organ systems: oral and pharynx

this lecture talked about various aspects of the pharynx, including muscles, tonsils, and innervation. the first section covered structures of the mouth and teeth: philtrum is the median shallow groove in the upper lip, labia frenulum is the fold of mucosal membrane that attaches the lip to the gums, and lingual frenulum is the fold that connects the tongue to the base of the mouth. there are 32 teeth, 8 in each half of each jaw: 2 incisors, 1 canine, 2 pre-molar, and 3 molars. the crowns of the teeth are made up of dentine and enamel, and the pulp cavity inside contains nerves and blood vessels, which travel through the tooth in root canals and exit via the apical foramen. teeth are anchored to bone via the cementum and peridontium layers.

there are intrinsic muscles inside the tongue and extrinsic muscles of the tongue that attach to various structures in the pharynx and move the tongue in different directions. this includes the genioglossus, which attaches to the mental spine of the mandible and protrudes and depresses the tongue, the hyoglossus, which attaches to the hyoid bone and depresses the tongue, the styloglossus, which attaches to the styloid process of the mandible and retracts the tongue, and the palatoglossus, which attaches to the soft palate and raises the tongue. the first three tongue muscles are innervated by the hypoglossal nerve (CNXII), and the palatoglossus is innervated by the vagal nerve.

the tongue's sensory innervation can be divided into two aspects: somatosensory innervation delivers pain, touch, heat sensation from the filiform papillae of the tongue, while viscerosensory information delivers the taste information from the chemoreceptors from the valate and fungiform papillae on the tongue. on the top 1/3 of the tongue, both somatosensory and viscerosensory innervation is provided by the glossopharyngeal nerve (CNIX) while in the bottom 2/3 of the tongue, viscerosensory innervation is provided by the facial nerve (CNVII) and somatosensory by the lingual nerve (V3).

the next topic in the lecture was the pharyngeal and palatine muscles. there are several pharyngeal constrictor muscles which constrict the pharynx, all originate from the posterior pharyngeal raphe, and are all innervated by the vagus nerve. the superior constrictor attaches to the buccinator by way of the pteromandibular raphe, the middle constrictor attaches to the hyoid, and the inferior constrictor attaches to the cricoid and thyroid cartilage. the palatine muscles include the palatopharyngeus, which attaches the soft palate to the back of the throat and serves to lower the soft palate and the palatoglossus, which was covered above. the tensor veli palatini (innervated by CN V3), which originates on the base of the skull, hooks around the hamulus and tautens the palate while the levator veli palatini (innervated by the vagus nerve) lifts the palate.

tonsils are masses of lymphoid tissue which are present in 4 main places in the pharynx: the pharyngeal tonsils in the upper nasopharynx, the tubular tonsils near that auditory tube, the lingual tonsils on the posterior tongue, and the palatine tonsils, which are between the palatoglossus and the palatopharyngeus. lymph from these nodes ultimately drains into the deep cervical lymph nodes and into the venous system.

questions
lips and tongue...
1. what is the philtrum?
2. what is the labia frenulum?
3. what is the lingual frenulum?
4. what are sublingual veins used for?

teeth...
5. what are the crowns of teeth made up of?
6. what attaches the root of the teeth to the bone?
7. what is the pulp cavity made up of?
8. how many teeth are there? what are the different types?
9. which nerves innervates the teeth?

origins, insertions, actions, innervations:
10. genioglossus
11. hyoglossus
12. styloglossus
13. palatoglossus

tongue innervation...
14. which tongue muscles does the hypoglossal nerve innervate?
15. what are the two categories of sensory innervation of the tongue?
16. which nerves provide somatosensory and viscerosensory innervation to the lower 2/3 of the tongue?
17. which nerves provide somatosensory and viscerosensory innervation to the upper 1/3 of the tongue?
18. which nerves provide somatosensory and viscerosensory innervation to the palate and epiglottis?
19. what is the difference between the filiform, fungiform, and vallate papillae?

pharyngeal muscles...
20. where do the pharyngeal constrictor muscles all originate?
21. what are the pharyngeal constrictor muscles innervated by?
22. where does the superior constrictor insert?
23. where does the middle constrictor insert?
24. where does the inferior constrictor insert?

palate muscles...
25. how does the soft palate help regulate the passage of air and food?
26. how does the epiglottis help regulate the passage of air and food?
27. tensor veli palatini...
28. levator veli palatini...
29. palatopharyngeus...
30. salpingopharyngeus...
31. snoring is associated with...
32. palatopharyngeus and palatoglossus forms a ... space which contains the ...

tonsils...
33. what is waldeyer's ring?
34. what is unique about the nasopharyngeal tonsils?
35. where is the tubal tonsil located?
36. where is the palatine tonsil located?
37. where is the lingual tonsil located?

nerves and lymph nodes...
38. which nerve innervates the upper section of the oral and nasal cavities?
39. what part of the pharynx does the glossopharygeal nerve innervate?
40. what other sensations or reflexes in the pharynx does the glossopharyngeal nerve mediate?
41. which nerve innervates the lower pharynx and larynx?
42. superficial lymph nodes all drain into...

answers
1. the median shallow groove in the upper lip.
2. folds of mucous membrane that connects the lips to the gingiva.
3. folds of mucous membrane that connects tongue to the base of the mouth.
4. ingestion of medicine directly into the blood.

5. enamel and dentine.
6. cementum and peridontial membrane.
7. a root canal that exits through the apical foramen. also contains nerves and blood vessels.
8. 32 total; 8 in each half of each jaw. 2 incisors, 1 canine, 2 premolar, 3 molar.
9. upper teeth: superior alveolar (V2). lower teeth: inferior alveolar (V3).

10. O: mental spine of the mandible, I: body of tongue, N: hypoglossal (CNXII) A: depress and protrude tongue.
11. O: hyoid bone, I: body of tongue, N: hypoglossal nerve, A: depress tongue.
12. O: styloid process of mandible, I:body of tongue, N: hypoglossal nerve, A: retract tongue.
13. O: soft palate, I: body of tongue, N: vagal nerve, A: elevate tongue.

14. the extrinsic muscles of the tongue (except the palatoglossus) and the intrinsic muscles of the tongue.
15. somatosensory includes tactile, pain, temperature sensation and viscerosensory is the taste sensation.
16. SS: lingual nerve (V3), VS: facial nerve (VII)
17. glossopharyngeal (IX)
18. vagus (X)
19. filiform is pain, temperature, touch receptor; valate and fungiform are taste receptors.

20. the posterior pharyngeal raphe.
21. vagus nerve
22. buccinator via the pteromandibular raphe.
23. hyoid bone
24. thyroid and cricoid cartilage.

25. during breathing it lowers down against the tongue and during eating it raises against the pharyngeal wall.
26. ascends against the tongue during breathing and folds down over larynx during eating.
27. O: pterygoid plates, I: palatine aponeurosis, N: V3, A: tauten palate, open auditory tube.
28. O: base of skull I: pterygoid processes, N: vagus A: raise soft palate and open auditory tubes.
29. O: thyroid cartilage, I: soft palate, N: vagus, A: depress soft palate
30. O: auditory tube, I: pharynx, N: vagus, A: open auditory tubes.
31. obstructions in the soft palate region.
32. triangular space which contains the palatine tonsil.

33. the ring of lymphoid tissue that contains: pharyngeal, tubal, palatine, lingual tonsils.
34. they are the uppermost part of the nasopharynx and can commonly become inflamed (enlarged adenoids) and block the passage of air.
35. near the auditory tube.
36. between the "pillars of fauces".
37. on the posterior surface of the tongue.
38. trigeminal: V2,V3
39. upper pharynx, auditory tube, tonsils
40. gag reflex, sore throat pain.
41. vagus
42. deep cervical lymph nodes.

organ systems: glucose regulation

this lecture focused on glucose metabolism: specifically, the interplay of insulin and glucagon secretion and their effect of glucose metabolism and storage in different organs and tissues. the pancreatic islets of langerhans secrete glucagon from alpha cells, insulin from beta cells, and somatostatin from delta cells. glucagon is secreted in response to low blood sugar and has a variety of effects which ultimately serve to raise blood glucose levels. in the liver, glycogenolysis is initiated, freeing glucose units from storage (see the biochem chapter on glycogen for more detail), gluconeogenesis creates glucose from non-carbon precursors such as amino acids. additionally, triacylglyceride stores are converted into fatty acids, which can be cleaved into ketone bodies, which are used as an alternative fuel source. glucagon is released in response to hypoglycemic (low blood sugar) conditions. other mechanisms are in place to raise blood sugar: sympathetic stimulation, cortisol, growth hormone. the symptoms from severe hypoglycemia are caused by these mechanisms; hunger by the hypothalamus and anxiety/tremors/sweating by sympathetic stimulation.

on the other hand, insulin is released in hyperglycemic conditions (high blood sugar) and facilitates uptake of glucose into cells. it accomplishes this by binding to receptors that translocate glucose transport proteins to surface of cell membranes, thereby allowing glucose to enter. there are 5 categories of glucose transport proteins, with different affinities for glucose and found in different locations of the body (see the carb digestion biochem chapter for some more physiology of the GLUT transporters): GLUT1 are found everywhere in the body and also present in placenta. GLUT2 transporters are in the pancreas, liver, kidney, and intestine. GLUT3 transporters are everywhere in the body. GLUT4 transporters are in muscle and adipose tissue and are the only insulin dependent glucose transporters. GLUT5 transporters are in the jejunum.

insulin has a variety of actions on organs and tissues; in the liver it initiates glycogen storage, fatty acid synthesis and subsequent triacylglyceride synthesis. in adipose tissue it stimulates uptake of glucose, triacylglyceride synthesis, and triacylglyceride release (through VLDL's). in muscle it stimulates uptake of glucose and amino acids and promotes glycogen storage from the excess glucose. insulin release is stimulated by a variety of factors- primarily high blood glucose levels, but also via parasympathetic stimulation, amino acids, growth hormone, and various GI hormones. insulin release is inhibited by catecholamines, somatostatin, and glucagon. note: glucagon and insulin reciprocally regulate each other- the release of one inhibits the release of the other. in addition, the release of somatostatin inhibits the release of both insulin and glucagon- preventing "rapid nutrient exhaustion".

diabetes type I is caused by an autoimmune destruction of pancreatic beta cells, resulting in low insulin levels and therefore low glucose metabolism and therefore a shift to ketone body metabolism. this also results in increased glucose levels in the urine, which can cause polyuria (excess urine volume), polydipsia (excess thirst), and polyphagia (excess hunger). type II diabetes is a resistance to insulin that is associated with high visceral fat deposits with high lipolytic activity (releasing fatty acids into the bloodstream) that are resistant to the anti-lipolytic properties of insulin. this can be induced by high free fatty acid, cortisol, or testesterone levels.

questions
glucagon...
1. what are the three types of cells in the pancreatic islets of langerhans and what do they secrete?
2. describe glucagon's effect on the liver.
3. what are the specific processes that occur that release glucose and ketones from the liver?
4. what is glucagon release from alpha cells stimulated by?
5. what is glucagon release from alpha cells inhibited by?
6. how does somatostatin "prevent rapid nutrient exhaustion"?
7. glucagon corrects...
8. what are the other ways that the body corrects for hypoglycemia?
9. what are the symptoms of severe hypoglycemia and what are they caused by?
10. what is reactive hypoglycemia and what is it caused by?

insulin...
11. describe the general function of insulin.
12. how does insulin facilitate the uptake of glucose into cells?
13. where are GLUT1-GLUT5 found?
14. which glucose transporter protein requires insulin?
15. describe insulin's action on muscle.
16. describe insulin's action on the liver.
17. describe insulin's action on adipose tissue.
18. what are some factors that facilitate release of insulin from the pancreas?
19. what are inhibitors of insulin release?

hormonal regulation...
20. describe the "reciprocal regulation" of insulin and glucagon.
21. describe the concept of a "basin of attraction" in regards to glucose regulation.

diabetes...
22. what is IDDM? what is it caused by?
23. what do high glucose levels in urine cause?
24. what is type II diabetes? what is it caused by and what does it result in?

answers
1. alpha cells secrete glucagon, beta cells secrete insulin, delta cells secrete glucagon.
2. increases glucose and ketone production and secretion.
3. glycogenolysis, gluconeogenesis, lipolysis, ketogenesis.
4. amino acids, decreased bloods sugar, CCK, VIP, catecholamines.
5. insulin/glucose, somatostatin.
6. by inhibiting both alpha and beta cell secretion of glucagon and insulin secretion.

7. hypoglycemia.
8. sympathetic stimulation, cortisol, growth hormone.
9. anxiety, tremors, sweating are caused by sympathetic action and hunger is caused by hypothalamus.
10. low blood sugar levels after a meal that results from excess release of insulin triggered by high content of high glycemic index carbohydrates (or insufficient protein).

11. to store metabolic fuels.
12. by binding to receptors which translocate glucose transporter proteins into the cell membrane.
13. GLUT1- ubiquitous, placenta, GLUT2- beta cell, liver, kidney, intestine, GLUT3- ubiquitous, GLUT4- muscle,adipose, GLUT5-jejunum.
14. GLUT4.
15. causes uptake of amino acids and sugar (and therefore promotes glycogen storage).
16. glycogen synthesis, fatty acid synthesis.
17. uptake of glucose and converion into fatty acids and glycerols, triglyceride synthesis, and uptake of fatty acids from blood lipoproteins.
18. high glucose levels, amino acids, parasympathetic stimulation (cephalic phase of pancreatic secretion), growth hormone, cortisol, GI hormones such as gastrin, secretin, CCK, GIP.
19. somatostatin, catecholamines.

20. insulin and glucagon inhibit each other's release from islet cells via paracrine actions.
21. the basin of attraction is the set of homeostatic variables which the body settles into over time; long term changes in hormone levels or autonomic activity can shift this basin of attraction to a new equilibrium point.

22. autoimmune destruction of pancreatic beta cells which results in low levels of insulin, and thus a shift from glucose metabolism to ketone body metabolism.
23. polyuria (excess urine volume), polydipsia (excess thirst), polyphagia (excess hunger)
24. type II diabetes is an insulin resistance that is caused by excess fatty acids, cortisol, or testosterone, which blocks insulin's anti-lipolytic effect on adipose tissue. can not be compensated by excess insulin secretion.

organ systems: GI embryology and vascular structures

this lecture describes the development of the gut tube starting from the infolding of the yolk sac in the development and positioning of the different sections of the intestines and stomach. early development: the epithelium and mucosa are derived from the endoderm layer while the muscularis is derived from the mesoderm layer. the gut tube is surrounded by two peritoneal sacs that form the visceral and parietal peritoneum. the dorsal mesogastrium is the section of the peritoneum early in development that connects the gut tube to the posterior abdominal wall. the greater omentum is part of the peritoneal layer that folds down over the intestines and serves as a repository for visceral fat (as well as having an active role in the immune system). the mesentary is the portion of the dorsal mesogastrium that attaches to the posterior gut tube and contains neurovascular bundles within its layers.

the gut tube itself undergoes several revolutions and many convolutions during its development, starting with a 90 degree rotation that positions the stomach to the left and the liver to the right of the abdominal cavity. the midgut then herniates and forms a U shaped loop in the 6th week, within which the small intestine develops. the formation of this long section of gut tube causes a bulging of the tube into the vitelline duct (?) and a subsequent entry into the abdominal cavity. the order of re-entry determines whether the section of the gut tube is classified as retroperitoneal or intraperitoneal-- retroperitoneal sections are affixed to the posterior abdominal wall and includes the duodenum, ascending, and descending colons. intraperitoneal are loosely suspended by mesentary and includes the small intestine and transverse colon. if the abdominal cavity closes before reentry of the gut tube is complete, this can result in a persistent vitelline duct, which might lead to such pathologies as vitelline cyst, vitelline fistula, or diverticulosis.

the gut tube is divided into three sections: foregut, midgut, hindgut. each section corresponds to multiple sections of the GI tract as we know it and also corresponds to a different major artery. for example, the foregut includes the stomach and duodenum and has blood supplied by the celiac artery. the midgut includes the jejunum, ileum, and ascending/transverse large intestine, and has blood supplied by the superior mesenteric artery. the hindgut includes the transverse and descending large intestine, rectum, and anal canal. as mentioned before, the mesentery that suspends the small intestine contains neurovascular bundles within its folds; there are two types of arteries that supply blood to the gut- vasa recta and arcade arteries. vasa recta arteries are more prevalent in the jejunum, arcades in the ileum.

sympathetic activity can constrict arteries, either in response to stress or a drop in blood pressure and activation of the RAAS system, decreasing blood and oxygen flow to the intestinal mucosa. eventually, the autoregulatory escape mechanism kicks in and brings the blood pressure in the intestines back to normal even with continued sympathetic activity. the sympathetic response to stress can ultimately result in toxemia due to the weakened epithelial wall (because of reduced oxygen flow) allowing in more microorganisms and toxins. this same result can come about due to ischemia caused by decreased cardiac output or decreased blood pressure as well.

questions
basic structures...
1. what is the gut tube made from? when does it start to develop?
2. the epithelium and mucosa of the gut tube are derived from...
3. smooth muscle is derived from...
4. describe the origin of the peritoneum.
5. what is the dorsal mesogastrium? what does it form?
6. what is the greater omentum? what are some of its properties?
7. spleen splits the greater omentum into...
8. describe the formation of the mesentery.
9. what travels between the layers of mesentery?

rotation and differentiation...
10. describe what happens in peritoneal rotation.
11. how does the large intestine come to surround the small intestine?
12. what does it mean for a section of the gut tube to be retroperitoneal and what is an example?
13. what does it mean for a section of the gut tube to be intraperitoneal and what is an example?
14. what determines whether a section of the gut tube will be retroperitoneal vs. intraperitoneal?
15. what is a persistent vitelline duct and what pathologies can it result in?
16. what is omphalocoele?

gut divisions and blood supply...
17. which arteries define the three sections of the GI tract?
18. what does the foregut form?
19. what does the midgut form?
20. what does the hindgut form?
21. which branches of the superior mesenteric artery supply the jejunum and ileum?
22. which branches of the superior mesenteric artery supply the ascending and transverse colon?
23. what are the two types of arteries that branch off and anastamose in the jejunum and ileum?
24. sympathetics constrict arteries in response to...
25. what is autoregulatory escape?
26. what are the two ways in which ischemia of the gut can occur?
27. how can toxemia result from ischemia of the gut?

answers
1. from the yolk sac during the 4th week.
2. endoderm
3. mesoderm
4. during the 5th and 6th weeks, two peritoneal sacs press against either side of the liver and stomach and form the visceral and parietal peritoneum.
5. the dorsal section of the peritoneal fold- forms the greater omentum and mesentery.
6. part of the dorsal mesogastrium that folds down over the intestine and is a repository for visceral fat. also has strong immune stimulating properties.
7. gastrolienal and lienorenal ligaments.
8. mesentary is formed from the portion of the dorsal mesogastrium that is attached to the posterior wall of the stomach.
9. neurovascular bundles to the visceral organs.

10. due to the 90 degree rotation of the peritoneal cavity, the stomach ends up to the left and the liver to the right (whereas they were both in the center before)
11. the midgut "herniates" and forms a U shaped loop during the 6th week, rotating 270 degrees around the superior mesenteric artery.
12. the portions that are affixed to the posterior wall of the abdominal wall and partially covered by peritoneum: examples are the ascending and descending large instestine and the duodenum.
13. the portion that is surrounded by the visceral peritoneum and is relatively mobile, suspended by mesentary. example is the small intestine and transverse colon.
14. the order of "reentry" into the abdominal cavity.
15. the vestiges of the vitelline duct which can result in a connection between the ileum and abdominal wall- potentially causing meckel's diverticulum, vitelline cyst, or a vitelline fistula.
16. a section of intestine trapped by early closing of the abdominal cavity before full retraction.

17. celiac artery: foregut, superior mesenteric: midgut, inferior mesenteric: hindgut.
18. stomach, duodenum
19. jejunum, ileum, proximal large intestine (ascending and transverse)
20. transverse, descending, sigmoid large intestine, rectum, anal canal.
21. sequential branches
22. ileocolic, right and middle colic arteries.
23. vasa recta in jejunum, arcades in ileum.
24. exercise or a drop in blood pressure
25. a compensatory mechanism which will allow vasodilation to offset excess sympathetic activity.
26. either by occlusion of the mesenteric arteries or decreased cardiac output/continuous vasoconstriction.
27. toxemia can develop by bacterial / toxin entry into intestinal epithelium which might occur when oxygen flow to the mucosa is decreased because blood flow is decreased (oxygen diffuses from arterioles to venules rather than to mucosa)

organ systems: the liver and lipid digestion

this unit reviewed some basic concepts about fat digestion and went into some more depth about the anatomy and physiology of the liver and gall bladder. the liver is located in the upper right quadrant of the abdomen, deep to the 5-10th ribs. it is suspended by the lesser omentum ligament, which attaches it to the intestine and the stomach, and the falciform ligament, which attaches it to the anterior of the abdominal wall. it has four lobes- left, right, quadrate, and caudate. the ligamentum teres (round ligament) is the vestigial remains of the umbilical vein that brought blood from the placenta. finally, the porta hepatis is the "hilum" or root of the liver (similar to the hilum of the lung) and contains the bile duct, hepatic portal vein and hepatic artery.

the liver receives nutrient rich and oxygen poor blood from the GI tract- specifically the gastric, splenic, and mesenteric arteries, which comes into the liver via the hepatic portal vein. it receives nutrient poor, oxygenated blood from the hepatic artery which branches off of the celiac artery. the liver cells, hepatocytes, are in hexagonal arrangements which have portal "triads" in each corner which contain bile ducts, hepatic portal veins, and hepatic arteries. in the center of the hexagons is the central vein, which leads to the hepatic vein, which leads to the inferior vena cava back to the heart. running from the edges of the hexagonal "lobule" are the sinuosoids where most of the functional activity of the liver takes place. the liver acinus theory describes the functional unit of the liver as the triangle between two portal triad corners and a central vein-- which is divided into three zones: zone 1 is closest to the central vein and although has lowest oxygen / nutrient content, is the site of most detoxification and chemical activity.

portal hypertension can occur from blockages in liver blood flow, resulting in a backpressure in portal circulation. this can cause a number of pathologies such as caput medusa, esophageal varicosities, and hemorrhoids. additionally, excess lymph can be drained from the liver (lymph drains into the space of disse, the tiny canals between the hepatocytes and sinusoids) and can collect in the peritoneal cavity, resulting in ascites. in this condition, the loss of fluid in the circulatory system must be compensated by renal devices which increase fluid retention such as aldosterone and renin secretion.

bile is secreted by hepatocytes and flows to the periphery of the hexogonal lobule, draining into the bile ducts, which drain into the right and left hepatic ducts. these combine to form the common hepatic duct, which combines with the bile duct from the gall bladder, called the cystic duct, to form the common bile duct. the common bile duct intersects with the main pancreatic duct at the hepatopancreatic ampulla and exits into the duodenum at the major duodenal papilla. the tissue around this point forms a sphincter called the sphincter of odie which contracts between meals or during fasting, which causes bile to stored in the gall bladder instead of being released into the duodenum.

bile stored in the gall bladder is made of bile salts, cholesterol, phospholipids, water, and can be concentrated over time via water reabsorption, or secretion of bile salts and cholesterol. if the bile becomes too concentrated in the gall bladder, over long periods of time with no contraction, then gall stones can precipitate out. in normal function, CCK and secretin are released from duodenal I and S cells, respectively, in response to protein, fat, or acid in the intestine (see "intestinal phase" in last lecture), causing an increase in pancreatic secretion, decrease in gastric secretion/motility, and bile release from gall bladder via contraction of the gall bladder and relaxation of the sphincter of odie. vagal stimulation can have the same effect. once in the intestine, bile surrounds fat molecules and aids in their absorption. the chapter in biochem covers this in much greater detail than what was presented in this lecture.

questions
location and anatomy...
1. where is the liver located?
2. what are the two ligaments that suspend the liver and where are they?
3. what are the lobes of the liver?
4. what is the ligamentum teres of the liver?
5. what is the porta hepatis?

physiology...
6. what are some of the functions of the liver?
7. how much blood does the liver receive (in terms of percentage of cardiac output)?
8. how does the liver get its oxygenated blood?
9. what does the portal vein bring to the liver? where does it bring it from?
10. what are sinusoids lined with?
11. what do the hepatic veins do?

lobules...
12. what is the classical lobule model of the liver?
13. what are the portal triads and what do they contain?
14. what is in the middle of the classical lobule?
15. what is the liver acinus model of the liver?
16. what are the three zones in the liver acinus model?
17. which zone is most susceptible to hypoxia and toxic damage?

hypertension and other pathologies...
18. where are the spaces of disse? what flows in them?
19. what is meant by "portal hypertension"?
20. what are some pathologies that portal hypertension can contribute to?
21. what is ascites?
22. how does ascites affect blood pressure?

bile secretion...
23. describe bile secretion by hepatocytes.
24. what are bile secretions made of?
25. what do the right and left hepatic ducts do?
26. ...common hepatic duct?
27. ...cystic duct
28. ...common bile duct
29. ...hepatopancreatic ampulla
30. ...main pancreatic duct
31. ...major duodenal papilla

gall bladder...
32. what are the three parts to the gall bladder?
33. what are three functions of the gall bladder?
34. how does the sphincter of oddi help store bile in the gall bladder?
35. describe two ways in which bile can be released by the gall bladder.
36. besides gall bladder emptying, what else does CCK mediate?
37. what effect does secretin have on the gall bladder and pancreas?
38. how are gallstones created?
39. what are two functions of bile?

micelles...
40. what is the general scheme for fat digestion?
41. about how big are micelles?
42. what pH is optimal for the action of pancreatic lipase?
43. which enzyme hydrolyzes cholesterol?
44. what are micelles made of?
45. how are bile salts formed?
46. what happens to the micelle contents at the enterocyte?
47. where does most of the reabsorption of bile acids and salts occur in the intestine?

chylomicrons and lipoproteins...
48. what are chylomicrons composed of?
49. 80-90% of chylomicrons are transported into...
50. how is the processing of short and medium chain fatty acids different?
51. what are the roles of: chylomicrons, VLDL, LDL, and HDL?
52. what makes feces brown and urine yellow?
53. jaundice is caused by...

answers
1. upper right abdomen between ribs 5-10.
2. lesser omentum between liver and stomach/intestine, falciform ligament between liver and anterior abdominal wall.
3. left, right, quadrate, caudate.
4. the round ligament, which is a vestigal remains of the umbilical vein carrying blood from the placenta to the fetus.
5. the "hilum" of the liver that contains bile ducts, hepatic arteries, and portal vein.

6. glycogen storage, gluconeogenesis, synthesis of TG's, cholesterol, phospholipids, fatty acid oxidation, protein synthesis, urea cycle, storage of vitamins and iron, detoxification, bile secretion.
7. 29%
8. via the celiac artery which branches off of the aorta
9. nutrient filled, deoxygenated blood from the gastric, splenic, and mesenteric veins.
10. hepatocytes
11. bring blood out of the superior aspect of the liver into the inferior vena cava.

12. divides hepatocytes into hexagonal "lobule" arrangements.
13. the corners of the hexagon in the classical lobule which contain the bile duct, hepatic artery and portal vein.
14. the central vein, which leads to the hepatic vein.
15. a model which has a functional "acinus" unit which is the triangle between two portal triads and a central vein.
16. zone 1 is closest to the portal triads and has the highest concentration of oxygen and nutrients. zone 2 is in the middle, zone 3 is closest to central vein and receives least nutrients but is primary site of alcohol and drug detoxification.
17. zone 3.

18. between hepatocytes and endothelium of sinusoids. lymph flows from sinusoids into space of disse, and sent to thoracic duct or inferior vena cava.
19. when a blockage of blood flow in the liver leads to backpressure in the portal circulation.
20. hemorrhoids, caput medusae, esophageal varicosities.
21. when portal hypertension causes excess lymph to flow in the space of disse, causing buildup of fluid in the peritoneal cavity.
22. since blood volume is lost to the lymph fluid that is trapped in the peritoneal cavity, blood pressure drops and the kidneys compensate by increasing salt and fluid retention until pressure is restored.

23. bile is secreted by hepatocytes and flows to the periphery of the portal lobules.
24. bile acids, phospholipids, cholesterol, along with bicarbonate and bile pigments (bilirubin)
25. bile outflow from the liver
26. junction between right and left hepatic ducts.
27. outflow from gall bladder.
28. outflow of bile from both gall bladder and liver.
29. junction of bile and pancreatic ducts.
30. outflow from pancreas.
31. bile and pancreatic secretion into duodenum.

32. body, neck, fundus.
33. store bile, concentrate bile, release bile into duodenum.
34. by contracting between meals, it allows backflow of bile from common bile duct into cystic duct into gall bladder.
35. CCK release triggered by fat or protein reach chyme entering the duodenum causes the sphincter of oddi to relax and the gall bladder to contract. vagus nerve stimulation has the same effect.
36. inhibits gastric mixing and secretion, stimulates intestinal mixing, stimulates pancreatic secretion.
37. increased water and bicarbonate secretion from duct cells.
38. either too much absorption of water (can be due to inflammation of epithelium), or high cholesterol content in stored bile (from too much absorption of bile salts, or too much secretion of cholesterol into bile)
39. to aid in fat digestion, and also elimination of various endogenous and exogenous substances such as cholesterol, bilirubin, drugs, heavy metals.

40. pancreatic lipase hydrolyzes triacylglycerides into free fatty acids, which are packaged into micelles via bile droplets. fatty acids are absorbed into enterocytes and bile is reabsorbed. fatty acids are reconverted to triacylglycerides, packaged into chylomicrons and transported in the blood.
41. ~1um
42. pH 8.
43. cholesterol esterase.
44. bile acids, phospholipids, cholesterol, and the fat that is trapped in the lipophilic core
45. bile acids are conjugated in the liver to form bile salts.
46. fatty acids are repackaged into triacylglycerol and cholesterol is esterified in the enterocyte, then packaged into a chylomicron in the ER.
47. the ileum.
48. cholesterol and triglycerides in a phospholipid shell with apoproteins.
49. lacteals and thoracic duct.
50. they are not packaged into chylomicrons and instead are transported directly into the venous system and stored in the liver and adipose.
51. chylomicrons transport fat from intestine into the blood. VLDL's transport triacylglycerides from the liver into the blood. LDL's are produced in plasma and trasnport cholesterol esters from liver to organs and tissues. HDL's are produced in plasma and transport cholesterol from peripheral tissues to the liver.
52. bilirubin is converted by colonic bacteria into urobilinogen, which can be excreted in the urine or converted to stercobilin and excreted in feces.
53. excess bilirubin

organ systems: carbohydrate and protein digestion, pancreatic secretion

[image courtesy of erica newon zelfand]

this unit focused on pancreatic secretions and their role in carbohydrate and protein digestion in the intestine. each day, the pancreas secretes 1L of pancreatic enzymes, among which are enzymes that break down carbohydrates into monosaccharides, enzymes that break down proteins into peptides, lipases which break down triacylglycerols into fatty acids. these digestive enzymes are secreted by the "acinar" cells of the pancreatic ducts, while water and electrolytes such as bicarbonate are secreted by duct cells (a similar strategy to salivary and gastric secretion). the bicarbonate from duct cells comes from carbonic acid, which is formed in duct cells by carbonic anhydrase. bicarbonate is transported into the duct lumen in exchange for a chloride ion by the CFTR transporter. the acinar cells can be stimulated to produce more secretion either directly by vagal stimulation or by different neuropeptides such as CCK, GRP, SubP, VIP. duct cells are stimulated to increase water and bicarbonate production mainly by secretin (which functions to reduce acidity in the intestine and as such also inhibits gastric secretion and emptying).

as with gastric secretion, pancreatic secretions can be divided into three phases (refer to comparison chart), cephalic, gastric, and intestinal. in the cephalic phase, thoughts or sensation of food causes increase of pancreatic secretion via vagal stimulation. in the gastric phase, gastric distention triggers vagal stimulation of pancreatic secretion. the most important phase for pancreatic secretion is the intestinal phase, where intestinal distention, high acid levels, or other digestive products trigger hormonal release that modify pancreatic secretion. CCK is released from I cells in response to fat and proteins, which stimulates acinar cells to increase enzymatic secretion. secretin is released from S cells in response to acid and fat, which stimulates bicarbonate and water secretion from pancreatic duct cells.

carbohydrate digestion, already initiated with salivary alpha amylase, continues with the secretion of pancreatic alpha amylase into the intestinal lumen. polysaccharides are cleaved into smaller di and tri saccharides, and then further digested by the brush border enzymes (see the biochem chapter for a much more detailed description). different sugars are absorbed into the enterocyte and bloodstream by different transporters: for example, glucose and galactose are absorbed into the enterocyte by SGLT1, a sodium co-transporter, while fructose is facilitatively absorbed by GLUT 5. the pancreas also secretes enzymes that digest proteins, all of which are activated by enterokinase, which activates trypsinogen into trypsin, which activates the other zymogens procarboxypeptidase, chymotrypsinogen, proelastase (see the biochem protein digestion chapter).

an interesting note about the role of tight junctions: most absorption of nutrients occurs through the membrane of the enterocyte, or transcellularly. however, in the case of macromolecules that are too large to be absorbed transcellularly, paracellular transport can occur via modulation of the tight junctions between enterocytes, which can occur reversibly via the molecule zonulin. paracellular transport can also occur in "leaky gut", hyperpermeability of the tight junctions, caused by excess glucose levels, alcohol abuse, NSAID/steroidal use,food allergies, crohn's disease. there is a distinct but underexplored relationship between tight junctino permeability and autoimmune disease; people with dysregulation of tight junction permeability have a higher susceptibility for autoimmune diseases.

questions
1. enzymes digest carbohydrates, fats, proteins by what type of reaction?
2. what is SGLT1 and what does it do?

describe the absorption of these substances from the intestinal lumen into the enterocyte, and from there into the blood stream:
3. glucose
4. lactose
5. fructose
6. glycogen
7. sodium

tight junctions...
8. describe the absorptive pathway from the intestinal lumen to the mucosal capillary.
9. what is a function of tight junctions in intestinal epithelium that is not commonly discussed?
10. what is the relationship of tight junctions and the immune system?
11. what are tight junctions made of?
12. what is "leaky gut" and what are some factors that cause it?
13. what is zonulin and what does it do?
14. what is lactulose and how is related to leaky gut?

pancreas...
15. where is the pancreas?
16. how much liquid does the pancreas secrete per day?
17. what do the acinar and duct cells secrete?
18. what are the electrolytes that are secreted by duct cells?
19. describe the secretion of bicarbonate by duct cells.
20. what are the enzymes that are secreted by the pancreas that digest proteins?
21. how are the protein digestion enzymes activated?
22. what does pancreatic amylase do?
23. what are the pancreatic enzymes that digest lipids?
24. what are the different ways in which pancreatic acinar cells are stimulated?
25. what are the actions of secretin?

pancreatic phases...
26. what are the three phases of pancreatic secretion?
27. describe the cephalic phase of pancreatic secretion.
28. describe the gastric phase of pancreatic secretion.
29. describe the intestinal phase of pancreatic secretion.
30. describe the secretion and actions of CCK.
31. describe the secretion and actions of secretin.
32. how does enzymatic secretion adapt to different dietary compositions?

carbohydrate digestion...
33. what are the approximate proportions of the different types of carbohydrates ingested?
34. pancreatic and salivary amylase digests starch into...
35. how are di and trisaccharides digested into monosaccharides?
36. what are the two ways that glucose and galactose can be transported into the intestinal epithelium?
37. compare the absorption of glucose and fructose.
38. describe the negative feedback that can occur in carbohydrate digestion.
39. how can malfunctioning carbohydrate digestion cause diarrhea?
40. what is the hydrogen breath test?
41. what effect does celiac disease has on the intestinal lining?

protein digestion and absorption...
42. how are proteins digested in the stomach?
43. how are proteins digested in the intestine?
44. how are polypeptides digested and absorbed in the intestine?

pancreatic tests...
45. what is the stool chymotrypsin test?
46. what is the pancreatic elastase test and why might it be more reliable than the stool chymotrypsin test?


answers
1. hydrolysis reactions.
2. it is a sodium / glucose co-transporter, facilitating absorption of glucose, galactose

3. glucose is transported into the enterocyte via SGLT1, then into the blood via GLUT2.
4. lactose is broken down into glucose and galactose via the brush border enzyme lactase, and glucose and galactose are absorbed and transported in the same way as question 3.
5. fructose is transported into enterocytes via GLUT5, and absorbed into blood via GLUT2.
6. glycogen is broken down into oligsaccharides and alpha limit dextrins by alpha amylase, and then broken down further into monosaccharides by brush border enzymes and absorbed the same way as in question 3.
7. sodium is transported along with glucose or galactose via the SGLT1 co-transporter.

8. intestinal lumen -> unstirred layer of fluid -> glycocalxces on microvilli of enterocytes -> cell membranes and cytoplasm -> basement membrane -> capillary
9. tight junctions can facilitate absorption of macromolecules, nutrients that are too big to be absorbed directly into enterocytes.
10. when tight junction regulation of macromolecule absorption is dysregulated, this can sometimes lead to intestinal and extraintestinal autoimmune disorders.
11. occludins, claudin family of proteins, junctional adhesion molecules.
12. hyperpermeability of the intestinal epithelium. caused by alcohol abuse, high sugar intake, food allergies, NSAIDS/steroid drugs, celiac disease and crohn's disease.
13. a molecules that facilitates the permeability of tight junctions and as such is involved in the absorption of fluid and macromolecules across the intestinal barrier, and also protect the intestine from being colonized by microorganisms.
14. a macromolecule that can only be absorbed paracellularly; its presence in the blood as compared to mannose (which is absorbed transcellularly) is a good indicator of leaky gut.

15. the body of the pancreas lies deep to the stomach and the tail extends to the spleen.
16. 1L per day
17. acinar cells secrete enzymes, duct cells secrete water and electrolytes.
18. bicarbonate and sodium.
19. bicarbonate is formed from carbonic acid which is formed by carbonic anhydrase and CO2. H+ is absorbed into blood, and bicarbonate is transported into the lumen by the transmembrane regulator CFTR (cystic fibrosis transmembrane regulator) which exchanges a chloride ion for a bicarbonate ion.
20. trypsinogen, proelastase, chymotrypsinogen, procarboxypeptidase.
21. trypsinogen is activated by the brush border protease enterokinase, forming trypsin, which activates the other enzymes.
22. an endoglucosidase that hydrolyzes carbohydrates into di and tri-saccharides.
23. pancreatic lipase, cholesterol esterase, phospholipase.
24. directly via the vagus nerve, or indirectly via stimulation of the vagus nerve by CCK, VIP, GRP, SubP.
25. stimulates duct cells to release bicarbonate, inhibits gastric secretion and emptying- overall effect is to raise pH.

26. cephalic, gastric, intestinal
27. stimulated by thoughts or sensation of food, vagus nerve stimulates pancreas secretion.
28. gastric distention causes vagal stimulation, which causes pancreas secretion.
29. the most important phase for pancreatic secretion; digestive products or low pH trigger release of hormones that control secretion.
30. CCK is secreted from I cells in the intestinal epithelium in response to proteins or fats. chief among its many effects is to stimulate pancreatic acinar secretion of enzymes.
31. secretin is released from S cells in the intestine in response to acid or fat-- its main effect is to increase water and bicarbonate secretion by pancreatic duct cells, thereby raising the pH of the intestinal lumen. it also decreases gastric motility and emptying.
32. CCK can up or downregulate the protein digesting proteases and the carbohydrate digesting amylases depending on the ratio of protein to carbohydrates in the diet.

33. 50% starch, 20% sucrose, 6% lactose, 1-2% maltose.
34. di and trisaccharides.
35. by the brush border enzymes.
36. transcellularly via the SGLT1 Na+ cotransporter or paracellularly with water with high glucose concentrations (see section on tight junctions)
37. fructose absorption is slower and uses a facilitated transporter rather than a co-transporter. (see question 5)
38. chemo and osmotic receptors sense high glucose levels in the duodenum and jejunum and trigger the vasovagal reflex, which decreases gastric motility and emptying.
39. in the case of lactose intolerance, lactose remains undigested and cause a hyperosmolar intestinal lumen from excess sugar as well as products from bacterial processing of these sugars; causing water to accumulate in the lumen and cause diarrhea.
40. a test which measures amount of hydrogen in breath, which is produced from bacteria that metabolize lactose in the intestine in lactose intolerant people.
41. destroys villi.

42. gastric pepsinogen is secreted and converted to pepsin by the low pH environment of the stomach. it cleaves proteins into smaller polypeptides.
43. in the intestine, proteins are digested by different pancreatic enzymes: trypsin, chymotrypsin, carboxypeptidase, elastase. trypsin activates the other three enzymes, which cleave large polypeptides into small polypeptides.
44. small polypeptides are cleaved further into smaller polypeptides and amino acids, which are then transported into the enterocyte and then absorbed into the blood by carrier proteins.

45. a marker for pancreatic output; normal is >9U/g stool, low is <>200 mcg/g stool, low is <100>
46. another test for pancreatic output, which might be more accurate because elastase is only produced by human pancreatic cells. normal is >200 mcg/g stool, low is <100>

organ systems: salivary and gastric secretion

this lecture covered the salivary and gastric enzymes; what they are, where they come from, what triggers and inhibits them. salivary glands and ducts have acinar cells and duct cells- acinar cells basically produce saliva, which contains a mixture of water, mucus, protective substances, and digestive enzymes. among the digestive enzymse are salivary alpha amylase (recall from carbohydrate digestion that this is the endoglucosidase that starts carbohydrate digestion), lingual lipase, mucins, and antimicrobial elements (such as lysozyme). duct cells regulate the electrolytic content of saliva, generally reabsorbing Na+ and Cl+ and secreting K+ and bicarbonate. the overall pH of saliva that is produced is 7.0, but can range from 6.5 to 8.0.

when these glands are innervated parasympathetically, they produce a watery saliva by three mechanisms: contraction of myoepithelial cells around acinar cells, vasodilation to increase blood supply, and augmentation of cell activity/division. the route for parasympethic innervation of the parotid gland begins at the inferior salivatory nucleus, then the glossopharyngeal nerve (CN IX), synapses at the otic ganglion, then follows the auriculotemporal nerve (recall from the face unit that this is part of the mandibular division of the trigeminal nerve) to the parotid. the sublingual and submandibular innervation starts at the superior salivatory nucleus, follows the facial nerve (CN XII), synapses at the submandibular ganglion, and follows the lingual nerve to the glands. sympathetic stimulation of the glands produce a more concentrated saliva- the sympathetic innervation begins at the nerves exiting the T1 level, which synapses at the superior cervical ganglion, and follows the arterial system to the salivary glands.

the gastric glands can be divided into two categories: oxyntic glands are in the fundus and body of the stomach and contain the H+ secreting parietal cells, histamine secreting enteroendocrine cells, pepsinogen secreting chief cells, and mucus cells (see more detailed descriptions at the histology lecture from last semester). pyloric glands are in the pylorus of the stomach and contain mucus cells and gastrin secreting G cells. parietal cells are the pivotal cells which secrete the H+ which lowers the pH of the stomach. the mechanism for H+ secretion is by production of carbonic acid via carbonic anhydrase, followed by dissociation into bicarbonate and H+, which is pumped into the duct lumen by a H+/K+ ATPase pump. parietal cell secretion of H+ can be stimulated by: acetylcholine/vagal nerve stimulation, gastrin, and histamine. it can also be inhibited by GIP, and factors that decrease gastrin secretion by G cells- namely, somatostatin and secretin.

the process of gastric secretion can be divided into three phases: cephalic, gastric, intestinal. cephalic is initiated by thoughts or sensation of food and causes the limbic system to activate the vagal nerve, which stimulates acid production by parietal cells and gastrin production by G cells. the gastric phase is initiated by gastric distention, or presence of amino acids, caffiene, or calcium, and also causes acid / gastrin secretion. the intestinal phase is triggered by amino acids in the duodenum, triggering gastrin release from duodenal G cells and thereby stimulating acid production.


questions
salivary glands and secretions...
1. what are the 4 types of salivary glands in the mouth?
2. where does the submandibular gland open up into?
3. what do acinar cells secrete?
4. what are the digestive enzymes that are secreted by the acinar cells?
5. how do duct cells affect salivary composition?
6. which ions are reabsorbed vs. secreted by the duct cells?
7. what is the range of salivary pH? what is the average pH?

innervation...
8. describe the parasympathetic route of innervation of the parotid gland.
9. describe the parasympathetic route of innervation of the submandibular and sublingual glands.
10. what are the three effects of parasympathetic stimulation of salivary glands?
11. what is the overall product of parasympathetic stimulation?
12. describe the sympathetic route of innervation of the salivary glands.
13. what is the product of sympathetic stimulation of the salivary glands?
14. what are some factors that increase salivation?
15. what are some factors that decrease salivation?

gastric glands and secretions...
16. what are the two types of glands / ducts in the stomach and where are they located?
17. what are the secretory cells in oxyntic glands and what do they secrete?
18. what are the secretory cells in the pyloric glands and what do they secrete?
19. describe the mechanism of parietal cell's secretion of H+.
20. what are some factors that stimulate parietal cell secretion of H+?
21. what is cimetidine and what cells does it affect?

three phases...
22. what happens in the cephalic phase and what is it initated by?
23. ...gastric phase?
24. ...intestinal phase?

other enzymes...
25. describe the activation and actions of pepsin.
26. what is the purpose of mucus and what is its secretion stimulated by?
27. what are three hormones that inhibit the release of H+ from gastric ducts?
28. describe the secretion and actions of somatostatin.
29. describe the secretion and actions of secretin.
30. describe the secretion and actions of GIP.
31. what are two examples of "positive feedback" of acid secretion?
32. what are two examples of "negative feedback" of acid secretion?
33. peptic ulcers are due to...
34. what happens when gastric acid enters the mucosal lining?
35. what is the role of Intrinsic Factor in digestion?


answers
1. parotid, submandibular, sublingual, palatine.
2. the sublingual papillae.
3. water, mucus, protective substances, digestive enzymes.
4. alpha-amylase, lingual lipase, mucins, lysozyme, calcium/phosphate/flouride (for teeth)
5. they regulate the electrolyte content of saliva.
6. sodium and chloride are reabsorbed and potassium and bicarbonate are secreted.
7. salivary is generally pH 7.0 but can range from 6.5 to 8.0.

8. begins in the inferior salivatory nucleus, glossopharyngeal nerve (CN IX), synapses at otic ganglion, auriculotemporal nerve to parotid.
9. begins in the superior salivatory nucleus, facial nerve (CN VII), synapses at submandibular ganglion, lingual nerve to submandibular and sublingual glands.
10. constriction of myoepithelial cells around acinar cells produces more saliva, vasodilation of nearby blood vessels increases blood supply, and augmentation of cell activity promotes growth and division.
11. produces a copious, watery saliva.
12. begins at the T1 level, synapses at the superior cervical ganglion, follows the arterial system to the salivary glands.
13. produces a enzyme rich saliva that is not very watery.
14. sensations or thoughts about food, and nausea to some extent (to neutralize upcoming vomit)
15. dehydration, negative emotions, sleep, fatigue.

16. oxyntic ducts are in the fundus and body of the stomach and pyloric ducts are in the pylorus of the stomach.
17. parietal cells secrete H+, chief cells secrete pepsinogen, enteroendocrine cells secrete histamine, mucus cells secrete mucus.
18. G cells secrete gastrin and mucus cells secrete mucus.
19. carbonic acid is created from intracellular CO2 via carbonic anhydrase, and dissociates into bicarbonate (which reenters the bloodstream) and H+, which is pumped out into the lumen of the gland by a H+ / K+ ATPase pump.
20. gastrin, acetylcholine (from vagal nerve stimulation), histamine.
21. a histamine blocker which blocks only the histamine receptors on parietal cells, not enterochromaffin like cells (a type of enteroendocrine cell that secretes histamine)

22. it is initated by thoughts or sensation of food (see question 14): the limbic system activates the vagal nerve, which stimulates the parietal cells to secrete more H+ and the G cells to secrete more gastrin.
23. gastric distention, presence of amino acids/peptides, caffiene, or calcium triggers the gastric phase- which also produces more H+ by parietal cells and gastrin by G cells.
24. amino acids/peptides in the duodenum triggers gastrin release from duodenal G cells.
25. pepsin is released from chief cells in the inactivate form, pepsinogen, which is auto cleaved at the low stomach pH. it cleaves proteins into smaller polypeptides.
26. to protect the gastric lining from digestion by acids, stimulated by vagus nerve, chemical stimulants (such as alcohol), and roughage.
27. somatostatin, secretin, GIP.
28. somatostatin is released from somatostatin cells in response to high acid levels in the stomach. somatostatin inhibits gastrin release from G cells, thereby reducing H+ levels.
29. secretin is released from duodenal secretin cells in resposne to high acid and fat levels in the stomach. secretin inhibits G cells gastrin release.
30. GIP is released from duodenal G cells in response to high acid and fat levels in the stomach. GIP directly inhibits parietal cells H+ release.
31. amino acids/peptides stimulating gastrin release, which stimulates acid secretion. vagus nerve stimulates acid secretion while inhibiting somatostatin release.
32. somatostatin inhibits gastrin release (see question 28), acid stimulates somatostatin release.
33. imbalance between aggressive digestive enzymes and protective factors such as mucus and bicarbonate.
34. inflammatory effects such as histamine release, edema, hemorrhage, leakage, etc.
35. it aids in vitamin B12 digestion: vitamin B12 is initially bound to dietary or gastric R proteins, then dissociated by pepsin and bound to intrinsic factor, which allows for its absorption into the ileum.

organ systems: GI physiology lecture II

the second lecture by Dr. SSL focused on small and large intestine "motility". in general, the intestines move the chyme (the half digested bolus) in two different ways; segmental, for mixing and absorption, and peristalstic, for moving the chyme along the digestive tract. the submucosal plexus is the nerve cluster in the submucosa of the intestines that are associated with the former, and the myenteric plexus is in between the muscularis mucosa layers and are associated with the latter.

once the bolus enters the small intestine, it takes 3-5 hours to move down to the ileum, where it reaches the ileocecal valve, a thickening of the tissue that prevents chyme from leaking into the cecum of the large intestine. as with all valves in the digestive tract, it is normally closed- when the valve loses tone, it can cause diarrhea, malabsorption, and a backflow of bacteria from the comparatively bacteria rich large intestine. the gastroileac reflex is when gastric or duodenal distention causes the relaxation of the valve. gastric distention can also induce peristalsis in the intestine (also controlled by the current mix of hormones in the lumen), called the gastroenteric reflex. the migrating motor complex is a peristaltic movement from the stomach to the ileum that occurs between meals, at approximately 90 minute intervals.

the large intestine's mixing function is accomplished by "haustration", which is a segmental mixing which aids in the absorption of water and further mixes the chyme. "mass movements" expel the colon's contents, and occur 1-3 times a day: each episode is 10-30 minutes long, with 30 second long contractions occuring every 2-3 minutes. a few reflexes that can induce mass movements: gastrocolic reflex is a mass movement in response to gastric distention or irritation, duodenalcolic is in response to duodenal distention or irritation, and orthocolic is in response to waking up or movement in the morning.

defecation can be induced intrinsically, meaning the distention of the rectum directly causes peristalsis in the descending and sigmoid colon, relaxes the internal and constricts the external anal sphincter. it can also be induced by the parasympathetic nervous system, by pelvic parasympathetic neurons stimulating relaxation of the internal and constriction of the external anal sphincters. in contrast, the sympathetic nervous system inhibits passage of rectal contents, and constricts the internal anal sphincter. lastly, stress causes loss of contractility in stomach and duodenum, as well as expelling fecal matter from large intestine, and chronic stress can ultimately lead to alternating bouts of constipation and diarrhea.


questions
introductory ideas...
1. describe the difference in blood appearance in stool depending on where the bleeding starts in the GI tract. 2. how far can a colonoscope reach?
3. what are the two nerve plexuses in the SI?
4. what is the submucosal plexus mainly involved with?
5. what is the myenteric plexus mainly involved with?
6. what gets absorbed in the duodenum and upper jejunum?
7. what are the upper and lower digestive system separated by?

small intestine motility...
8. what are the two types of contraction in the SI?
9. describe segmental contraction.
10. how long does it take for the bolus to move from the pylorus to ileocecal valve?
11. what is the gastroenteric reflex?
12. what is the gastroileac reflex?
13. what is the ileocecal valve?
14. what happens when the ileocecal valve loses tone?
15. how is appendicitis related to constipation?
16. what is the migrating motor complex?
17. how is the migrating motor complex activated?

large intestine / colon motility...
18. what is the function of the colon?
19. what is "haustration" of the colon?
20. describe the mass movements of the colon.
20b. describe the contractions during each mass movement.
21. what is the gastrocolic reflex?
22. what is the duodenalcolic reflex?
23. what is the orthocolic reflex?
24. how does nicotine affect the contraction of the colon?

reflexes and external influences...
25. describe the intrinsic reflex of defecation.
26. describe the parasympathetic reflex of defecation.
27. how is the external sphincter controlled?
28. what effect does the sympathetic nervous system have on bowel movements?
29. what effect does stress have on digestion?
30. what effect does chronic stress have on digestion?

answers
1. if the bleeding starts in upper GI tract, blood will have coagulated- darker stool. if bleeding in lower GI tract- reddish stool.
2. the terminal ileum.
3. myenteric, submucosal
4. secretion, absorption
5. motility
6. sugars, folic acid, calcium, iron.
7. ligament of treitz.

8. segmental contraction, peristalsis
9. more for mixing and mucosal contact.
10. 3-5 hours.
11. gastric and duodenal distention stimulates the myenteric plexus which stimulates peristalsis. hormones both stimulate and inhibit peristalsis.
12. food entering stomach stimulates relaxation of ileocecal valve.
13. last bit of ileum which delays entrance of chyme into cecum.
14. malabsorption, diahrrea, and backflow of bacteria from long bowel to small bowel.
15. appendicitis irritates the cecum around the ileocecal valve, which can cause it to remain closed.
16. a peristaltic wave that goes from the stomach to the ileum between meals, every 90 minutes.
17. the enteric nervous system, motilin.

18. absorb water and electrolytes, store and expel fecal matter.
19. a segmentation mixing of the large intestine that allows for mixing of chyme and greater absorption of water.
20. propulsive contractions of 20cm portions of the large intestine that occur 1-3 times per day.
21. each mass movement lasts 10-30 minutes, with contractions occuring every 2-3 minutes- with each contraction lasting 30 seconds.
21. when distention or irritation in the stomach triggers mass movement in intestines.
22. distention or irritation of duodenum triggers mass movement in intestines.
23. waking up / movement in the morning triggers mass movement in colon.
24. slows it down.

25. distention of rectum triggers peristalsis in descending and sigmoid colon, followed by relaxation of internal sphincter and contraction of external sphincter.
26. afferent neurons stimulate pelvic parasympathetic nerves to relax the internal sphincter and contract the external sphincter; happens from the splenic flexure to the anus.
27. voluntarily by the pudendal nerve.
28. inhibits passage in rectum, tightens internal spincter.
29. stomach and small intestine lose contraction ability, large intestine expels fecal matter.
30. alternative bouts of constipation and diarrhea.

organ systems: face and mastication

this lecture covered the bones, muscles, and nerves of the face. the bones related to the face are the maxilla (front teeth), mandible (jaw), frontal bone (forehead), nasal bone (bridge of nose), and zygomas (cheeks). the muscles involved in facial expression: for the eyes, the orbicularis oculi acts as a sphincter around the eye, while the frontalis is above the eye. the orbicularis oris is a sphincter muscle around the mouth, while the zygomaticus, labii, anguli, and platymas act as dilators of the lips.

the face muscles are innervated by the facial nerve, cranial nerve V, which is separated into three divisions: the opthamalic division is the topmost division, from the supraorbital nerve to the forehead and scalp area, contains the supraorbital foramen, and the supratrochlear, infratrochlear, external nasal, and lacrimal nerves. below this is the maxillary division, which runs from the infraorbital nerve to the bottom of the eyes, contains the infraorbital foramen, and the zygomaticofacial and zygomaticotemporal nerves.

the lowest division is the mandibular division, which is the mental nerve and chin area, and contains the mental foramen, as well as the mental nerve, inferior alveolar nerve, and the auriculotemporal nerve, which innervates the lateral scalp, temporomandibular junction (TMJ), and the tympanic membrane of the ear-- this is why injury to the TMJ area can potentially cause hearing loss. these nerves branch out from the mandibular nerve, which branches from the facial nerve, passes through the foramen ovale, into the inferotemporal fossa, and branches into the auriculotemporal and inferior alveolar nerve, which then passes through the mental foramen and becomes the mental nerve.

the facial muscles with respect to their actions on the mandible: the medial and lateral pterygoid both protrude and move the mandible from side to side, but the medial pterygoid elevates while the lateral pterygoid depresses the mandible. the temporalis and masseter both elevate the mandible but the temporalis retracts it as well, while the masseter protrudes it. finally, the digastric muscle runs from the mastoid processes to the digastric fossa and depresses the mandible.

the temporal mandibular joint is the connection between the condylar processes of the mandible and the mandibular fossa and articular tubercle of the temporal bone. in between the two bones are the articular disks, which allows the condylar process to move forward smoothly, allowing the lower mandible to rotate back and open the mouth- this motion is restricted by the temporomandibular ligament. the TMJ "click" is an abrupt movement of the condylar process against the articular tubercle which can be caused by a deformed articular tubercle or an articular plate with low compliance.

the last topic covered was the pterygoid venous plexus, which lies in and around the lateral pterygoid. it pools blood from local structures and the cavernous sinus, which collects blood from the deep facial and opthamalic vein. opening the mouth compresses the lateral pterygoid, which drains blood from the cavernous sinus, allowing for arterial blood to flow upwards-- this is one of the hypotheses for why we open our mouths so wide when we yawn.

questions
bones and muscles...
1. what are the bones of the face?
2. where are the "mental foramen"?
3. what are the muscles around the eyes?
4. what is the sphincter muscle around the mouth called?
5. what are the dilator muscles of the face?
6. what are the five layers to the scalp?
7. what is the nerve that innervates the facial muscles? describe its path.
8. what is bell's palsy?

innervation...
9. what is the trigeminal nerve and what are its divisions?
10. what are the boundaries of the opthamalic division and what are some nerves contained in it?
11. what are the boundaries of the maxillary division and what are some nerves contained in it?
12. what are the boundaries of the mandibular division and what are some nerves contained in it?
13. what are the foramen contained in each division of the trigeminal nerve?
14. how can damage to the TMJ cause hearing loss?
15. what are the nerves that innervate the back of the head? where do the nerves exit?

facial muscles: origins, insertions, innervations, actions:
16. temporalis...
17. masseter...
18. medial pterygoid...
19. lateral pterygoid...
20. digastric...

temporal mandibular joint...
21. describe the point of articulation for the TMJ.
22. what is the function of the articular disc in the TMJ?
23. which ligament of the TMJ restricts posterior motion of mandible?
24. what are the muscles that rotate the mandible around the TMJ axis?
25. describe what occurs in dislocation of the TMJ.
26. what does the "click" come from in the TMJ?

mandibular nerve...
27. describe the location and path of the mandibular nerve.
28. what nerves branch off of the mandibular nerve and what do they innervate?

pterygoid venous plexus...
29. what is the pterygoid venous plexus?
30. cavernous sinus connects with...
31. describe the potential for infection of the cavernous sinus.
32. what is a possible role of the pterygoid venous plexus in yawning?
33. what are the three actions that propel venous blood to the heart upon waking?

answers
1. frontal bones, zygomas, nasal, maxilla, mandible
2. in the body of the mandible.
3. frontalis, orbicularis oculi
4. orbicularis oris
5. the zygomaticus, labii, anguli, and platysma
6. SCALP: Skin, Connective tissue (dense), Aponeurosis, Loose connective tissue, Periosteum
7. cranial nerve VII, exits stylomastoid foramen, goes through the parotid duct.
8. a lesion of the facial nerve which leads to paralysis or weakness of facial muscles on one side of face.

9. cranial nerve 5, the nerve that receives sensory input from the face and scalp; has opthamalic, maxillary, mandibular divisions.
10. from the supraorbital nerve to the forehead and scalp. nerves are supra and infratrochlear, lacrimal, external nasal nerves
11. from the infraorbital nerve to the bottom of the eyes, zygomaticofacial and zygomaticotemporal nerves.
12. from the mental nerve to the chin area, contains auriculotemporal nerve.
13. opthamalic: supraorbital foramen, maxillary: infraorbital foramen, mandibular: mental foramen.
14. by damage to the auriculotemporal nerve, which innervates the tympanic membrane in the ear.
15. the greater and lesser occipital nerves, exit at the C2 level.

16. O: temporal fossa, I: coronoid processes, N: mandibular division of trigeminal nerve, A: elevate, retract mandible
17. O: zygomatic arch, I: ramus, angle, coronoid process of mandible, N: V3, A: elevate, protrude mandible
18. O: maxilla, lateral pterygoid plates, I: medial surface of angle of mandible, N: V3, A: elevate, protrude, side to side motion of mandible
19. O: pterygoid process, I: condylar process, articular disc of TMJ, N: V3, A: protrude, depress, side to side motion of mandible
20. O: mastoid process, I: digastric fossa, N: facial nerve (posterior belly), mylohyoid branch of V3 (anterior belly), A: depress mandible

21. the TMJ is a joint between the condylar processes of the mandible and the mandibular fossa / articular tubercle of the temporal bone.
22. allows for the upper portion of condylar processes to move anteriorly, and lower portion to rotate
23. temporomandibular ligament.
24. lateral pterygoid and digastric
25. excess anterior movement of mandible places condylar process anterior to articular tubercle.
26. a distorted articular tubercle or an articular disk with less compliance, which can cause abrupt movement of condylar process.

27. comes from facial nerve mandibular division, through foramen ovale, into inferotemporal fossa, innervates masticating muscles.
28. the auriculotemporal nerve, which innervates the lateral scalp, TMJ, and tympanic membrane. the inferior alveolar nerve, which innervates the lower teeth and goes through the mental foramen and turns into the mental nerve.

29. valveless veins near and around the lateral pterygoids which drains blood from cavernous sinus and other local structures.
30. deep facial and opthamalic veins.
31. infection of the nose or cheek area (via an infected pimple, for example) can carry from the opthamalic vein or deep facial vein into the cavernous sinus, which might carry into the brain, causing serious illnesses such as meningitis or even death.
32. compression of the pterygoid venous plexus by contraction of the lateral pterygoid will drain the blood from the cavernous sinus and allow for arterial blood flow, which will increase O2 flow to the brain.
33. the yawning action described above, extending limbs engages the extensor muscles which propel venous blood back to the heart, and taking a deep breath pushes down on the abdominal area, which pushes venous blood up into the thorax.

organ systems: GI physiology lecture 1

this is the first lecture in the series of GI physiology by Dr. Steven Sandburg Lewis. we covered a few introductory concepts: basal electric rhythms, some basic anatomy of the mouth and esophagus, gastric motility, and vomiting.

basal electrical rhythms are slow depolarizations that are initiated in GI tissue by the interstitial cells between the two layers of the muscularis mucosa. they generally occur on the frequency of 3-12 per minute, and if they reach the threshold frequency, an action potential will be induced and contraction of the muscle will occur. distention of the lumen in the GI tract, as well as parasympathetic and hormonal stimulation can depolarize the basal rhythm, bringing it closer to the threshold potential and therefore increasing the AP frequency. sympathetic activity and norepinephrine can have the opposite effect, hyperpolarizing the BER and lowering AP frequency.

the act of swallowing is an event in the pharanx is very much a coordinated event: the uvula is tissue in the back of the pharynx that prevents food (the bolus) from entering the nasal canal. the epiglottis is a flap of tissue that opens the esophagus and closes off the trachea. the bolus must pass through the upper esophageal sphincter (UES) which is normally closed to prevent air from entering the stomach. the bolus is then transported down by peristaltic motion to the lower esophageal sphincter (LES), which is normally closed to prevent gastric reflux.

three types of peristalsis are described: primary peristalsis occurs as a direct reaction to swallowing food. secondary peristalsis occurs even without swallowing- it is initiated when there is already a bolus stuck in the esophagus. tertiary peristalsis occurs in response to stress or loud noise, and contracts the entire length of the esophagus simultaneously- which in effect prevents peristalsis.

when the bolus passes through the LES and into the stomach, it induces "receptive relaxation" and peristalsis in the stomach muscularis layers as well. the stomach generally mixes on the frequency of 3 "constrictor waves" per minute, and includes an action called "retropulsion"- a backwards movement of the gastric contents to aid in mixing. (note: the fundus and body of the stomach can accomodate up to 1.5 L of food)

the last topic in this lecture was vomiting. there are three stages to vomiting: nausea, retching, and vomiting. nausea can be induced by a variety of events such as distention of organs, altered body chemistry, extreme fear or stress, etc. in the GI tract, this is manifested as antiperistaltic motion in the jejunum, relaxing of gastric muscle tone, and eventual reflux of duodenal contents into the stomach. in the next phase, wretching, the stomach contracts and pushes upwards into the thorax, against the closed LES. finally, vomiting occurs when the food gets ejected through the UES.

questions
BER's..
1. what are BER's? what are they generated by?
2. how is an action potential produced from a BER?
3. how is the maximum rate of muscle contraction set?
4. how does depolarization relate to action potential production? what causes depolarization of BER?
5. how does hyperpolarization relate to action potential production? what causes hyperpolarization of BER?

the mouth and esophagus...
6. dysphagia is...
7. what does the uvula do?
8. what does the UES do?
9. what does the LES do?
10. what is the difference between the three types of peristalsis in the esophagus?
11. when is tertiary peristalsis painful?
12. what is the relaxation of LES mediated by?
13. what foods relax LES tone?

gastric motility and emptying...
14. what is the first response of the stomach to the entering bolus?
15. fundus and body can accommodate up to...
16. what is the frequency of gastric mixing?
17. how does stress affect gastric contraction?
18. what is retropulsion?
19. how does fat content relate to gastric contraction
20. how many episodes of gastric reflux does the average person have per meal?

vomiting...
21. three phases of vomiting...
22. what occurs during nausea?
23. what occurs during retching?
24. what might happen due to excessive wretching?
25. what occurs during vomiting?
26. what is the vomiting center in the brain affected by?
27. what is an emetic? what are some examples?

answers
1. basal electrical rhythm, generated by interstitial cells between the circular and longitudinal muscularis mucosa.
2. when the BER reaches the threshold potential, an action potential is initiated.
3. by the slow wave frequency.
4. increases the AP frequency, cased by distention of lumen, parasympathetic and hormonal stimulation.
5. decreases AP frequency, caused by sympathetic activity, NE

6. difficulty swallowing.
7. prevents efflux of food into the nasal pharynx.
8. prevents air from getting into the stomach.
9. prevents gastric secretions from entering esophagus.
10. primary is in response to swallowing food. secondary is peristalsis without swallowing- when something is stuck in the esophagus. tertiary has no known function- can be stimulated by loud noises or stress and contracts the whole esophagus.
11. it can cause chest pain in individuals with esophageal motility problems.
12. vagus nerve, VIP, nitric oxide
13. alcohol, antacids, proton pump inhibitors, mint, chocolate, viagra (by way of NO), opiates, drugs to treat angina, bronchodilators. progesterone.

14. "receptive relaxation"
15. 1.5 L
16. 3 constrictor waves / minute.
17. it can cause contraction of the entire stomach (similar to tertiary esophageal contraction) which blanches blood to the brain/muscles and eventually can cause ulcers.
18. the backward motion of contents (to aid in mixing)
19. causes the gastric contents to mix longer. fats float on top and are emptied last.
20. about 3.

21. nausea, retching, vomiting.
22. relaxing of gastric tone, antiperistalsis begins in the jejunum, and eventual reflux of duodenal contents into stomach.
23. upward contraction of stomach, with LES closed.
24. a hiatal hernia.
25. food gets ejected through UES.
26. distention or irritation of viscera, cerebral events, or altered body chemistry. could be stimulated from GI or kidneys.
27. a substance which induces vomiting, such as ipecacuanha.

organ systems: reproductive anatomy and embryology

this lecture covered the anatomy and embryology of the male and female reproductive systems, first introduced in histology last semester. first it went through basic anatomical features of the female reproductive system. at the end of the vagina is the cervix, which is the opening to the uterus (the areas beside the cervix are called "fornices"). the uterus has four sections, the cervix, isthmus, body, and fundus. the uterine tubes branch off of the uterus and are divided into section as well: isthmus, ampula (where fertilization takes place), infundibulum, ending in the fimbria which open up into the peritoneal cavity. the uterus itself can be tilted forward, called anteversion, and additionally bent forward, called anteflexion. it is held in place by the round ligament, the uterosacral ligament, and the transverse sacral ligament. the ovaries are held in place by suspensory and ovarian ligaments.

the male reproductive anatomy basically follows spermatogenesis as it begins in the testes and ends at the penis. spermatogenesis occurs in the seminiferous tubules of the testis, aided by sertoli cells and leydig cells (which secrete testosterone). the spermatogonia in the walls of the tubules develop into spermatocytes, into spermatids, into spermatozoans, which are then released from the tubules. they travel into the rete testis, and into the ductus epididymus, which is a 4-5m long highly coiled tube where spermatozoans mature. from there they travel up the ductus deferens, which goes through the inguinal canal and behind the bladder, encountering the first of the ducts which combine with sperm to create seminal fluid.

the first of these is the seminal vesicles, which secrete a whitish viscous fluid containing fructose (recall the polyol pathway from biochemistry, and how sperm cells use fructose instead of glucose for metabolism). next is the ejaculatory ducts, which meet the urethra at the urethric crest of the prostate. next is the prostatic ducts in the prostate. finally, the bulbourethral gland is embedded in the external urethral sphincter and lubricates the penile urethra as well as neutralizing acidity from the urine.

some homologies of external genitalia between males and females are discussed: the penis and clitoris are both formed from the "genital tubercle". the "labiascrotal swelling" forms the scrotum in males and the labia majora in females. the urethral folds forms the urethra in males and the labia minora in females.

next we discuss the embryology of the reproductive systems. male/female differentiation begins around 4 weeks during development. before this point, germ cells in both sexes migrate from the yolk sac to the sex cords, forming the precursor to the gonads. in males, the mesonephric ducts (wolffian) develop while the paramesonephric (mullerian) ultimately degrade. the mesonephric ducts form the efferent ductules, ductus deferens, seminiferous tubules, and ejaculatory ducts.

in females, the follicles (recall the anatomy from the histology lecture) are formed by sex cords which form cortical cords, which form follicles. inside the follicles are oogonia, which began forming and dividing from the germ cells that migrated from the yolk sac. as mentioned above, the mesonephric duct eventually disappears and the paramesonephric duct develops into the female reproductive anatomy: the top of the ducts form the uterine tubes, ending in the infundibulum, and the bottom of the ducts form the uterus and vagina. the sinovaginal bulb is formed by the fusion of the urogenital sinus and the paramesonephric ducts, and the opening to the vagina forms by the hollowing out of the sinovaginal bulb.

some pathologies in development: hypospadias is the opening of the urethra in the ventral side of the penis instead of at the glans. chryptorchism is incomplete descent of the testis due to abnormal androgen production. congenital inguinal hernia is when the intestines come through the inguinal canal into the scrotal area. hydrocele is the acculumulation of fluid in the tunica vaginalis, which covers the testis.


questions
anatomy...
1. greater and lesser pelvis separated by...
2. what is the pelvic diaphragm made of?
3. what are the four parts of the uterus?
4. what are anteversion and anteflexion?
5. what is the connective tissue that holds the uterus?
6. what are the sections of the uterine tube?
7. what is the ovary held in place by?
8. what is the broad ligament formed from?
9. what are the fornices?

10. what is the tunica albuginea?
11. leydig cells secrete...
12. sertoli cells support...
13. describe spermatogenesis. (not on test)
14. describe the pathway of the sperm out from the seminiferous tubules to the ductus deferens.
15. describe the epididymus.
16. ductus deferens transports sperm cells through...
17. what do the seminal vescicles do?
18. where do the ejaculatory ducts open into the urethra?
19. prostate gland secrete into urethra via...
20. where is the bulbourethral gland? what does it do (2)?
21. what forms the seminal fluid?

22. what are the layers to the prostate?
23. what are the zones of the prostate?
24. what zones does hypertrophy of the prostate affect?
25. what zones does prostate cancer affect?
26. what does the prostate gland secrete? (4)
26b. what is an indicator for prostate cancer?

27. where is the superficial inguinal ring?
28. where is the deep inguinal ring?
29. conjoint tendon is the lowest part of...
30a. describe the path of the spermatic cord.
30b. what is the equivalent of the spermatic cord in the female and where does it pass through?
31. what is the pampiniform plexus?
32. what is the cremaster muscle?
33. what is an inguinal hernia?
34. what is the difference between a direct and indirect inguinal hernia?

what is the analogous erectile tissue on the female:
35. penis
36. corpus cavernosum
37. corpus spongiosum
38. bulb of penis and glans penis

39. what is it that imparts turgidity during an erection?
40. describe the corpus spongiosum.
41. describe the general purpose of the ischiocavernous muscle in males and females.
42. describe the general purpose of the bulbospongiosus muscle in males and females.
43. describe the general purpose of the transverse perinei muscle in males and females.
44. what gland on females is analogous to the bulbourethral gland in males?
45. what gland on females is analogous to the prostate gland in males?

46. describe the blood supply for erectile tissue.
47. describe the nervous system's role in producing an erection.
48. what is detumescence and how does it occur?

embryology...
49. urogenital ridge is formed from...
50. germ cells arise from... and migrate to...
51. in male genital development, seminiferous tubules are formed from...
52. mesonephric duct becomes...
53. some mesonephric ducts become...

54. in female genital development, follicles are formed from...
55. describe oogonia development.
56. paramesonephric duct is formed by which hormones?
57. what does the cranial end of the paramesonephric duct grow into?
58. what does the caudal end grow into?
59. where does the sinovaginal bulb form?
60. what does the vagina form from?
61. what is uterine duplication caused by?
62. what are the characteristics of female pseudohermaphrotidism?

63. what does the genital tubercle develop into in males and females?
64. what does the urethral fold develop into in males and females?
65. what does the labioscrota develop into in males and females?
66. what is hypospadias?

67. testes descend through...
68. piece of peritoneum is retained as...
69. what is chryptorchism?
70. what is a congenital inguinal hernia?
71. what is a hydrocele?


answers
1. pelvic brim
2. levator ani+coccygeus, pudendal nerve, muscle suspended across lesser pelvis
3. body, isthmus, cervix, fundus
4. anteversion is the tilting of the uterus forward onto the bladder. anteflexion is the further bending of the uterus forward. (retroversion and retroflexion are the opposite)
5. round, transverse cervical, and uterosacral ligaments.
6. isthmus, ampula, infundibulum, ovary.
7. suspensory ligaments, ovarian ligaments
8. the parietal layer of the peritoneum that covers the reproductive organs.
9. the spaces in the vagina around the cervix.

10. the inner covering of the testis
11. testosterone
12. spermatogenesis
13. spermatogonia->spermatocytes->spermatids->mature sperm cells
14. leave the seminiferous tubule via the rete testis, which then dumps into the efferent ductules, which then converges into the epididymus, then to the ductus deferens.
15. a highly coiled tube that is 4-6 meters long, the site for sperm maturation.
16. inguinal canal
17. secretes viscous whitish-yellow fluid containing fructose
18. urethral crest of prostate.
19. prostatic ducts
20. embedded in the external urethral sphincter, lubricates penile urethra and neutralizes acid from urine. the last contributor to seminal fluid.
21. bulbourethral, seminal vescicle, prostate secretions.

22. main, submucosal, mucosal.
23. peripheral, central, transitional, periurethral. (from largest to most focused)
24. central and transitional.
25. peripheral zone.
26. prostatic acid phosphatase (PAP), fibrinolysin, citric acid, and prostate-specific antigen.
26b. increased PAP and PSA levels.

27. in the external oblique
28. in the transversalis fascia
29. transverus and internal oblique muscles
30a. through the inguinal canal and into scrotum
30b. the round ligament of the uterus, passes through inguinal canal to labia majora.
31. the venae comitantes that maintain thermoregulation in the spermatic cord.
32. the muscle innervated by genitofemoral nerve that raises the testes for thermoregulation.
33. protrusion of intestine through abdominal wall
34. direct is via a weakened conjoint tendon, indirect is through the inguinal canal.

35. clitoris
36. corpus cavernosum
37. labia minora
38. bulb of vestibule and glans clitoris

39. the tunica albuginea
40. separated by the vagina in females but surrounds the urethra in males. has less CT, therefore less turgidity.
41. overlies corpus cavernosus
42. overlies bulb of penis/vestibule
43. tauten perineal membrane
44. greater vestibular
45. urethral and paraurethral

46. internal iliac artery to internal pudendal artery to deep artery of the penis/clitoris
47. during erection, parasympathetic nerves (S2,3,4) dilate helicine arteries and allow blood to flow into erectile tissue
48. sympathetic nervous activity constricts helicine arteries and reroutes blood into venous plexus and deep dorsal vein.

49. intermediate mesoderm
50. yolk sac and gonad
51. sex cords
52. ductus deferens, seminal vesicles, ejaculatory duct.
53. efferent ductules

54. sex cords which form cortical cords, which form follicles.
55. oogonia form from germ cells, and undergo mitosis during fetal development. after birth no more oogonia are formed.
56. maternal or placental estrogens.
57. uterine tubes, ending in infundibulum that opens up into peritoneum.
58. uterus and vagina
59. where the paramesonephric ducts fuse with the urogenital sinus
60. the fusion of the bulbs, which begin to hollow out.
61. improper fusion or development of paramesonephric ducts.
62. masculinization of female external genitalia: partial fusion of labia majora, clitoral hypertrophy, and persistent urogenital sinus.

63. penis and clitoris
64. penile urethra and labia minora
65. scrotum and labia majora.
66. urethral openings on the ventral surface of the penis rather than at the glans.

67. inguinal canal, along gubernaculum.
68. tunica vaginalis
69. abnormal androgen production produces undescended testes.
70. patency of inguinal canal which allows intestines to enter scrotum
71. excess fluid in the tunica vaginalis.