point. the transferase portion of the debrancher enzyme transfers the end three residues onto another chain, where it can be acted on by the glycogen phosphorylase enzyme. the alpha-1,6 glucosidase portion of the debrancher enzyme then hydrolyzes the final glucosyl residue on the branch to glucose.
7. the liver's glycogenolytic activity is regulated by glucagon, insulin, and epinephrine levels: when fasting, glucagon is high and insulin is low, which stimulates glycogenolysis and inhibits glycogen synthesis. during a high carbohydrate meal, insulin levels are high and glucagon levels are low -- stimulating glycogen synthesis and inhibiting glycogen breakdown. during exercise, epinephrine stimulates glycogen breakdown and inhibits glycogen synthesis as well.
8. epinephrine, AMP, and Ca2+. higher levels of all three molecules signal the need for greater energy production, which stimulates glycogen degradation and inhibits glycogen synthesis.
9. while both are employed by the liver to replenish blood glucose levels, glycogenolysis is both faster and supplies more glucose.
10. glucagon and insulin regulate glycogen synthesis / breakdown via a mechanism involving phosphorylating the glycogen synthase and glycogen phosphorylase enzymes between inactive and active states. for example, during fasting, high glucagon stimulates phosphorylation of glycogen phosphorylase to the active form, beginning glycogen degradation, while also phosphorylating glycogen synthase to an inactive form, inhibiting glycogen synthesis.
11. the phosphorylation of glycogen synthase into the inactive form is much more complex than that of glycogen phosphorylase into the active form, in that it has up to 10 different phosphorylation sites. "synergistic phosphorylation" is the process by which glycogen synthase is inactivated, where phosphorylation of one site (by protein kinase A) changes the conformation of the enzyme and facilitates phosphorylation at the remaining sites. (analogous to oxygen binding to hemoglobin)
12. hepatic PP-1 is a protein phosphatase that works in opposition to the protein kinase A in that it removes the phosphates from phosphorylase kinase and glycogen phosphorylase (thereby inhibiting glycogen breakdown), and glycogen synthase (thereby stimulates glycogen synthesis).
13. because its levels change to a greater degree in response to changing blood sugar levels than glucagon.
14. high glucose levels inhibit glycogen breakdown almost immediately (faster than the effect of glucagon's cAMP and protein kinase A pathway, which takes 10-15 minutes). glucose stimulates protein phosphatases to remove the phosphates from glycogen synthase b and phosphorylase a, the net effect being inhibition of glycogen degradation.
15. when epinephrine binds to beta receptors in the liver, it stimulates adenylate cyclase to produce cAMP and activate protein kinase A in a similar fashion as glucagon.
16. when epinephrine binds to alpha receptors, it activates the PIP-Ca2+ signal transduction system which increases intracellular levels of Ca2+.
17. because skeletal muscle has no glucose 6-phosphatase to facilitate the conversion to glucose.
18. glucagon has no effect on skeletal muscle regulation of glycogen synthesis/degradation and therefore glycogen levels in skeletal muscle do not vary much depending on food intake.
19. AMP represents the usage of ATP and activates the muscle isozyme of glycogen phosphorylase.
Saturday, December 6, 2008
organ systems: gas transport
this unit covered a few basic biochemical ideas about the way that oxygen and carbon dioxide are transported by the blood. oxygen is mainly transported in the bound form to hemoglobin, oxyhemoglobin, and thus the uptake and release of oxygen to and from the blood is governed by the oxyhemoglobin saturation curve, a sigmoidal shaped curve which describes the relative saturation of oxygen for a given PO2. this graph ties in with the previous lecture on gas exchange, in which we covered all the PO2 and PCO2s for the atmosphere, arteries, body tissues, and veins. looking at these numbers using the dissociation curve, we find that at the arterial PO2 of 95 mmHg, hemoglobin is ~97% saturated and at the venous PO2 of 40 mmHg, hemoglobin is ~70% saturated -- this difference in saturation represents oxygen's unloading from the blood. we then look at factors that can shift the dissociation curve to the right (essentially saying that for a given partial pressure, hemoglobin affinity for oxygen has decreased). these factors are: increased H+ production, which causes conformational changes in hemoglobin that reduces its affinity to oxygen, increased temperature, and increased 2,3-DPG, which competes for O2 binding sites on Hb.
carbon dioxide is transported as a dissolved gas (7%), bound to hemoglobin (23%), but mainly in the form of bicarbonate ion (70%). this conversion to bicarbonate is facilitated by carbonic anhydrase, which converts dissolved CO2 into carbonic acid, H2CO3, which then dissociates into H+ and bicarbonate ion, HCO3-. this reaction is important because it also is the common pathway which describes the mechanism for both the bohr and the haldane effect. the bohr effect can be summed up as: increased CO2 production in body tissues and uptake into the blood facilitates O2 release into tissues. this occurs when CO2 is converted to carbonic acid, and thus H+ and bicarbonate-- the H+ binds to hemoglobin and as described above decreases its affinity for O2, allowing it to be released into the tissues. the haldane effect is the opposite: increased O2 uptake in the lungs facilitates CO2 release. this happens because O2 binds to hemoglobin and causes the release of H+ protons, which then combine with bicarbonate and form carbonic acid, which is converted back into CO2 via carbonic anhydrase, which is then released into the air.
questions
1. what are the ways in which O2 is transported in the blood and the relative percentage of each?
2. what is the saturation level of hemoglobin in arterial blood?
3. what is the saturation level of hemoglobin in venous blood?
4. what would the saturation level of hemoglobin be if PO2 was at 160mmHg, the atmospheric PO2?
5. what are three factors that can shift the hemoglobin saturation curve to the right?
6. what are the ways in which CO2 is transported in the blood and the relative percentage of each?
7. describe the formation of bicarbonate ion from dissolved CO2.
8. what is the enzyme that catalyzes the formation of carbonic acid?
9. what is the "chloride shift"?
10. describe the bohr effect.
11. describe the haldane effect.
answers
1. 3% as a dissolved gas, 97% bound to hemoglobin.
2. ~97%
3. 70%
4. >99%
5. decreased pH, increased temperature, increased concentration of 2,3-DPG
6. 7% as a dissolved CO2 gas, 23% bound to hemoglobin, 70% as bicarbonate ion.
7. dissolved CO2 + H2O -> H2CO3 (carbonic acid) -> H+ and bicarbonate ion.
8. carbonic anhydrase.
9. Cl- moving into cells to balance the H+ that is being dissociated from carbonic acid.
10. the bohr effect refers to hemoglobin's decreased affinity for O2 in the tissues which is caused by the increase in H+ concentration which binds to hemoglobin and changes its conformation. the increased H+ concentration in the tissues is due to higher CO2 levels from metabolism, which is converted into carbonic acid, which dissociates into H+ and bicarbonate. in short: increased CO2 in the tissues causes decreased hemoglobin affinity for O2.
11. the haldane effect is analogous to the bohr effect except in the reverse order; increased O2 in the lungs causes CO2 to be released from the blood.
carbon dioxide is transported as a dissolved gas (7%), bound to hemoglobin (23%), but mainly in the form of bicarbonate ion (70%). this conversion to bicarbonate is facilitated by carbonic anhydrase, which converts dissolved CO2 into carbonic acid, H2CO3, which then dissociates into H+ and bicarbonate ion, HCO3-. this reaction is important because it also is the common pathway which describes the mechanism for both the bohr and the haldane effect. the bohr effect can be summed up as: increased CO2 production in body tissues and uptake into the blood facilitates O2 release into tissues. this occurs when CO2 is converted to carbonic acid, and thus H+ and bicarbonate-- the H+ binds to hemoglobin and as described above decreases its affinity for O2, allowing it to be released into the tissues. the haldane effect is the opposite: increased O2 uptake in the lungs facilitates CO2 release. this happens because O2 binds to hemoglobin and causes the release of H+ protons, which then combine with bicarbonate and form carbonic acid, which is converted back into CO2 via carbonic anhydrase, which is then released into the air.
questions
1. what are the ways in which O2 is transported in the blood and the relative percentage of each?
2. what is the saturation level of hemoglobin in arterial blood?
3. what is the saturation level of hemoglobin in venous blood?
4. what would the saturation level of hemoglobin be if PO2 was at 160mmHg, the atmospheric PO2?
5. what are three factors that can shift the hemoglobin saturation curve to the right?
6. what are the ways in which CO2 is transported in the blood and the relative percentage of each?
7. describe the formation of bicarbonate ion from dissolved CO2.
8. what is the enzyme that catalyzes the formation of carbonic acid?
9. what is the "chloride shift"?
10. describe the bohr effect.
11. describe the haldane effect.
answers
1. 3% as a dissolved gas, 97% bound to hemoglobin.
2. ~97%
3. 70%
4. >99%
5. decreased pH, increased temperature, increased concentration of 2,3-DPG
6. 7% as a dissolved CO2 gas, 23% bound to hemoglobin, 70% as bicarbonate ion.
7. dissolved CO2 + H2O -> H2CO3 (carbonic acid) -> H+ and bicarbonate ion.
8. carbonic anhydrase.
9. Cl- moving into cells to balance the H+ that is being dissociated from carbonic acid.
10. the bohr effect refers to hemoglobin's decreased affinity for O2 in the tissues which is caused by the increase in H+ concentration which binds to hemoglobin and changes its conformation. the increased H+ concentration in the tissues is due to higher CO2 levels from metabolism, which is converted into carbonic acid, which dissociates into H+ and bicarbonate. in short: increased CO2 in the tissues causes decreased hemoglobin affinity for O2.
11. the haldane effect is analogous to the bohr effect except in the reverse order; increased O2 in the lungs causes CO2 to be released from the blood.
Thursday, December 4, 2008
histology: the respiratory system
this section traces the passage of air from the trachea to the capillaries in the alveolus. the trachea is the largest tube in the respiratory system which is bolstered by 20 or so cartilage rings and smooth muscle. it has a PSCC epithelium with goblet cells and tracheal glands in the submucosa. the trachea then branches into the brochi, which have smatterings of cartilage and are like smaller versions of the trachea. bronchioles (from organ systems: primary for each lung, secondary for each lobe, tertiary for each bronchopulmonary segment) have no cartilage, and epithelium which begins to transition from PSC to simple columnar. terminal bronchioles are the last section of the airway that does not take place in gas exchange, and they have simple columnar epithelium with no goblet cells. next comes the respiratory bronchioles, where gas exchange begins to take place, which have simple cuboidal epithelium and the beginnings of alveoli protruding out from the walls. these transition into alveolar ducts, which are basically smaller respiratory bronchioles with simple squamous epithelium and many alveolar sacs. finally, the air reaches the alveolar sac, which is the end of the passageway.
between the alveolar sacs is the interalveolar septum, where gas exchange with blood actually takes place. this border is lined with type 1 and 2 pneumocytes, involved in gas exchange and surfactant secretion, respectively. thus, in order to reach the blood, gas has to diffuse through: type 1 pneumocyte cell, type 1 pneumocyte basement membrane, endothelial basement membrane, endothelial cell. also between the interalveolar septum are some fibroblasts, alveolar phagocytes, and a scant CT matrix called the zona diffusa.
questions
1. describe the passage of air from the trachea to the alveoli.
2. describe the physical support of the trachea
3. describe the layers of the trachea.
distinguishing characteristics of:
4. bronchi...
5. bronchiole...
6. terminal bronchiole...
7. respiratory bronchiole...
8. alveolar duct...
9. alveolar sac...
10. what are the two alveolar surfaces formed by epithelia?
11. what is inside the interalveolar septa?
12. describe the barrier between blood and air in the alveoli.
answers
1. trachea, bronchi, bronchioles, terminal bronchioles, respiratory bronchioles, alveolar ducts, alveolar sacs, alveoli.
2. ~20 cartilage rings with smooth muscle (trachealis) spanning the posterior openings.
3. PSCC in mucosa with goblet cells, sometimes diffuse lymphatic tissue. submucosa of CT and tracheal glands. hyaline cartilage layer, then adventitia.
4. fragmented hyaline cartilage, PSCC with goblet cells.
5. smooth muscle but no cartilage, PSCC to simple columnar epithelium with goblet cells.
6. simple columnar, cilia but no goblet cells. clara cells secrete lipoprotein surfactant.
7. beginning of gas exchange; alveoli begin to protrude through walls. simple cuboidal epithelium with no cilia.
8. like a smaller respiratory bronchiole with many alveolar sacs.
9. terminal room of alveoli at ends of ducts, simple squamous epithelium.
10. type 1 pneumocytes which allow for gas exchange and type 2 pneumocytes which secrete surfactant.
11. CT matrix called zona diffusa, fibroblasts, alveolar phagocytes, capillaries. zone fiber phago cap
12. pneumocyte, pneumocyte basement membrane, endothelium basement membrane, endothelium.
between the alveolar sacs is the interalveolar septum, where gas exchange with blood actually takes place. this border is lined with type 1 and 2 pneumocytes, involved in gas exchange and surfactant secretion, respectively. thus, in order to reach the blood, gas has to diffuse through: type 1 pneumocyte cell, type 1 pneumocyte basement membrane, endothelial basement membrane, endothelial cell. also between the interalveolar septum are some fibroblasts, alveolar phagocytes, and a scant CT matrix called the zona diffusa.
questions
1. describe the passage of air from the trachea to the alveoli.
2. describe the physical support of the trachea
3. describe the layers of the trachea.
distinguishing characteristics of:
4. bronchi...
5. bronchiole...
6. terminal bronchiole...
7. respiratory bronchiole...
8. alveolar duct...
9. alveolar sac...
10. what are the two alveolar surfaces formed by epithelia?
11. what is inside the interalveolar septa?
12. describe the barrier between blood and air in the alveoli.
answers
1. trachea, bronchi, bronchioles, terminal bronchioles, respiratory bronchioles, alveolar ducts, alveolar sacs, alveoli.
2. ~20 cartilage rings with smooth muscle (trachealis) spanning the posterior openings.
3. PSCC in mucosa with goblet cells, sometimes diffuse lymphatic tissue. submucosa of CT and tracheal glands. hyaline cartilage layer, then adventitia.
4. fragmented hyaline cartilage, PSCC with goblet cells.
5. smooth muscle but no cartilage, PSCC to simple columnar epithelium with goblet cells.
6. simple columnar, cilia but no goblet cells. clara cells secrete lipoprotein surfactant.
7. beginning of gas exchange; alveoli begin to protrude through walls. simple cuboidal epithelium with no cilia.
8. like a smaller respiratory bronchiole with many alveolar sacs.
9. terminal room of alveoli at ends of ducts, simple squamous epithelium.
10. type 1 pneumocytes which allow for gas exchange and type 2 pneumocytes which secrete surfactant.
11. CT matrix called zona diffusa, fibroblasts, alveolar phagocytes, capillaries. zone fiber phago cap
12. pneumocyte, pneumocyte basement membrane, endothelium basement membrane, endothelium.
histology: the integument
the integument is divided into three basic layers: on the surface is the epidermis, then the dermis, then the hypodermis. the epidermis itself has several layers, the deepest of which is called the stratum basale which is on the basement membrane of the epidermis and contains mitotically active keratinocytes, which are epithelial cells containing keratin, which is a sulfur bound protein. also scattered in this layer are other cells such as melaninocytes which produce melanin, Langerhans cells which are antigen presenting cells, and Merkel cells which are involved in light touch perception. the next layer up is the stratum spinosum. which is a thick layer containing keratinocytes that are held together by desmodomes. above the spinosum is a thin layer called stratum granulosum which is composed of dying keratinocytes. the last layer is the stratum corneum, which is basically a thick layer of keratin, of variable thickness depending on the location on the body.
beneath the epidermis is the dermis, and the border between the two contains projections upwards from the dermis called papillary ridges and projections downwards from the epidermis called rete pegs. the dermis has two layers, a thin papillary layer and the reticular layer. the reticular layer makes up the bulk of the dermis and is made of dense irregular CT and is highly vascularized and innervated. inside the dermis are two types of pressure receptors- meissner's corpuscle senses light pressure in the papillary layer and is made from helically wound schwann cells around a nerve axon ending. pacinian corpuscles sense deep pressure in the reticular layer and are made of concentric schwann cell wrappings around the end of the axon.
questions
1. what are the 3 basic layers to the skin?
2. describe the epidermis.
3. describe the dermis.
4. describe the hypodermis.
5. what are the layers of the epidermis?
6. describe the stratum basale.
7. what are the cells that might appear in the stratum basale?
8. describe the stratum spinosum.
9. describe the stratum granulosum.
10. describe the stratum corneum.
11. what are the two layers of the dermis?
12. describe the papillary layer of the dermis.
13. describe the reticular layer of the dermis.
14. what is a meissner's corpuscle?
15. what is a pacinian corpuscle?
16. what is the smooth muscle strip associated with hair follicles?
17. describe the structure of a sweat gland.
18. describe the structure of a sebaceous gland.
answers
1. epidermis, dermis, hypodermis.
2. nonvascularized and minimally innervated, keratinized stratified squamous, made almost entirely of keratinocytes.
3. well vascularized and innervated, mostly dense irregular CT
4. mostly loose CT and adipose tissue.
5. stratum basale, spinosum, granulosum, corneum.
6. single layer of mitotically active cuboidal cells sitting on basement membrane.
7. melanocyte, which produces melanin. langerhans cell, which is an antigen presenting immune cell. merkel cell, involved in light touch sensation.
8. keratinocytes which are held together by extensive desmodomes. form a layer of variable thickness.
9. granular layer a few layers thick with dying keratinocytes.
10. keratinized layer of many dead keratinocytes, sometimes with a clear bottom portion called the stratum lucidum.
11. papillary layer, reticular layer
12. thin, undulating, with upward projections called dermal papillas and downward projections from epidermis called rete pegs.
13. thicker layer with dense irregular CT with elastin, highly vascularized and innervated.
14. touch sensor in dermal papillae. small, helical wound Schwann cells on an axon.
15. a deep pressure and vibration sensor in the deep dermis or hypodermis. large, with concentric layers of schwann cells.
16. arrector pili muscle
17. simple tubular gland extending deep into the dermis.
18. simple acinar gland off of hair follicles that produces sebum.
beneath the epidermis is the dermis, and the border between the two contains projections upwards from the dermis called papillary ridges and projections downwards from the epidermis called rete pegs. the dermis has two layers, a thin papillary layer and the reticular layer. the reticular layer makes up the bulk of the dermis and is made of dense irregular CT and is highly vascularized and innervated. inside the dermis are two types of pressure receptors- meissner's corpuscle senses light pressure in the papillary layer and is made from helically wound schwann cells around a nerve axon ending. pacinian corpuscles sense deep pressure in the reticular layer and are made of concentric schwann cell wrappings around the end of the axon.
questions
1. what are the 3 basic layers to the skin?
2. describe the epidermis.
3. describe the dermis.
4. describe the hypodermis.
5. what are the layers of the epidermis?
6. describe the stratum basale.
7. what are the cells that might appear in the stratum basale?
8. describe the stratum spinosum.
9. describe the stratum granulosum.
10. describe the stratum corneum.
11. what are the two layers of the dermis?
12. describe the papillary layer of the dermis.
13. describe the reticular layer of the dermis.
14. what is a meissner's corpuscle?
15. what is a pacinian corpuscle?
16. what is the smooth muscle strip associated with hair follicles?
17. describe the structure of a sweat gland.
18. describe the structure of a sebaceous gland.
answers
1. epidermis, dermis, hypodermis.
2. nonvascularized and minimally innervated, keratinized stratified squamous, made almost entirely of keratinocytes.
3. well vascularized and innervated, mostly dense irregular CT
4. mostly loose CT and adipose tissue.
5. stratum basale, spinosum, granulosum, corneum.
6. single layer of mitotically active cuboidal cells sitting on basement membrane.
7. melanocyte, which produces melanin. langerhans cell, which is an antigen presenting immune cell. merkel cell, involved in light touch sensation.
8. keratinocytes which are held together by extensive desmodomes. form a layer of variable thickness.
9. granular layer a few layers thick with dying keratinocytes.
10. keratinized layer of many dead keratinocytes, sometimes with a clear bottom portion called the stratum lucidum.
11. papillary layer, reticular layer
12. thin, undulating, with upward projections called dermal papillas and downward projections from epidermis called rete pegs.
13. thicker layer with dense irregular CT with elastin, highly vascularized and innervated.
14. touch sensor in dermal papillae. small, helical wound Schwann cells on an axon.
15. a deep pressure and vibration sensor in the deep dermis or hypodermis. large, with concentric layers of schwann cells.
16. arrector pili muscle
17. simple tubular gland extending deep into the dermis.
18. simple acinar gland off of hair follicles that produces sebum.
Wednesday, December 3, 2008
MS anatomy: deep back and neck
this lecture covered the anatomy of the spine as well as the muscles of the deep back, head, and neck. the spine is made of 7 cervical vertebrae, 12 thoracic vertebrae, and 5 lumbar vertebrae and a sacrum at the bottom which is made up of 5 fused vertebrae. notable differences between the three vertebral sections: cervical vertebrae have short, split spines, while thoracic vertebrae have long, downward sloping ones. lumbar vertebrae have extra processes next to the transverse processes called mamillary processes. range of movement is wide for cervical and lumbar sections but narrow for thoracic. the spine has two opposite curves, called kyphotic and lordotic. the sacrum and the thoracic spine are kyphotic, folding the body inwards, while the the lumbar and cervical spine have the lordotic curve which has the opposite shape.
some unique features about the top two vertebrae, the atlas (C1) and axis (C2). the atlas lacks a vertebral body and just has anterior and posterior arch. resting in the anterior arch, secured by the transverse ligament, is an upward protrusion from C2, called the "dens" of the axis, which is actually the fusion of the vertebral bodies of C1 and C2. the dens and the atlas form the atlanto-axis pivot joint and allow for rotational movement of the head. the joint between the atlas and the occiput is called the atlanto-occipital joint and is stabilized by a host of muscles that attach to the occiput around it (more to come) as well as the atlanto occipital membrane, a ligament that spans from the posterior occiput to the spinous process of C1. the joint itself is between the superior articular facets of the atlas and the condyles of the occiput.
we then look at the muscles of the back, neck, and head, starting with the muscles of the deep back. these include the erector spinae, the superficial and larger group of back muscles that span from the sacrum to the base of the skull. these include the spinalis, the longissimus, and the iliocostalis. the transversospinalis are a deeper and more intricate set of back muscles that lie in the groove between the transverse and spinous processes-- originating from transverse processes, inserting into spinous processes. the semispinalis covers the upper 1/3 of the spine and each muscle group has a span of 5-8 vertebrae, the multifidus is prominent near the sacrum and spans 3-4 vertebrae a piece, and the rotatores go all along the spine and cover 1-2 vertebrae each. in general, the erector spinae (the larger muscles) are more involved in extension and the transverospinalis muscles (smaller muscles) are more involved in lateral flexion and rotation.
the muscles that aid in movement of the head can be divided into three sections: suboccipital muscles, anterior neck muscles, and lateral neck muscles. suboccipital muscles include the rectus capitis posterior major and minor, and the inferior and superior oblique. for these muscles, when a muscle is oriented vertically, it is involved in extension, and when it is oriented diagonally or horizontally, it is involved in rotation. the anterior neck muscles include the rectus capitis anterior and longus colli and capitis. the lateral neck muscles are the scalenes and SCM. the suboccipital muscles are innervated by the posterior rami of C1, the anterior neck muscles are innervated by C1-4, and the lateral neck muscles are innervated by C2,3 and cranial nerve XI.
questions
vertebrae anatomy
1. spinous process is formed by...
2. transverse process is formed by...
3. mamillary processes...
4. vertebral canal is formed by...
5. zygapophyseal/facet joint is formed by...
6. what are the primary and secondary curves of the spine called?
cervical, thoracic, lumbar vertebrae:
7. body...
8. spines...
9. costotransverse foramen...
10. range of movement...
11. movements...
12. 5 sacral foramen fuse after...
13. sacral foarmina convey...
14. sacral promontory is...
15. what are the sacral crests and what are they made from?
16. sacral canal ends at...
17. what is the coccyx?
18. what is the sacralization of L5?
19. what is the lumbarization of S1?
20. what type of joint is the intervertebral joint?
21. describe the composition of the intervertebral joint.
22. what are the ligaments that support the intervertebral joints?
23. what is a herniated disc?
24. what type of joint is the facet joint?
25. supraspinous ligament...
26. interspinous ligament...
27. ligamentum flavum...
28. what are the anatomical features of C1?
29. what is unique about C2?
30. what is the atlanto-axis joint?
31. what is the transverse ligament?
32. alar and apical ligaments...
33. what is the atlanto-occipital joint and what movement does it allow?
34. what is the atlanto-occipital membrane penetrated by?
deep back muscles
35. what are the erector spinae muscles and where do they originate from?
36. spinalis...
37. longissimus...
38. iliocostalis...
39. what are the transverospinalis muscles?
40. semispinalis...
41. semispinalis capitis is...
42. multifidus...
43. rotatores...
44. what is the splenius and where do the two types attach?
45. describe the difference in action between the long and short deep back muscles.
46. what are deep back muscles innervated by?
suboccipital muscles- origins, insertions, actions
47. inferior oblique...
48. superior oblique...
49. rectus capitis posterior major...
50. rectus capitis posterior minor...
51. which nerve innervates the suboccipital muscles?
anterior neck muscles
52. rectus capitis anterior and lateralis...
53. longus colli and capitis...
54. which nerve innervates the anterior neck muscles?
lateral neck muscles
55. anterior scalenes...
56. posterior scalenes...
57. SCM...
58. flexion of head is mainly due to which muscles?
59. extension of head is mainly due to which muscles?
answers
1. fusion of two pedicles.
2. fusion of pedicles and laminae.
3. are on lumbar vertebrae and can be confused with transverse processes.
4. column of vertebral foramen and houses the spinal cord.
5. joining of superior and inferior articular facets.
6. primary = kyphotic in the thoracic spine and sacrum. secondary = lordotic in the cervical and lumbar spine.
7. oblong, heart shaped, oblong
8. short / bifid, long / downward sloping, intermediate / horizontal
9. transverse foramen, costotransverse, no foramen
10. wide, narrow, wide
11. flex/extend/abduct/some rotation, rotation, flex/extend/abduct/some rotation
12. 20 years
13. anterior and posterior rami of sacral nerves
14. prominent body of S1
15. median crest made from fused SP's, lateral crest from fused TVP's.
16. sacral hiatus
17. 4 small fused vertebrae at the bottom of the sacrum which serve as the origin for pelvic muscles and ligaments.
18. total or partial fusion of L5 to sacrum.
19. total or partial separation of S1 from sacrum.
20. symphysis joint.
21. outer layer is fibrous CT called annulus fibrosus, gelatinous center called nucleus pulposus.
22. anterior and posterior longitudinal ligaments.
23. when pressure between the vertebrae causes the nucleus pulposa to herniate out of the annulus fibrosus and potentially compress spinal nerves against the articular processes.
24. synovial joint.
25. joins tips of vertebral spines
26. spans between vertebral spines
27. elastic CT helps extend vertebral column
28. the "atlas" has an anterior and posterior arch and no vertebral body.
29. the "axis" has an upward protrusion called the "dens" which is the fusion of the bodies of the atlas and axis.
30. the joint that is formed by the dens and the anterior arch of the atlas which allows for the rotation of the head.
31. anchors the dens to the anterior arch.
32. anchor dens to margin of foramen magnum and limits rotational movement.
33. joint between the occipital condyles of the head and the superior articular facets of the atlas. permits flexion and extension of head.
34. C1, vertebral artery.
35. iliac crest and sacrum.
36. interconnects thoracic spinous processes.
37. runs along costovertebral region, also has a capitis portion.
38. goes from iliac crest to ribs.
39. semispinalis, multifidus, rotatores- muscles that span from sacrum to base of skull. lie within groove between transverse and spinous processes and go from TP's to SP's.
40. semispinalis spans 5-8 vertebrae, are in the upper 1/2 of vertebral column.
41. strongest extensor of the skull.
42. spans 3-4 vertebrae, thickest over sacrum
43. span 1-2 vertebrae throughout spine.
44. muscle that goes from spinous processes to TP's or to skull. capitis attaches to mastoid process, cervicis attaches to TP's.
45. long deep back muscles more extension, short deep back muscles more rotation and lateral flexion.
46. posterior rami of spinal nerves.
47. O: spine of axis I: TP of axis A: rotate
48. O: TP of axis I: occiput A: extend
49. O: spine of axis I: occiput A: extend and rotate
50. O: posterior tubercle of atlas I: occiput A: extend
51. posterior ramus of C1
52. O: TP of atlas I: occiput A: flexion and lateral flexion and stabilization of altantoocciptal joint.
53. O: body and TP's of cervical vertebrae I: same, plus occiput A: flexion
54. C1-4
55. O: upper TP's I: 1st rib A: flexion of head, raise ribs N: lower cervical nerves
56. O: upper TP's I: 2nd rib A: flexion of head, raise ribs N: lower cervical nerves
57. O: manubrium, clavicle I: mastoid process A: flexion, lateral flexion, rotation, raise ribs N: motor-spinal accessory (cranial nerve XI), C2,3
58. SCM, rectus capitis anterior, longus capitis / colli
59. trapezius, rectus capitis posterior, superior oblique
some unique features about the top two vertebrae, the atlas (C1) and axis (C2). the atlas lacks a vertebral body and just has anterior and posterior arch. resting in the anterior arch, secured by the transverse ligament, is an upward protrusion from C2, called the "dens" of the axis, which is actually the fusion of the vertebral bodies of C1 and C2. the dens and the atlas form the atlanto-axis pivot joint and allow for rotational movement of the head. the joint between the atlas and the occiput is called the atlanto-occipital joint and is stabilized by a host of muscles that attach to the occiput around it (more to come) as well as the atlanto occipital membrane, a ligament that spans from the posterior occiput to the spinous process of C1. the joint itself is between the superior articular facets of the atlas and the condyles of the occiput.
we then look at the muscles of the back, neck, and head, starting with the muscles of the deep back. these include the erector spinae, the superficial and larger group of back muscles that span from the sacrum to the base of the skull. these include the spinalis, the longissimus, and the iliocostalis. the transversospinalis are a deeper and more intricate set of back muscles that lie in the groove between the transverse and spinous processes-- originating from transverse processes, inserting into spinous processes. the semispinalis covers the upper 1/3 of the spine and each muscle group has a span of 5-8 vertebrae, the multifidus is prominent near the sacrum and spans 3-4 vertebrae a piece, and the rotatores go all along the spine and cover 1-2 vertebrae each. in general, the erector spinae (the larger muscles) are more involved in extension and the transverospinalis muscles (smaller muscles) are more involved in lateral flexion and rotation.
the muscles that aid in movement of the head can be divided into three sections: suboccipital muscles, anterior neck muscles, and lateral neck muscles. suboccipital muscles include the rectus capitis posterior major and minor, and the inferior and superior oblique. for these muscles, when a muscle is oriented vertically, it is involved in extension, and when it is oriented diagonally or horizontally, it is involved in rotation. the anterior neck muscles include the rectus capitis anterior and longus colli and capitis. the lateral neck muscles are the scalenes and SCM. the suboccipital muscles are innervated by the posterior rami of C1, the anterior neck muscles are innervated by C1-4, and the lateral neck muscles are innervated by C2,3 and cranial nerve XI.
questions
vertebrae anatomy
1. spinous process is formed by...
2. transverse process is formed by...
3. mamillary processes...
4. vertebral canal is formed by...
5. zygapophyseal/facet joint is formed by...
6. what are the primary and secondary curves of the spine called?
cervical, thoracic, lumbar vertebrae:
7. body...
8. spines...
9. costotransverse foramen...
10. range of movement...
11. movements...
12. 5 sacral foramen fuse after...
13. sacral foarmina convey...
14. sacral promontory is...
15. what are the sacral crests and what are they made from?
16. sacral canal ends at...
17. what is the coccyx?
18. what is the sacralization of L5?
19. what is the lumbarization of S1?
20. what type of joint is the intervertebral joint?
21. describe the composition of the intervertebral joint.
22. what are the ligaments that support the intervertebral joints?
23. what is a herniated disc?
24. what type of joint is the facet joint?
25. supraspinous ligament...
26. interspinous ligament...
27. ligamentum flavum...
28. what are the anatomical features of C1?
29. what is unique about C2?
30. what is the atlanto-axis joint?
31. what is the transverse ligament?
32. alar and apical ligaments...
33. what is the atlanto-occipital joint and what movement does it allow?
34. what is the atlanto-occipital membrane penetrated by?
deep back muscles
35. what are the erector spinae muscles and where do they originate from?
36. spinalis...
37. longissimus...
38. iliocostalis...
39. what are the transverospinalis muscles?
40. semispinalis...
41. semispinalis capitis is...
42. multifidus...
43. rotatores...
44. what is the splenius and where do the two types attach?
45. describe the difference in action between the long and short deep back muscles.
46. what are deep back muscles innervated by?
suboccipital muscles- origins, insertions, actions
47. inferior oblique...
48. superior oblique...
49. rectus capitis posterior major...
50. rectus capitis posterior minor...
51. which nerve innervates the suboccipital muscles?
anterior neck muscles
52. rectus capitis anterior and lateralis...
53. longus colli and capitis...
54. which nerve innervates the anterior neck muscles?
lateral neck muscles
55. anterior scalenes...
56. posterior scalenes...
57. SCM...
58. flexion of head is mainly due to which muscles?
59. extension of head is mainly due to which muscles?
answers
1. fusion of two pedicles.
2. fusion of pedicles and laminae.
3. are on lumbar vertebrae and can be confused with transverse processes.
4. column of vertebral foramen and houses the spinal cord.
5. joining of superior and inferior articular facets.
6. primary = kyphotic in the thoracic spine and sacrum. secondary = lordotic in the cervical and lumbar spine.
7. oblong, heart shaped, oblong
8. short / bifid, long / downward sloping, intermediate / horizontal
9. transverse foramen, costotransverse, no foramen
10. wide, narrow, wide
11. flex/extend/abduct/some rotation, rotation, flex/extend/abduct/some rotation
12. 20 years
13. anterior and posterior rami of sacral nerves
14. prominent body of S1
15. median crest made from fused SP's, lateral crest from fused TVP's.
16. sacral hiatus
17. 4 small fused vertebrae at the bottom of the sacrum which serve as the origin for pelvic muscles and ligaments.
18. total or partial fusion of L5 to sacrum.
19. total or partial separation of S1 from sacrum.
20. symphysis joint.
21. outer layer is fibrous CT called annulus fibrosus, gelatinous center called nucleus pulposus.
22. anterior and posterior longitudinal ligaments.
23. when pressure between the vertebrae causes the nucleus pulposa to herniate out of the annulus fibrosus and potentially compress spinal nerves against the articular processes.
24. synovial joint.
25. joins tips of vertebral spines
26. spans between vertebral spines
27. elastic CT helps extend vertebral column
28. the "atlas" has an anterior and posterior arch and no vertebral body.
29. the "axis" has an upward protrusion called the "dens" which is the fusion of the bodies of the atlas and axis.
30. the joint that is formed by the dens and the anterior arch of the atlas which allows for the rotation of the head.
31. anchors the dens to the anterior arch.
32. anchor dens to margin of foramen magnum and limits rotational movement.
33. joint between the occipital condyles of the head and the superior articular facets of the atlas. permits flexion and extension of head.
34. C1, vertebral artery.
35. iliac crest and sacrum.
36. interconnects thoracic spinous processes.
37. runs along costovertebral region, also has a capitis portion.
38. goes from iliac crest to ribs.
39. semispinalis, multifidus, rotatores- muscles that span from sacrum to base of skull. lie within groove between transverse and spinous processes and go from TP's to SP's.
40. semispinalis spans 5-8 vertebrae, are in the upper 1/2 of vertebral column.
41. strongest extensor of the skull.
42. spans 3-4 vertebrae, thickest over sacrum
43. span 1-2 vertebrae throughout spine.
44. muscle that goes from spinous processes to TP's or to skull. capitis attaches to mastoid process, cervicis attaches to TP's.
45. long deep back muscles more extension, short deep back muscles more rotation and lateral flexion.
46. posterior rami of spinal nerves.
47. O: spine of axis I: TP of axis A: rotate
48. O: TP of axis I: occiput A: extend
49. O: spine of axis I: occiput A: extend and rotate
50. O: posterior tubercle of atlas I: occiput A: extend
51. posterior ramus of C1
52. O: TP of atlas I: occiput A: flexion and lateral flexion and stabilization of altantoocciptal joint.
53. O: body and TP's of cervical vertebrae I: same, plus occiput A: flexion
54. C1-4
55. O: upper TP's I: 1st rib A: flexion of head, raise ribs N: lower cervical nerves
56. O: upper TP's I: 2nd rib A: flexion of head, raise ribs N: lower cervical nerves
57. O: manubrium, clavicle I: mastoid process A: flexion, lateral flexion, rotation, raise ribs N: motor-spinal accessory (cranial nerve XI), C2,3
58. SCM, rectus capitis anterior, longus capitis / colli
59. trapezius, rectus capitis posterior, superior oblique
histology: vascular system
this lecture covers the circulatory system and the lymphatic system. the main types of blood vessels are reviewed (we covered this in organ systems already in much greater detail). arteries supply oxygenated blood to tissues and have three basic layers: the innermost layer is the tunica intima and has a squamous endothelium, subendothelial CT, and internal elastic lamina. the middle layer is the tunica media and has smooth muscle and external elastic lamina. the outermost layer is the tunica adventitia which has connective tissue that blends in with surrounding CT, with a network of blood vessels (vasa vasorum) and nerves (nervi vascularis). arterioles are the next level after arteries, which have a thicker smooth muscle tunica media layer which aids in their function, which is mainly to regulate blood flow to capillary beds. there are three types of capillaries which are distinguished by size and continuity of the endothelium: type 1 continuous, which have a tight endothelium which do not allow much leakage, type 2 fenestrated, which allow for some leakage and are present in the renal glomerulus, and type 3 discontinuous, which are much larger and have huge holes that allow for entire cells to pass through- found in the bone marrow, spleen, and liver. after the capillaries come the venules and veins, which are different from arteries in that they have no internal elastic lamina, a thinner tunica media, and rely on the contraction of skeletal muscle and a series of valves for blood flow back to the heart.
the lymphatic system is a sort of complementary system to the circulatory system in that it recirculates body fluids which have been picked up from the interstitial space outside of capillaries. it also functions in red blood cell production and destruction, aids in immunodefense (in the production and circulation of lymphocytes), and aids in fat absorption in the GI tract (think of the central lacteal in the lamina propria of the small intestine). there are several orders of lymphatic organization, the first of which is diffuse lymph tissue, which is just a scattering of lymphocytes in a general area, such as right underneath the epidermis in the airways or GI tract. next is nodular lymph tissue, which are more discrete aggregations of lymphocytes which might have germinal centers in the middle for profilerating new cells- such as the Peyer's patches in the ileum. next is a lymph node, which is an encapsulated "inline filter" for lymph vessels, a small container into which lymph gets poured in through many afferent lymphatic vessels, filtered through the subcapsular and medullary sinuses, and poured back out through a larger efferent lymphatic vessel.
finally, we get to the lymph organs, which are large scale lymph and blood filtering factories. first is the spleen, the functional part of which is called the splenic pulp, which comes in two varieties- red and white. the red is the bulk of the spleen and is filled with RBC's, and white pulp are little islands of lymphocytes that are found alongside blood vessels. the tonsils are another lymph organ, consisting of a series of lymphatic tissue masses covered by a stratified squamous epithelium which is thrown into "crypts". the thymus is the third and last lymph organ, and is a bi-lobed organ beneath the sternum in which t-lymphocytes are trained to differentiate self from non-self.
questions
1. what are the three basic layers to arteries?
2. describe the tunica intima layer of arteries.
3. describe the tunica media layer of arteries.
4. describe the tunica adventitia layer of arteries.
5. what is an arteriole?
6. what are three major differences between veins and arteries?
7. what is a venule?
8. what are the three types of capillaries?
9. describe type I capillaries.
10. describe type II capillaries.
11. describe type III capillaries.
12. what are the main functions of the lymphatic system?
13. describe lymphatic vessels.
14. what are the two types of lymphoid tissue?
15. describe diffuse lymphoid tissue.
16. describe nodular lymphoid tissue.
17. what are the four examples of lymph organs?
18. describe the structure of a lymph node.
19. what is the flow through a lymph vessel?
20. describe the structure of the spleen.
21. what is the thymus?
22. describe the structure of the tonsils.
answers
1. tunica intima, tunica media, tunica adventitia.
2. tunica intima is the innermost layer of an artery and contains squamous endothelium, sub endothelial CT, and internal elastic lamina.
3. tunica media is the middle, thickest layer that contains smooth muscle with elastin.
4. tunica adventitia is the outermost layer containing CT with a network of blood vessels (vasa vasorum) and nerves (nervi vascularis)
5. an artery with a luminal diameter of less than 100um that plays a role in distributing and controlling entry of blood into capillary beds.
6. no internal elastic lamina, relatively thin tunica media, and endothelium is thrown into valves to prevent backflow.
7. a vein with a luminal diameter of less than 200um.
8. type 1 continuous, type 2 fenestrated, type 3 discontinuous.
9. the most common capillary in the body, the endothelium is held tightly together and is relatively leak proof.
10. small holes in endothelium allow some leakage, seen in glomerulus, exocrine ducts, choroid plexus.
11. larger (up to 30um) diameter with large holes in endothelium that allow entire cells to pass, seen in liver, bone marrow, spleen.
12. recirculation of body fluids, defense, hematopoeisis (adding lymphocytes), recycling RBC's (spleen), absorption of fat in GI tract. recirculate blood in defense of fat recycling.
13. vessels that gather and remove excess tissue fluid from capillaries and circulate back into venous system. rely on skeletal muscle and valve system for pumping (much like veins).
14. diffuse and nodular
15. scattering of lymphocytes; often associated with epithelial linings of GI tract and respiratory airways.
16. semi discrete (but unencapsulated) mass of lymphocytes, sometimes with a germinal center where new cells proliferating.
17. lymph nodes, spleen, tonsils, thymus.
18. encapsulated mass of lymph nodules that serves as an in line filter (for lymph) with multiple afferent "feeder" lines and one or two efferent "drainer" lines.
19. afferent lymph vessel, subcapsular sinus, medullary sinus, efferent lymphatic vessel.
20. inline filter (for blood) with two types of "pulp" in the parenchyma: red pulp is the bulk of the spleen and has masses of RBC's, white pulp is small lymphocytes islands associated with blood vessels.
21. a bilobed t-lymphocyte manufacturing center underneath the sternum
22. series of masses of lymphoid tissue with stratified squamous epithelium thrown into crypts that cover aggregations of nodules.
the lymphatic system is a sort of complementary system to the circulatory system in that it recirculates body fluids which have been picked up from the interstitial space outside of capillaries. it also functions in red blood cell production and destruction, aids in immunodefense (in the production and circulation of lymphocytes), and aids in fat absorption in the GI tract (think of the central lacteal in the lamina propria of the small intestine). there are several orders of lymphatic organization, the first of which is diffuse lymph tissue, which is just a scattering of lymphocytes in a general area, such as right underneath the epidermis in the airways or GI tract. next is nodular lymph tissue, which are more discrete aggregations of lymphocytes which might have germinal centers in the middle for profilerating new cells- such as the Peyer's patches in the ileum. next is a lymph node, which is an encapsulated "inline filter" for lymph vessels, a small container into which lymph gets poured in through many afferent lymphatic vessels, filtered through the subcapsular and medullary sinuses, and poured back out through a larger efferent lymphatic vessel.
finally, we get to the lymph organs, which are large scale lymph and blood filtering factories. first is the spleen, the functional part of which is called the splenic pulp, which comes in two varieties- red and white. the red is the bulk of the spleen and is filled with RBC's, and white pulp are little islands of lymphocytes that are found alongside blood vessels. the tonsils are another lymph organ, consisting of a series of lymphatic tissue masses covered by a stratified squamous epithelium which is thrown into "crypts". the thymus is the third and last lymph organ, and is a bi-lobed organ beneath the sternum in which t-lymphocytes are trained to differentiate self from non-self.
questions
1. what are the three basic layers to arteries?
2. describe the tunica intima layer of arteries.
3. describe the tunica media layer of arteries.
4. describe the tunica adventitia layer of arteries.
5. what is an arteriole?
6. what are three major differences between veins and arteries?
7. what is a venule?
8. what are the three types of capillaries?
9. describe type I capillaries.
10. describe type II capillaries.
11. describe type III capillaries.
12. what are the main functions of the lymphatic system?
13. describe lymphatic vessels.
14. what are the two types of lymphoid tissue?
15. describe diffuse lymphoid tissue.
16. describe nodular lymphoid tissue.
17. what are the four examples of lymph organs?
18. describe the structure of a lymph node.
19. what is the flow through a lymph vessel?
20. describe the structure of the spleen.
21. what is the thymus?
22. describe the structure of the tonsils.
answers
1. tunica intima, tunica media, tunica adventitia.
2. tunica intima is the innermost layer of an artery and contains squamous endothelium, sub endothelial CT, and internal elastic lamina.
3. tunica media is the middle, thickest layer that contains smooth muscle with elastin.
4. tunica adventitia is the outermost layer containing CT with a network of blood vessels (vasa vasorum) and nerves (nervi vascularis)
5. an artery with a luminal diameter of less than 100um that plays a role in distributing and controlling entry of blood into capillary beds.
6. no internal elastic lamina, relatively thin tunica media, and endothelium is thrown into valves to prevent backflow.
7. a vein with a luminal diameter of less than 200um.
8. type 1 continuous, type 2 fenestrated, type 3 discontinuous.
9. the most common capillary in the body, the endothelium is held tightly together and is relatively leak proof.
10. small holes in endothelium allow some leakage, seen in glomerulus, exocrine ducts, choroid plexus.
11. larger (up to 30um) diameter with large holes in endothelium that allow entire cells to pass, seen in liver, bone marrow, spleen.
12. recirculation of body fluids, defense, hematopoeisis (adding lymphocytes), recycling RBC's (spleen), absorption of fat in GI tract. recirculate blood in defense of fat recycling.
13. vessels that gather and remove excess tissue fluid from capillaries and circulate back into venous system. rely on skeletal muscle and valve system for pumping (much like veins).
14. diffuse and nodular
15. scattering of lymphocytes; often associated with epithelial linings of GI tract and respiratory airways.
16. semi discrete (but unencapsulated) mass of lymphocytes, sometimes with a germinal center where new cells proliferating.
17. lymph nodes, spleen, tonsils, thymus.
18. encapsulated mass of lymph nodules that serves as an in line filter (for lymph) with multiple afferent "feeder" lines and one or two efferent "drainer" lines.
19. afferent lymph vessel, subcapsular sinus, medullary sinus, efferent lymphatic vessel.
20. inline filter (for blood) with two types of "pulp" in the parenchyma: red pulp is the bulk of the spleen and has masses of RBC's, white pulp is small lymphocytes islands associated with blood vessels.
21. a bilobed t-lymphocyte manufacturing center underneath the sternum
22. series of masses of lymphoid tissue with stratified squamous epithelium thrown into crypts that cover aggregations of nodules.
Tuesday, December 2, 2008
histology: urinary system
this unit provided a brief histological overview of the kidneys and the tubular architecture of the urinary system. the basic function of the kidneys is to filter the blood and excrete waste through the urine, which leaves the kidney via the ureter, is pooled in the bladder, then goes from the bladder to the body's exterior by means of the urethra. inside the kidney itself there is an outer layer called the cortex and an inner layer called the medulla, which contains triangular shaped lobes called medullary pyramids. the pyramids collect urine at their tips, called area cribosa, into the calyces, which drain into the renal sinuses, renal pelvis, and out to the ureter. the kidney is filled with functional tubular units called the nephron, of which there are two types: juxtamedullary and cortical, depending on their location.
the site of filtration of blood occurs at the glomerulus, which is a ball of type 2 fenestrated capillaries inside a Bowman's capsule. the Bowman's capsule is similar to a pericardium or pleura in that it has a visceral and parietal layer and a space in between; in this case, the visceral layer is made up of the layer of podocytes that encase the ball of capillaries and provide an extra filtration layer, outside of which there is the bowman's space, and then the parietal bowman's capsule. the blood supply to the ball of capillaries comes from the afferent arteriole and leaves through the efferent arteriole; this end of the glomerulus is called the vascular pole. on the other side of the glomerulus is the urinary pole, which collects the filtrate from the blood into the proximal tubule, which is a convoluted tubule made of simple cuboidal epithelium with extensive apical microvilli. this tubule descends into the medullary region and becomes the loop of Henle, which is thin and squamous on the way down and thick and cuboidal on the way up. this turns into the distal convoluted tubule, which comes back to the glomerulus to form the juxtamedullary complex, which is a junction of the distal tubule and the efferent arteriole, with a group of cells called the macula densa in between. the distal tubule then dumps into a collecting duct, which empties into the papillary ducts that empty into the area cribrosa of the medullary pyramids, and out the body as covered above.
the blood flow in and out of the kidney is as follows: the visceral abdominal aorta supplies the blood to the renal artery, which branches into the interlobular arteries, which branch into the arcuate arteries, which branch into the interlobular arteries, which branch into the intralobular arteries, which turn into afferent arterioles and enter the glomerulus. the blood is filtered in the capillaries in the glomerulus, then flows out through the efferent arteriole, then enters peritubular capillaries, which are small capillaries that run alongside nephron tubules and are the link between the arteries and veins in the kidneys. from the peritubular capillaries, blood flows into veins and exits in the opposite order: intralobular, interlobular, etc etc.
some details about the epithelium of the plumbing of the urinary system: there is transitional epithelium basically from the ureter to the end of the urethra, which switches to non-keratinized stratified squamous. the muscularis externa of the ureter and urethra has opposite layers than other tubes of the body in that has an inner longitudinal and outer circular layer. the urinary bladder has a thick and choatic muscularis externa.
questions
1. what are four functions of the urinary system?
2. describe the anatomy of the kidney.
3. describe the blood flow in and out of the kidney.
4. what are the two types of nephrons?
5. describe the anatomy of a glomerulus.
6. what are the two poles in a glomerulus?
7. what is the glomelular membrane composed of?
8. describe the proximal tubule.
9. describe the loop of Henle.
10. describe the distal tubule.
11. what is a juxtaglomerular apparatus?
12. describe the collecting ducts.
13. describe juxtaglomerular cells.
14. what are peritubular capillaries?
15. describe the ureter.
16. describe the urinary bladder.
17. describe the epithelium of the urethra.
18. describe the muscularis externa of the urethra.
answers
1. chemically balance the blood, remove wastes, regulate blood pressure, and regulate red blood cell production.
2. kidneys have an outer layer called cortex and inner layer called medulla. in the medulla there are medullary pyramids from which urine is collected from the tips (area cribrosa) to the minor and major calyces, which converge into the renal sinuses, which converge into the renal pelvis, which leads out to the ureter.
3. renal artery to interlobar artery to arcuate artery to interlobular artery to intralobular artery to afferent arteriole to glomelular capsule to intralobular vein to interlobular vein to arcuate vein to interlobar vein to renal vein.
4. cortical nephrons and juxtamedullary nephrons.
5. 1-20 type II capillaries held together by a mesangium, encased in podocytes which make up the visceral Bowman's capsule, outside of which is the Bowman's space, and then the parietal Bowman's capsule.
6. vascular pole contains the afferent and efferent arterioles. urinary pole is on the other end of the glomerulus, where the proximal tubule starts.
7. type II capillary endothelium, endothelial basement membrane, podocyte basement membrane, podocyte, occasional mesangial cell.
8. long, convoluted, does most of the absorption, simple cuboidal with extensive apical microvilli.
9. has a thin, squamous descending section and a thick, ascending, cuboidal section.
10. simple suboidal, no microvilli. convolutes and feeds into a collecting duct.
11. the junction between a distal tubule and a vascular pole, with a macula densa in between
12. a large diameter tube that is the common collecting point for a number of nephrons, and merges into papillary ducts to the area cribrosa. simple cuboidal with rounded apical surfaces.
13. modified smooth muscle cells that secrete renin, which catalyzes formation of angiotensin-- regulates blood pressure.
14. the capillaries found of the back sides of nephric tubules and serve as points for absorption, the link between arterial and venous blood vasculature.
15. long muscular tube from renal pelvis to bladder with transitional epithelium and lamina propria (but no muscularis mucosa) muscularis externa has "reversed" layers -- inner longitudinal outer circular.
16. distensible sac with transitional epithelium and lamina propria but no muscularis mucosa. muscularis externa thick and chaotic.
17. PSC epithelium, near bladder is more transitional, near exterior is more non keratinzed stratified squamous. muscularis externa has inner longitudinal, outer circular.
the site of filtration of blood occurs at the glomerulus, which is a ball of type 2 fenestrated capillaries inside a Bowman's capsule. the Bowman's capsule is similar to a pericardium or pleura in that it has a visceral and parietal layer and a space in between; in this case, the visceral layer is made up of the layer of podocytes that encase the ball of capillaries and provide an extra filtration layer, outside of which there is the bowman's space, and then the parietal bowman's capsule. the blood supply to the ball of capillaries comes from the afferent arteriole and leaves through the efferent arteriole; this end of the glomerulus is called the vascular pole. on the other side of the glomerulus is the urinary pole, which collects the filtrate from the blood into the proximal tubule, which is a convoluted tubule made of simple cuboidal epithelium with extensive apical microvilli. this tubule descends into the medullary region and becomes the loop of Henle, which is thin and squamous on the way down and thick and cuboidal on the way up. this turns into the distal convoluted tubule, which comes back to the glomerulus to form the juxtamedullary complex, which is a junction of the distal tubule and the efferent arteriole, with a group of cells called the macula densa in between. the distal tubule then dumps into a collecting duct, which empties into the papillary ducts that empty into the area cribrosa of the medullary pyramids, and out the body as covered above.
the blood flow in and out of the kidney is as follows: the visceral abdominal aorta supplies the blood to the renal artery, which branches into the interlobular arteries, which branch into the arcuate arteries, which branch into the interlobular arteries, which branch into the intralobular arteries, which turn into afferent arterioles and enter the glomerulus. the blood is filtered in the capillaries in the glomerulus, then flows out through the efferent arteriole, then enters peritubular capillaries, which are small capillaries that run alongside nephron tubules and are the link between the arteries and veins in the kidneys. from the peritubular capillaries, blood flows into veins and exits in the opposite order: intralobular, interlobular, etc etc.
some details about the epithelium of the plumbing of the urinary system: there is transitional epithelium basically from the ureter to the end of the urethra, which switches to non-keratinized stratified squamous. the muscularis externa of the ureter and urethra has opposite layers than other tubes of the body in that has an inner longitudinal and outer circular layer. the urinary bladder has a thick and choatic muscularis externa.
questions
1. what are four functions of the urinary system?
2. describe the anatomy of the kidney.
3. describe the blood flow in and out of the kidney.
4. what are the two types of nephrons?
5. describe the anatomy of a glomerulus.
6. what are the two poles in a glomerulus?
7. what is the glomelular membrane composed of?
8. describe the proximal tubule.
9. describe the loop of Henle.
10. describe the distal tubule.
11. what is a juxtaglomerular apparatus?
12. describe the collecting ducts.
13. describe juxtaglomerular cells.
14. what are peritubular capillaries?
15. describe the ureter.
16. describe the urinary bladder.
17. describe the epithelium of the urethra.
18. describe the muscularis externa of the urethra.
answers
1. chemically balance the blood, remove wastes, regulate blood pressure, and regulate red blood cell production.
2. kidneys have an outer layer called cortex and inner layer called medulla. in the medulla there are medullary pyramids from which urine is collected from the tips (area cribrosa) to the minor and major calyces, which converge into the renal sinuses, which converge into the renal pelvis, which leads out to the ureter.
3. renal artery to interlobar artery to arcuate artery to interlobular artery to intralobular artery to afferent arteriole to glomelular capsule to intralobular vein to interlobular vein to arcuate vein to interlobar vein to renal vein.
4. cortical nephrons and juxtamedullary nephrons.
5. 1-20 type II capillaries held together by a mesangium, encased in podocytes which make up the visceral Bowman's capsule, outside of which is the Bowman's space, and then the parietal Bowman's capsule.
6. vascular pole contains the afferent and efferent arterioles. urinary pole is on the other end of the glomerulus, where the proximal tubule starts.
7. type II capillary endothelium, endothelial basement membrane, podocyte basement membrane, podocyte, occasional mesangial cell.
8. long, convoluted, does most of the absorption, simple cuboidal with extensive apical microvilli.
9. has a thin, squamous descending section and a thick, ascending, cuboidal section.
10. simple suboidal, no microvilli. convolutes and feeds into a collecting duct.
11. the junction between a distal tubule and a vascular pole, with a macula densa in between
12. a large diameter tube that is the common collecting point for a number of nephrons, and merges into papillary ducts to the area cribrosa. simple cuboidal with rounded apical surfaces.
13. modified smooth muscle cells that secrete renin, which catalyzes formation of angiotensin-- regulates blood pressure.
14. the capillaries found of the back sides of nephric tubules and serve as points for absorption, the link between arterial and venous blood vasculature.
15. long muscular tube from renal pelvis to bladder with transitional epithelium and lamina propria (but no muscularis mucosa) muscularis externa has "reversed" layers -- inner longitudinal outer circular.
16. distensible sac with transitional epithelium and lamina propria but no muscularis mucosa. muscularis externa thick and chaotic.
17. PSC epithelium, near bladder is more transitional, near exterior is more non keratinzed stratified squamous. muscularis externa has inner longitudinal, outer circular.
Monday, December 1, 2008
biochem: mark's medical biochemistry chapter 31- gluconeogenesis
gluconeogenesis is the process that occurs mainly in the liver in which glucose is produced from non-carbohydrate sources during times of fasting, exercise, or stress. it is essentially the opposite of glycolysis, in that instead of producing pyruvate from glucose, it synthesizes glucose from pyruvate. pyruvate itself is supplied by several different sources: lactate can be oxidized into pyruvate and is available from anaerobic glycolysis or by adipocytes in red blood cells. alanine can be transaminated into pyruvate and is produced from other amino acids released from the muscle. glycerol also serves as the precursor to an intermediate of gluconeogenesis, DHAP. the reactions of gluconeogenesis can be divided into three major sections:
conversion of pyruvate to phosphoenolpyruvate (PEP)
1. pyruvate is formed from alanine or lactate in the cytosol.
2. pyruvate diffuses into the mitochondria and is carboxylated to oxaloacetate via pyruvate carboxylase (recall that this is an anaplerotic reaction of the TCA cycle)
3. oxaloacetate is either transaminated to aspartate, or reduced to malate (using NADH as an electron source) and transported back out of the mitochondria.
4. oxaloacetate is reformed in the cytosol either by transamination of aspartate or oxidation of malate.
5. oxaloacetate is converted to phosphoenolpyruvate via phosphoenolpyruvate carboxykinase, using one GTP.
conversion of PEP to fructose 1,6 bisphosphate (reverse of glycolysis)
6. PEP is converted to 2-phosphoglycerate
7. 2-phosphoglycerate is converted to 3-phosphoglycerate
8. 3-phosphoglycerate is converted to 1,3-bisphosphoglycerate
9. 1,3-bisphosphoglycerate is converted to G3P.
10. for every two molecules of G3P that are formed, one isomerizes to DHAP
11. G3P condenses with DHAP to form fructose 1,6 bisphosphate.
conversion of fructose 1,6 bisphosphate to glucose (reverse of glycolysis)
12. fructose 1,6 bisphosphate is converted to fructose 6-phosphate via fructose 1,6 bisphosphatase.
13. fructose 6-phosphate is isomerized to glucose 6-phosphate via phosphoglucoisomerase.
14. glucose 6-phosphate is converted to glucose via glucose 6-phosphatase.
the reactions in bold are irreversible, endergonic reactions that use enzymes that are not used in the reverse glycolytic pathway. this is significant because the relative activity of these competing enzymes determines whether the reaction will proceed in the glycolytic or gluconeogenic pathway. the regulation of the first of these reactions, the conversion of oxaloacetate to PEP, is the most complex and is regulated by several enzymes in upstream reactions beginning with pyruvate production. the first, pyruvate dehydrogenase, is normally responsible for oxidizing pyruvate to acetyl CoA but is deactivated during gluconeogenesis, allowing pyruvate to instead be carboxylated into oxaloacetate. pyruvate carboxylase, the enzyme that catalyzes this reaction, is in turn activated by acetyl CoA, which is produced during the fatty acid oxidation which occurs during fasting or stress. these two reactions work in tandem during fasting conditions to ensure production of oxaloacetate from pyruvate rather than acetyl CoA.
the third enzyme which takes place in the regulation of the production of PEP is PEP carboxykinase, which converts oxaloacetate to PEP. in fasting conditions, glucagon and epinephrine stimulate cAMP to increase transcription of PEPCK enzymes, increasing the quantity of enzyme in the cell (called inducing). finally, the last enzyme involved is pyruvate kinase, which normally converts PEP back into pyruvate (recall the last step of glycolysis). high glucagon levels causes phosphorylation of the enzyme (using a mechanism involving cAMP and protein kinase A) and inactivates it-- thus allowing PEP to be used for gluconeogenesis instead of being uselessly cycled back to pyruvate. these four enzymes basically act as "switches" which first turn on the gluconeogenic pathway by allowing pyruvate to be converted to PEP.
the next places for enzymatic regulation of the gluconeogenic pathway are: the conversion of fructose 1,6-bisphosphate to fructose 6-phosphate, and the conversion of glucose 6-phosphate into glucose. both reactions are similar in that (as mentioned earlier) they use enzymes that are not the same as the reverse glycolytic reaction. in fasting conditions, the enzymes that catalyze the glycolytic reaction are deactivated, allowing the reaction to proceed in the gluconeogenic direction.
the book then talks about what happens in the liver and body tissues during, after, and long after a meal. during a high carbohydrate meal, blood glucose levels can rise from the normal 80-100 mg/dL to a high of 140 mg/dL. during this time insulin is secreted from the beta cells in the pancreas, and glucagon levels decrease. the net result is a storage of glucose in the liver as glycogen. within a few hours after eating, blood glucose and insulin levels fall back down, and glucagon levels start to rise- this initiates the process of glycogenolysis, which is the conversion of the stored glycogen in the liver back into glucose to maintain blood glucose levels. glucagon stimulates glycogenolysis and inhibits glycogen storage concurrently via production of cAMP, which stimulates protein kinase A to inactivate the enzyme related to glycogen synthesis as well as activate the glycogenolytic pathway. within 4 hours after a meal, as the liver's glycogen supply is decreasing (it takes about 30 hours to deplete the liver's supply of glycogen), gluconeogenesis is also stimulated by glucagon and falling blood sugar levels.
questions
1. what happens in the liver during fasting?
2. what is gluconeogenesis?
3. what are the three carbon sources for gluconeogenesis in humans?
4. describe the role of lactate as a gluconeogenic precursor.
5. describe the role of alanine as a gluconeogenic precursor.
6. describe the role of glycerol in gluconeogenesis.
7. describe the conversion of pyruvate to PEP.
8. what determines the path in which oxaloacetate will be converted and transported across the mitochondrial membrane?
9. describe the conversion of PEP to fructose 1,6 bisphosphate.
10. describe the conversion of fructose 1,6 bisphosphate to glucose.
11. describe the conversion of glycerol to DHAP.
12. what are other factors that can stimulate gluconeogenesis?
13. what are the three main reactions that are regulated in gluconeogenesis?
14. how does the fasting state deactivate pyruvate dehydrogenase?
15. how does the fasting state activate pyruvate carboxylase?
16. how is PEP carboxykinase regulated?
17. what is pyruvate kinase and how is it regulated?
18. describe the regulation of the reaction from fructose 1,6 bisphosphate to fructose 6-phosphate.
19. describe the regulation of the reaction from glucose 6-phosphate to glucose.
20. what is the energy consumption during gluconeogenesis and where does it happen?
21. what are normal blood glucose levels for fasting, right after a meal, 2 hours after a meal, and starvation?
22. describe the pancreas's actions after ingestion of a high glucose meal.
23. glycerol, glucagon, glycogen.
24. describe the stimulation of glycogenolysis in the liver.
25. describe what happens roughly 4 hours after a meal.
26. describe what happens during prolonged starvation.
27. how long does it take to deplete liver glycogen stores? (and therefore halt glycogenolysis)
answers
1. liver releases glucose into the blood via glycogenolysis and gluconeogenesis.
2. the process by which glucose is created in the liver from non carbohydrate sources.
3. lactate, glycerol, and amino acids- particularly alanine.
4. lactate is produced by anaerobic glycolysis through reduction of pyruvate or by adipocytes in the fed state or by red blood cells. lactate is oxidized into pyruvate, which is a precursor for gluconeogenesis.
5. alanine is produced in the muscle from other amino acids (whenever insulin is low or stress hormones are high) and from glucose. it is converted to pyruvate via alanine aminotransferase.
6. glycerol is released from adipose tissue whenever insulin levels are low or stress hormones are high. it is converted to DHAP, which is a gluconeogenetic intermediate (as well as a glycolytic one)
7. pyruvate is created from alanine or lactate in the cytosol, and then travels into the mitochondria, where it is carboxylated to oxaloacetate via pyruvate carboxylate (an anaplerotic reaction of the TCA cycle). oxaloacetate is then transaminated to aspartate or reduced to malate and transported back out into the cytosol, and reformed back into oxaloacetate (via oxidation or transamination). in the cytosol, oxaloacetate is decarboxylated by phosphoenolpyruvate carboxylkinase to form PEP.
8. the reduction of oxaloacetate into malate requires reducing equivalents; if the mitochondria has need for reducing equivalents for other reactions, it will use the other venue, the conversion to aspartate.
9. PEP is converted to fructose 1,6 bisphophate through a reversal of the glycolytic reactions. PEP is converted into 2-phosphoglycerate, to 3-phosphoglycerate, to 1,3 bisphosphoglycerate, and reduced to G3P. for every two molecules of G3P produced, one isomerizes to DHAP. G3P and DHAP condense to form fructose 1,6 bisphosphate.
10. fructose 1,6 bisphosphate has a phosphate removed by fructose 1,6bisphosphatase to form fructose 6 phosphate. fructose 6 phosphate is isomerized to glucose 6 phosphate by phosphoglucose isomerase. glucose 6 phosphate has a phosphate removed by glucose 6-phosphatase, producing glucose.
11. glycerol is converted to glycerol 3-phosphate via glycerol kinase, and then oxidized to DHAP.
12. prolonged exercise, stress, and a high protein diet.
13. OAA to PEP, fructose 1,6 bisphosphate to fructose 6 phosphate, glucose 6 phosphate to glucose. all three reactions use regulatory enzymes which are not involved in the reverse glycolytic pathway.
14. during the fasting state, fatty acids are released from adipose tissue and undergo beta oxidation, producing NADH, acetyl CoA, and ATP. the higher ATP / ADP ratio phosphorylates pyruvate dehydrogenase into the inactive form.
15. fatty acid oxidation produces acetyl CoA, which activates pyruvate carboxylase.
16. glucagon is released during fasting and EP is released during exercise/stress, both of which stimulate production of cAMP, which increases transcription of PEPCK genes.
17. pyruvate kinase is the enzyme that catalyzes the conversion of PEP back into pyruvate. when glucagon levels are high, pyruvate kinase is phosphorylated and inactive through a mechanism involving cAMP and protein kinase A.
18. this reaction occurs via the fructose 1,6 bisphosphotase enzyme, and normally would compete with the reverse reaction from glycolysis, fructose 6-phosphate to fructose 1,6 biphosphate via PFK-1. however, under conditions favoring gluconeogenesis, the enzymes that stimulate PFK-1 are inactive, allowing the reaction to head towards the production of glucose.
19. low insulin and glucose levels deactivate the enzyme for the glycolytic forward reaction and allow the glucose synthesis to occur.
20. for every mole of glucose that is produced, 6 moles of ATP and 2 moles of NADH are used. 2 moles of ATP at the conversion of pyruvate to oxaloacetate, 2 moles of ATP at the conversion of oxaloacetate to PEP, 2 moles of ATP at the conversion from 3-phosphoglycerate to 1,3 bisphosphoglycerate, and 2 moles of NADH at the reduction of 1,3 bisphospholycerate to G3P. (2 moles at each reaction because 2 molecules of pyruvate combine into one molecule of glucose)
21. fasting: 80-100mg/dL. right after a meal: up to 140mg/dL. 2 hours after a meal: back to 80-100mg/dL. starvation: not lower than 65mg/dL.
22. during a meal, the high glucose concentration in the blood stimulates the beta cells of the pancreas to increase insulin production. glucagon levels decrease in response to a high carbohydrate meal but increase in response to a high protein meal.
23. glycerol is released from adipose whenever levels of insulin are low and levels of glucagon is high-- and is converted into DHAP. glucagon is a hormone released by the alpha cells of the pancreas in response to decreasing blood glucose levels-- stimulating gluconeogenesis. glucagon also activates production of cAMP in liver cells, which activates protein kiase A, which inactivates glycogen synthase-- thus high glucagon levels inhibit glycogen production. glycogen is synthesized from glucose and stored in the liver.
24. high glucagon levels stimulate adenylate cyclate, which synthesizes cAMP. cAMP activates protein kinase A, which inactivates glycogen synthase, and activates phosphorylase kinase. phosphorylase activates phosphorylase b, which converts glycogen to glucose 1-P, which is then converted to glucose 6-P and then free glucose in the liver, which can then enter the blood.
25. in addition to supplementing blood glucose levels with glycogenolysis, gluconeogenesis is stimulated by the release of precursor material such as glycerol, alanine, and lactate from peripheral body tissues.
26. the body switches to fatty acid and ketone body oxidation and requires much less glucose.
27. ~30 hours
conversion of pyruvate to phosphoenolpyruvate (PEP)
1. pyruvate is formed from alanine or lactate in the cytosol.
2. pyruvate diffuses into the mitochondria and is carboxylated to oxaloacetate via pyruvate carboxylase (recall that this is an anaplerotic reaction of the TCA cycle)
3. oxaloacetate is either transaminated to aspartate, or reduced to malate (using NADH as an electron source) and transported back out of the mitochondria.
4. oxaloacetate is reformed in the cytosol either by transamination of aspartate or oxidation of malate.
5. oxaloacetate is converted to phosphoenolpyruvate via phosphoenolpyruvate carboxykinase, using one GTP.
conversion of PEP to fructose 1,6 bisphosphate (reverse of glycolysis)
6. PEP is converted to 2-phosphoglycerate
7. 2-phosphoglycerate is converted to 3-phosphoglycerate
8. 3-phosphoglycerate is converted to 1,3-bisphosphoglycerate
9. 1,3-bisphosphoglycerate is converted to G3P.
10. for every two molecules of G3P that are formed, one isomerizes to DHAP
11. G3P condenses with DHAP to form fructose 1,6 bisphosphate.
conversion of fructose 1,6 bisphosphate to glucose (reverse of glycolysis)
12. fructose 1,6 bisphosphate is converted to fructose 6-phosphate via fructose 1,6 bisphosphatase.
13. fructose 6-phosphate is isomerized to glucose 6-phosphate via phosphoglucoisomerase.
14. glucose 6-phosphate is converted to glucose via glucose 6-phosphatase.
the reactions in bold are irreversible, endergonic reactions that use enzymes that are not used in the reverse glycolytic pathway. this is significant because the relative activity of these competing enzymes determines whether the reaction will proceed in the glycolytic or gluconeogenic pathway. the regulation of the first of these reactions, the conversion of oxaloacetate to PEP, is the most complex and is regulated by several enzymes in upstream reactions beginning with pyruvate production. the first, pyruvate dehydrogenase, is normally responsible for oxidizing pyruvate to acetyl CoA but is deactivated during gluconeogenesis, allowing pyruvate to instead be carboxylated into oxaloacetate. pyruvate carboxylase, the enzyme that catalyzes this reaction, is in turn activated by acetyl CoA, which is produced during the fatty acid oxidation which occurs during fasting or stress. these two reactions work in tandem during fasting conditions to ensure production of oxaloacetate from pyruvate rather than acetyl CoA.
the third enzyme which takes place in the regulation of the production of PEP is PEP carboxykinase, which converts oxaloacetate to PEP. in fasting conditions, glucagon and epinephrine stimulate cAMP to increase transcription of PEPCK enzymes, increasing the quantity of enzyme in the cell (called inducing). finally, the last enzyme involved is pyruvate kinase, which normally converts PEP back into pyruvate (recall the last step of glycolysis). high glucagon levels causes phosphorylation of the enzyme (using a mechanism involving cAMP and protein kinase A) and inactivates it-- thus allowing PEP to be used for gluconeogenesis instead of being uselessly cycled back to pyruvate. these four enzymes basically act as "switches" which first turn on the gluconeogenic pathway by allowing pyruvate to be converted to PEP.
the next places for enzymatic regulation of the gluconeogenic pathway are: the conversion of fructose 1,6-bisphosphate to fructose 6-phosphate, and the conversion of glucose 6-phosphate into glucose. both reactions are similar in that (as mentioned earlier) they use enzymes that are not the same as the reverse glycolytic reaction. in fasting conditions, the enzymes that catalyze the glycolytic reaction are deactivated, allowing the reaction to proceed in the gluconeogenic direction.
the book then talks about what happens in the liver and body tissues during, after, and long after a meal. during a high carbohydrate meal, blood glucose levels can rise from the normal 80-100 mg/dL to a high of 140 mg/dL. during this time insulin is secreted from the beta cells in the pancreas, and glucagon levels decrease. the net result is a storage of glucose in the liver as glycogen. within a few hours after eating, blood glucose and insulin levels fall back down, and glucagon levels start to rise- this initiates the process of glycogenolysis, which is the conversion of the stored glycogen in the liver back into glucose to maintain blood glucose levels. glucagon stimulates glycogenolysis and inhibits glycogen storage concurrently via production of cAMP, which stimulates protein kinase A to inactivate the enzyme related to glycogen synthesis as well as activate the glycogenolytic pathway. within 4 hours after a meal, as the liver's glycogen supply is decreasing (it takes about 30 hours to deplete the liver's supply of glycogen), gluconeogenesis is also stimulated by glucagon and falling blood sugar levels.
questions
1. what happens in the liver during fasting?
2. what is gluconeogenesis?
3. what are the three carbon sources for gluconeogenesis in humans?
4. describe the role of lactate as a gluconeogenic precursor.
5. describe the role of alanine as a gluconeogenic precursor.
6. describe the role of glycerol in gluconeogenesis.
7. describe the conversion of pyruvate to PEP.
8. what determines the path in which oxaloacetate will be converted and transported across the mitochondrial membrane?
9. describe the conversion of PEP to fructose 1,6 bisphosphate.
10. describe the conversion of fructose 1,6 bisphosphate to glucose.
11. describe the conversion of glycerol to DHAP.
12. what are other factors that can stimulate gluconeogenesis?
13. what are the three main reactions that are regulated in gluconeogenesis?
14. how does the fasting state deactivate pyruvate dehydrogenase?
15. how does the fasting state activate pyruvate carboxylase?
16. how is PEP carboxykinase regulated?
17. what is pyruvate kinase and how is it regulated?
18. describe the regulation of the reaction from fructose 1,6 bisphosphate to fructose 6-phosphate.
19. describe the regulation of the reaction from glucose 6-phosphate to glucose.
20. what is the energy consumption during gluconeogenesis and where does it happen?
21. what are normal blood glucose levels for fasting, right after a meal, 2 hours after a meal, and starvation?
22. describe the pancreas's actions after ingestion of a high glucose meal.
23. glycerol, glucagon, glycogen.
24. describe the stimulation of glycogenolysis in the liver.
25. describe what happens roughly 4 hours after a meal.
26. describe what happens during prolonged starvation.
27. how long does it take to deplete liver glycogen stores? (and therefore halt glycogenolysis)
answers
1. liver releases glucose into the blood via glycogenolysis and gluconeogenesis.
2. the process by which glucose is created in the liver from non carbohydrate sources.
3. lactate, glycerol, and amino acids- particularly alanine.
4. lactate is produced by anaerobic glycolysis through reduction of pyruvate or by adipocytes in the fed state or by red blood cells. lactate is oxidized into pyruvate, which is a precursor for gluconeogenesis.
5. alanine is produced in the muscle from other amino acids (whenever insulin is low or stress hormones are high) and from glucose. it is converted to pyruvate via alanine aminotransferase.
6. glycerol is released from adipose tissue whenever insulin levels are low or stress hormones are high. it is converted to DHAP, which is a gluconeogenetic intermediate (as well as a glycolytic one)
7. pyruvate is created from alanine or lactate in the cytosol, and then travels into the mitochondria, where it is carboxylated to oxaloacetate via pyruvate carboxylate (an anaplerotic reaction of the TCA cycle). oxaloacetate is then transaminated to aspartate or reduced to malate and transported back out into the cytosol, and reformed back into oxaloacetate (via oxidation or transamination). in the cytosol, oxaloacetate is decarboxylated by phosphoenolpyruvate carboxylkinase to form PEP.
8. the reduction of oxaloacetate into malate requires reducing equivalents; if the mitochondria has need for reducing equivalents for other reactions, it will use the other venue, the conversion to aspartate.
9. PEP is converted to fructose 1,6 bisphophate through a reversal of the glycolytic reactions. PEP is converted into 2-phosphoglycerate, to 3-phosphoglycerate, to 1,3 bisphosphoglycerate, and reduced to G3P. for every two molecules of G3P produced, one isomerizes to DHAP. G3P and DHAP condense to form fructose 1,6 bisphosphate.
10. fructose 1,6 bisphosphate has a phosphate removed by fructose 1,6bisphosphatase to form fructose 6 phosphate. fructose 6 phosphate is isomerized to glucose 6 phosphate by phosphoglucose isomerase. glucose 6 phosphate has a phosphate removed by glucose 6-phosphatase, producing glucose.
11. glycerol is converted to glycerol 3-phosphate via glycerol kinase, and then oxidized to DHAP.
12. prolonged exercise, stress, and a high protein diet.
13. OAA to PEP, fructose 1,6 bisphosphate to fructose 6 phosphate, glucose 6 phosphate to glucose. all three reactions use regulatory enzymes which are not involved in the reverse glycolytic pathway.
14. during the fasting state, fatty acids are released from adipose tissue and undergo beta oxidation, producing NADH, acetyl CoA, and ATP. the higher ATP / ADP ratio phosphorylates pyruvate dehydrogenase into the inactive form.
15. fatty acid oxidation produces acetyl CoA, which activates pyruvate carboxylase.
16. glucagon is released during fasting and EP is released during exercise/stress, both of which stimulate production of cAMP, which increases transcription of PEPCK genes.
17. pyruvate kinase is the enzyme that catalyzes the conversion of PEP back into pyruvate. when glucagon levels are high, pyruvate kinase is phosphorylated and inactive through a mechanism involving cAMP and protein kinase A.
18. this reaction occurs via the fructose 1,6 bisphosphotase enzyme, and normally would compete with the reverse reaction from glycolysis, fructose 6-phosphate to fructose 1,6 biphosphate via PFK-1. however, under conditions favoring gluconeogenesis, the enzymes that stimulate PFK-1 are inactive, allowing the reaction to head towards the production of glucose.
19. low insulin and glucose levels deactivate the enzyme for the glycolytic forward reaction and allow the glucose synthesis to occur.
20. for every mole of glucose that is produced, 6 moles of ATP and 2 moles of NADH are used. 2 moles of ATP at the conversion of pyruvate to oxaloacetate, 2 moles of ATP at the conversion of oxaloacetate to PEP, 2 moles of ATP at the conversion from 3-phosphoglycerate to 1,3 bisphosphoglycerate, and 2 moles of NADH at the reduction of 1,3 bisphospholycerate to G3P. (2 moles at each reaction because 2 molecules of pyruvate combine into one molecule of glucose)
21. fasting: 80-100mg/dL. right after a meal: up to 140mg/dL. 2 hours after a meal: back to 80-100mg/dL. starvation: not lower than 65mg/dL.
22. during a meal, the high glucose concentration in the blood stimulates the beta cells of the pancreas to increase insulin production. glucagon levels decrease in response to a high carbohydrate meal but increase in response to a high protein meal.
23. glycerol is released from adipose whenever levels of insulin are low and levels of glucagon is high-- and is converted into DHAP. glucagon is a hormone released by the alpha cells of the pancreas in response to decreasing blood glucose levels-- stimulating gluconeogenesis. glucagon also activates production of cAMP in liver cells, which activates protein kiase A, which inactivates glycogen synthase-- thus high glucagon levels inhibit glycogen production. glycogen is synthesized from glucose and stored in the liver.
24. high glucagon levels stimulate adenylate cyclate, which synthesizes cAMP. cAMP activates protein kinase A, which inactivates glycogen synthase, and activates phosphorylase kinase. phosphorylase activates phosphorylase b, which converts glycogen to glucose 1-P, which is then converted to glucose 6-P and then free glucose in the liver, which can then enter the blood.
25. in addition to supplementing blood glucose levels with glycogenolysis, gluconeogenesis is stimulated by the release of precursor material such as glycerol, alanine, and lactate from peripheral body tissues.
26. the body switches to fatty acid and ketone body oxidation and requires much less glucose.
27. ~30 hours
Saturday, November 29, 2008
histology: digestive system
this lecture provided a histological perspective on the different sections of the digestive system, focusing on tissue and cell types. the digestive system is introduced as one long tube which starts in the pharynx, becomes the esophagus, stomach, small intestine, large intestine, then rectum. within all of these sections, there are generally four different layers: the mucosa is the innermost layer and contains the epithelium (either stratified squamous or simple columnar), a loose or reticular CT lamina propria, and a layer of muscle named the muscularis mucosa. beneath this is the submucosa, which contains blood vessels and nerves (and in the small intestine, the meissner's plexus). beneath this is the muscularis externa, which is generally composed of an inner circular layer, middle plexus of ganglia ("myenteric" plexus), and outer longitudinal layer. finally, on the outside of the tube is the serosa (or adventitia in some places, such as the esophagus above the diaphragm), which is made up of connective tissue and mesothelium. all of the sections of the digestive system are made up of variants of these four layers depending on location and function.
the first section, the esophagus, is unique in that its epithelia is made up of non-keratinized stratified squamous (presumably to deal with the abrasion of food coming in, and non-keratinized because waterproofing isn't an issue), which is thrown into esophageal glands that begin the lubricating process. the muscularis layer is also unique in that the top part of the esophagus is mainly skeletal muscle, gradually blends with smooth muscle in the middle, and by the bottom is mainly smooth muscle. the esophagus ends in the esophageal-cardiac junction, where the epithelial layer transitions from the non-keratinized stratified of the esophagus to the simple columnar of the stomach.
the stomach has four sections, from top to bottom: the cardiac, fundic, body, pyloric regions. the mucosa of the stomach is thrown into gastric glands, which contain specialized secretory cells which aid in digestion: surface mucous cells and mucous neck cells secrete mucous near the tops and bottoms of the glands, respectively. parietal cells secrete HCl near the tops of the glands, and chief cells secrete pepsinogen near the base of the glands. the muscularis of the stomach is also unique in that it has an inner oblique layer, middle circular, and outer longitudinal layer. the fundus is the most representative region of the stomach, and the other three regions are variations on this region. for example, the epithelia in both the cardiac and pyloric regions contain only mucous cells, and the muscularis layers are tightened into the cardiac and pyloric sphincters on either end.
after the stomach comes the small intestine, which is divided into three regions, the duodenum, jejunum (the most representative region), and ileum. the intestinal mucosa is unique in that it is folded into large intestinal glands called "Krypts of Lieberkuhn", covered with columnar absorptive/secretory cells called enterocytes, with goblet cells scattered throughout. also present in the epithelium are enteroendocrine cells, which secrete hormone like substances, as well as Paneth cells, which secrete lysozymes to regulate the bacterial flora in the gut. the lamina propria of the intestine is well vascularized with type 2 fenestrated capillaries, with occasional lymph nodes called Peyer's Patches. additionally, there is often a "central lacteal" inside the villi, which is a large lymph vessel that aids in absorption of larger molecules. the muscularis of the small intestine generally contains an inner circular layer, followed by a nerve "net" called the myenteric plexus, followed by an outer longitudinal muscle layer.
the large intestine is similar to the small intestine, the main differences being: more goblet cells, lymph rich, but no microvilli, paneth cells, or enteroendocrine cells. it has two main sections, the colon and the rectum, and at the "end of the line", the rectal-anal junction, there are four notable changes: the transition from the simple columnar absorptive cells of the small intestine to the non-keratinized stratified squamous of the rectum, the patchy muscularis mucosa, the huge blood vessels in the submucosa, and the presence of skeletal muscle in the muscularis externa. (notice how this is similar to the esophagus)
the role of the pancreas and liver in digestion is then looked at: the pancreas is a mostly exocrine gland which secretes from compound acinar glands a variety of enzymes-- carboxypeptidase, chymotrypsinogen, trypsinogen for digestion of proteins, amylase for digestion of carbohydrates, lipase for digestion of lipids, and bicarbonate to neutralize the acidity from gastric digestion. it also functions as an endocrine gland with its "Islets of Langerhans", which contain alpha, beta, and delta cells which release glucagon, insulin, and somatostatin, respectively. the liver also functions as both an endocrine / exocrine gland which aids in digestion by releasing bile for digestion of fats (exocrine) and filtering and adding to blood (endocrine). the liver has many functions, such as processing of glycogen, fetal blood cell production, production of blood clotting factors, and detoxification of the blood.
the basic cell type of the liver is called the hepatocyte, and they are arranged in roughly hexagonally shaped functional units called "lobules". on the borders of the lobules, on roughly every other corner of the hexagon, are "portal triads" which contain hepatic portal veins (which supply oxygen poor, nutrient rich blood to the liver from the intestine), hepatic arteries (supplying fresh blood to the liver), and bile ducts. in the center of the lobules are "central veins" which carry away deoxygenated blood. the last aspect of the liver that's looked at is the liver acinus theory, which states that blood flows from the portal triad laterally to the adjacent central veins, forming a diamond shaped functional unit overlayed on two lobules.
questions
1. what are the four primary layers in the entire digestive system?
2. what is the mucosa composed of?
3. what is in the submucosa?
4. what is the muscularis composed of?
5. what is the serosa composed of?
esophagus
6. describe the mucosa of the esophagus.
7. describe the muscularis of the esophagus.
8. describe the outer wall of the esophagus.
9. what is the esophageal-cardiac junction?
stomach- surface mucosa, mucosa neck, chief, parietal,
10. what are the four parts to the stomach?
11. describe the mucosa of the stomach.
12. what are some other cells that function in the mucosa of the stomach?
13. describe the muscularis externa of the stomach.
14. how does the cardiac region of the stomach differ from the body region?
15. how does the pyloric region of the stomach differ from the body region?
small intestine- lieberkuhn, enterocytes, paneth, meissner's, peyer's patch, brunner's
16. what are the three parts to the small intestine?
17. describe the mucosa of the small intestine.
18. what is unique about the surface of the mucosa of the small intestine?
19. what are the crypts of Lieberkuhn?
20. which digestive enzymes are secreted by the pancreas to aid in digestion in the small intestine?
21. what is secreted from the liver to help in digestion in the small intestine?
22. what are some of the cells in the mucosal epithelium of the small intestine?
23. describe the lamina propria of the small intestine.
24. describe the submucosa of the small intestine.
25. describe the myenteric plexus and what role it plays.
26. the serosa of the small intestine is the...
27. what are brunner's glands and what do they do? where are they found?
28. what are some distinguishing characteristics of the ileum?
large intestine-
29. describe the mucosa of the large intestine.
30. what are the four characteristics of the rectal-anal junction?
accessory glands- salivary glands, pancreas, liver,
31. what are the three types of salivary glands and what do they secrete?
32. describe the exocrine function of the pancreas.
33. describe the endocrine function of the pancreas.
34. name five major functions of the liver.
35. describe how the liver operates both as an exocrine and endocrine gland.
36. what is the hepatic portal vein?
37. what is the hepatic artery?
38. what type of capillaries are in the liver?
39. what is the basic cell type in the liver and what are they assembled into?
40. describe the architecture of the lobule.
41. what is the liver acinus theory? why is it the most likely scheme of blood flow in the liver?
answers
1. mucosa, submucosa, muscularis, serosa
2. epithelium (mostly simple columnar), lamina propria, muscularis mucosa
3. connective tissue with blood vessels and nerves, sometimes a submucosal plexus (meissner's)
4. inner circular layer of smooth muscle, middle plexus of ganglia (myenteric/auerbach's), outer longitudinal smooth muscle
5. CT, mesothelium
6. non-keratinzed stratified squamous epithelium, has esophageal glands for lubrication.
7. upper 1/3 made of skeletal muscle, middle 1/3 mix of skeletal and smooth muscle, lower 1/3 smooth muscle.
8. has adventitia, serosa seen only after tube penetrates diaphragm.
9. the end of the esophagus, an abrupt change from stratified squamous to simple columnar epithelium.
10. cardiac, fundus, body, pylorus
11. simple columnar epithelium with gastric glands for digestion, lamina propria which is richly vascularized, loose / reticular CT.
12. surface mucous cells, mucous neck cells secrete mucous on surface and at base of gastric pits. parietal cells secrete HCl at top of gland proper. chief cells secrete pepsinogen near base of gland.
13. inner oblique, middle circular, outer longitudinal. thickened at either end of stomach to form cardiac and pyloric sphincter.
14. cardiac region glands only have mucous cells, and there is an abrupt change from the esophagus.
15. pyloric region glands only have mucous cells. glands branch more and have deeper pits.
16. duodenum, jejunum, ileum.
17. simple columnar epithelium thrown into glandular tubes called intestinal glands (crypts of Lieberkuhn) and projections called villi.
18. they have a striated border formed from microvilli.
19. intestinal glands that both secrete and absorb.
20. trypsinogen, chymotrypsinogen, carboxypeptidase (for protein), amylase (for carbohydrates), lipase (for lipids)
21. bile salts (for lipids)
22. primarily composed of enterocytes which are columnar absorptive cells with microvilli, with mucous secreting goblet cells throughout, as well as enteroendocrine cells which are at the base of the glands and secrete hormone like substances, and paneth cells which secretes lysozyme to control bacterial flora.
23. well vascularized, type II capillaries, may have a central lacteal for absorption of larger molecules, may have lymph nodules called Peyer's patches.
24. may have a meissner's plexus, which assists in regulating secretion and blood flow.
25. a nerve net in the muscularis layer which helps coordinate peristaltic contractions of muscularis externa.
26. visceral peritoneum.
27. in the submucosa of the duodenum, secretes alkaline-mucoid material and urogastrone.
28. greatest amount of "GALT", Peyer's patches, fewer villi and more goblet cells.
29. simple columnar epithelia with intestinal glands but no villi. abundant goblet cells and lymph rich lamina propria, but no entero-endocrine or paneth cells.
30. epithelial transition from simple columnar to non-keratinized stratified squamous, patchy muscularis mucosa, huge blood vessels in submucosa, skeletal muscle in muscularis externa. transition, patchy, blood, skeletal.
31. parotid secretes mainly serous, submandibular secretes a mixture of mucous and serous, and sublingual secretes mostly mucous.
32. the pancreas' function is mainly to serve as an exocrine gland which secrete digestive enzymes (see question 20), composed of compound acinar glands. it also secretes alkaline bicarbonate in order to neutralize the acidity from gastric digestion.
33. 2% of the pancreas is used for endocrine function, in the form of "islets of langerhans" which are clumped glands which consist of alpha, beta, and delta cells which secrete glucagon, insulin, and somatostatin, respectively.
34. fetal hematopoesis (before shifting to bone marrow), glucagon processing, plasma protein production (such as clotting factors), bile production, and detoxification. blood, glucagon, clotting, bile, detox. detox clotting blood into a bile of glucagon.
35. exocrine because it dumps bile into the intestine, endocrine because it filters blood and adds to it.
36. the vein that brings oxygen poor but potentially nutrient rich blood into the liver from the GI tract.
37. the artery that brings fresh blood to the liver itself.
38. type three discontinuous.
39. basic cell type is the hepatocyte and they are arranged into lobules.
40. hexagonal shaped cell with a large central vein in the middle and a trio of vessels at every other corner of the border of the cell, called the portal area: containing hepatic portal vein (question 36), hepatic artery (question 37), and bile duct.
41. the liver acinus theory of blood flow says that blood flows laterally from the portal areas to the adjacent central vein (creating a diamond shaped functional unit overlayed on top of two lobules). this theory is backed up by the patterns of degradation during liver poisoning.
the first section, the esophagus, is unique in that its epithelia is made up of non-keratinized stratified squamous (presumably to deal with the abrasion of food coming in, and non-keratinized because waterproofing isn't an issue), which is thrown into esophageal glands that begin the lubricating process. the muscularis layer is also unique in that the top part of the esophagus is mainly skeletal muscle, gradually blends with smooth muscle in the middle, and by the bottom is mainly smooth muscle. the esophagus ends in the esophageal-cardiac junction, where the epithelial layer transitions from the non-keratinized stratified of the esophagus to the simple columnar of the stomach.
the stomach has four sections, from top to bottom: the cardiac, fundic, body, pyloric regions. the mucosa of the stomach is thrown into gastric glands, which contain specialized secretory cells which aid in digestion: surface mucous cells and mucous neck cells secrete mucous near the tops and bottoms of the glands, respectively. parietal cells secrete HCl near the tops of the glands, and chief cells secrete pepsinogen near the base of the glands. the muscularis of the stomach is also unique in that it has an inner oblique layer, middle circular, and outer longitudinal layer. the fundus is the most representative region of the stomach, and the other three regions are variations on this region. for example, the epithelia in both the cardiac and pyloric regions contain only mucous cells, and the muscularis layers are tightened into the cardiac and pyloric sphincters on either end.
after the stomach comes the small intestine, which is divided into three regions, the duodenum, jejunum (the most representative region), and ileum. the intestinal mucosa is unique in that it is folded into large intestinal glands called "Krypts of Lieberkuhn", covered with columnar absorptive/secretory cells called enterocytes, with goblet cells scattered throughout. also present in the epithelium are enteroendocrine cells, which secrete hormone like substances, as well as Paneth cells, which secrete lysozymes to regulate the bacterial flora in the gut. the lamina propria of the intestine is well vascularized with type 2 fenestrated capillaries, with occasional lymph nodes called Peyer's Patches. additionally, there is often a "central lacteal" inside the villi, which is a large lymph vessel that aids in absorption of larger molecules. the muscularis of the small intestine generally contains an inner circular layer, followed by a nerve "net" called the myenteric plexus, followed by an outer longitudinal muscle layer.
the large intestine is similar to the small intestine, the main differences being: more goblet cells, lymph rich, but no microvilli, paneth cells, or enteroendocrine cells. it has two main sections, the colon and the rectum, and at the "end of the line", the rectal-anal junction, there are four notable changes: the transition from the simple columnar absorptive cells of the small intestine to the non-keratinized stratified squamous of the rectum, the patchy muscularis mucosa, the huge blood vessels in the submucosa, and the presence of skeletal muscle in the muscularis externa. (notice how this is similar to the esophagus)
the role of the pancreas and liver in digestion is then looked at: the pancreas is a mostly exocrine gland which secretes from compound acinar glands a variety of enzymes-- carboxypeptidase, chymotrypsinogen, trypsinogen for digestion of proteins, amylase for digestion of carbohydrates, lipase for digestion of lipids, and bicarbonate to neutralize the acidity from gastric digestion. it also functions as an endocrine gland with its "Islets of Langerhans", which contain alpha, beta, and delta cells which release glucagon, insulin, and somatostatin, respectively. the liver also functions as both an endocrine / exocrine gland which aids in digestion by releasing bile for digestion of fats (exocrine) and filtering and adding to blood (endocrine). the liver has many functions, such as processing of glycogen, fetal blood cell production, production of blood clotting factors, and detoxification of the blood.
the basic cell type of the liver is called the hepatocyte, and they are arranged in roughly hexagonally shaped functional units called "lobules". on the borders of the lobules, on roughly every other corner of the hexagon, are "portal triads" which contain hepatic portal veins (which supply oxygen poor, nutrient rich blood to the liver from the intestine), hepatic arteries (supplying fresh blood to the liver), and bile ducts. in the center of the lobules are "central veins" which carry away deoxygenated blood. the last aspect of the liver that's looked at is the liver acinus theory, which states that blood flows from the portal triad laterally to the adjacent central veins, forming a diamond shaped functional unit overlayed on two lobules.
questions
1. what are the four primary layers in the entire digestive system?
2. what is the mucosa composed of?
3. what is in the submucosa?
4. what is the muscularis composed of?
5. what is the serosa composed of?
esophagus
6. describe the mucosa of the esophagus.
7. describe the muscularis of the esophagus.
8. describe the outer wall of the esophagus.
9. what is the esophageal-cardiac junction?
stomach- surface mucosa, mucosa neck, chief, parietal,
10. what are the four parts to the stomach?
11. describe the mucosa of the stomach.
12. what are some other cells that function in the mucosa of the stomach?
13. describe the muscularis externa of the stomach.
14. how does the cardiac region of the stomach differ from the body region?
15. how does the pyloric region of the stomach differ from the body region?
small intestine- lieberkuhn, enterocytes, paneth, meissner's, peyer's patch, brunner's
16. what are the three parts to the small intestine?
17. describe the mucosa of the small intestine.
18. what is unique about the surface of the mucosa of the small intestine?
19. what are the crypts of Lieberkuhn?
20. which digestive enzymes are secreted by the pancreas to aid in digestion in the small intestine?
21. what is secreted from the liver to help in digestion in the small intestine?
22. what are some of the cells in the mucosal epithelium of the small intestine?
23. describe the lamina propria of the small intestine.
24. describe the submucosa of the small intestine.
25. describe the myenteric plexus and what role it plays.
26. the serosa of the small intestine is the...
27. what are brunner's glands and what do they do? where are they found?
28. what are some distinguishing characteristics of the ileum?
large intestine-
29. describe the mucosa of the large intestine.
30. what are the four characteristics of the rectal-anal junction?
accessory glands- salivary glands, pancreas, liver,
31. what are the three types of salivary glands and what do they secrete?
32. describe the exocrine function of the pancreas.
33. describe the endocrine function of the pancreas.
34. name five major functions of the liver.
35. describe how the liver operates both as an exocrine and endocrine gland.
36. what is the hepatic portal vein?
37. what is the hepatic artery?
38. what type of capillaries are in the liver?
39. what is the basic cell type in the liver and what are they assembled into?
40. describe the architecture of the lobule.
41. what is the liver acinus theory? why is it the most likely scheme of blood flow in the liver?
answers
1. mucosa, submucosa, muscularis, serosa
2. epithelium (mostly simple columnar), lamina propria, muscularis mucosa
3. connective tissue with blood vessels and nerves, sometimes a submucosal plexus (meissner's)
4. inner circular layer of smooth muscle, middle plexus of ganglia (myenteric/auerbach's), outer longitudinal smooth muscle
5. CT, mesothelium
6. non-keratinzed stratified squamous epithelium, has esophageal glands for lubrication.
7. upper 1/3 made of skeletal muscle, middle 1/3 mix of skeletal and smooth muscle, lower 1/3 smooth muscle.
8. has adventitia, serosa seen only after tube penetrates diaphragm.
9. the end of the esophagus, an abrupt change from stratified squamous to simple columnar epithelium.
10. cardiac, fundus, body, pylorus
11. simple columnar epithelium with gastric glands for digestion, lamina propria which is richly vascularized, loose / reticular CT.
12. surface mucous cells, mucous neck cells secrete mucous on surface and at base of gastric pits. parietal cells secrete HCl at top of gland proper. chief cells secrete pepsinogen near base of gland.
13. inner oblique, middle circular, outer longitudinal. thickened at either end of stomach to form cardiac and pyloric sphincter.
14. cardiac region glands only have mucous cells, and there is an abrupt change from the esophagus.
15. pyloric region glands only have mucous cells. glands branch more and have deeper pits.
16. duodenum, jejunum, ileum.
17. simple columnar epithelium thrown into glandular tubes called intestinal glands (crypts of Lieberkuhn) and projections called villi.
18. they have a striated border formed from microvilli.
19. intestinal glands that both secrete and absorb.
20. trypsinogen, chymotrypsinogen, carboxypeptidase (for protein), amylase (for carbohydrates), lipase (for lipids)
21. bile salts (for lipids)
22. primarily composed of enterocytes which are columnar absorptive cells with microvilli, with mucous secreting goblet cells throughout, as well as enteroendocrine cells which are at the base of the glands and secrete hormone like substances, and paneth cells which secretes lysozyme to control bacterial flora.
23. well vascularized, type II capillaries, may have a central lacteal for absorption of larger molecules, may have lymph nodules called Peyer's patches.
24. may have a meissner's plexus, which assists in regulating secretion and blood flow.
25. a nerve net in the muscularis layer which helps coordinate peristaltic contractions of muscularis externa.
26. visceral peritoneum.
27. in the submucosa of the duodenum, secretes alkaline-mucoid material and urogastrone.
28. greatest amount of "GALT", Peyer's patches, fewer villi and more goblet cells.
29. simple columnar epithelia with intestinal glands but no villi. abundant goblet cells and lymph rich lamina propria, but no entero-endocrine or paneth cells.
30. epithelial transition from simple columnar to non-keratinized stratified squamous, patchy muscularis mucosa, huge blood vessels in submucosa, skeletal muscle in muscularis externa. transition, patchy, blood, skeletal.
31. parotid secretes mainly serous, submandibular secretes a mixture of mucous and serous, and sublingual secretes mostly mucous.
32. the pancreas' function is mainly to serve as an exocrine gland which secrete digestive enzymes (see question 20), composed of compound acinar glands. it also secretes alkaline bicarbonate in order to neutralize the acidity from gastric digestion.
33. 2% of the pancreas is used for endocrine function, in the form of "islets of langerhans" which are clumped glands which consist of alpha, beta, and delta cells which secrete glucagon, insulin, and somatostatin, respectively.
34. fetal hematopoesis (before shifting to bone marrow), glucagon processing, plasma protein production (such as clotting factors), bile production, and detoxification. blood, glucagon, clotting, bile, detox. detox clotting blood into a bile of glucagon.
35. exocrine because it dumps bile into the intestine, endocrine because it filters blood and adds to it.
36. the vein that brings oxygen poor but potentially nutrient rich blood into the liver from the GI tract.
37. the artery that brings fresh blood to the liver itself.
38. type three discontinuous.
39. basic cell type is the hepatocyte and they are arranged into lobules.
40. hexagonal shaped cell with a large central vein in the middle and a trio of vessels at every other corner of the border of the cell, called the portal area: containing hepatic portal vein (question 36), hepatic artery (question 37), and bile duct.
41. the liver acinus theory of blood flow says that blood flows laterally from the portal areas to the adjacent central vein (creating a diamond shaped functional unit overlayed on top of two lobules). this theory is backed up by the patterns of degradation during liver poisoning.
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