USMLE27

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USMLE27
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2015-03-09 13:35:30
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  1. What are the effects of carotid massage?
    • Causes reflex vagal discharge to the SA node, atrial myocytes and AV node → ⇩heart rate and cardiac output
    • Note: PaO2 and PaCO2 are NORMAL
  2. What causes the formation of a complete mole?
    Sperm fertilizes an ovum that has lost its maternal chromosomes
  3. This type of hydatidiform mole does not contain fetal parts.
    Complete mole - 46 XX, 46 XY
  4. In this type of hydatidiform mole, there are extremely high β-hCG levels.
    Complete mole - 46 XX, 46 XY
  5. This type of hydatidiform mole presents with an enlaged uterus "size greater than dates"
    Complete mole - 46 XX, 46 XY
  6. This type of hydatidiform mole presents with a normal uterine size
    Partial mole - 69 XXX or XXY
  7. This type of hydatidiform mole contains fetal parts
    Partial mole - 69 XXX or XXY
  8. With this type of hydatidiform mole, 2% progress to choriocarcinoma.
    Complete mole - 46 XX, 46 XY
  9. This type of hydatidiform mole has a 46 XX or XY karyotype
    Complete mole - 46 XX, 46 XY
  10. This type of hydatidiform mole has a 69 XXX or XXY karyotype
    Partial mole - 69 XXX or XXY
  11. What causes the formation of a partial mole?
    Result from fertilization of an egg by 2 or more sperm
  12. Describe the migration of the testes.
    The testes originate in the abdomen and migrate to the scrotal sac via the inguinal canal.
  13. Which cells are affected in patients with cryptorchidism? How are they affected?
    Sertoli cells-line the seminiferous tubules.  The seminiferous tubules become atrophic and hyalinized as a result of temperature-induced damage → ⇩sperm count & ⇩inhibin





  14. Describe the findings of each in BILATERAL cryptorchidism.
    LH
    Testosterone
    Inhibin
    FSH
    • LH: ⇧
    • Testosterone: ⇩ (but NORMAL in unilateral)
    • Inhibin: ⇩
    • FSH: ⇧
  15. Describe the findings of each in UNILATERAL cryptorchidism.
    LH
    Testosterone
    Inhibin
    FSH
    • LH: ⇧
    • Testosterone: NORMAL  (but decreased in bilateral)
    • Inhibin: ⇩
    • FSH: ⇧
  16. This urine crystal is characteristic of?
    Hexagonal crystals- Cystine kidney stone
  17. Hexagonal crystals are characteristic of which type of kidney stone?
    Cystine
  18. What causes the formation of cystine kidney stones?
    Defect in a transporter in the PCT that normally reabsorbs cystine, lysine, arginine and ornithine.
  19. Where do most renal cell carcinomas originate from?
    From the PROXIMAL CONVOLUTED TUBULE
  20. This carcinoma originates from the proximal convoluted tubule.
    Renal cell carcinoma
  21. Describe the microscopic findings of renal cell carcinoma.
    • Tumors are composed of polygonal cells with abundant clear cytoplasm and eccentric nuclei.
    • They are filled with accumulated LIPDS and CARBOHYDRATES
  22. This type of tumor is composed of polygonal clear cells filled with accumulated lipids and carbohydrates.
    Renal cell carcinoma
  23. Describe the pathology seen below.
    • Renal cell carcinoma
    • Golden yellow mass
  24. Where does Renal onocytoma arise from?
    Collecting ducts
  25. This tumor arises from the collecting ducts.
    Renal oncocytoma
  26. Where do Transitional cell carcinomas arise from?
    • Renal pelvis - 90%
    • Renal calyces, ureters, bladder
  27. This type of tumor often arises from the renal pelvis.
    Transitional cell carcinoma
  28. Describe the phases of acute tubular necrosis.
    • 1. Initiation/ inciting phase- ischemic injury to renal tubules by hemorrage, acute MI, sepsis, surgery
    • 2. Maintenance phase⇩urine output (oliguria), risk of HYPERKALEMIA, metabolic acidosis, Uremia (urea in blood)⇧BUN/Cr
    • 3. Recovery phase- ⇧urine output, ⇩BUN/Cr, risk of HYPOKALEMIA,  ⇩concentrations of K, Mg, PO4 and Ca
  29. What happens in the recovery phase of acute tubular necrosis?
    • Recovery phase
    • ⇧urine output, 
    • ⇩BUN/Cr
    • Risk of HYPOKALEMIA
    • ⇩concentrations of K, Mg, PO4 and Ca
  30. What happens in the maintainence phase of acute tubular necrosis?
    • Maintenance phase
    • ⇩urine output (oliguria)
    • Risk of HYPERKALEMIA
    • Metabolic acidosis
    • Uremia (urea in blood)
    • ⇧BUN/Cr
  31. In this phase of acute tubular necrosis, there is decreased urine output.
    • Maintenance phase
    • ⇩urine output (oliguria)
    • Risk of HYPERKALEMIA
    • Metabolic acidosis
    • Uremia (urea in blood)
    • ⇧BUN/Cr
  32. In this phase of acute tubular necrosis, there is increased urine output.
    • Recovery phase
    • ⇧urine output, 
    • ⇩BUN/Cr
    • Risk of HYPOKALEMIA
    • ⇩concentrations of K, Mg, PO4 and Ca
  33. In this phase of acute tubular necrosis, there is risk of hyperkalemia.
    • Maintenance phase
    • ⇩urine output (oliguria)
    • Risk of HYPERKALEMIA
    • Metabolic acidosis
    • Uremia (urea in blood)
    • ⇧BUN/Cr
  34. In this phase of acute tubular necrosis, there is risk of hypokalemia.
    • Recovery phase
    • ⇧urine output, 
    • ⇩BUN/Cr
    • Risk of HYPOKALEMIA
    • ⇩concentrations of K, Mg, PO4 and Ca
  35. Metabolic acidosis occurs in this phase of acute tubular necrosis.
    • Maintenance phase
    • ⇩urine output (oliguria)
    • Risk of HYPERKALEMIA
    • Metabolic acidosis
    • Uremia (urea in blood)
    • ⇧BUN/Cr
  36. Urea in blood is characteristic of this phase of acute tubular necrosis.
    • Maintenance phase
    • ⇩urine output (oliguria)
    • Risk of HYPERKALEMIA
    • Metabolic acidosis
    • Uremia (urea in blood)
    • ⇧BUN/Cr
  37. ⇩BUN/Cr is characteristic of this phase of acute tubular necrosis.
    • Recovery phase
    • ⇧urine output, 
    • ⇩BUN/Cr
    • Risk of HYPOKALEMIA
    • ⇩concentrations of K, Mg, PO4 and Ca
  38. Patients complain of double vision when walking downstairs. Which cranial nerve is affected?
    Trochlea- CN4
  39. Alkaline phosphatase refects activity of?
    Osteoblasts
  40. Urinary deoxypyridinoline refelects activity of?
    • Osteoclasts.
    • It is released into circulation when bone is absorbed/ broken down by osteoclasts.
  41. Where is the most common location for hematogenous osteomyelitis in children?
    • Metaphysis of long bone
  42. The rotator cuff is made up of tendons of which muscles?
    • Supraspinatus
    • Infraspinatus
    • Teres minor
    • Subscapularis
  43. What is the most commonly injured structure in rotator cuff syndrome?
    Tendon of the supraspinatus muscle
  44. What is Glanzmann thromblasthenia?
    ⇩GpIIb/IIIa → defect in platelet-platelet aggregation
  45. Defect in platelet to platelet aggregation is characteristic of which disease?
    • Glanzmann thrombasthenia
    • ↓GpIIb/ IIIa
  46. What does decreased GpIIb/IIIa results in?
    • Defective platelet-platelet aggregation
    • Glanzmann thromboblasthenia
  47. Where do gastric erosions extend to vs gastric ulcer?
    • Erosions- do not fully extend through the muscularis mucosa 
    • Ulcers- penetrate muscularis mucosa and can extend to submucosal layers
  48. What prevents lactation during pregnancy?
    ⇧levels of PROGESTERONE and ESTROGEN (which also promotes breast growth)
  49. What secretes β-hCG? What is its function?
    • hCG is secreted by the syncytiotrophoblast.
    • It serves to maintain the corpus luteum until the placenta can assume responsibility for estrogen and progesterone levels
  50. Which drugs can be used for acute gout attacks?
    • 1. NSAIDs: Naproxen, Indomethacin
    • 2. Glucocorticoids 
    • 3. Colchicine
  51. What is the MOA and use of Colchicine?
    • MOA: Binds and stabilizes tubulin to inhibit microtubule polymerization.
    • USE: Acute gout attacks
  52. This drug binds and stabilizes tubulin to inhibit microtubule polymerization.
    Colchicine- acute gout
  53. What are the side effects of Cochicine therapy?
    • GI effects- nausea, abdominal pain, diarrhea
    • Avoid in ppts with renal dysfunction
  54. What type of cell is seen below?
    • Reed-sternberg cells- Hodgkin's lymphoma
    • Owl eyes
  55. What is the mechanism of Digoxin?
    Inhibits the Na+/K+ ATPase causing an increase in intracellular Na+, which in turn inhibits the Na+/Ca2+ exchanger causing an increase in intracellular Ca2+
  56. Describe the pathology seen below?
    A diamond-shaped (crescendo-decrescendo) systolc murmur is characteristic for aortic stenosis
  57. What are the effects of beta-agonistis on the uterus?
    • β2-agonist
    • Uterine relaxation (tocolysis)
  58. Which receptor is responsible for uterine relaxation?
    β2 agonist
  59. What are the effects of menopause on bone?
    ⇩estrogen levels accelerate the loss of bone mass through a ⇩in osteoblastic activity and an ⇧in osteoclastic activity
  60. What are the major types of bone present in adult skeleton?
    • Tarabecular/ Spongy bone
    • Cortical/ Long bone
  61. Where are osteoporotic fractures most commonly at?
    Most commonly at VERTEBRAL BODIES and second most  common at the NECK OF THE FEMUR
  62. Which type of bone does Osteoporosis primarily affect?
    Trabecular/ spongy bone
  63. Trabecular thinning with fewer interconnections are characteristic of which disease?
    Osteoporosis
  64. Describe the bone changes in Osteoporosis?
    Trabecular/ Spongy bone loss mass and interconnections
  65. Excessive accumulation/ deposition of unmineralized osteoid is characteristic of?
    Vitamin D deficiency
  66. Describe the microscopic bone findings in vitamin D deficiency.
    Excessive accumulation/ deposition of  unmineralized OSTEOID 
  67. What does the arrow point to in this bone pathology?
    • Cement lines
    • In Paget's disease of the bone, irregular patterns of lamellar bone are linked by cement lines (which represent PREVIOUS AREAS OF BONE RESORPTION)
  68. Describe the histological findings in Osteopetrosis?
    Persistence of primary, unmineralized spongiosa in the medullary canals, with no mature trabeculae.
  69. The persistence of primary unmineralized spongiosa in the medullary canals are characteristic of?
    Osteopetrosis (marble bone disease)
  70. What is the main difference between post-traumatic stress disorder and acute stress disorder?
    • They present with identical symptoms (recurrent nightmares and flashbacks, potential memory loss)
    • Acute stress disorder - between 3 days and 1 month
    • PSTD- greater than 1 month
  71. Describe the oxidative reaction of the HMP shunt.
    • Glucose-6-Phosphate 6-phosphogluconate ⇨ Ribulose-5-Phosphate
    • CO2 and 2NADPH are produced
  72. NADPH produced by the HMP shunt is used in which reactions?
    • 1. Cholesterol and fatty acid synthesis
    • 2. Reducing glutathionine (and this repairing oxidative damage) available to RBCs
  73. In this disease, the muscle fibers of the calf are replaced by fat and connective tissue.
    Duchenne muscle dystrophy
  74. Cytosine is converted to uracil by?
    Spontaneous deamination
  75. Ultraviolet rays damage DNA through the formation of?
    Thymine dimers
  76. This microorganism is latent in the sacral ganglia.
    HSV-2
  77. Hepatocyte ballooning degeneration are characterisitic of?
    Acute hepatitis
  78. What are Councilman bodies and in which diseases are they commonly found?
    Eosinophilic apoptotic hepatocytes - Viral hepatitis or Yellow fever
  79. Eosinophilic apoptotic hepatocytes are characteristic of?
    Councilman bodies
  80. Blood levels of this microbial component correlate with morbidity and mortality in patients with meningitis by Neisseria.
    Lipooligosaccharide
  81. Lipooliogaccharide is a component of which microbacterium?
    • Neisseria meningitidis
    • Responsible for the many of the toxic effects of meningitis
  82. Deficiency of these complement components results in an inability to form the membrane attack complex.
    C5b-C9
  83. Which complement components form the membrane attack complex?
    C5-C9
  84. Deficiency of these complement components predisposes to recurrent infections by Neisseria.
    C5-C9
  85. What is the function of ceruloplasmnin?
    • Serum carrier protein for copper
    • Decreased in Wilson's disease

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