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USMLE 25

  1. Describe the findings of each in 11β-hydroxylase deficiency: Mineralocorticoids, Cortisol, Sex hormones, Blood pressure, K+, Renin activity
    • Mineralocorticoids: ⇩
    • Sex hormones: ⇧
    • Blood pressure: ⇧
    • K+: ⇩
    • Renin activity: ⇩
  2. What is the function of 11β-hydroxylase?
    Converts 11-deoxycorticosterone to Corticosterone
  3. Describe the presentation/ findings of 11β-hydroxylase deficiency.
    • Ambiguous genetalia
    • Hypertension (due to ⇧11-deoxycorticosterone)
    • Fluid & Salt retention
  4. What bone is most common of the carpal bone fractures?
    Scaphoid fractures
  5. What frequently causes a scaphoid fractures?
    • They frequently result from falls onto an outstretched arm that cause axial compression or wrist hyperextension.
    • Image Upload 2
  6. Describe the presentation of a scaphoid fracture.
    Patients present with persistent wrist pain and tenderness in the anatomical snuffbox following a fall on outstretched hand
  7. Scaphoid fractures are at risk for?
    • Avascular necrosis - retrograde blood supply
    • Nonunion
  8. Describe the blood supply of the scaphoid bone.
    • Supplied by the dorsal scaphoid branch of the radial artery.
    • Image Upload 4
    • Blood supply to the proximal pole proceeds in a retrograde manner and can be easily interrupted by a fracture.
  9. What is the pathology seen below?
    Image Upload 6
    Scaphoid fracture
  10. Label the diagram below.
    Image Upload 8
    Image Upload 10
  11. What other diseases/ conditions is carpal syndrome associated with?
    • Repetitive wrist movements
    • Hypothyroidism
    • Diabetes mellitus
    • Rheumatoid arthritis
  12. A fall on an outstretched hand that damages the hook of hamate can cause?
    Ulnar nerve injury
  13. Dislocation of the lunate may cause?
    Acute carpal tunnel syndrome
  14. What congential cardiac defect is Marfan syndrome associated with?
    • Mitral valve prolapse
    • Cystic medial necrosis of the aorta ⇨ dissecting aortic aneurysms, Aortic regurgitation
  15. What is the most important prognostic indicator for patients with malignant melanoma?
    Measurement of the depth of invasion (Breslow thickness)
  16. Melanomas in the vertical growth phase indicate?
    Increased risk of metastasis
  17. What is the pathology seen below?
    Image Upload 12
    • Porcelain gallbladder
    • Calcified gallbladder
  18. What is the pathology seen below?
    Image Upload 14
    • Porcelain galbladder
    • Calcified gallbladder
  19. What is a Porcelain gallbladder? What causes it? How do we treat?
    • Calcified gallbladder due to chronic cholecystitis (inflammation)
    • Treatment: Cholecystectomy due to high rates of GALLBLADDER CARCINOMA
  20. Rim of calcium deposits that outline the gallbladder is characteristic of which pathology?
    Porcelain gallbladder
  21. What is the difference between Salk and Sabin polio vaccine?
    • Salk- Killed (INJECTED)
    • Sabin- Live attenuated (ORAL)
  22. One patient is given a live attenuated polio vaccine and another a killed polio vaccine. The level of which poliovirus antibodies will differ the most between the patients?
    Oropharyngeal/ Intestinal mucosal IgA would increase more with the live attenuated - Sabin which is ORAL vs the killed - Salk which is injected.
  23. High peak in the gamma-globulin region on serum electrophoresis represents?
    M spike- consists of an overproduced monoclonal immunoglobulin
  24. Describe an M spike. Which diseases is it characteristic of?
    • M spike is an M protein consisting of an overproduced monoclonal immunoglobulun. 
    • Serum protein electrophoresis shows a high peak in gamma-globulin region.
  25. The absolute risk reduction of drug A versus standard therapy was 4%. The incidence of recurrent PE in the standard therapy group was 6%. There were 24 patients who developed recurrent PE in the drug A group. How many total subjects were there in the drug A group?
    • Absolute Risk Reduction= Event Rate control- Event rate treatment
    • 4%= 6%- Event rate treatment
    • Event rate treatment= 2%= 0.2
    • Event rate treatment= Number of events in the treatment arm/ Number of subjects in the treatment arm
    • Number of subjects in the treatment arm= 24/0/02= 1200
  26. How do we calculate absolute risk reduction?
    ARR= Event rate control- Event rate treatment
  27. How do we calculate event rate treatment?
    ER treatment= Number of events in the treatment arm/ Number of subects in the treatment arm
  28. What is the MOA and use of Diphenoxylate?
    • Binds mu opiate receptors in the GI tract and SLOWS MOTILITY
    • Use: Diarrhea
  29. What is the MOA and use of Loperamide?
    • Binds mu opiate receptors in the GI tract and SLOWS MOTILITY
    • Use: Diarrhea
  30. What is the MOA and use of Bosentan?
    • MOA: Antagonize endothelin-1-receptors→ ⇩pulmonary vascular resistance
    • Use: Pulmonary hypertension
  31. This drug inhibits endothelin-1 receptors.
    Bosentan- used in the treatment of pulmonary hypertension
  32. What is the MOA and use of Etanercept?
    • MOA: Fusion protein that works as a receptor for tumor necrosis factor
    • Use: Rheumatoid arthritis, Psoriasis, Ankylosing spondylitis
  33. This drug is a fusion protein that works as a receptor for tumor necrosis factor α.
    Etanercept
  34. What causes the familial/ heritable form of Pulmonary arterial hypertension?
    Mutation in BMPR2 gene which normally inhibits vascular smooth muscle proliferation.
  35. What is the function of the BMPR2 gene?
    Inhibits vascular smooth muscle proliferation.
  36. Describe the pathogenesis of idiopathic pulmonary artery hypertension.
    • 1. Muscularization of small arteries
    • 2. Medial hypertrophy and intimal hyperplasia
    • 3. Intimal fibrosis (onion skinning)
    • 4. Formation of capillary turfts (plexiform lesion)
  37. What is the function of pyruvate kinase?
    • Converts phosphoenolpyruvate to Pyruvate
    • One molecule of ATP is generated.
  38. This enzyme converts phosphoenolpyruvate to pyruvate.
    Pyruvate kinase
  39. What stimulates the activity of pyruvate kinase?
    Fructose 1, 6-bisphosphate
  40. How does Pyruvate kinase deficiency cause hemolytic anemia?
    Due to failure or glycolysis (pyruvate kinase stimulates glycolysis) and failure to regenerate sufficient ATP to maintain erythrocyte structure.
  41. This type of anemia results from failure to generate sufficient ATP to maintain erythrocyte structure.
    Pyruvate kinase deficiency
  42. These drugs are analogues of pyrophosphate.
    Bisphosphonates- Alendronate and other -dronates
  43. What toxicity is associated with the use of Bisphosphonates? How can we avoid this?
    • Can cause CORROSIVE ESOPHAGITIS
    • Patients are advised to take with water and remain upright for 30 mins
  44. Patient develops right-sided weakness and numbness, with his arm more severely affected than his leg. He understands everything that is said to him, but cannot speak. Which artery has been occluded?
    LEFT Middle meningeal artery
  45. Describe the symptoms of an occlusion to the Middle cerebral artery.
    • Contralateral loss of sensation/ paralysis of UPPER LIMB and FACE
    • APHASIA- loss of ability to understand/ express speech
  46. A lesion to broca's area manifests as? What artery supplies this area?
    Inability to speak or write, but preserved comprehension of the spoken and written word
  47. Where is Broca's area located?
    Inferior frontal gyrus in the dominant (left) hemisphere
  48. This structure is located in the inferior frontal gyrus in the dominant (left) hemisphere.
    Brocas area
  49. Loss of ability to speak or write but preserved comprehension of the spoken and written word is associated with a lesion to?
    Brocas area- inferior frontal gyrus in the dominant (left) hemisphere
  50. A lesion of the left anterior cerebral artery leads to?
    Right sided loss of sensory and motor functions in the lower limb
  51. What causes hyperestrinism in alcoholic cirrhosis and what are the manifestations of that?
    • Hyperestrinism in alcoholic cirrhosis is caused by:
    • 1. ⇩catabolism of estrogens (by nonfunctional liver)
    • 2. ⇧sex hormone binding globulin which binds more testosterone than estrogen

    • This leads to:
    • Gynecomastia
    • Testicular atrophy
    • Decreased body hair
    • Spider angiomata
  52. What are the manifestations of hyperestrinism in alcoholic cirrhosis?
    • 1. Gynecomastia
    • 2. Testicular atrophy
    • 3. Decreased body hair
    • 4. Spider angiomata
  53. What causes pedal/ ankle edema in cirrhosis?
    • Cirrhotic liver produces insufficient amounts of proteins, such as albumin.
    • Hypoalbuminema→  ⇩Intravascular oncotic pressure → Fluid moves into the extravascular space → Pitting edema
  54. What is Fetor hepaticus and what is it characteristic of?
    Malodorous breath- Alcoholic cirrhosis
  55. What causes Fector hepaticus?
    • Breath smells musty
    • Caused by Hyperammonemia
  56. What are the effects of portal hypertension in cirrhosis?
    • 1. Esophageal varices hematemesis
    • 2. Melena (due to peptic ulcer)
    • 3. Splenomegaly
    • 4. Caput medusae, ascites
    • 5. Portal hypertensive gastropathy
    • 6. Anorectal varices
  57. What is Caput medusae?
    • Distended paraumbilical veins
    • Alcoholic cirrhosis
  58. Ppt presents with shortness of breath. Analysis of expiratory gases reveals: 
    Tracheal pO2: 150 mmHg
    Alveolar pO2: 145 mmHg
    Alveolar pCO2: 5 mm Hg
    What causes the result of this patients pulmonary gas analysis?
    • Normal Tracheal pO2 = 150 mmHg
    • Normal alveolar pO2 = 104 mmHg
    • Normal alveolar pCO2 = 40 mmHg
    • Patient is suffering frrom a very poor alveolar perfusion evidenced by failure of the alveolar gas to reach its normal equilibrium point.
  59. What is diffusion-limited gas exchange?
    Gas does not equilibiriate by the time blood reaches the end of the capillary
  60. In which situation can O2 equilibrium become diffusion-limited?
    • Emphysema
    • Pulmonary fibrosis
    • In states of ⇧pulmonary flow (e.g. exercise)
  61. What is the clinical use of thiazide diuretics?
    • Hypertension
    • Heart failure
    • Hypercalciuria ⇨ Ca2+ oxalate kidney stones
    • Nephrogenic DI
    • Osteoporosis
  62. How to we treat calcium kidney stones?
    • 1. Hydration
    • 2. THIAZIDE diuretics
    • 3. Citrate
  63. Which diuretic increases Ca2+ excretion?
    • Loops lose calcium
    • Furosemide, Bumetanide, Toresemide
  64. What are the effects of loop diuretics on Ca+?
    ⇧Serum Ca2+ excretion
  65. What is restless leg syndrome and how do we treat?
    • Uncomfortable urge to move the legs due to an uncomfortable sensation in the legs. 
    • It is worst at rest or when falling alseep.
    • Tx: Dopamine agonsit - ROPINIROLE, PRAMIPEXOLE
  66. In this disorder, there is an uncomfortable urge to move the legs due to an uncomfortable sensation in the legs. It occurs especially when one is about to go to sleep. How do we treat?
    • Restless leg syndrome
    • Dopamine agonist- Ropinirole, pramipexole
  67. What is the MOA and use of Ropinirole?
    • MOA: Dopamine agonist (non-egot (preferred))
    • USE: Parkinsonism
  68. What is the MOA and use of Pramipexole?
    • MOA: Dopamine agonsit (non-ergot (preferred))
    • USE: Parkinsonism
  69. What are the dopamine agonists?
    • Bromocriptine - ergot
    • Pramipexole, Ropinirole- non-ergot
  70. What is cataplexy and how can we treat?
    • A feature of Narcolepsy
    • Characterized by sudden loss of muscle tone, often triggered by strong emotional stimulus such as laughter.
    • Tx: Muscarinic antagonists
Author
rere_girl4ever
ID
297679
Card Set
USMLE 25
Description
USMLE 25
Updated

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