this is the second lecture on blood chemistry in lab diagnosis II. we covered glucose levels, various glucose testing, BUN, creatinine, calcium, albumin, and globulin.
questions
glucose and fasting glucose tests...
1. blood glucose levels are controlled primarily by which two hormones?
2. blood glucose levels are influenced secondarily by...
3. what is the normal range for fasting glucose levels?
4. what is the critical high value for FG?
5. after age 50, how do fasting glucose levels generally change?
6. what are some interfering factors for the fasting glucose test?
7. what are some factors that can cause increased glucose levels?
8. what are some factors that can cause decreased glucose levels?
9. what is the glucose level that is used to diagnose diabetes mellitus?
10. what is the glucose level that is used to diagnose "pre-diabetes"?
two hour post prandial...
11. what is the 2hrgpp?
12. what level on the 2hrgpp corresponds to the dx of pre-diabetes?
13. what level on the 2hrgpp corresponds to the dx of diabetes?
14. what factors will cause falsely elevated levels on the 2hrgpp?
15. what factors will cause falsely ∂ecreased levels on the 2hrgpp?
16. what are the advantages of a 2hrgpp over a fasting blood glucose test?
GTT and HbA1c...
17. what is the glucose tolerance test?
18. GTT sometimes used in conjunction with insulin levels to diagnose...
19. what is the HbA1c test?
20. 8% on the HbA1c test corresponds to what level of blood glucose?
BUN...
21. blood urea nitrogen is an indirect measure of the function of which two organs?
22. urea is an end product of metabolism of what substance?
23. what is the most common etiology of increased BUN?
24. what is renal azotemia?
25. what is post-renal azotemia?
26. what are some general factors that could lead to a decreased BUN?
27. what are some factors that could interfere with BUN level testing?
28. what is the normal range for BUN levels?
29. what is the critical high level for BUN levels?
creatinine...
30. creatinine is produced from metabolism of...
31. describe the variability of creatinine throughout the day.
32. relationship of creatinine and kidney function?
33. relationship of creatinine and liver function?
34. in renal disease, which level rises first, creatinine or BUN?
35. what are some factors that could increase creatinine levels?
36. what are some factors that could decrease creatinine levels?
37. what are some factors that interfere in the testing of creatinine levels?
38. what are the normal values for creatinine levels in males and females?
39. what is the critical high level for creatinine?
40. what do BUN/creatinine ratios of 10:1, 20:1 correspond to?
bound calcium...
41. calcium tests are useful in determining...
42. what form is calcium found in the blood?
43. what are 3 mechanisms in the body used to maintain calcium homeostasis?
44. what is the general relationship between calcium and phosphorous in the blood?
45. what are the most common causes of hypercalcemia?
46. what are some causes of hypocalcemia?
47. what is the normal and critical range for calcium in the blood?
ionized calcium...
48. what is the relationship between ionized calcium and serum albumin?
49. ionized calcium might be a better indicator for what disorder?
50. ionized calcium levels is used as a monitor for what procedures?
51. what are some factors that could cause decreased ionized calcium levels?
52. what are some factors that could lead to increased ionized calcium levels?
53. how do the normal and critical ranges of ionized calcium compare to bound calcium?
54. what are some factors that might interfere with calcium measurements in general?
55. what time during the day is calcium generally highest?
total protein...
56. what percentage of protein in the serum does albumin account for?
57. where are globulins synthesized?
58. increase in total proteins are either from...
59. what is total protein used to measure?
60. what is the normal range for total protein?
61. what are some factors that could interfere with the measurement of total protein?
62. what are some drugs that could falsely increase the measurement of total protein?
63. what are some drugs that could falsely decrease the measurements of total protein?
serum albumin...
64. where is serum albumin synthesized?
65. describe the importance of serum albumin in the vascular system.
66. what is the normal range for serum albumin?
67. what are some factors that could increase serum albumin levels?
68. what are some factors that could decrease serum albumin levels?
globulins...
69. globulins form the building blocks of which molecules?
70. serum globulin reflects the damage of which system?
71. where are alpha, beta, and gamma globulins synthesized?
72. what is the normal range of globulins?
73. what are some factors that cause increased globulin levels?
74. what are some factors that cause decreased globulin levels?
75. what is the ratio of albumin to globulin generally?
76. decreased A/G ratio can be caused by...
answers
1. glucagon and insulin.
2. ACTH, corticosteroids, EP, thyroxine.
3. 70-100 mg/dl.
4. 400 mg/dl.
5. increases 1 mg/dl per year.
6. stress, caffiene, pregnancy, delayed testing time, drugs.
7. DM, stress/fever, hyperthyroid, cushing's, chronic renal failure, pancreatitis, pheochromocytoma. [damn that stress- try crushing your liver with your pancreas and some chromosomes]
8. insulinoma, hypothyroid, hypopituitarism, addison's, severe liver disease, glucagon deficiency, reactive hypoglycemia. [low insults adds leverage to the reactivity of glucagon]
9. 126 mg/dl, two samples.
10. 100-125 mg/dl, two samples.
11. glucose levels taken 2 hours after eating.
12. 140-199 mg/dl.
13. >200 mg/dl.
14. smoking, stress, eating.
15. vomiting, a small meal.
16. less expensive and less patient discomfort.
17. a series of blood glucose measurements before glucose ingestion and at set intervals afterwards.
18. delayed onset hypoglycemia and impaired glucose tolerance.
19. a test that measures the percentage of glucose attached to hemoglobin A1c.
20. glucose above 200mg/dl.
21. liver and kidney.
22. proteins.
23. pre-renal azotemia such as CHF.
24. any kidney damage that leads to decreased excretory capabilities leads to increased BUN in the blood.
25. obstruction after the kidneys: kidney stones in the ureters, bladder neck, decreased urine excretion.
26. liver failure, overhydration, negative nitrogen balance, early pregnancy, nephrotic syndrome (loss of BUN through kidneys). [buns filled with water and nitrous never failed the overly-negative pregnant woman]
27. abnormal water or protein consumption, late pregnancy, increased muscle mass.
28. 6-20 mg/dl.
29. >50 mg/dl.
30. creatine phosphate in muscle.
31. slightly low at 7AM, slightly high at 7PM.
32. completely excreted by kidneys and thus a useful measure of GFR.
33. generally is not affected.
34. BUN rises first.
35. renal disease, acromegaly, rhabdomylosis, muscular dystrophy, myasthenia gravis, urinary obstruction, high protein diet. [creatine kid- like a tall rabbit with muscles, pees protein against gravity]
36. decreased muscle mass, inadequate protein, pregnancy, small stature. [short, skinny, pregnant]
37. high meat diets, ketoacidosis, some drugs.
38. 0.8-1.3 mg/dl for males, 0.6-1.1 mg/dl for females.
39. >4 mg/dl.
40. 10:1 can be normal or renal azotemia. 20:1 can be pre or post renal azotemia.
41. calcium metabolism and parathyroid function.
42. 50% bound to albumin, 50% ionized.
43. PTH controls calcium resorption from bone, reabsorption from kidney, and vitamin D increases Ca2+ absorption in intestines.
44. they have a roughly inversely proportional relationship.
45. hyperparathyroid, malignancies.
46. decreased serum albumin, hypoparathyroidism, vitamin D deficiency, some others.
47. 8.8-10.4 mg/dl normal, less than 7.0 critical.
48. no relationship to serum albumin.
49. hyperparathyroidism.
50. open heart surgery and organ transplants.
51. acute pancreatitis, hypoparathyroidism, vitamin D deficiency, magnesium deficiency, multiple organ failure, toxic shock. [acute, PTH, D, mg, organ failure, toxic shock] [IC: to damp]
52. hyperparathyroidism, PTH producing tumors, excess vitamin D. [PTH, PTH, D]
53. roughly half the levels.
54. vitamin D intoxication, decreased pH (increases levels), increased pH (decreases levels).
55. around 9pm.
56. about 60%.
57. the reticuloendothelial system, the liver.
58. increase in globulins or dehydration (albumin generally not affected)
59. liver dysfunction, nutritional status, chronic edema, immune system disorders, SLE, protein wasting, cancer. [liver, nutrition, edema, immune, SLE, cancer]
60. 6.4-8.3 mg/dl.
61. prolonged tourniquet application, drugs, dehydration/overhydration.
62. anabolic steroids, growth hormone, insulin, progesterone.
63. OCP's, estrogen, hepatoxic drugs, nephrotoxic drugs.
64. in the liver.
65. maintains oncotic pressure. important transport protein for drugs, hormones, enzymes, calcium.
66. 3.5-5.0 g/dl.
67. dehydration.
68. liver disease, nephrotic syndrome, ascites, severe burns, increased capillary permeability (SLE), overhydration, inflammation, malnutrition.
69. antibodies, glycoprotein, lipoproteins, clotting factors, acute phase reactants.
70. the RE system in the liver.
71. alpha and beta by the liver, gamma by WBC's.
72. 2.3-3.4 mg/dl.
73. MM, waldenstrom's macroglobulinemia, acute inflammation, chronic inflammation, cirrhosis, infectious disease, dehydration, autoimmune hepatitis.
74. genetic disorders that limit antibody production, secondary immune deficiencies, over-hydration.
75. generally much more albumin than globulin.
76. conditions that cause loss of albumin such as SLE, in which increased capillary permeability causes loss of albumin but not globulin.
Showing posts with label calcium. Show all posts
Showing posts with label calcium. Show all posts
Wednesday, January 27, 2010
Tuesday, February 3, 2009
organ systems: acid base balance and urinary system
this lecture is an introduction to body pH and the mechanisms that regulate it: the kidneys, the lungs, and chemical buffers. it also talks about the development of kidney stones and the physiology of the bladder.
body pH is largely determined by the balance between the acidic carbon dioxide and the basic bicarbonate. recall from respiratory physiology that carbon dioxide combines with water in cells via carbonic anhydrase to form carbonic acid, which then dissociates into bicarbonate and H+. the body can develop alkalosis or acidosis due to an imbalance of these molecules; acidosis can occur either by hypoventilation (retaining too much CO2) or through metabolic pathways- loss of bicarbonate through diarrhea, renal failure, buildup of lactic acid from exercise, excess ketone body production in the case of diabetes mellitus. alkalosis can occur by hyperventilation (loss of too much CO2 from lungs) or by ingestion of antacids, excess secretion of H+ in the kidneys due to hypertension, or vomiting of acidic HCl.
in order to regulate the pH, the body can increase or decrease the ventilation rate to regulate blood CO2 levels. another main source of pH regulation is in the kidneys via the balance between reabsorption and excretion of bicarbonate and H+. bicarbonate in the blood is filtered in the kidneys and combines with H+ secreted by the epithelial cells of the proximal tubule. this forms carbonic acid, which can be converted back into CO2 and H2O via carbonic anhydrase. the CO2 then diffuses back into the epithelial cells, where it reforms bicarbonate and H+ through the reverse reaction. in this way 99% of bicarbonate filtered through the kidney is reabsorbed.
if the acidity in the blood is too high, then H+ secreted into the lumen will be higher than the bicarbonate in the filtrate, and excess H+ will be bound to ammonia and phosphate buffers and excreted, raising the pH. conversely, if the blood is basic, then there will be more bicarbonate than H+, and the excess will be unable to be reabsorbed as CO2 and thus be excreted, lowering the pH. angiotensin II and aldosterone can both cause excess H+ secretion, resulting in low pH- angiotensin II stimulates the PCT Na+/H+ cotransporters in the tubular epithelia, while aldosterone stimulates the Na+/H+ antiporter, as well as stimulating intercalated cell secretion of H+. this means that the high angiotensinII and aldosterone levels associated with hypertension also result in a lower pH.
a brief look at kidney stones: when there is excess insoluble material in the filtrate or excess water reabsorption, sometimes stones can develop in the kidney and block urine passage. the most common is the calcium oxalate stone, which develops from a hyper-reabsorption of calcium and oxalate from the intestines, which then combine in the kidneys. a second type of kidney stone is struvite, which forms from a bacterial enzyme, urease, which degrades urea into NH3, which raises pH and forms MgNH4PO4 stones.
the urine that forms in the kidney then goes out via the ureters into the bladder. the bladder is surrounded by the detrusor muscle, and has openings that lead out into the urethra, which leads out into the outside world. the urethral sphincter has two layers, the inner sphincter, which is controlled by parasympathetic smooth muscle, and the outer layer, which is controlled by voluntary striated muscle (pudendal nerve, S2,3,4). when the bladder is filling, the detrusor muscle relaxes and the inner sphincter contracts. during the micturition (urination) reflex, the detrusor muscle contracts and the inner sphincter relaxes.
questions
1. what is blood pH regulated by?
2. what is the main chemical buffer in the blood?
3. how do the lungs regulate pH?
4. how do the kidneys regulate pH?
5. what are the pH limits of the body and what occurs beyond the limits?
6. what are the sources of acidity in the body?
7. acidity depends on the ratio between...
8. the reaction that produces bicarbonate from CO2 is catalyzed by...
9. what is the pKa of bicarbonate and what happens at the physiologic pH of 7.4?
10. why is urine continuously acidified?
11. what are the two sources for production of CO2 in the body?
12. describe the ultimate fate of CO2.
13. describe the reabsorption of bicarbonate in the proximal convoluted tubules of the kidney.
14. describe the reabsorption of bicarbonate in the proximal convoluted tubules when there is an acid load.
15. describe acid secretion in the distal convoluted tubules.
16. what is the phosphate buffer? what does it do?
17. what is the major buffer system for excess H+ ions?
18. ammonium buffer produced from...
19. describe the path of the ammonium buffer through the nephron.
20. what is "bicarbonate addition"?
21. how do low potassium levels contribute to an acid urine?
22. what effect does angiotensin II have on H+ secretion?
23. what are the three ways in which aldosterone increases H+ secretion?
24. what is the body's response to respiratory acidosis?
25. what is the body's response to respiratory alkalosis?
26. what are four potential causes of metabolic acidosis?
27. what is the body's response to metabolic acidosis?
28. what are three potential causes of metabolic alkalosis?
29. what is the body's response to metabolic alkalosis?
30. what is the cause of kidney stones?
31. what is the most common type of kidney stone and what is it caused by?
32. what are struvite stones and how are they formed?
33. what is the muscle that contracts in the bladder?
34. what is the trigone?
35. in males, external and internal urethral sphincters are separated by...
36. how long is the urethra in males vs. females?
37. describe the difference between the internal vs. external urethral sphincters in females.
38. bladder filling is mediated by the...
39. baroreceptor sensory neurons in the bladder stimulates...
40. pressure waves are ...
41. what is the nerve that controls the external urethral sphincter?
answers
1. chemical buffers, kidneys, lungs.
2. bicarbonate
3. expiration of CO2 reduces acidity.
4. excess H+ ions are excreted, bound to phosphate and other buffers.
5. a pH below 7.0 results in a depressed CNS state- leading to coma and death. a pH above 7.8 results in an overactive CNS: leading to nervousness, muscle tetany, convulsions.
6. CO2 is derived from metabolism and is a volatile source of acidity. phosphoric, sulfuric, and hydrochloric acids are non volatile sources of acids and are derived from nucleic acid/protein/amino acid metabolism.
7. bicarbonate to carbon dioxide.
8. carbonic anhydrase.
9. pKa of bicarbonate is 6.1- at the body's pH of 7.4, CO2 is constantly removed.
10. because the basic bicarbonate is being selectively reabsorbed to maintain the buffer system, and the excess H+ from the dietary acid loads are being filtered and excreted.
11. metabolism produces CO2. H+ from non volatile acids can also combine with bicarbonate and create CO2.
12. CO2 combines with water to form carbonic acid, which dissociates into bicarbonate and H+ ion. in the kidney, H+ is secreted and bicarbonate is reabsorbed.
13. hydrogen ion is secreted into the lumen, where it combines with bicarbonate to form carbonic acid, which is converted to CO2 and H2O by carbonic anhydrase. CO2 then diffuses through the epithelial membrane and reforms bicarbonate, which is then reabsorbed into circulation.
14. when there is an acid load, there is more H+ than the level of bicarbonate- excess H+ is bound to ammonia and phosphate and excreted. (any excess bicarbonate is simply excreted)
15. bicarbonate has been mostly reabsorbed in the proximal tubules, so H+ is simply secreted by the ATPase pumps in the intercalated cells and lowers the pH of the lumen to approximately 4.5.
16. the phosphate buffer combines with excess H+ secreted into the lumen and aids in its excretion.
17. the ammonia buffer system.
18. glutamine in proximal convoluted tubule
19. ammonia combines with H+ in the proximal tubule, and is reabsorbed in the thick ascending limb, and is then secreted back into the tubule at the distal convoluted tubule and the collecting duct.
20. each H+ ion that is secreted, buffered, and excreted is dissociated from carbonic acid, forming bicarbonate which can then reenter circulation.
21. low blood potassium levels pull K+ ions out via a K+/H+ antiporter, thereby pulling in H+ ions which are then secreted into the urine.
22. angiotensin II stimulates the PCT Na/H contransporters, which facilitate Na reabsorption and H secretion.
23. aldosterone stimulates the intercalated cell secretion of H+, stimulates the Na/H antiporter, and upregulates the Na/K pump (thereby stimulating the Na/H antiporter)
24. the excess H+ that is produced by excess CO2 in the body is secreted and bound to ammonia and phosphate buffers and excreted, thereby raising pH. every H+ ion that is excreted also corresponds to a new bicarbonate ion which can be used to buffer the pH further.
25. less H+ is secreted, allowing excess bicarbonate to be excreted.
26. excess bicarbonate being lost through diarrhea, renal failure (H+ not being secreted fast enough), acidic ketone bodies created from diabetes mellitus, and lactic acid produced from anaerobic respiration.
27. H+ secretion and bicarbonate addition in the kidneys, as well as hyperventilating reducing CO2 levels in the blood.
28. ingestion of antacids, excess H+ loss due to aldosterone or hypokalemia, or loss of HCl through vomiting.
29. less H+ is secreted, allowing excess bicarbonate to be excreted from the kidneys. hypoventilation also raises CO2 levels in the blood.
30. excess insoluble materials or water reabsorption causes stones to precipitate out.
31. calcium oxalate, due to both high calcium levels (from intestinal hyperabsorption or defective renal absorption) and high oxalate levels (intestinal over-absorption)
32. MgNH4PO4, caused by urease action of bacterial infection.
33. detrusor muscle.
34. the triangular area in the bladder between the two ureteric orifices and the urethral opening.
35. the prostate.
36. 20cm in males, 4 cm in females
37. internal urethral sphincter is involuntary, smooth muscle, controlled by autonomic nervous system, and relaxes when bladder is expanded. exteral sphincter is voluntary, striated muscle, controlled by pudendal nerve.
38. sympathetic nervous system
39. relaxation of detrusor muscle and constriction of internal urethral sphincter.
40. parasympathetic micturition reflexes- alternating detrusor contraction and relaxation along with internal urethral sphincter relaxation.
41. pudendal (S2,3,4)
body pH is largely determined by the balance between the acidic carbon dioxide and the basic bicarbonate. recall from respiratory physiology that carbon dioxide combines with water in cells via carbonic anhydrase to form carbonic acid, which then dissociates into bicarbonate and H+. the body can develop alkalosis or acidosis due to an imbalance of these molecules; acidosis can occur either by hypoventilation (retaining too much CO2) or through metabolic pathways- loss of bicarbonate through diarrhea, renal failure, buildup of lactic acid from exercise, excess ketone body production in the case of diabetes mellitus. alkalosis can occur by hyperventilation (loss of too much CO2 from lungs) or by ingestion of antacids, excess secretion of H+ in the kidneys due to hypertension, or vomiting of acidic HCl.
in order to regulate the pH, the body can increase or decrease the ventilation rate to regulate blood CO2 levels. another main source of pH regulation is in the kidneys via the balance between reabsorption and excretion of bicarbonate and H+. bicarbonate in the blood is filtered in the kidneys and combines with H+ secreted by the epithelial cells of the proximal tubule. this forms carbonic acid, which can be converted back into CO2 and H2O via carbonic anhydrase. the CO2 then diffuses back into the epithelial cells, where it reforms bicarbonate and H+ through the reverse reaction. in this way 99% of bicarbonate filtered through the kidney is reabsorbed.
if the acidity in the blood is too high, then H+ secreted into the lumen will be higher than the bicarbonate in the filtrate, and excess H+ will be bound to ammonia and phosphate buffers and excreted, raising the pH. conversely, if the blood is basic, then there will be more bicarbonate than H+, and the excess will be unable to be reabsorbed as CO2 and thus be excreted, lowering the pH. angiotensin II and aldosterone can both cause excess H+ secretion, resulting in low pH- angiotensin II stimulates the PCT Na+/H+ cotransporters in the tubular epithelia, while aldosterone stimulates the Na+/H+ antiporter, as well as stimulating intercalated cell secretion of H+. this means that the high angiotensinII and aldosterone levels associated with hypertension also result in a lower pH.
a brief look at kidney stones: when there is excess insoluble material in the filtrate or excess water reabsorption, sometimes stones can develop in the kidney and block urine passage. the most common is the calcium oxalate stone, which develops from a hyper-reabsorption of calcium and oxalate from the intestines, which then combine in the kidneys. a second type of kidney stone is struvite, which forms from a bacterial enzyme, urease, which degrades urea into NH3, which raises pH and forms MgNH4PO4 stones.
the urine that forms in the kidney then goes out via the ureters into the bladder. the bladder is surrounded by the detrusor muscle, and has openings that lead out into the urethra, which leads out into the outside world. the urethral sphincter has two layers, the inner sphincter, which is controlled by parasympathetic smooth muscle, and the outer layer, which is controlled by voluntary striated muscle (pudendal nerve, S2,3,4). when the bladder is filling, the detrusor muscle relaxes and the inner sphincter contracts. during the micturition (urination) reflex, the detrusor muscle contracts and the inner sphincter relaxes.
questions
1. what is blood pH regulated by?
2. what is the main chemical buffer in the blood?
3. how do the lungs regulate pH?
4. how do the kidneys regulate pH?
5. what are the pH limits of the body and what occurs beyond the limits?
6. what are the sources of acidity in the body?
7. acidity depends on the ratio between...
8. the reaction that produces bicarbonate from CO2 is catalyzed by...
9. what is the pKa of bicarbonate and what happens at the physiologic pH of 7.4?
10. why is urine continuously acidified?
11. what are the two sources for production of CO2 in the body?
12. describe the ultimate fate of CO2.
13. describe the reabsorption of bicarbonate in the proximal convoluted tubules of the kidney.
14. describe the reabsorption of bicarbonate in the proximal convoluted tubules when there is an acid load.
15. describe acid secretion in the distal convoluted tubules.
16. what is the phosphate buffer? what does it do?
17. what is the major buffer system for excess H+ ions?
18. ammonium buffer produced from...
19. describe the path of the ammonium buffer through the nephron.
20. what is "bicarbonate addition"?
21. how do low potassium levels contribute to an acid urine?
22. what effect does angiotensin II have on H+ secretion?
23. what are the three ways in which aldosterone increases H+ secretion?
24. what is the body's response to respiratory acidosis?
25. what is the body's response to respiratory alkalosis?
26. what are four potential causes of metabolic acidosis?
27. what is the body's response to metabolic acidosis?
28. what are three potential causes of metabolic alkalosis?
29. what is the body's response to metabolic alkalosis?
30. what is the cause of kidney stones?
31. what is the most common type of kidney stone and what is it caused by?
32. what are struvite stones and how are they formed?
33. what is the muscle that contracts in the bladder?
34. what is the trigone?
35. in males, external and internal urethral sphincters are separated by...
36. how long is the urethra in males vs. females?
37. describe the difference between the internal vs. external urethral sphincters in females.
38. bladder filling is mediated by the...
39. baroreceptor sensory neurons in the bladder stimulates...
40. pressure waves are ...
41. what is the nerve that controls the external urethral sphincter?
answers
1. chemical buffers, kidneys, lungs.
2. bicarbonate
3. expiration of CO2 reduces acidity.
4. excess H+ ions are excreted, bound to phosphate and other buffers.
5. a pH below 7.0 results in a depressed CNS state- leading to coma and death. a pH above 7.8 results in an overactive CNS: leading to nervousness, muscle tetany, convulsions.
6. CO2 is derived from metabolism and is a volatile source of acidity. phosphoric, sulfuric, and hydrochloric acids are non volatile sources of acids and are derived from nucleic acid/protein/amino acid metabolism.
7. bicarbonate to carbon dioxide.
8. carbonic anhydrase.
9. pKa of bicarbonate is 6.1- at the body's pH of 7.4, CO2 is constantly removed.
10. because the basic bicarbonate is being selectively reabsorbed to maintain the buffer system, and the excess H+ from the dietary acid loads are being filtered and excreted.
11. metabolism produces CO2. H+ from non volatile acids can also combine with bicarbonate and create CO2.
12. CO2 combines with water to form carbonic acid, which dissociates into bicarbonate and H+ ion. in the kidney, H+ is secreted and bicarbonate is reabsorbed.
13. hydrogen ion is secreted into the lumen, where it combines with bicarbonate to form carbonic acid, which is converted to CO2 and H2O by carbonic anhydrase. CO2 then diffuses through the epithelial membrane and reforms bicarbonate, which is then reabsorbed into circulation.
14. when there is an acid load, there is more H+ than the level of bicarbonate- excess H+ is bound to ammonia and phosphate and excreted. (any excess bicarbonate is simply excreted)
15. bicarbonate has been mostly reabsorbed in the proximal tubules, so H+ is simply secreted by the ATPase pumps in the intercalated cells and lowers the pH of the lumen to approximately 4.5.
16. the phosphate buffer combines with excess H+ secreted into the lumen and aids in its excretion.
17. the ammonia buffer system.
18. glutamine in proximal convoluted tubule
19. ammonia combines with H+ in the proximal tubule, and is reabsorbed in the thick ascending limb, and is then secreted back into the tubule at the distal convoluted tubule and the collecting duct.
20. each H+ ion that is secreted, buffered, and excreted is dissociated from carbonic acid, forming bicarbonate which can then reenter circulation.
21. low blood potassium levels pull K+ ions out via a K+/H+ antiporter, thereby pulling in H+ ions which are then secreted into the urine.
22. angiotensin II stimulates the PCT Na/H contransporters, which facilitate Na reabsorption and H secretion.
23. aldosterone stimulates the intercalated cell secretion of H+, stimulates the Na/H antiporter, and upregulates the Na/K pump (thereby stimulating the Na/H antiporter)
24. the excess H+ that is produced by excess CO2 in the body is secreted and bound to ammonia and phosphate buffers and excreted, thereby raising pH. every H+ ion that is excreted also corresponds to a new bicarbonate ion which can be used to buffer the pH further.
25. less H+ is secreted, allowing excess bicarbonate to be excreted.
26. excess bicarbonate being lost through diarrhea, renal failure (H+ not being secreted fast enough), acidic ketone bodies created from diabetes mellitus, and lactic acid produced from anaerobic respiration.
27. H+ secretion and bicarbonate addition in the kidneys, as well as hyperventilating reducing CO2 levels in the blood.
28. ingestion of antacids, excess H+ loss due to aldosterone or hypokalemia, or loss of HCl through vomiting.
29. less H+ is secreted, allowing excess bicarbonate to be excreted from the kidneys. hypoventilation also raises CO2 levels in the blood.
30. excess insoluble materials or water reabsorption causes stones to precipitate out.
31. calcium oxalate, due to both high calcium levels (from intestinal hyperabsorption or defective renal absorption) and high oxalate levels (intestinal over-absorption)
32. MgNH4PO4, caused by urease action of bacterial infection.
33. detrusor muscle.
34. the triangular area in the bladder between the two ureteric orifices and the urethral opening.
35. the prostate.
36. 20cm in males, 4 cm in females
37. internal urethral sphincter is involuntary, smooth muscle, controlled by autonomic nervous system, and relaxes when bladder is expanded. exteral sphincter is voluntary, striated muscle, controlled by pudendal nerve.
38. sympathetic nervous system
39. relaxation of detrusor muscle and constriction of internal urethral sphincter.
40. parasympathetic micturition reflexes- alternating detrusor contraction and relaxation along with internal urethral sphincter relaxation.
41. pudendal (S2,3,4)
Monday, February 2, 2009
organ systems: calcium and phosphate
this is the 5th lecture in the series on the kidney and talks about the kidneys' role in the regulation of calcium and phosphate levels. the kidney is one of three regulatory sites for calcium blood levels, the other two being the intestine and the bone. falling blood calcium levels trigger the release of parathyroid hormone from the parathyroid glands, which has a multifaceted effect that ultimately raises blood calcium levels.
in the kidney, the 60% of calcium that is filtered (meaning not bound to blood proteins) is mainly reabsorbed in the proximal convoluted tubule in a fashion similar to the reabsorption of sodium. PTH regulation plays a role in the reabsorption of calcium in the thick ascending limb and distal convoluted tubule; by upregulating calcium channels and pumps in the tubular epithelium. it also downregulates phosphate transporters, leading to the simultaneous decreasing of phosphate reabsorption. the rationale behind this is that high phosphate levels and calcium levels would lead to mineralization in non-bone tissues.
in the intestines, PTH stimulates calcium absorption from the gut by way of regulating the synthesis of vitamin D into its active form. vitamin D then activates calcium channels and calbindin, which transports calcium across the cells.
in the bones, PTH regulates blood calcium levels by maintaining the balance between calcium being deposited onto new bone surfaces by osteoblasts (deposition) vs. calcium being released into the bloodstream by the breakdown of bone by osteoclasts (resorption). in general, PTH stimulates osteoclast activity by signalling apoptosis in osteoblasts, thereby raising calcium levels. if PTH is pulsed, however, osteoblast apoptosis is inhibited and deposition by osteoblasts can actually be stimulated.
a few pathologies related to calcium regulation: hyperparathyroidism results in the excess secretion of PTH and thus excessively high blood Ca2+ levels, as well as a loss of calcium levels in the bone. hypoparathyroidism is the opposite condition which results in low blood calcium levels. osteomalacia is a demineralization of the bone which results from a deficiency of calcium or vitamin D. osteoporosis is also a demineralization of the bone which results in the loss of bone matrix, not just calcium.
questions
1. what are calcium and phosphate used for in the body?
2. how closely regulated are calcium levels in the body?
3. where are the main sites for homeostatic control of calcium levels?
4. what are the primary hormones that provide homeostatic maintenance of calcium and phosphate levels?
5. what form is calcium found in the body? how much is filtered in the kidney?
6. how does acidosis relate to Ca2+ in the blood? what does it result in?
7. how does alkalosis relate to Ca2+ in the blood? what does it result in?
8. PTH is secreted in response to...
9. describe the reabsorption of Ca2+ in the kidney.
10. describe PTH's control over phosphate reabsorption.
11. why does PTH stimulate reabsorption of Ca2+ and simultaneous excretion of PO4-?
12. describe vitamin D's role in intestinal calcium absorption.
13. describe PTH's role in vitamin D synthesis.
14. describe vitamin D's role in intestinal phosphate absorption.
15. what are the two factors that regulate bone formation and remodeling?
16. describe how stress regulates remodeling of bone.
17. calcium and phosphate are stored in bone in the form of...
18. how is hydroxyapetite formation inhibited in non bone tissues?
19. how do osteoblasts overcome the solubilizing of calcium and phosphate by pyrophosphate in bone?
20. what is calcitonin and where is it released from?
21. how does calcitonin lower blood Ca+ levels?
22. how does PTH stimulate deposition of bone?
23. how does PTH stimulate resorption of bone?
24. how is PTH used to control the balance between deposition/resorption of bone?
25. what effect does hyperparathyroidism have on Ca2+ levels?
26. what effect does hypoparathyroidism have on Ca2+ levels?
27. osteomalacia is...
28. osteoporosis is...
answers
1. muscle contraction, secretion of neurotransmitters, hormones, enzymes, etc.
2. very closely, varying only 1-2% daily or weekly
3. kidney, bone, intestines
4. parathyroid hormone, vitamin D, calcitonin
5. 40% protein bound (and thus not filterable by the kidney), 10% in Ca2+ form, 50% bound to anions. 60% filtered in the kidney.
6. H+ compete with Ca2+ for sites on albumin, which transports the ions in the blood. if the pH is low, then there is less protein bound calcium and thus more free ionized form. this causes decreased neural activity and muscle weakness.
7. if there are less H+ in the blood, then Ca2+ binds to proteins in the blood and reduces the free ionized form. this causes neuromuscular irritability and CNS problems.
8. a fall in blood Ca2+ level.
9. 2/3 of the Ca2+ is reabsorbed in the proximal convoluted tubule, and 1/3 is reabsorbed in the thick ascending loop and distal convoluted tubule. PTH provides fine control over Ca2+ reabsorption in the ascending loop and distal convoluted tubule.
10. PTH inhibits reabsorption of phosphate in the proximal convoluted tubule, where most phosphate reabsorption takes place.
11. because raising both phosphate and calcium levels could create calcium phosphate in soft tissues.
12. vitamin D upregulates of calcium membrane transporters as well as calbindin, which carries calcium across the cell.
13. PTH, secreted in response to falling Ca2+ levels, regulates the synthesis of 1,25 hydroxylated vitamin D- the active form.
14. vitamin D upregulates Na-PO4 cotransporter in intestinal cells.
15. hormones and physical stress.
16. stress creates a piezoelectric effect that initiates osteoblast (bone building) and osteoclast (bone destroying) activity on opposing surfaces which remodels bone.
17. hydroxyapetite: Ca10(PO4)6OH2
18. it remains in soluble form by pyrophosphate.
19. osteoblasts contain alkaline phosphatases that cleave pyrophosphates, freeing calcium and phosphate to form bone.
20. a hormone that is released in response to rising Ca2+ levels that counters the effects of PTH. released from parafollicular cells of the thyroid.
21. by inhibiting osteoclast activity; free Ca2+ is then used to deposit bone by osteoblasts.
22. PTH stimulates osteoclast activity, which can induce release of growth factors from bone matrix which can in turn stimulate osteoblast deposition of bone.
23. PTH stimulates osteoblast to initiate RANK/RANKL paracrines which activates osteoclasts and thus stimulates bone resorption.
24. if PTH is secreted intermittently, osteoblast apoptosis is inhibited and deposition occurs. if PTH is secreted continuously, osteoblasts continue to undergo apoptosis and osteoclast activity resorbs bone.
25. excess secretion of PTH causes blood Ca2+ levels to rise and bone density to fall.
26. reduction in osteoclastic activity reduces resorption of calcium and lowers blood calcium levels.
27. demineralization of bone resulting from deficiency in calcium or vitamin D.
28. loss of bone matrix
in the kidney, the 60% of calcium that is filtered (meaning not bound to blood proteins) is mainly reabsorbed in the proximal convoluted tubule in a fashion similar to the reabsorption of sodium. PTH regulation plays a role in the reabsorption of calcium in the thick ascending limb and distal convoluted tubule; by upregulating calcium channels and pumps in the tubular epithelium. it also downregulates phosphate transporters, leading to the simultaneous decreasing of phosphate reabsorption. the rationale behind this is that high phosphate levels and calcium levels would lead to mineralization in non-bone tissues.
in the intestines, PTH stimulates calcium absorption from the gut by way of regulating the synthesis of vitamin D into its active form. vitamin D then activates calcium channels and calbindin, which transports calcium across the cells.
in the bones, PTH regulates blood calcium levels by maintaining the balance between calcium being deposited onto new bone surfaces by osteoblasts (deposition) vs. calcium being released into the bloodstream by the breakdown of bone by osteoclasts (resorption). in general, PTH stimulates osteoclast activity by signalling apoptosis in osteoblasts, thereby raising calcium levels. if PTH is pulsed, however, osteoblast apoptosis is inhibited and deposition by osteoblasts can actually be stimulated.
a few pathologies related to calcium regulation: hyperparathyroidism results in the excess secretion of PTH and thus excessively high blood Ca2+ levels, as well as a loss of calcium levels in the bone. hypoparathyroidism is the opposite condition which results in low blood calcium levels. osteomalacia is a demineralization of the bone which results from a deficiency of calcium or vitamin D. osteoporosis is also a demineralization of the bone which results in the loss of bone matrix, not just calcium.
questions
1. what are calcium and phosphate used for in the body?
2. how closely regulated are calcium levels in the body?
3. where are the main sites for homeostatic control of calcium levels?
4. what are the primary hormones that provide homeostatic maintenance of calcium and phosphate levels?
5. what form is calcium found in the body? how much is filtered in the kidney?
6. how does acidosis relate to Ca2+ in the blood? what does it result in?
7. how does alkalosis relate to Ca2+ in the blood? what does it result in?
8. PTH is secreted in response to...
9. describe the reabsorption of Ca2+ in the kidney.
10. describe PTH's control over phosphate reabsorption.
11. why does PTH stimulate reabsorption of Ca2+ and simultaneous excretion of PO4-?
12. describe vitamin D's role in intestinal calcium absorption.
13. describe PTH's role in vitamin D synthesis.
14. describe vitamin D's role in intestinal phosphate absorption.
15. what are the two factors that regulate bone formation and remodeling?
16. describe how stress regulates remodeling of bone.
17. calcium and phosphate are stored in bone in the form of...
18. how is hydroxyapetite formation inhibited in non bone tissues?
19. how do osteoblasts overcome the solubilizing of calcium and phosphate by pyrophosphate in bone?
20. what is calcitonin and where is it released from?
21. how does calcitonin lower blood Ca+ levels?
22. how does PTH stimulate deposition of bone?
23. how does PTH stimulate resorption of bone?
24. how is PTH used to control the balance between deposition/resorption of bone?
25. what effect does hyperparathyroidism have on Ca2+ levels?
26. what effect does hypoparathyroidism have on Ca2+ levels?
27. osteomalacia is...
28. osteoporosis is...
answers
1. muscle contraction, secretion of neurotransmitters, hormones, enzymes, etc.
2. very closely, varying only 1-2% daily or weekly
3. kidney, bone, intestines
4. parathyroid hormone, vitamin D, calcitonin
5. 40% protein bound (and thus not filterable by the kidney), 10% in Ca2+ form, 50% bound to anions. 60% filtered in the kidney.
6. H+ compete with Ca2+ for sites on albumin, which transports the ions in the blood. if the pH is low, then there is less protein bound calcium and thus more free ionized form. this causes decreased neural activity and muscle weakness.
7. if there are less H+ in the blood, then Ca2+ binds to proteins in the blood and reduces the free ionized form. this causes neuromuscular irritability and CNS problems.
8. a fall in blood Ca2+ level.
9. 2/3 of the Ca2+ is reabsorbed in the proximal convoluted tubule, and 1/3 is reabsorbed in the thick ascending loop and distal convoluted tubule. PTH provides fine control over Ca2+ reabsorption in the ascending loop and distal convoluted tubule.
10. PTH inhibits reabsorption of phosphate in the proximal convoluted tubule, where most phosphate reabsorption takes place.
11. because raising both phosphate and calcium levels could create calcium phosphate in soft tissues.
12. vitamin D upregulates of calcium membrane transporters as well as calbindin, which carries calcium across the cell.
13. PTH, secreted in response to falling Ca2+ levels, regulates the synthesis of 1,25 hydroxylated vitamin D- the active form.
14. vitamin D upregulates Na-PO4 cotransporter in intestinal cells.
15. hormones and physical stress.
16. stress creates a piezoelectric effect that initiates osteoblast (bone building) and osteoclast (bone destroying) activity on opposing surfaces which remodels bone.
17. hydroxyapetite: Ca10(PO4)6OH2
18. it remains in soluble form by pyrophosphate.
19. osteoblasts contain alkaline phosphatases that cleave pyrophosphates, freeing calcium and phosphate to form bone.
20. a hormone that is released in response to rising Ca2+ levels that counters the effects of PTH. released from parafollicular cells of the thyroid.
21. by inhibiting osteoclast activity; free Ca2+ is then used to deposit bone by osteoblasts.
22. PTH stimulates osteoclast activity, which can induce release of growth factors from bone matrix which can in turn stimulate osteoblast deposition of bone.
23. PTH stimulates osteoblast to initiate RANK/RANKL paracrines which activates osteoclasts and thus stimulates bone resorption.
24. if PTH is secreted intermittently, osteoblast apoptosis is inhibited and deposition occurs. if PTH is secreted continuously, osteoblasts continue to undergo apoptosis and osteoclast activity resorbs bone.
25. excess secretion of PTH causes blood Ca2+ levels to rise and bone density to fall.
26. reduction in osteoclastic activity reduces resorption of calcium and lowers blood calcium levels.
27. demineralization of bone resulting from deficiency in calcium or vitamin D.
28. loss of bone matrix
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