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535 Cards in this Set
- Front
- Back
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MINERAL & BONE METABOLISM
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MINERAL & BONE METABOLISM
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1. _______ is the balance between osteoblasts and osteoclasts.
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1. Bone modeling
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2. ____% of skeletal minerals are exchanged yearly by adults.
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2. 20%
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3. Mineral and bone metabolism is reliant on _______, _______, and _______.
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3. Intestinal absorption, renal clearance, and hormonal regulation
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4. Where is most calcium found in the body?
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4. Bone
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5. What are the functions of calcium?
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5. bone structure, coagulation, plasma membrane potential, muscle contraction and neurotransmission, enzyme cofactor
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6. A decrease in calcium causes _______ neuromuscular excitiability and ________
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6. increased, tetany
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7. _______ displaces Ca++ from pH dependent proteins.
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7. Acidosis
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8. What are the two most important functions of phosphorus?
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8. bone mineralization and phospholpid stucture in cell membranes
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9. ____% of phosphorus is found in the bone.
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9. 50%
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10. What is the bone pool?
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10. Quickly accesible calcium at the surface of a bone
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11. Plasma ionized Ca, PO4, and Mg facilitate _____________________.
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11. interchange between excellular fluid & bone, urine, and intestinal contents
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12. PTH is produced by ______, and are released when _______ is low.
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12. Cheif cells, plasma calcium
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13. PTH functions to increase _______, _______, and _______. Its decreases ________.
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13. bone resorption, calcitrol, calcium reabsorption by kidneys :: PO4 reabsorption by kidneys
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14. Calcitrol stimulates the kidneys to ______________.
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14. Increase reabsorption of Calcium and phosphorus
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15. Calcitonin stimulates the kidneys to ______________.
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15. Decrease reabsorption of Ca and PO4
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16. What produces PTH related protein? (PTHrP)
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16. Normal squamous and breast epithelial cells (heavy amounts from tumors)
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17. What does PTHrP do?
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17. Acts like PTH, increases plasma Ca significantly
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18. What are the two major causes of hypercalcemia?
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18. Primary Hyperparathyroism or Malignancy
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19. Why can multiple myeloma cause hypercalcemia?
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19. Increase in IgG, and calcium binds to to IgG
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20. What is the most common cause of hypocalcemia? Secondary?
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20. Hypoalbuminemia :: Hypoparathyroidism
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21. The rare hypermagnesemia causes _______, ______, _______, and _______.
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21. respiratory paralysis, cardiac arrest, muscle injury, and severe dehydration
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22. Hypomagnesemia is associated with what symptoms?
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22. Tetany, agitation, delerium, muscle weakness, and cardiac arrest
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23. Hypomagnesemia is found in alcoholics, so what else would you associate with it?
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23. cirrhosis, malabsorption syndromes and hypo-mineralnamehere
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24. Alkaline phosphatase is an ____ found in the _______ and _______.
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24. enzyme, bone, liver
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25. ALP tends to be elevated in _________ and _________ disease.
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25. bone, hepatobiliary
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26. Bone ALP increase whenever there is increased _______ activity.
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26. osteoblastic
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27. Osteoporosis is the ____ loss of ____________.
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27. balanced loss of bone & matrix
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28. What is the most useful test to monitor Vitamin D deficiency and Paget's?
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28. Bone ALP
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RENAL FUNCTION AND URINALYSIS
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RENAL FUNCTION AND URINALYSIS
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29. Who makes erythropoietin?
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29. Kidney
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30. A disease that is pre-renal, such as ______, results in _____ & _________.
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30. Congestive Heart Failure, decrease blood flow & increase blood urea
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31. What three things are typically measured to determine renal function?
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31. BUN, Creatinine, and uric acid
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32. Which kidney assessment is not affected by daily living changes?
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32. Creatinine
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33. What is the prime indicator of glomerular filtration/clearance rate?
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33. Creatinine
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34. Why is creatine such a good indicator of filtration rate?
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34. Neither absorbed nor secreted in the tubules
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35. Uric acid is the product of _____________.
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35. purine breakdown by the liver
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36. What can cause hyperuricemia?
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36. Renal disease, hypertension (anything that slows excretion rates)
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37. Describe the lab findings in gout.
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37. Increase uric acid, WBCs, ESR, and CRP
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38. What are the risk factors for gout?
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38. Hyperuricemia, alcohol, purine diet, genetics, diurectics
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39. What are the renal complications of gout?
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39. Nephrolithiasis, acute gouty nephropathy, chronic gouty nephropathy
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40. What is the typical kidney stone of gout? Why is it so dangerous?
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40. Staghorn Calculus :: often becomes infected
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41. Urine is mostly ________ & ________.
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41. water and urea
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42. When is a midstream catch indicated?
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42. When a sterile collection is needed
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43. What are the three stages of a routine urinalysis?
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43. Physical, chemical, and microscopic
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44. What is checked during the physical stage of urinalysis?
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44. color & turbidity
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45. When is a microscopic exam required?
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45. When there is blood, protein, leukocyte esterase, or nitrites
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46. What is the first indication of renal disease? When is this normal?
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46. proteinuria :: when its low level mucous
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47. What are the benign causes of proteinuria?
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47. dehydro, stress, exercise, fever, orthostatic, non-renal acute illness
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48. What is orthostatic proteinuria?
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48. increase proteins in an upright position, normal when supine
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49. More than ______ grams of protein per day always suggest glomerular problems.
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49. 4.0 grams
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50. Which collagen disease may lead to proteinuria?
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50. SLE
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51. Trauma, infection, renal stones, and malaginancy can all cause _________.
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51. hematuria
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52. The dipstick measures ________, not ______; the microscope does that.
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52. hgB, RBCs
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53. What is the difference between hemoglobinuria & hematuria?
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53. Hematuria only includes intact RBCs
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54. If the urine is hemoglobin positive, but no RBCs are visible, __________ has occurred.
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54. Intravascular hemolysis
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55. More than ____ of WBCs in the urine is called _______.
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55. Pyuria
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56. If WBC casts are seen you should suspect __________.
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56. pyelonephritis
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57. If you are nitrite negative, are you free of infection? Why or why not?
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57. No, yeast & some (+) bacteria do not make nitrites
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58. What group commonly gets UTIs?
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58. Females & diabetics
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59. An acidic diet may lead to __________ stones.
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59. Uric acid stones
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60. An alkaline diet may lead to __________ stones.
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60. Calcium stones
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61. Who tends to have ketonuria?
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61. Diabetics
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62. What is the renal threshold for releasing glucose into the urine?
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62. 180 mg/dl
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63. ASO is for what?
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63. Group A beta hemolytic strep
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PLASMA PROTEINS
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PLASMA PROTEINS
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64. Which plasma proteins are not produced in the liver?
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64. Peptide hormones, von Willy, and immunoglobulins
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65. A negative nitrogen balance would signify what?
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65. More protein breakdown than synthesis
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66. What can determine the protein families? How many signatures are there?
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66. Electrophoretic migration :: 5
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67. __________ stimulate hepatic synthesis of acute phase reactants.
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67. Cytokine IL-1 & IL-6
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68. What are acute phase reactants?
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68. proteins that modify inflammatory response (the acute phase of an illness)
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69. What transport proteins are not synthesized during acute inflammatory states?
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69. albumin & transferrin
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70. What is total protein composed of?
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70. Albumin & globulins
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71. What changes total protein?
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71. H20 level, concentration of protein
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72. What can cause hyperproteinemia?
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72. dehydro, gammopathy, inflammation, infection
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73. What can cause hyperalbuminemia?
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73. dehydration
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74. Albumin is a sensitive marker for _______ & _______ integrity.
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74. glomerular & Blood-brain-barrier
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75. What does the A/G ratio tell us?
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75. That albumin should be higher in levels than all other globulins combined
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76. What is an important protease inhibitor involved in emphysema or infintile hepatitis?
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76. alpha1-antitrypsin
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77. _____ transports free hgB.
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77. Haptoglobulin
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78. Haptoglobulin is used to monitor what? When will it increase? Decrease?
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78. Acute phase reactions & hemolysis :: inflammation & nephrotic syndrome :: intravascular hemolysis
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79. What is ceruloplasmin?
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79. Enzyme that allows for iron binding and metabolism
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80. When does ceruloplasmin decrease? Increase?
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80. Wilson's disease (Cu is in tissues) :: inflammation & Cu toxicity
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81. Transferrin increases in _________, while decreases in __________.
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81. IDA, inflammation
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82. What can be used to detect pathologies during pregnancy?
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82. C-reactive protein (CRP)
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83. CRP is non-specific but is the _________ acute phase reactant, thus its used to monitor _______.
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83. most sensitive, inflammation
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84. Who reacts quicker, CRP or Neutrophils? Which disperses quicker?
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84. CRP :: CRP
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85. Immunoglobulins are composed of one ______ and one to three _________.
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85. light chain, heavy chain
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86. How many antigens is a plasma cell sensitive too? This is known as a _________ immunoglobulin.
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86. Only for 1 antigen :: monoclonal
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87. Who is the memory immunoglobulin? Most abundant in blood?
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87. IgG :: IgG
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88. What is the most common immunoglobulin in the body?
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88. IgA
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89. Who is the rapid response immunoglobulin?
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89. IgM
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90. What is a monogammopathy?
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90. spike of a particular globulin clone (such as MM's Bence Jones)
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91. What will lead to hypoproteinemia & hypoalbumemia?
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91. nephrotic syndrome, blood loss, burns, inflammation, malignancy, liver disease, intake
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92. In essence, what does A/G ratio tell us?
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92. Albumin should be in greater numbers than total other globulins, if not, uh oh!
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93. Alpha1-antitrypsin is a ______ inhibitor, preventing tissue breakdown by _______.
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93. protease, neutrophils
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94. A lack of alpha1-antitrypsin results commonly in __________.
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94. emphysema
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95. During pregnancy for determining illness, _________ is useful & __________ is not.
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95. c-reactive protein :: SED rate
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96. Immunoglobulin production by multiple clones is known as __________.
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96. polyclonal
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97. Polyclonal gammopathies are caused by ______________________.
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97. general immune stimulation (inflammation, autoimmune disease)
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98. What can be used to visualize monoclonal gammopathies?
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98. Immunoelectrophoresis
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99. What is a benign monoclonal gammopathy? What percentage becomes malignant?
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99. Monoclonal gammopathy of undetermined significance :: 33%
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100. MM is a monoclonal malignant proliferation of plasma cells, what clone is elevated in MM?
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100. IgG
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101. In about a 5th of MM cases, only the ____ chain is produced.
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101. light chain
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102. In over half of MM cases the _________ protein is seen, which is a __________.
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102. Bence Jones Protein, free light chains in urine
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103. Name a IgM monoclonal gammopathy.
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103. Waldenstrom Macroglobulinemia
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104. How does Waldenstrom Macroglobulinemia present?
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104. Bleeding, thick blood leading to headache & visual problems, and renal failure
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105. Hypogammaglobulinemia tends to be due to _______, and thus often have recurrent ________.
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105. CLL, bacterial infections
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106. A hypogammaglobulinemia due to increased secretion would likely be in a case of __________.
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106. nephrotic syndrome
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107. What prevents immune complexes & antigens from circulation removal?
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107. Portal hypertension (due to cirrhosis)
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108. Portal hypertension results in what gammopathy?
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108. Polyclonal IgG & IgA hypergammopathy
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109. If you viewed an electrophoresis graph that had a wide beta + gamma lump, what is suspected?
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109. Cirrhosis
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HEPATIC BILIARY DISORDERS
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HEPATIC BILIARY DISORDERS
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110. What breaks down substances into waste for elimination?
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110. Liver
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111. What happens to coagulation protein levels in end stage liver disease? Clinical symptom?
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111. Decrease levels :: bruising
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112. What are synthesized in the liver?
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112. plasma proteins, lipids, lipoproteins, bile acids
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113. What are the names for insoluble bilirubin?
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113. uncongugated or indirect
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114. What bilirubin is measured typically by serum labs?
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114. direct (because it seperates)
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115. What are the three phases of bilirubin?
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115. Uptake (hepatocytes), conjugation (hepatocytes), excretion (bile, rate limiting)
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116. Unconjugated bilirubin is bound to _________, and thus ____ be excreted in bile or urine.
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116. albumin, cannot
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117. Does unconjugated bili cross the placenta? BBB?
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117. yes, yes (because lipid soluble)
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118. Interference of the enzyme ____________ leads to jaundice.
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118. UDP-glucuronyl
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119. When does conjugated bilirubin appear in the urine?
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119. increased plasma levels
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120. What reduces bilirubin in the intestines? What does it become?
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120. anaerobic bacteria :: urobilinogen
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121. What is a metabolite of urobilinogen that colors the stool?
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121. stercobilin
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122. Most of the body’s urobiligen is __________; 20% is __________.
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122. excreted in stool (a little in urine) ; reabsorbed
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123. What colors urine?
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123. urobilin
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124. What bilirubin is meant when referring to urine?
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124. direct (water soluble)
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125. Jaundice bilirubin deposition occurs where?
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125. skin, sclerae (conjunctiva actually), gums, nail beeds, tympanic membranes, soft palate
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126. What is a yellowish patch in the eye due to chronic sun exposure?
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126. pinguecula
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127. What is a serious cause of silent jaundice?
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127. pancreatic carcinoma
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128. Excess _______ can cause pruritis and scratching.
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128. Bilirubin
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129. What are the three forms of hyperbilirubinemia?
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129. Prehepatic, hepatic, and post-hepatic
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130. Jaundice is often _____-causal.
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130. multi
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131. Pre-hepatic jaundice is predominantly _______________ hyperbilirubinemia with a _______ liver.
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131. unconjugated, normal
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132. What is the most common cause of pre-hepatic jaundice?
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132. hemolytic anemia
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133. What are the laboratory findings of Pre-hepatic jaundice?
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133. elevated indirect bilirubin / urobilinogen, possible elevated direct bilirubin
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134. ____ jaundice is a problem of the hepatocytes resulting in possible trouble with ____, _____, or ____.
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134. Hepatic jaundice, uptake, conjugation, excretion (Cholestasis)
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135. What can cause decreased uptake, conjugation, and excretion?
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135. hepatitis
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136. What can cause decreased uptake, and conjugation?
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136. Gilbert's syndrome
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137. What can cause decreased conjugation?
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137. Crigler-Najjar syndrome
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138. What can cause decreased excretion?
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138. Primary biliary cirrhosis (or anything that interferes w/ transport of conjugated bilirubin)
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139. Why does direct bilirubin elevates in hepatitis?
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139. The bilirubin that is conjugated is returned to the plasma so levels increase
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140. Urine is often _______ colored in acute hepatitis.
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140. amber
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141. Who tends to get Gilbert's syndrome? What type of bilirubin is involved?
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141. Fasting alcoholic men :: unconjugated
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142. Crigler-Jajjar syndrome is a _______ disorder that causes _________ hyperbilirubinemia.
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142. genetic, unconjugated
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143. _____ is the progressive destruction of interlobular bile ducts resulting in _______ and _______.
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143. Primary Biliary cirrhosis, cholestasis, liver cirrhosis
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144. What is the common mechanism of post hepatic jaundice?
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144. Common bile duct obstruction
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145. In post hepatic jaundice, since no _____ gets to the GI tract, no _______ is produced.
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145. bilirubin, urobilinogen
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146. What are the lab findings of post hepatic jaundice?
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146. High direct, total, and urine bilirubin
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147. How does the urine appear in post-hepatic jaundice? Feces?
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147. Amber, steatorheaa or clay colored
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148. What can indicate bile duct obstruction in the presence of liver disease?
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148. alkaline phosphatase
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149. What is the most sensitive to chronic liver disease?
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149. GGTP
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150. AST, formally ______, is sensitive to ________ since its made in the ________.
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150. SGOT, liver damage, liver
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151. ALT was formally known as _____.
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151. SGPT
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152. LDH 1 & 2 is found where? LDH 5?
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152. RBCS, heart, & kidneys :: Liver
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153. Serum albumin & cholesterol _______ in long-standing liver disease.
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153. decrease (liver makes em')
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154. Hepatatis is considered acute if ____________.
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154. lasts less than 6 months
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155. What are the symptoms of acute viral hepatitis?
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155. jt pain, myalgia, steatorrhea, bilirubinemia, uticaria
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156. What are the common physical findings of acute viral hepatitis?
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156. hepatomegaly, splenomegaly, jaundice, & fever
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157. What are the lab findings of acute viral hepatitis?
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157. Increase AST/ALT/ALP/DirectBilirubin/UrineBilirubin
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158. What are primarily measured in HAV?
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158. anti-HAV IgM (sometimes IgG)
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159. Hepatitis A (HAV), aka _________, is transmitted via _________.
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159. infectious HAV, fecal-oral route
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160. What is the most common cause of cirrohosis & liver cancer worldwide? Transmission?
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160. Hepatis B :: Sex & Injection
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161. What are the states of HBV?
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161. Active, carrier, and chronic
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162. HBV surface antigen (HBsAg) is elevated when? Antiobody levels?
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162. current infection :: past infection
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163. How is Hep C transmitted? What is the incubation of hep C? Lab test?
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163. transfusion & drugs :: 15 weeks (normal) up to 30 years :: Anti-HCV
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164. The delta agen, Hep D, is a defective _________ that needs ______ to infect.
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164. RNA virus, HBV
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165. What is the mode of transmission of HEV?
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165. Fecal oral (tropical regions)
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HEPATIC BILIARY DISORDERS PART II
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HEPATIC BILIARY DISORDERS PART II
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166. Is fatty liver reversible? Cirrhosis?
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166. Yes : no
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167. How would a fatty liver & alcoholic liver disease appear on a lab?
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167. Increase ALT, AST, GGTP
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168. In what conditions is RUQ pain seen?
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168. Fatty Liver, Alcoholic hepatitis, Acute cholelithiasis
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169. What are the symptoms of Alcoholic hepatitis?
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169. anorexia, nausea/vomiting, hepatomegaly, fever, splenomegaly, jaundice
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170. Why is repetitive hepatocellular regeneration bad?
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170. Results in fibrous scarring and distorted architecture leading to portal hypertension
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171. _____ grams of alcohol for 10-15 years increases liver disease risk in men. Women?
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171. 40-60, sooner, (10 = 1 beer), but can vary greatly
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172. What are the features of portal hypertension?
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172. splenomegaly, ascites, caput medusae, bleeding esophageal varices, hemmroids
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173. What are the lab findings of cirrhosis?
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173. Hyper-bilirubinemia, hypo-albuminemia, prolonged bleeding/PT, « K/cholesterol, macrocytic anemia
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174. Why does gynecomastia occur in cirrhosis?
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174. Improper sex hormone processing
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175. Ascities is ________ portal hypertension
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175. secondary
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176. ________ may manifest in late stage Hep B or C?
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176. Hepatic Cancer
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177. What are the lab findings of hepatic cancer?
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177. leukocytosis, elevated hematocrit/ALP/erythropoetin, Hep B antigen, alpha fetoprotein
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178. Most stones are composed of a ________.
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178. cholesterol
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179. ______________ is a supersaturation of bile in the gall bladder.
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179. Cholelithiasis
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180. What is the MC cause of pancreatitis? 2nd most common?
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180. Booze :: Gall stones
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181. Where does cholelithiasis tend to lodge?
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181. Cystic duct
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182. What is the difference between a gallstone & acute gallstone/biliary attack?
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182. the stone can't get out , 'gallstones' can
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183. What are the symptoms of acute cholelithiasis?
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183. nausea/vomiting, RUQ & RLQ pain, spine pain, NO FEVER
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184. What are the lab findings of acute cholelithiasis?
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184. usually none
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185. Are gallstones painful?
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185. May or not be, dependent on how many stones are expelled
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186. Mixed content gallstones often exhibit ___________ sign.
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186. Mercedes Benz
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187. What is used to usually visulize gallstones?
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187. Ultrasound
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188. In rare cases acute cholecystitis results from _________. MC cause?
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188. Viscous bile (usually trauma related) :: Cystic duct obstruction
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189. Cholecystitis obstruction leads to _____ and _____.
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189. inflammation (w/ fever) and secondary gallbladder infection
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190. Cholecystitis is very dangerous to what type of individual?
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190. Diabetic
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191. In acute cholecystitis there is a ____________ that the patient may exhibit __________.
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191. Palpable Gall Bladder :: Murphy's SIGN
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192. What is Murphy's sign?
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192. arrest of inspiration during costal angle palpation
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193. What is seen in an acute cholecystitis laboratory?
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193. Mild leukocytosis, increased bilirubin/amylase/ALP/ALT/AST
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194. What is a bile duct stone?
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194. Chole-doch-olith-iasis
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195. What is an infection of the common bile duct (CBD)? What syncope suggests this?
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195. cholangitis (life threatening) :: Charcot's triad
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196. Where are most CBD stones from? Where else can they form?
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196. gall bladder :: biliary tree
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197. Charcot's triad consists of ______, ______, and _______.
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197. fever, jaundice, and biliary pain
|
|
|
198. So.... when I say CHOLE-whatever lab findings, you say...
|
198. Elevated ALP/AST/ALT/Bilirubin/Amylase
|
|
|
199. What is a precursor to Gall bladder or biliary carcinoma? Describe it.
|
199. Porcelain gallbladder (calcification of gall bladder due to excess inflammation)
|
|
|
PANCREAS & GASTROINTESTINAL
|
PANCREAS & GASTROINTESTINAL
|
|
|
200. What is the major cause of peptic ulcer?
|
200. Helicobacter pylori
|
|
|
201. What stimulates the secreton of HCl and gastric enzymes?
|
201. Gastrin
|
|
|
202. How is gastrin formation evaluated?
|
202. fasting endoscopy
|
|
|
203. Puked up blood from a deep gastric ulcer is desribed as ____________.
|
203. coffee ground emesis
|
|
|
204. What often happens to the fecus with gastric ulcers?
|
204. steatorrhea or hematochezia
|
|
|
205. What does the Guaiac test measure?
|
205. peroxidase activity of heme (occult blood in fecus)
|
|
|
206. What are the pancreatic enzymes?
|
206. amylase, lipase, trypsin & chymotrypsin
|
|
|
207. What is the most common pancreatic disease? What is occuring in it?
|
207. acute pancreatitis :: exocrine enzyme leakage leading to self-digestion & inflammation (very bad!)
|
|
|
208. What is the most common cause of acute pancreatitis?
|
208. alcohol abuse
|
|
|
209. What can cause severe midepigastric pain?
|
209. ulcers, gallstones, acute pancreatitis
|
|
|
210. In acute pancreatitis, what can be seen?
|
210. Lipase and amylase rise (but rise is lessened the longer the problem presents)
|
|
|
211. What is enzyme is sensitive for acute pancreatitis? Specific?
|
211. amylase :: lipase
|
|
|
212. What is discoloration of the flanks and groin in pancreatitis?
|
212. Grey-Turner sign
|
|
|
213. What is the major tumor marker of pancreatic cancer?
|
213. CA 19-9 (Carbohydrate antigen)
|
|
|
214. Chronic pancreatitis may lead to _________, ________, ________, or ________.
|
214. Secondary Type I Diabetes, Pancreatic calcification, steatorrhea, death
|
|
|
215. Why does malabsorption occur in chronic pancreatis?
|
215. decrease pancreatic enzymes
|
|
|
ENDOCRINOLOGY
|
ENDOCRINOLOGY
|
|
|
216. What makes calcitonin for calcium regulation?
|
216. parafollicular cells
|
|
|
217. What do follicular cells produce?
|
217. T4 (thyroxine) & T3 (triiodothyronine)
|
|
|
218. ______ is oxidized in the thyroid and binds to ___________ to make thyroid hormones.
|
218. Iodine, thyroglobulin
|
|
|
219. T3 and T4 are primarily transported by ____________.
|
219. Thyroid binding globulin
|
|
|
220. Give an example of a primary hyperthyroidism? Secondary?
|
220. Graves :: Pituitary Tumor
|
|
|
221. What is the most common initial test for thyroid disease?
|
221. TSH
|
|
|
222. Thyroid hormones exert their effects once they bind and _________.
|
222. deiodate
|
|
|
223. The ______ thyroglobulin in the gland that is elevated in ________ and ________.
|
223. prohormone, thyroid carcinoma and hyperthyroidism
|
|
|
224. What test is used to assess the available binding sites on TBG?
|
224. T3 Resin Uptake
|
|
|
225. In the T3U, the amount of T3 removed by resin is ________ related to the binding sites.
|
225. Inversly related
|
|
|
226. What do we actually care more about, free thyroxin or TBG bound thyroxin?
|
226. Free thyoxin (they are the active players)
|
|
|
227. In pregnancy, the total T3/T4 can make an appearance of __-thyroid, while T3U can appear __-thyroid.
|
227. hyper, hypo
|
|
|
228. What would happen to T3U in hyperthyroidism?
|
228. Increase
|
|
|
229. Increase T3 resin uptake tells us that there is _______ binding sites.
|
229. less
|
|
|
230. If TBG increase _______ increases, while ________ is unaffected.
|
230. Total T4/T3, free T4/T3 (T4/T3 tends follow TBG availability)
|
|
|
231. How effective is testing antithyroid antibodies?
|
231. good, but 15% of normal patients have them
|
|
|
232. TSH receptor antibodies can ___________ the effecter.
|
232. Turn Off or Turn On
|
|
|
233. What are the general lab findings of hyperthyroidism?
|
233. Increase T3/T4, decrease TSH
|
|
|
234. A thryoid nodule that produces excessive thyroid hormones is a __________.
|
234. Toxic Goiter
|
|
|
235. Hyperthyroidism patients are what type of temperature sensitive?
|
235. Heat
|
|
|
236. __________ is a protrusion of the eyeball due to inflammatory infiltrate.
|
236. Grave's opthalmopathy
|
|
|
237. Grave's disease is caused by _________________ against ________.
|
237. antagonistic thyroid-stimulating immunoglobulins, TSH receptors
|
|
|
238. Pregnancy increases _____________.
|
238. TBG (total bound T4/T3 too, but NO FREE CHANGE)
|
|
|
239. Lid lag, pretibial myxedema, vitilago, & pseudoclubbing (thyroid acropathy) of the nails are seen in _____________.
|
239. grave's disease
|
|
|
240. Toxic goiters are the clinical picture of _______________.
|
240. hyperthyroidism
|
|
|
241. What are the lab findings of primary hypothyroidism?
|
241. Increase TSH, decrease T4/T3
|
|
|
242. What are the lab findings of secondary hypothyroidism?
|
242. Decrease TSH and T4/T3
|
|
|
243. The onset of hypothyroidism is usually __________.
|
243. insidious
|
|
|
244. What neuromuscular symptoms of hypothyroidism are of particular importance?
|
244. myalgia, CTS, adhesive capsulitis, and delayed reflexes
|
|
|
245. What happens to the skin and hair in hypothyroidism?
|
245. becomes coarse, reckless, dry, and cold
|
|
|
246. How would the lab appear with primary hypothyroidism?
|
246. increase TSH and decrease T4/T3
|
|
|
247. What is Hashimoto's Thyroiditis?
|
247. anti-TPO/Thyroglobulin antibodies resulting in hypothyroid
|
|
|
248. What is a reversible autoimmune hypthyroidism?
|
248. postpartum thyroiditis
|
|
|
249. How would the lab appear with secondary hypothyroidism?
|
249. Decrease TSH & T4/T3
|
|
|
250. What drug can cause goiter? Food type? Mineral?
|
250. Lithium :: Goitrogens (cabbage) :: iodine
|
|
|
251. ________ goiter is one that lacks iodine.
|
251. Endemic
|
|
|
252. What is the most important test in the differential diagnosis of hypercalcemia?
|
252. Serum PTH
|
|
|
253. PTH increase serum ______ and decreases serum _____.
|
253. Ca, PO4
|
|
|
254. What is the most common cause of secondary hypocalcemia is _______ or _________.
|
254. vitamin D defiency, renal disease w/ Ca loss
|
|
|
255. Primary hypoparathyroidism is typically caused by ________.
|
255. surgery
|
|
|
256. ___________ is the resistance of the tissues to the action of PTH.
|
256. Pseudohypoparathyroidism
|
|
|
257. ________ is the endproduct of production and tests for adrenal medullary ________ production.
|
257. Vanillylmandelic Acid (VMA), catecholamines (epinephrine)
|
|
|
258. VMA is measured from what sample?
|
258. Urine
|
|
|
259. What is a pheochromocytoma?
|
259. benign/malignant chromaffin cell tumor (results in explosive personality changes)
|
|
|
260. What assess adrenal androgen production?
|
260. DHEA, ketosteroids (by urine)
|
|
|
261. What is the important glucocorticosteroid produced in the adrenal cortex?
|
261. Cortisol
|
|
|
262. Excessive GH is most commonly caused by a ______________.
|
262. adenoma of pituitary gland
|
|
|
TUMOR MARKERS
|
TUMOR MARKERS
|
|
|
263. What is a tumor marker?
|
263. some generic protein that elevates in the blood during the presence of cancer
|
|
|
264. Which tumor marker is specific enough to screen for carcinoma in an asymptomatic person?
|
264. PSA
|
|
|
265. What are general tumor markers effective for?
|
265. Tumor staging, monitoring, detecting recurrence, monitor therapeutic response
|
|
|
266. What are the two tumor classifications?
|
266. Ectopic proteins, normal cells products in excess via tumor
|
|
|
267. CA 125 is seen primarily in ___________ and __________ cancer monitoring.
|
267. ovarian and endometrial
|
|
|
268. CA 19-9 is used primarily for ___________ cancer screening.
|
268. pancreatic
|
|
|
269. CA 15-3 is used primarily for ___________ cancer screening.
|
269. breast
|
|
|
270. The _______ antigen, CEA, was the ______ tumor marker.
|
270. oncofetal antigen, first used
|
|
|
271. CEA is used primarily for _______ & _______ cancer screening.
|
271. Colorectal & GI
|
|
|
272. CEA often increases with what lifestyle choice?
|
272. Smoking
|
|
|
273. ____________ is a general oncogenic antigen often elevated in chronic hepatitis.
|
273. Alpha-fetoprotein
|
|
|
274. hCG is used to monitor _____________ and ______________.
|
274. trophoblastic & germ cell tumors
|
|
|
275. PSA is a protein found in the _________.
|
275. seminal plasma
|
|
|
AUTOIMMUNE DISORDERS
|
AUTOIMMUNE DISORDERS
|
|
|
276. The presentation of Autoimmune disorders are _______ from person to person
|
276. highely variable
|
|
|
277. What are the common mechanisms of autoimmune disorders?
|
277. antibodies on cell surfaces, immune complexes, autoreactive cytotoxic cells
|
|
|
278. What is the major laboratory screening test in autoimmune disease?
|
278. ANA
|
|
|
279. ANA is a _______ of antibodies that detect _______.
|
279. class :: antibodies that react with nucleic acid
|
|
|
280. What are the major ANA antigens?
|
280. anything found in a nucleus
|
|
|
281. What test that is less subjective can be used to assess autoimmune diseases?
|
281. specific autoantibody titer
|
|
|
282. Auto antibodies are _______ to autoimmune diseases.
|
282. not unique
|
|
|
283. RF is a _______ autoantibody that reacts with the _______.
|
283. IgM, IgG
|
|
|
284. Autoimmune patients will usually have _____ CBC, _____ ESR, and _____ complement.
|
284. Normochromic normocytic anemia, increased, altered
|
|
|
285. What organs are impacted the most in SLE?
|
285. Joints, skin, and kidneys
|
|
|
286. In SLE, 98% of the time they are _________ positive.
|
286. ANA (especially dsDNA & SM)
|
|
|
287. What test often results in a false positive when a patient has lupus?
|
287. RPR/VDRL (syphillus test)
|
|
|
288. How does the CBC appear in lupus?
|
288. Anemiac with leukocytopenia
|
|
|
289. ____________ is the autoimmune destruction of lacrimal and salivary glands. Does ANA work?
|
289. Sjogren's Syndrome :: Mostly (75%)
|
|
|
290. What test measures tear production?
|
290. Schirmer's (the eye shimmers)
|
|
|
291. Scleroderma is characterized by excessive _______ deposition throughout the body.
|
291. Collagen
|
|
|
292. In scleroderma, the ANA will have a _______ appearance.
|
292. Speckled
|
|
|
HEMOSTASIS
|
HEMOSTASIS
|
|
|
1. What is a purpura under 2mm in diameter? Greater than 2cm?
|
1. Petechia, Ecchymosis
|
|
|
2. What are the three majors components of the haemostatic system?
|
2. vasconstriction, platlet activation/aggregation (primary), blood coagulation (secondary)
|
|
|
3. What are the four steps of homeostasis in order?
|
3. Adhesion, release, aggregation, provision of phospholipid surfaces
|
|
|
4. What mediates adhesion to collagen during vascular injury?
|
4. Glycoproteins & von Willebrand
|
|
|
5. What is synthesized when platelets release their contents?
|
5. Prostaglandin thromboxan A2
|
|
|
6. What does Prostaglandin thromboxan A2 do?
|
6. Platelet aggregation & vasoconstrictor
|
|
|
7. During aggregation, platelet _______ increases while integrin can bind to __________.
|
7. binding capacity, fibrinogen
|
|
|
8. What is the importance of the provision of phospholipid surface?
|
8. organizes & promotes interaction of clotting factors
|
|
|
9. Secondary homeostasis is ______________________.
|
9. blood proteins reactions through a cascade process
|
|
|
10. What are the three pathways of secondary homeostasis?
|
10. intrinsic, extrinsic, common
|
|
|
11. What triggers the extrinsic pathway?
|
11. Tissue factor exposure post endothelium trauma
|
|
|
12. What triggers the intrinsic pathway?
|
12. Collegen exposure post endothelium trauma
|
|
|
13. What are the four major factor groups of the coagulation cascade?
|
13. Activators, Vit K dependent factors, cofactors, fibrinogen
|
|
|
14. Tissue factor activates _______. Collagen activates _________.
|
14. Factor VII :: Contact phase proteins
|
|
|
15. What are the vitamin K dependent factors? What are they collectively known as?
|
15. Factor II, VII, IX, X :: Prothrombin
|
|
|
16. Prothrombin is synthesized in the _____, are modified by _______, and are necessary for _________.
|
16. liver, Carboxylase, Ca binding and enzymatic activity
|
|
|
17. What inhibits Vitamin K?
|
17. Coumadin (anti-coagulants)
|
|
|
18. Fibrinogen becomes ________ which forms a __________.
|
18. fibrin, clot
|
|
|
19. Tissue plasminogen activator convert _________ to __________.
|
19. plasminogen to plasmin
|
|
|
20. What does plasmin do?
|
20. degrads fibrin (thus no more clots)
|
|
|
21. What is a naturally occurring anti-coagulant?
|
21. Antithrombin III
|
|
|
22. Protein C inhibits coagulation & is vit C dependent, thus what drug could affect it?
|
22. Coumadin
|
|
|
23. At what number does spontaneous bleeding occur?
|
23. 20,000
|
|
|
24. What does bleeding time assess?
|
24. Platlet function (adhesion & aggregation) & qualitative defects
|
|
|
25. What is the reference range for bleeding time?
|
25. 3-8 minutes
|
|
|
26. What is a platelet aggregation assay used for?
|
26. detect aggregation abnormalites
|
|
|
27. What does a bone marrow differentiate?
|
27. Decrease platlet production (decrease megakaryocytes) from platelet destruction (more megas)
|
|
|
28. What measures the extrinsic coagulation pathway?
|
28. Prothrombin Time (PT)
|
|
|
29. What is added to a PT to form the fibrin clot?
|
29. Tissue factor & Ca
|
|
|
30. PT is usually used to monitor what therapy?
|
30. Coumadin
|
|
|
31. What measures the intrinsic coagulation pathway?
|
31. APTT
|
|
|
32. Fibrinogen levels are assessed by adding _______.
|
32. bovine toxine
|
|
|
33. Thrombin time evaluates _________, and is used to screen for __________.
|
33. Fibrinogen to fibrin, inadequate conversion (dysfibrinogemia)
|
|
|
34. What is the major cause of morbidity in people with platelet disorders?
|
34. intracranial hemorrhage
|
|
|
35. What are the two categories of platelets disorders?
|
35. Decrease platelets, abnormal platelets
|
|
|
36. What are the two general reasons for an acquired decrease of platelets?
|
36. decreased bone marrow production, increased peripheral destruction
|
|
|
37. Idiopathic Thrombocytopenic purpura has ______ directed against _____, usually because of ______.
|
37. autoantibody, platelets, heparin/drugs
|
|
|
38. Describe the lab findings of ITP?
|
38. Decrease platelets, normal PT/APTT & bone marrow, positive anti-platelets
|
|
|
39. What is Disseminated Intravascular Coagulation?
|
39. overactive coagulation --> too many clots --> infactions or hemmorhage
|
|
|
40. When does DIC occur?
|
40. during traumatic tissue damage
|
|
|
41. Describe the lab findings of DIC?
|
41. Decrease platelets & fibrinogen, Increase PT/APTT
|
|
|
42. What is the congenital platelet function disease?
|
42. Von Willebrand's Disease
|
|
|
43. What is Von Willebrand's Disease?
|
43. deficient VQ factor
|
|
|
44. What is von willebrand's factor?
|
44. Cofactor for factor VIII activity and platelet adhesion/aggregation
|
|
|
45. Describe the lab findings of von Willy?
|
45. BT increased, decreased aggregation, antigens, normal platelets, increase APTT
|
|
|
46. What are the two categories of coagulation disorders?
|
46. decreased activity of procoagulants (bleed) , decreased anticoagulants (infarct)
|
|
|
47. Cascade disorders usually result in bleeding in the __________.
|
47. joints
|
|
|
48. What are the common causes for acquired cascade disorders?
|
48. Portal HTN or Hepatocellular damage = disrupted coagulation factors synthesized in the liver
|
|
|
49. Hemophilia is a ____________ trait.
|
49. X linked (so men get it more)
|
|
|
50. Hemophilia A is a __________ deficiency resulting in a _________ APTT.
|
50. factor VIII, increased
|
|
|
51. Hemophilia B is a __________ deficiency resulting in a _________ APTT.
|
51. Factor IX, increased
|
|
|
LIPIDS & CARDIAC MONITORING
|
LIPIDS & CARDIAC MONITORING
|
|
|
52. What are the two most prominent lipids in the plasma?
|
52. cholesterol & triglycerides
|
|
|
53. What are lipoproteins?
|
53. lipid transport packages (chylomicrons, VLDL, LDL, HDL)
|
|
|
54. What are alipoproteins?
|
54. protein portion that perform functions necessary for lipid metabolism
|
|
|
55. What is your long term energy storage?
|
55. triglycerides
|
|
|
56. For plasma triglyceride levels, _________ is essential.
|
56. fastin
|
|
|
57. Triglyceride levels are generally not considered an independent risk factor for___, but they are for ___.
|
57. atherosclerosis, heart disease (especially women)
|
|
|
58. What are the risk factors for atherosclerosis?
|
58. +45men/+55female, family history, current smoking, hypertension, DM, HDL/LDL imbalance
|
|
|
59. To find out exactly the lipid profile, a _____________ is needed.
|
59. Lipoprotein Electrophoresis
|
|
|
60. Type ______ lipids are caused by poor diet and can be restored with proper dieting.
|
60. Type IIB
|
|
|
61. All other lipid types are liver dependent, thus _______ doesn't necessarily have any positive effects.
|
61. diet
|
|
|
62. Almost all endrogenous cholesterol is synthesized by the ________ & _________.
|
62. liver & gut
|
|
|
63. What is the key element of myelin?
|
63. phospholipids
|
|
|
64. What is used to assess risk of atherosclerosis? (type of lipid)
|
64. lipoproteins
|
|
|
65. Familial hypercholesterolemia is an inherited defect in ___________ with a defective ___________.
|
65. hepatocyte LDL receptors (physio), feedback inhibition (diet)
|
|
|
66. What is secondary hypercholesterolemia?
|
66. acquired disorders of increased lipoprotein synthesis due to an underlying disorders
|
|
|
67. There is a inverse correlation between triglycerides and _________.
|
67. HDL
|
|
|
68. Most increased triglycerides is due to ________, and secondarily to _______________________.
|
68. Diet :: alcohol, DM, Renal failure
|
|
|
69. Cholesterol levels should be __________.
|
69. Less than 200 mg/dl
|
|
|
70. LDL cholesterol levels should be ___________.
|
70. less than 130 mg/dl
|
|
|
71. HDL cholesterol levels should be ___________.
|
71. more than 55 mg /dl
|
|
|
72. HDL cholesterol is __________ related with the risk of atherosclerosis.
|
72. inversly
|
|
|
73. Myoglobin is a muscle protein that optimizes uptake of ____.
|
73. O2
|
|
|
74. Muscle cell damage is reversible if reperfusion occurs within _______ of an ischemic event.
|
74. 15-20 minutes
|
|
|
75. What are the phases of an ischemic event?
|
75. 1) Jeopardy, 2) injury, 3) infarction
|
|
|
76. What are the three common patterns for Myocardial Ischemia?
|
76. Chronic IHD, angina pectoris, and acute myocardial infarction (AMI)
|
|
|
77. What is the most common cause of myocardial ischemia?
|
77. atherosclerosis
|
|
|
78. Triglyceride levels should be _______, and can _______ daily. What must be done to get Trig levels?
|
78. less than 200 mg/dl, variate :: Fasting
|
|
|
79. For diagnosis of AMI, what 2 of 3 criteria must be met?
|
79. History of chest pain, ECG changes, typical cardiac enzyme rises/peaks/returns to reference ranges
|
|
|
80. What are the contractile proteins of cardiac muscle?
|
80. actin, myosin, troponin
|
|
|
81. What are the cardiac enzymes?
|
81. Creatine Kinase, Lactate Dehydrogenase, Aspartate Aminotransverase
|
|
|
82. When are cardiac proteins & enzymes released into circulation?
|
82. during irreversible damage
|
|
|
83. What does 'diagnostic window' mean?
|
83. Cardiac markers have characteristic rise, peaks, and normalizy return periods
|
|
|
84. Creatine Kinase (CK) is found in _____________ & _____________.
|
84. striated muscle & brain tissue
|
|
|
85. Why is CK of limited diagnostic value?
|
85. elevates in various diseases (not just MI)
|
|
|
86. What is the gold standard for early diagnosis of AMI? Why?
|
86. CKMB (CK2) :: It's fast (even if its not the most accurate)
|
|
|
87. What are the characteristic periods of CKMB?
|
87. Rise (2-6hrs), Peak (12-24hrs), Normalizes (2 days)
|
|
|
88. What are the subforms of CKMB and why are they significant?
|
88. CK-MB1 & CK-MB2 :: Usually even ratio, in MI the ratio is altered
|
|
|
89. _______ is involved in glucose metabolism.
|
89. LDH
|
|
|
90. How many LD isoenzymes are there?
|
90. five
|
|
|
91. What LD isoenzymes are pertinent to MI? What tissues are these found?
|
91. LD1 & LD2 :: cardiac muscle, kidneys, & RBCs
|
|
|
92. During a MI, LD1 & LD2 levels ________, leaving the plasma with more ________.
|
92. Flip, LD1
|
|
|
93. AST, aka _______, is a _____________ found in the ____, ____, and ____.
|
93. SGOT :: transaminase :: liver, skelatal, cardiac muscle
|
|
|
94. Why isn't SGOT levels regularly used for MI?
|
94. its too slow
|
|
|
95. What is a very sensitive marker for AMI?
|
95. Myoglobin (Fast too!)
|
|
|
96. What very specific MI marker can be used up to 2 weeks after a suspected MI?
|
96. Troponin TnT
|
|
|
97. What can be seen in a CBC related to a MI? Explain why.
|
97. Increase WBC/Neutrophils :: to clean up dead cells
|
|
|
98. Will ESR raise after an AMI?
|
98. yes (up to 2 weeks)
|
|
|
ELECTROLYTES
|
ELECTROLYTES
|
|
|
99. What are the primary negatively charged ions? What are they collectively known as?
|
99. Chloride, Bicarbonate, lactate :: Anions
|
|
|
100. What are the primary positively charged ions? What are they collectively known as?
|
100. Sodium, Potassium :: Cations
|
|
|
101. What are the functions of electrolytes?
|
101. Maintain Osmotic pressure/pH/muscles, oxidation-reduction reactions, act as cofactors to enzymes
|
|
|
102. What is the major extracellular cation? What are its major functions?
|
102. Sodium :: maintain water distrobution & osmotic pressure
|
|
|
103. What is the major intracellular cation? What are its major functions?
|
103. Potassium :: cellular metabolism, neuromuscular function
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104. When does potassium move into the cells?
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104. When there are increased glucose and insulin levels (ready to metabolize!)
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105. What is a potassium wasting medication?
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105. Furosmide
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106. What is the major extracellular anion? What does it do
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106. Chloride :: Water balence
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107. What is the "chloride shift"?
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107. calcium moves into cells as HCO3 leaves
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108. What is the major component of total plasma CO2 and thus the acid-base balance?
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108. Bicarbonate (HCO3)
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109. What is the anion gap used for? A high anion gap is often from what?
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109. to ddx metabolic acidosis :: lactic or ketoacidosis
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110. Intracellular fluid comprises of _________ total body water.
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110. 2/3
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111. How is H20 balance maintained?
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111. ingestion, excretion, renal contribution, and renin-angiotensin-aldosterone
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112. ADH increases ____________ and increases _______________.
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112. permability of collecting ducts, reabsorption of water
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113. What are the main regulators of plasma osmolality?
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113. sodium, chloride, urea, and glucose
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114. What are the causes of hypersomolality?
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114. dehydration, hyperglycemia, hypernatremia
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115. What is hypernatremia?
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115. excessive sodium in blood
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116. What are the two type of hypnatremia and give an example of each.
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116. Depletional (acidosis, addison's), delutional (edema, Congestive hear failure)
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117. Acidosis can result in ______-kalemia.
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117. Hyperkalemia
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118. What will cause a shift of intracellular K to extracellular?
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118. dehydration and diabetic ketoacidosis
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119. For hypokalemia, what will cause a shift from extracellular into intracellular K?
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119. alkalosis & insulin therapy
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CARBOHYDRATES
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CARBOHYDRATES
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120. Salivary amylase converts ________ into ________.
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120. starch, maltose
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121. What is glycolysis?
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121. anaerobic conversion of glucose into pyruvate/lactate (for ATP)
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122. What is glycogenesis?
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122. glycogen from glucose (stored in liver & muscle)
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123. What is glycogenolysis?
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123. Glycogen into glucose (for energy)
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124. What is gluconeogenesis?
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124. Glucose from noncarbohydrate sources
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125. Insulin ______ blood glucose.
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125. lowers
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126. What hormones increase blood glucose (thus counter-insulin/regulatory)?
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126. Glucagon, IGF, GH, cortisol, catecholamines, ACTH
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127. Pancreatic __-cells produce _______, which is then cleaved into ______ & ______.
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127. Beta, proinsulin, insulin & inactive C-peptide
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128. In Type ___ diabetes, INCREASED C-peptide levels are often seen.
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128. II
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129. C-peptide functions to repair _______ and helps with diabetic _________ & _________.
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129. muscular wall of arteries, diabetic neuropathy & nephropathy
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130. What is the major hormone of increased blood glucose?
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130. glucagon
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131. Glucagon stimulates ______________ & ______________.
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131. glycogenolysis & gluconeogenesis
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132. Cortisol, GH, & ACTH are _______ antagonists that affect _________ receptor binding.
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132. insulin, insulin
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133. Too much cortisol will result in Type ___ diabetes.
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133. Type II
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134. Catecholamines, such as _______, are produced by the __________ and they stimulate ____________.
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134. epinephrine, adrenal medulla, glycogenolysis
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135. Some tumors produce _____ associated with hypoglycemia.
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135. IGF-2
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136. What is the blood glucose threshold at which glycosuria tends to occur? (Not always though)
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136. 180 mg/dl
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137. What type of diabetes is less common? Which was formerly known as juvenile?
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137. Type I IDDM, Type I IDDM
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138. In type I DM, there is a _________ due to autoimmune destruction of ________________.
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138. insulin deficiency, beta cells
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139. The hallmark symptoms of abrupt poly's, weight loss, and ketoacidosis is seen in _________ diabetes.
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139. Type I
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140. Will exercise help a Type I patient? Type II?
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140. No, Yes
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141. Type II has either decreased insulin _________ or increased ______________.
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141. production, peripheral insulin resistance
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142. What are the typical symptoms of type II diabetes? What symptom typically starts diabetic awareness?
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142. Obesity, extremity pain, VISION disturbance
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143. Gestational diabetes is due to __________ and may be asymptomatic.
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143. insulin resistance
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144. Because gestational diabetes can be asymptomatic, ___________ are recommened.
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144. Universal screening (24 & 28 week of gestation)
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145. What secondary diabetes is associated with increased glucocorticosteroids?
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145. Cushing's Syndrome
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146. Diabetic ketoacidosis occurs when the ____ are severely compromised and ____ has been stimulated.
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146. Carbohydrate pathways, glycolysis
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147. Acidosis will exhibit what symptoms?
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147. Headache, Poly's, Kussmaul Breaths, Vommitting, & fruity breath
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148. What is a Kussmaul?
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148. Rapid deep breathing (to push acids out, CO2), as progresses it slows down
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149. What happens to the osmolarity of the blood in a DKA?
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149. increases (because more glucose)
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150. What is a nonketotic hyperosmolar coma? Who gets them?
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150. Excessive Insulin (1000+ mg/dl) leads to dehydration :: Type II diabetics
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151. What are the normal ranges for fasting blood glucose? What is it used for?
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151. 65-110 mg/dl, diagnose & monitor DM
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152. What is the criteria for diagnosis of diabetes mellitus?
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152. Fasting 126+ twice, or Fasting 126+ and classic symptoms
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153. An FBG of 110 to 125 is known as ________________.
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153. impaired fasting glucose tolerance
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154. What is a glucose tolerance test (GTT)?
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154. glucose loading test that measures ability to produce insulin
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155. The GTT is used for determine ________, ________, and ________.
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155. DM, Gestational DM, and hypoglycemia
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156. The 2 hour post prandial glucose test is used in conjunction with _____ to screen for DM.
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156. Fasting Blood Glucose
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157. What is a normal post prandial glucose?
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157. 120mg/dl or less
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158. The 1-hour post prandial screen is used for ____________.
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158. gestational diabetes
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159. What test is used to determine diabetic patient compliance & effectiveness of therapy?
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159. Glycated/Glycosalated Hemoglobin
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160. How long will glycated Hgb exist? What does glycated mean?
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160. 1-2 months :: Glucose-modifed proteins
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161. What glycated Hgb is typically monitored and what are the intended levels?
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161. Hgb A1C :: Less than 7.25%
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WBC DISORDERS
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WBC DISORDERS
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162. What is the process of WBC differentiation & proliferation?
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162. Leukopoiesis
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163. What are the granulocytes?
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163. Neutrophils, Eosinophils, and basophils
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164. Where are granulocytes produced? Maturated?
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164. Bone marrow :: Bone Marrow
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165. Seeing an immature cell in the blood is known as a _________.
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165. shift to the left
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166. What are the other names for a Neutrophil?
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166. Seg, Granulocyte, PMN
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167. Neutrophils are mediated to migrate to an infection/inflammation by _________________.
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167. chemotactic substances
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168. What WBCs cannot reenter the blood once they have entered tissues?
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168. PMNs, Monocytes/Macrophages
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169. Basophils function in ___________ reactions.
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169. Hypersensitivity
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170. Monocytes are produced in the ___________ from the same progenitor that produces ___________.
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170. bone marrow :: neutrophil
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171. Monocytes become _______ once they enter tissues, and they can live there for up to __________.
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171. macrophages, years
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172. Tissue macrophages can _________.
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172. proliferate
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173. Monocytes perform ___________ and kill their pray with their ___________.
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173. phagocytosis, enzyme filled granules
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174. What enhances the the adherance and ingestion of microrganisms?
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174. Surface Fc receptor on IgG's and complement
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175. Monocytes can aggrevate inflammation, how?
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175. Secrete mediators of inflammation (CSF, IL-1, Complement components)
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176. After maturation lymphocytes migrate to __________________.
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176. peripheral lymphoid tissues
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177. What cells can reenter circulation once in tissues?
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177. Lympocytes
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178. T-helper cells assist in the production of ______, activate ______, and induce _____________.
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178. antibodies, macrophages, cytotoxic properties of T cells
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179. MHC functions with ________.
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179. T-cells
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180. T-helper cells are what CD cells?
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180. CD4
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181. T-cytotoxin/suppressor, aka ____, does what?
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181. CD8 :: antigen dependent lysis & modulate immune reactions
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182. _____________ cells can cause cell death without antigen exposure.
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182. Natural Killer Cells
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183. Any prefix+cytosis means what?
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183. Increased number in circulation
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184. Any prefix+penia means what?
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184. Decreased number in circulation
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185. When assessing a sample for disease _________ should be used.
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185. absolute concentration
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186. How is absolute concentration figured?
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186. Total WBC * % of cell type
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187. A disease with an excess of neutrophils results in a ___ in lymphocytes, although ___ has not changed.
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187. relative :: absolute number
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188. Give in order of number the WBC types.
|
188. Neutro, Lympho, Mono, Eosino, Baso
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189. __________, _________, & _________ is useful in the differentiation of leukemia.
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189. Cytochemical stains, Flow cytometry, & bone marrow examination
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190. Myeloid is a ________.
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190. WBC
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191. Neutrophils are involved in _____________ reactions?
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191. acute bacterial
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192. What is a Leukemoid reaction?
|
192. WBC of 50,000+ or more than 5% immature cells
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|
|
193. What are common causes of Leukemoid reactions?
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193. Severe bacterial, bone tumor destruction, hemolysis or tissue destruction, & corticosteroid treatment
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|
194. Stab cells in peripheral blood signifies a _____________. What are stab cells also known as?
|
194. shift to the left :: Band
|
|
|
195. What is an inverted diff?
|
195. Lymphocytes > PMNs
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|
196. Atypical lymphocytes, aka ______, are a classic finding in ________________.
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196. reactive (react to virus), mononucleous
|
|
|
197. What do atypical cells look like?
|
197. Large w/ irregular nucleus & clear/basophilic cytoplasm
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198. What immunoglobin is involved in acute phase reactions?
|
198. IgM
|
|
|
199. What is typically decreased in lymphocytopenia?
|
199. Decreased antibody production
|
|
|
200. Eosinophilia is involved in what typically?
|
200. Allergic & parasitic reactions
|
|
|
201. What is eosinopenia associated with?
|
201. Acute inflammatory, stress, corticosteroid use
|
|
|
202. Stress results in __________ & ___________.
|
202. Eosinopenia & Neutrophilia
|
|
|
203. What is leukemia?
|
203. Malignancy of marrow origin w/ unregulated proliferation of cells
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|
|
204. What is a lymphoma?
|
204. Malignancy of lymphocyte origin
|
|
|
205. When granulocytes dominate a leukemia it is known as what? (3 names)
|
205. Myelocytic, Myelogenous, Nonlymphocytic
|
|
|
206. When lymphocytes dominate a leukemia it is known as what? (1 name)
|
206. Lymphocytic
|
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|
207. In acute leukemia, the WBC count is ___, the RBCs are ____ & ___, and the platelet count is _____.
|
207. Elevated/Normal, Normocytic/chromic, usually decreased
|
|
|
208. In chronic leukemias, the WBC count is ____, the RBCs are ___ & ___, and the platelet count is ___.
|
208. Elevated, Normocytic/chromic, Normal/Increased
|
|
|
209. Who tends to bruise more, Acute or Chronic? Why?
|
209. Acute :: Low platlet
|
|
|
210. What is a stem cell disorder w/ unregulated proliferation of immature cells? What cells are seen?
|
210. Acute Leukemias :: Blasts
|
|
|
211. What is the important diagnostic criteria of Acute Leukemias?
|
211. 30% or more blasts cells in Bone Marrow
|
|
|
212. What are the clinical findings of acute leukemia?
|
212. Low grade fever, weakness, anemia/bleeding, infection, bone pain
|
|
|
213. What is the cut off for a low grade fever?
|
213. 101 F
|
|
|
214. In Acute Lymphoblastic Leukemia (ALL), there is a proliferation of ______ and occurs MC in ______.
|
214. lymphoblasts, children
|
|
|
215. How is ALL & AML diagnosed?
|
215. Marrow & peripheral smear (better w/ cytochemical staining)
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|
|
216. In Acute Myelocytic Leukemia (AML), is a proliferation of ______, and occurs MC in ______.
|
216. Myelogenous/immature myeloid series, Middle age +
|
|
|
217. What occurs in AML?
|
217. Marrow cells replaced by immature then spill into periphery
|
|
|
218. What is a key finding in immature cells of AML?
|
218. Auer Rods (an inclusion body)
|
|
|
219. How is chronic leukemia typically found?
|
219. Routine physical or for nonspecific complaints (fatigue, enlarge nodes)
|
|
|
220. What type of cells are involved in Chronic Leukemias?
|
220. Mostly Mature (but not quite right)
|
|
|
221. Chronic Myelocytic Leukemia (CML) is MC in ______, and key exhibits the ____________.
|
221. 50 yr old adults, Philidephia Chromosome
|
|
|
222. What are the common symptoms of CML?
|
222. Fatigue, weight loss, anorexia, H/A, splenomegaly
|
|
|
223. During a CML _______, a peripheral blood shows 30% ____. Afterwards survival time is ________.
|
223. blast crisis, blast cells, 2-6 months
|
|
|
224. The WBC count in CML is ________________.
|
224. 50k-300k
|
|
|
225. In basic terms, what occurs in the philidelphia chromosome?
|
225. #9 switches with #22
|
|
|
226. What is the most common adulthood leukemia? Which has smudge cells?
|
226. CLL :: CLL
|
|
|
227. Chronic Lymphocytic Leukemia (CLL) is a proliferation of ________ that cannot become ________.
|
227. mature lymphocytes (usually B), plasma cells
|
|
|
228. In CLL since plasma cells are not formed, what occurs?
|
228. Hypogammaglobulinemia --> no antibodies, get sick loads!
|
|
|
229. How would the bone marrow appear in CLL?
|
229. Hypercellular w/ mature lymphocytes
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