USMLE 16

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USMLE 16
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2015-03-06 13:38:34
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  1. What is type 1 Rapidly progressive (crescentic) glomerulonephritis?
    Goodpasture syndrome
  2. What is Goodpastures syndrome? Describe the findings of it.
    • Linear GBM deposits of IgG and C3 on immunoflourescence.
    • Antibodies to GBM and alveolar basement membrane.
  3. Describe the characteristics of Urticaria (hives).
    Superficial dermal edema and lymphatic channel dilation.
  4. This skin disorder is characterized by superficial dermal edema and lymphatic channel dilation.
    Urticaria/ Hives
  5. What causes the formation of urticaria (hives).
    Pruritic wheals that form after mast cell degranulation.
  6. Describe the pathology seen below.
    • Urticaria (hives)
    • Pruritic wheals that form after mast cell degranulation.
    • Characterized by superficial dermal edema and lymphatic channel dilation.
  7. Describe the pathology seen below.
    • Acanthosis nigricans
    • Increase in thickness of stratum spinosum (prickle cell layer)
  8. Increase in the thickness of the stratum spinosum is characteristic of which disease?
    Acanthosis Nigricans
  9. What is spongiosis and what condition is it associated with?
    • Epidermal accumulation of edematous fluid in intercellular spaces.
    • Eczematous dermatitis
  10. Microscopic term associated with eczematous dermatitis.
    Spongiosis- epidermal accumulation of edematous fluid in intercellular spaces
  11. Epidermal accumulation of edematous fluid in intercellular spaces is characteristic of?
    Spongiosis- Eczematous dermatitis
  12. What is acantholysis and what condition is it associated with?
    • Separation of epidermal cells/ loss of cohesion between keratinocytes in the epidermis.
    • Pemphigus vulgaris
  13. Separation of epidermal cells is characteristic of?
    • Acantholysis
    • Pemphigus vulgaris
  14. What microscopic term is associated with Pemphigus vulgaris?
    Acantholysis- sepatation of epidermal cells.
  15. The malignant potential of adenomatous polyps is determined by?
    • 1. Size of the polyp: <1cm- unlikely to undego malignant transformation; >4cm- 40% risk of malignancy.
    • 2. Villous adenomas are more prone to be malignant than tubular adenomas.
    • 3. Degree of dysplasia.
  16. What is the pathology seen below?
    Villous adenoma of the colon
  17. What is the pathology seen below?
    Tubular adenoma of the colon
  18. Describe the series of gene mutations involved in the transformation of normal colon to colon carcinoma.
    • 1. Progression of normal mucosa of colon to small polyp (colon at risk). ⇨Mutation in APC tumor suppressor gene.
    • 2. Increase in the size of the polyps to an Adenoma. ⇨Mutation in K-ras protooncogene.
    • 3. Malignant transformation of adenoma to carcinoma. ⇨Mutation of p53 and DCC genes.
  19. Which gene mutations occur at A, B and C, respectively?
    • A: Loss of APC gene
    • B: KRAS mutation
    • C: Loss of p53 and DCC
  20. Which gene mutation facilitates the growth of adenomas?
    KRAS mutation
  21. Which genes facilitate the malignant transformation of adenoma into carcinoma?
    p53 and DCC
  22. Which gene mutation facilitates the progression of normal mucosa to a small polyp?
    APC tumor suppressor gene
  23. What is dyskeratosis and in which disease is it found?
    • Dyskeratosis- abnormal, premature keratinization of individual keratinocytes.
    • Squamous cell carcinoma
  24. The following measures the concentration of several substances over the length of the proximal tubule. Label it accordingly.
    •  PAH
    • Creatinine
    • Inulin
    • Urea
    •  Cl-
    • K+
    • Na+
    • HCO3-
    • Amino acids
    • Glucose
  25. What is positive punishment?
    Giving a punishment decreases behavior.
  26. Giving a punishment decreases behavior.
    Positive punishment
  27. What is negative punishment?
    Removal of a reward decreases behavior
  28. Removal of a reward decreases behavior.
    Negative punishment
  29. What is positive reinforcement?
    Giving a reward increases behavior
  30. Giving a reward increases behavior.
    Positive reinforcement
  31. What is negative reinforcement?
    Removal of punishment or consequence increases behavior
  32. Removal of punishment or consequence increases behavior.
    Negative reinforcement
  33. What trinucleotide repeat expansion is found in Fragile X syndrome?
    CGG
  34. CGG trinucleotide repeat expansion is found in which disease?
    Fragile X syndrome
  35. Holosystolic, harsh sounding murmur is characteristic of?
    VSD
  36. Holosystolic, high pitched blowing murmur is characterisitc of?
    Mitral/ Tricuspid Regurgitation
  37. This drug reduces mortality in patients with congestive heart failure.
    Spironolactone & Eplerenone- aldosterone antagonist (prevent heart remodeling by aldosterone)
  38. What are the aldosterone receptor antagonists?
    • Spironolactone 
    • Eplerenone
  39. What is the MOA and use of Spironolactone?
    • MOA: Aldosterone receptor antagonist
    • USE: Hyperaldosteronism, K+ depletion, Heart failure
  40. What is the MOA and use of Eplerenone?
    • MOA: Aldosterone receptor antagonist
    • USE: Hyperaldosteronism, K+ depletion, Heart failure
  41. Which drugs act here?
    K+ sparing diuretics- Spironolactone, Eplerenone, Triamterene, Amiloride
  42. What is the MOA of Hydrochlorothiazide?
    ↑excretion of Na+, Cl- and H20 in early DCT
  43. Which drug act here?
    Thiazide diuretics- Chlorthalidone, Hydrochlorothiazide
  44. This drug works by blocking Na+/Cl- symporters in the distal convoluted tubule.
    Hydrocholorothiazide, Chlorthalidone
  45. What is the MOA of Furosemide?
    Inhibits Na-K-2Cl symporters in the ascending limb of Henle → ↑excretion of Na+, Cl-
  46. This drug inhibits Na-K-2Cl symporters in the ascending limb of the loop of Henle.
    Furosemide, Bumetanide, Toresemide
  47. Which drug acts here?
    • Loop diuretics- Furosemide, Bumetanide, Torsemide
    • Ethacrynic acid
  48. What is the MOA and use of Triamterene?
    • MOA: Blocks Na+ channels in the cortical collecting tubules.
    • USE: Hyperaldosteronism, K+ depletion, Heart failure
  49. What is the MOA and use of Amiloride?
    • MOA: Blocks Na+ channels in the cortical collecting tubule.
    • USE: Hyperaldosteronism, K+ depletion, Heart failure
  50. This drug blocks Na+ channels in the cortical collecting tubule.
    • Triamterene
    • Amiloride
  51. Which drugs act here?
    • Acetazolamide
  52. What is Factor 5 Leiden mutation?
    Produces a Factor 5 resistant to inhibition by activated Protein C
  53. Describe the presentation and findings of Chronic mesenteric ishcemia.
    • Atherosclerotic narrowing of the celiac trunk, IMA and SMA
    • -Epigastric/ periumbilical abdominal pain occurs 30-60 mins after food intake. (Atherosclerotic arteries can't dilate in response to digestion and resorption)
    • - Weight loss- patient avoid pain associated with eating
    • - NORMAL GI endoscopy
  54. What is the normal range of serum potassium?
    3.5 - 5.5 mEq/L
  55. Which diuretics cause potassium loss?
    • Loop diuretics: Furosemide, Bumetanide, Toresmide
    • Thiazide diuretics 
  56. Which diuretics cause hyperkalemia?
    K+ sparing diuretics: Spironolactone, Eplerenone, Triamterene, Amiloride
  57. What is this type of breathing? What causes it?
    • Cheyne strokes-  gradually increasing then gradually decreasing tidal volumes followed by apnea.
    • Seen in Congestive heart failure, ↑intracranial pressure, stroke, brain tumor, traumatic brain injury
  58. What is this type of breathing? What causes it?
    • Kussmaul's respirations (Diabetic Ketoacidosis)
    • Deep and laboured breathing
  59. What type of breathing is this? What causes it?
    • Obstructive sleep apnea
    • Reductions or cessations of airflow with no cyclic variations in tidal volume
  60. What causes a shift from the blue curve to the red curve below?
    • Left shift (think O2 is LESS available to tissues)→ ↑affinity of Hb for O2
    • ⇧ pH
    • Temperature (hypothermia)
    • ⇩ 2,3 DPG
  61. What effect does decreased temperature (hypothermia) have on the O2-Hb dissociation curve?
    Left shift-  O2  is LESS available to issues → ↑affinity of Hb for O2

    Decreased temperature helps to stablilize the bond between O2 and Hb
  62. What effect does Anemia have on the O2-Hb dissociation curve?
    Anemia can cause lactic acidosis which will result in lower blood pH, shifting the curve to the right.  Facilitating unloading of O2, ↓affinity of Hb to O2



  63. What effect does hypoventilation have on the O2-Hb dissociation curve?
    Hypoventilation causes increased CO2 retention and respiratory acidosis that shifts the curve to the right. → Facilitating O2 unloading, ↓affinity of Hb for O2
  64. What is the most common side effect of aspirin?
    Gastrointestinal blood loss
  65. Ca2+ channel blocker that can lead to peripheral edema and flushing?
    • Amlodipine, Nifedipine
    • Works on vascular smooth muscle muscle → ⇩ muscle contractility
  66. What is the use of Verapamil?
    Used as a therapy for rate control in atrial fibrillation with rapid ventricular response due to its ability to slow conduction through the atrioventricular node.
  67. What are the most frequent adverse reactions noted with verapamil?
    Constipation and gingival hypertension.
  68. What is the MOA of Nitrates?
    Relax smooth muscle vasculature (dilate veins >>> arteries) through a mechanism where they are metabolized into endothelium derived relaxing factor, also known as nitric oxide. → ⇧cGMP
  69. What is the most common side effect of nitrates?
    Headaches, especially with sublingual nitroglycerin
  70. What is the function of hypoxanthine-guanine phosphoribosyltransferase?
    • Converts Hypoxanthine → Iosine monophosphate (IMP)
    • Guanine → Guanosine monophosphate (GMP)
  71. What happens if there is a deficiency of hypoxanthine-guanine phosphoribosyltransferase?
    • HGPRT converts hypoxanthine to iosine monophosphate and guanine to guanine monophosphate.
    • Deficiency of HGPT results in increased degradation of guanine and hypoxanthine bases to uric acid.
  72. Which enzyme activity is increased in Lesch-Nyhan syndrome and why?
  73. Where does the posterior cerebral artery supply?
    The occipital lobe, which contains the striate or primary visual cortex.
  74. This artery supplies the occipital lobe.
    Posterior cerebral artery
  75. This artery supplies the visual cortex
    Posterior cerebral artery
  76. Lesion to the posterior cerebral artery leads to?
    • Contralateral hemanopia with macular sparing
    • Lesion to the occipital lobe
  77. Where is the lesion?
  78. Describe the presentation and findings of Central retinal artery occlusion.
    • Acute painless monocular vision loss.
    • Retina cloudy with attenuated vessels and "cherry-red" spot at fovea (center of macula)
  79. What is the pathology seen below?
    • Central retinal artery occlusion
    • Retina cloudy with attenuated vessels and "cherry-red" spot at fovea (center of macula)
  80. Retina cloudy with attenuated vessels and cherry red spot at fovea (center of macula)
    Central retinal artery occlusion
  81. What does the red dot indicate with respect to airway, alveolar and intrapleural pressure?
    • The centrer of the airway, pressure-volume curve is the Functional residual capacity (FRC) of the lungs. 
    • FRC= volume of gas in lungs after normal respiration.
    • It identifies the resting state. At FRC, airway and alveolar pressure is 0 and intrapleural pressure is negative with a value of -5 cm H20
  82. What is functional residual capacity?
    Volume of gas in lungs after normal expiration
  83. What causes a constantly negative intrapleural pressure?
    • Tramautic injury that extends into the intrapleural space, such as a stab wound or accidental insertion of a needle (e.g. subclavian central catheter placement). 
    • When a puncture of the pleura allows intrapleural communication with the atmosphere (pressure: 0 cm H20).
  84. Describe the pathogenesis of Atherosclerosis
    • 1. Endothelial cell dysfunction.
    • 2. Macrophage and LDL accumulation
    • 3. Foam cell formation
    • 4. Fatty streaks
    • 5. Smooth muscle cell migration (involves PDGF and FGF) proliferation, and extracellular matrix deposition
    • 6. Fibrous plaque
    • 7. Complex atheromas
  85. Describe the characteristic of a mitral regurgitation murmur.
    Blowing, holosystolic murmur heard best over the cardiac apex with radiation to the axilla
  86. What accounts for dyspnea in heart failure patients?
    • Diastolic return of blood from the pulmonary circulation to the left atrium is impaired, thereby increasing pressure in the pulmonary veins and capillaries.
    • This causes the transudation of fluid from the pulmonary capillaries into the lung interstitum. 
    • The preence of fluid in the pulmonary intersitium DECREASES COMPLIANCE (Stretch)
  87. Dysnea, crackles at lung bases and the presence of an S3 sound suggest?
    Left heart failure
  88. In which diseases is the Functional residual capacity increased?
    • FRC- volume of gas in lung after normal expiration
    • FRC is increased in diseases that increase lung compliance (stretch) such as the obstructive lung diseases emphysema and chronic bronchitis.
  89. In which diseases is the Functional residual capacity decreased?
    • FRC- volume of gas in lung after normal expiration
    • FRC is decreased in diseases that decrease lung compliance (stretch) such as pulmonary fibrosis, pneumonia, pulmonary edema.
  90. What are the characteristics of Tuberous sclerosis?
    • Hamartomas in CNS and skin
    • Angiofibromas
    • Mitral regurgitation
    • Ash-leaf spot
    • Rhabdomyoma (cardiac; Tuberous sclerosis)
    • autosomal dOminant
    • Mental retardation
    • Angiomyolipoma
    • Seizures
    • Shagreen patches. 
  91. What is an angiomyolipoma and which condition is it associated with?
    • Renal benign tumor composed of blood vessels, smooth muscle and fat.
    • Tuberous sclerosis
  92. Histology of kidney, what is the pathology?
    Renal angiomyolipoma
  93. What is the pathology seen below?
    Angiofibromas- tuberous sclerosis
  94. Angiofibromas are characteristic of?
    Tuberous sclerosis
  95. What is the pathology below?
    Ash leaf spots- Tuberous sclerosis
  96. Leaf-shaped patches of skin lacking pigment are characteristic of ?
    Ash-leaf patches (Tuberous sclerosis)
  97. Cardiac rhabdomyomas are associated with which disease?
    Tuberous sclerosis

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