lab dx final study questions. (doesn't include thyroid and GI health lectures)
questions
cytology tests...
1. when is a sputum cytology test indicated?
2. what are some pathological findings on a sputum cytology test?
3. when is a urine cytology test indicated?
4. how would GU inflammation manifest on a urine cytology test?
5. how would viral infection manifest on a urine cytology test?
6. when is a nipple discharge cytology test indicated?
7. nipple discharge cytology can aid in the diagnosis of...
pap smear...
8. what are the indications for getting a pap smear?
9. what are the indications for getting a pap smear according to the ACE?
10. how often does the ACE recommend getting a pap smear?
11. what is the area on the cervix where the most abnormal cells changes occur?
12. what is the number 1 risk factor for cervical cancer?
13. what are the high risk strains of the microorganism in question 12?
14. what is the advantage to the "standard" pap smear collection technique?
15. what does the gardasil vaccine target?
cervical cancer classification...
16. what is the bethesda system?
17. what are the minimum requirements for specimen adequacy according to the bethesda system?
18. what do the CIN I-3 classifications indicate?
19. what is ASC-US and what is the significance?
20. what is an AGC and what is its significance?
21. what is the maturation index and what is its significance?
22. what might be seen in atrophic vaginitis?
liver enzymes...
23. which enzymes are a better indicator of liver function rather than the enzymes on a hepatic panel?√
24. what conditions might cause a marked increase in AST and ALT levels?√ √
25. what conditions is ALP markedly increased in?√X
26. an increase in which marker is associated with alcoholic hepatitis?√√
27. an AST/ALT ratio of >1 indicates...√√
28. an AST/ALT ratio of >2-3 indicates...√√
29. an AST/ALT ratio of <1>
Showing posts with label lab diagnosis II. Show all posts
Showing posts with label lab diagnosis II. Show all posts
Wednesday, March 24, 2010
Saturday, March 20, 2010
lab dx II: thyroid function tests
a review of the thyroid in the context of lab diagnosis in the context of cramming for finals.
the synthesis of thyroid hormones begins in the follicles of the thyroid, filled with a protein rich colloid where iodine is incorporated into thyroglobulin molecules to form mostly T4 (90%) and T3 (10%, the biologically active form). the thyroid is stimulated to release T4/T3 by TSH, which is released by the pituitary via stimulation by TRH, which is released by the hypothalamus. once released, T4 is converted to T3 in the periphery and mediate cellular growth, differentiation and metabolism.
in the periphery T4 and T3 are either free or bound; if bound they are most likely bound to TBG, or TBPA (20% of T4), or albumin (10% T4, 30% T3). T4 is converted to T3 mainly in the liver and skeletal muscle, which then has a ten times greater affinity for nuclear receptors within cells which mediate metabolic activity. only about 40% of T4 is converted directly to T3; the remaining T4 can be converted either to reverse T3 or T3AC, both of which are inactive isomers of T3 that can be activated by intestinal sulfatases.
more detail on T4: when in the blood, T4 is mostly bound (99.98%) rather than free. thus when levels of the main carrier for T4 goes up, TBG (as can happen in pregnancy), T4 levels may appear to be falsely elevated- however free, unbound T4 levels will remain normal. T4 levels less than 2.0 ug/mL are equivalent to "myxedema hypothyroidism" and can be caused by primary, secondary, or tertiary hypothryoidism-- lack of production at the level of the thyroid, pituitary, or hypothalamus, respectively. T4 greater than 20 ug/ml is considered a "thyroid storm" and can be from primary hyperthyroid (most commonly grave's disease), acute thyroiditis, struma ovarii, or a TBG increase.
a test that can provide an indirect measurement of T4 is the T3 resin uptake test, which measures relative saturation of TBG- because the T4 in the blood is nearly all bound to TBG. if T4 levels are elevated in hyperthyroidism or struma ovarii, TBG will be more saturated and not able to accommodate much T3, which will result in higher levels of T3 bound to resin rather than TBG-- leading to a high T3RU. conversely, hypothyroid states will leave TBG less saturated, allowing T3 to bind to it rather than to the resin-- leading to a low T3RU.
testing TSH levels is useful for differentiating between different types of hypothyroidism-- primary hypothyroid would present with high TSH levels and would not be responsive to exogenous TSH, whereas secondary or tertiary hypothyroid would have near zero TSH levels and would be responsive to exogenous TSH.
some more lab markers and what they indicate: total T3 levels (bound plus free) are useful for measuring hyperthyroidism. free T4 or T3 useful for patients with protein abnormalities. reverse T3 levels high in hyperthyroidism and with stressed physiology. autoantibodies can also be measured, to the thyroid gland (results in hyperthyroid), or TPO and thyroglobulin (hypothyroid).
primary hypo and hyperthyroid and most commonly caused by antibodies to the thyroid; in primary hyperthyroid, this results from defective suppressor genes which ultimately allow b cells to create anti TPO and TGLB antibodies. grave's can manifest with marked exophthalmos due to the targeting of TSH receptors in the retro orbital area by the anti thyroid antibodies. on the other end of the spectrum, hashimoto's is the result of an anti TPO antibody, and might initially present as hyperthyroidism, then progress to hypothyroidism with low T4, T3RU, and high TSH. compared to grave's, hashimoto's has a higher level of anti TPO antibodies.
questions
thyroid hormone synthesis...
1. what type of cell in the thyroid produces thyroid hormone?
2. what is contained inside the follicles?
3. what do the parafollicular cells produce?
4. what is the role of the hypothalamus and pituitary in thyroid function?
5. what form is thyroid hormone secreted in and which form is biologically active?
6. what is the role of TPO in the colloid of the follicles?
7. what is the T4:T3 ratio in the colloid?
8. what are the three fundamental physiological processes that thyroid hormones affect?
thyroid hormones in the wilderness...
9. which protein binds most T3 and T4 in the blood?
10. what does TBPA carry?
11. what does albumin carry?
12. which tissues does T4 conversion generally take place in?
13. compare the biological potency of T4 vs. T3.
14. under normal circumstances, what is T4 converted into besides T3?
15. are T3s and T3AC biologically active?
T4...
16. what percentage of T4 is protein bound?
17. what conditions might show falsely elevated T4 levels? how does this appear as a lab result?
18. what are congenital defects that can result from low T4 levels?
19. what are the critical high and low values for T4?
20. what are the most common factors for increased T4 levels?
21. what are the most common causes for decreased T4 levels?
T3RU...
22. what is T3RU a measure of?
23. what would be the T3RU for hyperthyroidism and why?
24. what would be the T3RU for hypothyroidism and why?
25. is T3RU better for assessing hyper or hypothyroidism?
26. what else can cause increased T3RU besides hyperthyroidism?
27. what else can cause decreased T3RU besides hypothyroidism?
28. what is the formula for FTI and what does it represent?
TSH...
29. TSH aids in the diagnosis of...
30. what are TSH levels in primary, secondary, tertiary hypothyroidism?
31. describe the diurnal variation seen in TSH levels.
32. what causes increased TSH levels?
33. what causes decreased TSH levels?
34. what does TRH assess?
total T3, free T4/T3, reverse T3, thyroid antibodies...
35. are total T3 levels better for diagnosing hyper or hypothyroidism?
36. what is T3 toxicosis and how does it present?
37. when are free T4 or T3 levels useful to measure?
38. when are reverse T3 levels high?
39. what did Dr. Dennis Wilson, MD propose in relation to reverse T3?
40. what are some examples of autoantibodies to the thyroid gland?
grave's and hashimoto's...
41. what is grave's disease?
42. what is the "suppressor defect" in the context of grave's disease?
43. what are the autoantibodies that are commonly seen in grave's?
44. why does grave's disease manifest with exophthalmos?
45. what is hashimoto's?
46. which gender is more likely to get hashimoto's?
47. early stages of hashimotos might present as...
48. early labs of hashimotos might show...
49. compare the antibody titer levels in grave's vs. hashimotos.
euthyroid sick syndrome...
50. what is ESS?
51. what are three specific physiogical processes that can cause ESS?
answers
1. follicular epithelium.
2. protein rich colloid, high in thyroglobulin.
3. calcitonin.
4. hypothalamus releases TRH, which stimulates release of TSH from pituitary, which is the main mediator of thyroid gland function.
5. 90% secreted as T4, then converted to biologically active T3 in cells.
6. thyroid peroxidases oxidize iodide to iodine for use in T3/T4.
7. 5:1.
8. cellular growth, differentiation, metabolism.
9. TBG, 70%.
10. 20% of T4 and no T3.
11. 10% of T4, 30% T3.
12. liver and skeletal muscle.
13. T3 has a 10 times greater affinity for DNA transcription factor receptors than T4.
14. 40% T3, 20% reverse T3, 20%T3S.
15. not unless they encounter sulfatases in the GI tract.
16. 99.98%.
17. pregnancy and oral contraceptives. high TBG but normal free T4.
18. cretinism, mental retardation.
19. less than 2.0 ug/ml- myxedema coma
more than 20 ug/ml- thyroid storm
20. primary hyperthyroid (grave's disease)
acute thyroiditis
struma ovarii
TBG increase
21. primary hypothyroid (hashimoto's)
secondary hypothyroid (pituitary dysfx)
tertiary hypothyroid (hypothalamus dysfx)
protein malnutrition
22. an indirect measurement of the amount of free binding sites on TBG and TBPA.
23. hyperthyroidism -> high T4 levels -> more saturated TBG -> more T3 bound to resin instead of TBG -> higher T3RU.
24. hypothyroidism -> low T4 -> more unsaturated TBG -> more T3 bound to TBG -> lower T3RU.
25. better for hyperthyroidism-- only 60% accurate for hypo.
26. hypoproteinemia, struma ovarii.
27. any factor that increases TBG like pregnancy, hepatitis / cirrhosis.
28. FTI=(T4*T3RU)/100, is an estimate for total T4 levels.
29. hypothyroidism.
30. primary- high TSH. secondary + tertiary: TSH almost 0.
31. lowest at 10AM, highest at 10PM.
32. primary hypothyroid
thyroiditis
thyroid agenesis
congenital cretinism
excess iodine intake
33. secondary, tertiary hypothyroid
hyperthyroid
self medication with T4
34. responsiveness of anterior pituitary to secrete TSH upon injection of TRH.
35. hyperthyroid.
36. normal T4 and high T3.
37. useful to measure thyroid functioning in patients who have protein abnormalities.
38. hyperthyroidism.
39. a stressed body might have a predisposition to converting T4 to rT3 instead of T3.
40. thyroid stimulating antibodies, resulting in hyperthyroidism. anti TPO antibody, inhibits thyroid peroxidase. anti TGLB, inhibits thyroglobulin.
41. most common form of hyperthyroid that results from TSI's stimulating TSHR's.
42. a defect in a suppressor gene allows t helper cells to interact with thyroid antigens, which then stimulate b cells to create thyroid stimulating immunoglobulin.
43. anti TPO, anti TGLB.
44. the TSH antibodies produced in grave's bind to TSH receptors in the retroorbital tissues which produces inflammation and swelling.
45. the most common cause of acquired hypothyroid.
46. females 8:1.
47. hyperthyroid.
48. normal T4 and TSH + anti TPO ab.
49. much higher in hashimotos.
50. thyroid dysfunction secondary to nonthyroidal systemic illness.
51. decreased peripheral conversion of T4 to T3,
decreased clearance of reverse T3
decreased binding of thyroid hormones to TBG
[conversion, clearance, binding]
the synthesis of thyroid hormones begins in the follicles of the thyroid, filled with a protein rich colloid where iodine is incorporated into thyroglobulin molecules to form mostly T4 (90%) and T3 (10%, the biologically active form). the thyroid is stimulated to release T4/T3 by TSH, which is released by the pituitary via stimulation by TRH, which is released by the hypothalamus. once released, T4 is converted to T3 in the periphery and mediate cellular growth, differentiation and metabolism.
in the periphery T4 and T3 are either free or bound; if bound they are most likely bound to TBG, or TBPA (20% of T4), or albumin (10% T4, 30% T3). T4 is converted to T3 mainly in the liver and skeletal muscle, which then has a ten times greater affinity for nuclear receptors within cells which mediate metabolic activity. only about 40% of T4 is converted directly to T3; the remaining T4 can be converted either to reverse T3 or T3AC, both of which are inactive isomers of T3 that can be activated by intestinal sulfatases.
more detail on T4: when in the blood, T4 is mostly bound (99.98%) rather than free. thus when levels of the main carrier for T4 goes up, TBG (as can happen in pregnancy), T4 levels may appear to be falsely elevated- however free, unbound T4 levels will remain normal. T4 levels less than 2.0 ug/mL are equivalent to "myxedema hypothyroidism" and can be caused by primary, secondary, or tertiary hypothryoidism-- lack of production at the level of the thyroid, pituitary, or hypothalamus, respectively. T4 greater than 20 ug/ml is considered a "thyroid storm" and can be from primary hyperthyroid (most commonly grave's disease), acute thyroiditis, struma ovarii, or a TBG increase.
a test that can provide an indirect measurement of T4 is the T3 resin uptake test, which measures relative saturation of TBG- because the T4 in the blood is nearly all bound to TBG. if T4 levels are elevated in hyperthyroidism or struma ovarii, TBG will be more saturated and not able to accommodate much T3, which will result in higher levels of T3 bound to resin rather than TBG-- leading to a high T3RU. conversely, hypothyroid states will leave TBG less saturated, allowing T3 to bind to it rather than to the resin-- leading to a low T3RU.
testing TSH levels is useful for differentiating between different types of hypothyroidism-- primary hypothyroid would present with high TSH levels and would not be responsive to exogenous TSH, whereas secondary or tertiary hypothyroid would have near zero TSH levels and would be responsive to exogenous TSH.
some more lab markers and what they indicate: total T3 levels (bound plus free) are useful for measuring hyperthyroidism. free T4 or T3 useful for patients with protein abnormalities. reverse T3 levels high in hyperthyroidism and with stressed physiology. autoantibodies can also be measured, to the thyroid gland (results in hyperthyroid), or TPO and thyroglobulin (hypothyroid).
primary hypo and hyperthyroid and most commonly caused by antibodies to the thyroid; in primary hyperthyroid, this results from defective suppressor genes which ultimately allow b cells to create anti TPO and TGLB antibodies. grave's can manifest with marked exophthalmos due to the targeting of TSH receptors in the retro orbital area by the anti thyroid antibodies. on the other end of the spectrum, hashimoto's is the result of an anti TPO antibody, and might initially present as hyperthyroidism, then progress to hypothyroidism with low T4, T3RU, and high TSH. compared to grave's, hashimoto's has a higher level of anti TPO antibodies.
questions
thyroid hormone synthesis...
1. what type of cell in the thyroid produces thyroid hormone?
2. what is contained inside the follicles?
3. what do the parafollicular cells produce?
4. what is the role of the hypothalamus and pituitary in thyroid function?
5. what form is thyroid hormone secreted in and which form is biologically active?
6. what is the role of TPO in the colloid of the follicles?
7. what is the T4:T3 ratio in the colloid?
8. what are the three fundamental physiological processes that thyroid hormones affect?
thyroid hormones in the wilderness...
9. which protein binds most T3 and T4 in the blood?
10. what does TBPA carry?
11. what does albumin carry?
12. which tissues does T4 conversion generally take place in?
13. compare the biological potency of T4 vs. T3.
14. under normal circumstances, what is T4 converted into besides T3?
15. are T3s and T3AC biologically active?
T4...
16. what percentage of T4 is protein bound?
17. what conditions might show falsely elevated T4 levels? how does this appear as a lab result?
18. what are congenital defects that can result from low T4 levels?
19. what are the critical high and low values for T4?
20. what are the most common factors for increased T4 levels?
21. what are the most common causes for decreased T4 levels?
T3RU...
22. what is T3RU a measure of?
23. what would be the T3RU for hyperthyroidism and why?
24. what would be the T3RU for hypothyroidism and why?
25. is T3RU better for assessing hyper or hypothyroidism?
26. what else can cause increased T3RU besides hyperthyroidism?
27. what else can cause decreased T3RU besides hypothyroidism?
28. what is the formula for FTI and what does it represent?
TSH...
29. TSH aids in the diagnosis of...
30. what are TSH levels in primary, secondary, tertiary hypothyroidism?
31. describe the diurnal variation seen in TSH levels.
32. what causes increased TSH levels?
33. what causes decreased TSH levels?
34. what does TRH assess?
total T3, free T4/T3, reverse T3, thyroid antibodies...
35. are total T3 levels better for diagnosing hyper or hypothyroidism?
36. what is T3 toxicosis and how does it present?
37. when are free T4 or T3 levels useful to measure?
38. when are reverse T3 levels high?
39. what did Dr. Dennis Wilson, MD propose in relation to reverse T3?
40. what are some examples of autoantibodies to the thyroid gland?
grave's and hashimoto's...
41. what is grave's disease?
42. what is the "suppressor defect" in the context of grave's disease?
43. what are the autoantibodies that are commonly seen in grave's?
44. why does grave's disease manifest with exophthalmos?
45. what is hashimoto's?
46. which gender is more likely to get hashimoto's?
47. early stages of hashimotos might present as...
48. early labs of hashimotos might show...
49. compare the antibody titer levels in grave's vs. hashimotos.
euthyroid sick syndrome...
50. what is ESS?
51. what are three specific physiogical processes that can cause ESS?
answers
1. follicular epithelium.
2. protein rich colloid, high in thyroglobulin.
3. calcitonin.
4. hypothalamus releases TRH, which stimulates release of TSH from pituitary, which is the main mediator of thyroid gland function.
5. 90% secreted as T4, then converted to biologically active T3 in cells.
6. thyroid peroxidases oxidize iodide to iodine for use in T3/T4.
7. 5:1.
8. cellular growth, differentiation, metabolism.
9. TBG, 70%.
10. 20% of T4 and no T3.
11. 10% of T4, 30% T3.
12. liver and skeletal muscle.
13. T3 has a 10 times greater affinity for DNA transcription factor receptors than T4.
14. 40% T3, 20% reverse T3, 20%T3S.
15. not unless they encounter sulfatases in the GI tract.
16. 99.98%.
17. pregnancy and oral contraceptives. high TBG but normal free T4.
18. cretinism, mental retardation.
19. less than 2.0 ug/ml- myxedema coma
more than 20 ug/ml- thyroid storm
20. primary hyperthyroid (grave's disease)
acute thyroiditis
struma ovarii
TBG increase
21. primary hypothyroid (hashimoto's)
secondary hypothyroid (pituitary dysfx)
tertiary hypothyroid (hypothalamus dysfx)
protein malnutrition
22. an indirect measurement of the amount of free binding sites on TBG and TBPA.
23. hyperthyroidism -> high T4 levels -> more saturated TBG -> more T3 bound to resin instead of TBG -> higher T3RU.
24. hypothyroidism -> low T4 -> more unsaturated TBG -> more T3 bound to TBG -> lower T3RU.
25. better for hyperthyroidism-- only 60% accurate for hypo.
26. hypoproteinemia, struma ovarii.
27. any factor that increases TBG like pregnancy, hepatitis / cirrhosis.
28. FTI=(T4*T3RU)/100, is an estimate for total T4 levels.
29. hypothyroidism.
30. primary- high TSH. secondary + tertiary: TSH almost 0.
31. lowest at 10AM, highest at 10PM.
32. primary hypothyroid
thyroiditis
thyroid agenesis
congenital cretinism
excess iodine intake
33. secondary, tertiary hypothyroid
hyperthyroid
self medication with T4
34. responsiveness of anterior pituitary to secrete TSH upon injection of TRH.
35. hyperthyroid.
36. normal T4 and high T3.
37. useful to measure thyroid functioning in patients who have protein abnormalities.
38. hyperthyroidism.
39. a stressed body might have a predisposition to converting T4 to rT3 instead of T3.
40. thyroid stimulating antibodies, resulting in hyperthyroidism. anti TPO antibody, inhibits thyroid peroxidase. anti TGLB, inhibits thyroglobulin.
41. most common form of hyperthyroid that results from TSI's stimulating TSHR's.
42. a defect in a suppressor gene allows t helper cells to interact with thyroid antigens, which then stimulate b cells to create thyroid stimulating immunoglobulin.
43. anti TPO, anti TGLB.
44. the TSH antibodies produced in grave's bind to TSH receptors in the retroorbital tissues which produces inflammation and swelling.
45. the most common cause of acquired hypothyroid.
46. females 8:1.
47. hyperthyroid.
48. normal T4 and TSH + anti TPO ab.
49. much higher in hashimotos.
50. thyroid dysfunction secondary to nonthyroidal systemic illness.
51. decreased peripheral conversion of T4 to T3,
decreased clearance of reverse T3
decreased binding of thyroid hormones to TBG
[conversion, clearance, binding]
Thursday, March 18, 2010
Wednesday, January 27, 2010
lab diagnosis II: blood chemistry- glucose and proteins
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.
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.
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