USMLE5

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USMLE5
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2015-02-01 23:57:10
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  1. What does elevated capillary hydrostatic pressure result in? What causes it?
    • Transudate edema
    • Results in increased plasma filtration into interstitum.
    • Abnormal arteriolar dilation (eg; use of dihydropyridine Ca2+ channel blockers)
    • Impairments in venous return (eg venous thrombosis, Right-sided heart failure)
  2. What does decreased plasma oncotic pressure result in? What causes it?
    • Transudate edema
    • Results in reduced amount of interstitial fluid returning to the circulation.
    • Oncotic pressure is generated by plasma proteins, especially albumin.
    • Decreased albumin conditions:- Nephrotic syndrome, Liver disease (CIRRHOSIS), malnutrition.
  3. What generates oncotic pressure?
    • Plasma proteins, especially albumin.
  4. How does sodium and water retention affect the intersitium?
    • Transudate edema
    • Increase intravascular volume, which ↑capillary hydrostatic pressure and ↓plasma oncotic pressure by diluting plasma proteins.

    Can be caused by kidney disease/ injury, congestive heart failure.
  5. Increased levels of acetylcholinesterase can be used to diagnose?
    Neural tube defects.
  6. Which disease has a high risk of Hirschsprung disease?
    Down syndrome
  7. What causes Hirschsprung disease?
    • Failure of neural crest cell migration leads to the absence of Auerbach and Meissner plexuses in segment of colon.
    • Congenital megacolon.
  8. How do we calculate the incidence of a disease?
    = new cases/ total population AT RISK
  9. In which diseases is anticipation common?
    • Trinucleotide repeat diseases:
    • Huntington
    • Friedreich ataxia
    • Myotonic dystrophy
  10. What is penetrance?
    The likelihood that the properties of a gene will be expressed.
  11. What is incomplete penetrance?
    The properties of a mutant gene is not expressed phenotypically.
  12. What is pleiotropy?
    • One gene mutation leads to multiple phenotypic abnormalities.
    • Phenylketonuria
  13. What is mosaicism? In which diseases is it seen in?
    • The presence of two populations of cells with different genotypes in one pateint. 
    • Person has a different genetic make up.
    • Turner
    • Klinefelter
    • Down syndrome
  14. Describe the presentation and findings of Polymyositis.
    Muscle weakness, mostly at shoulders.

    • ↑Expression of MHC I molecules on sarcolemma
    • CD8+ cytotoxic cells destroy myocyte.
    • ⇑Creatine kinase
  15. What disease is Lambert-Eaton myasthenic syndrome associated with?
    Small cell lung cancer
  16. What causes Lambert-Eaton mysathenic syndrome?
    • Autoantibodies to presynaptic Ca2+ channel →
    • ↓Ach release
  17. Muscle weakness that improves with activity is characteristic of which disease?
    Lambert-Eaton
  18. Describe the presentation of Lambert-Eaton myasthenic syndrome.
    • Muscle weakness (improves with use)
    • Dry mouth, impotence (autonomic symptoms)
  19. Why should non-selective beta blockers should not be used in diabetic patients?
    • It masks hypoglycemia in diabetics.
    • 1. Blockade of beta-2 receptors inhibit hepatic gluconeogenesis, glycogenolysis and lipolysis.
    • 2. The response to hypoglycemia (tremor, palpitations (tachycardia), hunger, nervousness, confusion, seizures) due to epinephrine and norepinephrine release is masked.
  20. What are the non-selective beta blockers?
    • Nadolol
    • Pindolol (partial antagonist)
    • Propranolol
    • Timolol
    • (N-Z)
  21. What pathology are Acanthocytes (spur cell) associated with?
    • Liver disease
    • Abetalipoproteinemia 
    • Irregularly shaped surface projections with vary in length and width.
  22. Which pathologic RBC form is seen in Liver disease?
    • -Acanthocyte 
    • -Target cell
  23. Which pathologic RBC form is seen in Abetalipoproteinemia?
    Acanthocyte
  24. What pathology are Schistocytes (helmet cell) associated with?
    • 1. DIC-gram- sepsis, acute pancreatitis, burn injury
    • 2. Thrombotic thrombocytopenic purpura (deficiency of ADAMTS 13/ vWF metalloprotease)
    • 3. Hemolytic Uremic syndrome
    • 4. HELLP syndrome
    • 5. Mechanical hemolysis (heart valve prosthesis)
  25. What pathology are Spherocytes  associated with?
    • -Hereditary spherocytosis
    • -Drug and infection induced autoimmune hemolysis
    • Small round cells without normal central pallor.
  26. What pathology are Target cells associated with?
    • HbC disease
    • Asplenia
    • Liver disease
    • Thalassemia
  27. Which ligament should be avoided during oophorectomy (removal of ovary)? Why?
    • Infundibulopelvic/ suspensory ligament-
    • 1.The nerves, arteries, veins and lymphatics supplying the ovary are delivered by this ligament. 
    • Can cause excess bleeding 
    • 2. Ureter at risk of injury 
  28. What does the infundibulopelvic/ suspensory ligament connect?
    • Ovaries to lateral pelvic wall.
  29. What causes the pathology seen below?
    Left ventricular free wall rupture



    Complication of transmural infarction (ST elevation) which generally occurs 3-14 days after the onset of ischemia, when coagulation necrosis, neutrophil infiltration and enzymatic lysis of connective tissue have sufficiently weakened the infarcted myocardium.
  30. What causes cardiac tamponade? Describe its presentation.
    • CAUSE: Rupture of the ventricular free wall as a result of an acute transmural MI.
    • Muffled heart sounds
    • Elevated jugular venous pressure
    • Profound HYPOTENSION
    • Cardiac tamponade limits ventricular filling during diastole, which decreases venous return -> Hypotension
  31. What is the function of Phenylalanine hydroxylase?
    Converts Phenylalanine to Tyrosine
  32. What is the function of Tyrosine hydroxylase?
    Converts tyrosine to Dihydroxyphenylalanine
  33. What is the function of Tyrosinase?
    Converts Dihydroxyphenylalanine to Melanin
  34. What is the function of DOPA decarboxylase?
    Converts Dihydroxyphenylalanine to Dopamine
  35. What is the function of Vitamin C in catecholamine synthesis?
    Converts Dopamine to NE
  36. What is the function of S-adenosyl methionine in catecholamine synthesis?
    Converts norepinephrine to Epinephrine
  37. What is the function of Phenylethanolamine-N-methyltransferase?
    Converts Norepinephrine to Epinephrine
  38. What converts norepinephrine to epinephrine? What stimulates this enzyme?
    • Phenylethanolamine-N methyltransferase
    • Cortisol stilulates this enyme.
  39. What causes this? What can be used to control it?
    • Exophthalmos- Graves disease
    • Infiltration of lymphocytes into the extraocular muscles and connective tissue.
    • Retro-orbital fibroblasts are then stmulated by TH1 cells to produce excessive amounts of glycosaminoglycans.
    • Tx: CORTICOSTEROIDS e.g Prednisone
  40. What mediates iodide uptake by the thyroid?
    • Sodium-iodide symporter
    • This uptake of iodide occurs against its concentration gradient.
  41. What is the function of the sodium-iodide symporter?
    Mediates iodide uptake by the thyroid against its concentration gradient.
  42. What is the MOA of Perchlorate?
    Inhibits the sodium-iodide symporter which mediates thyroid uptake of iodide.
  43. What is the MOA of Pertechnetate?
    Inhibits Sodium-iodide symporter which mediates the uptake of iodide by the thyroid.
  44. What is the MOA of Thiocyanate?
    Inhibits the sodium-iodide symporter which mediates thyroid uptake of iodide
  45. These anions can competitively inhibit the basolateral sodium-iodide symporter.
    • Perchlorate
    • Pertechnetate
    • Thiocyanate
  46. What is the function of thyroid peroxidase?
    • 1. Oxidation and organification of iodide
    • 2. Coupling of monoiodotyrosine and di-iodotyrosine
  47. This enzyme is used in the oxidation and organification of iodide.
    Thyroid peroxidase
  48. This enzyme couples iodide with tyrosine residues on thyroglobulin.
    Thyroid peroxidase
  49. Why is there such a high RBC chloride content in venous blood?
    • 1. Carbonic anhydrase activity forms bicarbonate from CO2 and water.
    • 2. Many of the bicarbonate diffuse out of the RBC into plasma.
    • 3. To maintain electrical neutrality, chloride ions diffuse into the RBC to take their place. ⇦CHLORIDE SHIFT
  50. Urethritis which cannot be cured by ceftriaxone indicates?
    • Nongonococcal urethritis-
    • Caused by Chlamydia trachomatis or Ureaplasma urealyticum
  51. Coagulase negative staphyloccus?
    • Staphyloccus epidermidis- Novobiocin sensitive
    • Staphyloccus aureus- Novobiocin resistant
  52. Coagulase positive staphyloccus?
    Staphyloccus aureus
  53. How does infection with Staphyloccus epidermidis occur?
    • Prosthetic devices (eg. hip implant, shunt, heart valve) and intravenous catheters.
    • Produce extracellular polysaccharide matrix
  54. This organism produces extracellular polysaccharide matrix.
    Staphyloccus epidermidis (biofilms)
  55. What enzyme is deficient in Xeroderma pigmentosum?
    ENDONUCLEASE
  56. How does DNA polymerase I takes out the RNA primer?
    5'→3' exonuclease
  57. How does DNA polymerase III proofread?
    3'→5' exonuclease
  58. This enzyme has 3'→5' exonuclease activity.
    DNA polymerase III- Proofreading
  59. This enzyme has 5'→3' exonuclease activity.
    DNA polymerase I - degrades RNA primer
  60. Defective repair of mismatched bases is associated with which disease?
    Hereditary nonpolyposis colorectal cancer
  61. Hereditary nonpolyposis colorectal cancer is due to a defect in?
    Defect in repair of mismatched bases.
  62. Birbeck granules are characteristic of this disease.
    Langerhans cell histiocytosis
  63. What are langerhans cells?
    Dendritic cells found in the skin that act as APCs.
  64. Where do langerhans cells come from and describe its characteristics.
    Derived from myeloid cell line and posess characteristic raquet-shaped intracytoplasmic granules known as Birbecks granules.
  65. Where are langerhans cells found?
    Skin and mucous membranes
  66. This cell has a characteristic tennis-raquet shaped intracytoplasmic granule.
    Langerhans cells
  67. Where are Kupffer cells found and what role do they play?
    • Macrophage-derived cell in LIVER.
    • Lie within hepatic sinusoids.
  68. What are osteoclasts? Where are they derived from?
    • Multinucleated cells that dissolve bone by secreting acid and collagenases.
    • Differentiate from monocytes, macrophages.
  69. What are mesangial cells? Where are they derived from?
    • Specialized  smooth muscle cells around blood vessels in the kidney, which function to regulate blood flow through the capillaries.
    • Are derived from MONOCYTES.
  70. What are the causes of Mirtal stenosis?
    Rheumatic fever
  71. What are the Mitral and Tricuspid valves derived from?
    Fused endocardial cushions of the AV canal
  72. Which murmurs can be caused by rheumatic fever?
    • Mitral Regurgitation/ Tricuspid regurgitation
    • Mitral stenosis
    • Mitral valve prolapse
    • Aortic Regurgitation
  73. What is the MOA of Cilostazol?
    • Phosphodiesterase III inhibitor;  Increases cAMP in platelets, resulting in inhibition of platelet aggregation.
    • Arteriolar VASODILATOR
  74. What is the MOA and use of Dipyridamole?
    • Phosphodiesterase III inhibitor;  Increases cAMP in platelets, resulting in inhibition of platelet aggregation.
    • Arteriolar VASODILATOR
  75. What is the MOA of Heparin?
    Activates antithrombin, which decreases thrombin and factor 10a
  76. What is the MOA and use of Agatroban?
    • Inhibit thrombin directly
    • tx: Heparin induced thrombocytopenia
  77. What is the MOA of Warfarin?
    Inhibitor of epoxide reductase (which converts Vitamin K from the oxidized to the reduced form) needed to produce factors 2, 7, 9, 10, Protein C and S.
  78. What is the MOA and use of tPA?
    • tPA/ Alteplase
    • Converts plasminogen to plasmin which cleaves thrombin and fibrin clots.
    • Tx: ST elevation MI, Pulmonary embolism
  79. What is the MOA and use of Alteplase?
    • tPA/ Alteplase
    • Converts plasminogen to plasmin which cleaves thrombin and fibrin clots.
    • Tx: ST elevation MI, Pulmonary embolism
  80. What are the effects of thromboxane A2?
    Platelet aggregation and vasoconstriction
  81. What is the MOA of Ticlopidine?
    • Inhibit platelet aggregation by irreversibly  blocking ADP receptors.
    • Prevent expression of GPIIb/IIIa on platelet surface
  82. What is the MOA of Clopidogrel?
    • Inhibit platelet aggregation by irreversibly  blocking ADP receptors.
    • Prevent expression of GPIIb/IIIa on platelet surface
  83. What is the MOA of Abciximab?
    • Bind to GPIIb/IIIa on platelets, preventing aggregaton.
    • Made from monoclonal antibody Fab fragments.
  84. What causes Cachexia (anorexia, anemia, malaise, weight loss)?
    • TNF-alpha (a.k.a Cachectin)
    • IFN-gamma
    • IL-1
    • IL-6
  85. What is the function of Transforming Growth Factor- Beta (TGF-B)?
    • Inhibits inflammatory response
    • Decrease T cell proliferation and cytokine production.
  86. What is parathyroid hormone-related peptide and in which neoplasms is it produced?
    • Squamous cell lung carcinoma
    • Renal cell carcinoma
    • Breast cancer
    • Causes hypercalcemia
  87. In this disease, even after administration of high dose dextamethasone, there are still elevated levels of ACTH and cortisol.
    Ectopic ACTH secretion e.g small cell lung cancer
  88. What happens after administration of high dose dextamethasone in ectopic ACTH secretion?
    There will still be elevated levels of ACTH and cortisol.
  89. In this condition, after administration of low-dose dextamethasone, cortisol levels are suppressed.
    • This could be either:
    • Adrenal adenoma
    • Exogenous corticosteroids
  90. This this condition, even after administration of low-dose dextamethasone, there are still elevated levels of ACTH and cortisol.
    • This could be either:
    • Pituitary adenoma
    • Ectopic ACTH production
  91. In this diesase, after administration of high dose dextamethasone, ACTH and cortisol levels are suppressed.
    Pituitary adenoma
  92. What is the most common cancer in men (in the US)?
    • 1. Prostate
    • 2. Lung
    • 3. Colon/ rectum
  93. What is the most common cancer in women (in the US)?
    • 1. Breast
    • 2. Lung
    • 3. Colon/ rectum
  94. Which cancers have the highest mortality rate in men the US?
    • 1. Lung
    • 2. Prostate
    • 3. Colon/ rectum
  95. Which cancers have the highest mortality rate in women in the US?
    • 1. Lung
    • 2. Breast
    • 3. Colon/ rectum
  96. How does B activation and class/ isotype switching occur?
    • Interaction with CD40 receptor on activated B cells with CD40 ligand (CD154) on activated T cells. 
    • The T cell secretes cytokines that determine Ig class switching of B cell
  97. Where does B cell activation/ isotype class switching occur?
    In the germinal centers of the lymph node.
  98. Explain the Pupillary light reflex
    Light enters eye ⇨ Retina transmitts information via the optic nerve bilaterally to the Pretectal nucleus, located in the superior colliculus ⇨ Fibers project to the ipsilateral and contralateral Edwinger-Westphal nucleus ⇨ Parasympathetic preganglionic neurons in the E.W nucleus transmits the info via the occlumotor nerve to the cilliary ganglion. ⇨ They synapse with parasympathetic postganglionic neurons ⇨ Innervate sphincter of iris
  99. What happens when light is shone in the left eye with a damaged optic nerve?
    • Light shone in left eye with damaged optic nerve: No constriction with left and right eye
    • Light shone in right eye with no damage to optic nerve: Contriction in left with damaged optic nerve and in right
  100. Describe the findings in Carbon monoxide poisoning with respect to Hb concentration, PaO2 (dissolved O2), % Saturation, Total O2 content (both dissolved and O2 attached to Hb).
    • Hb concentration: Normal
    • PaO2 (dissolved O2):Normal
    • % Saturation: ↓ (CO competes with O2)
    • Total O2 content(both dissolved and O2 attached to Hb): 
  101. Describe the findings in Anemia/ chronic blood loss with respect to Hb concentration, PaO2 (dissolved O2), % Saturation, Total O2 content (both dissolved and O2 attached to Hb).
    • Hb concentration
    • PaO2 (dissolved O2): Normal
    • % Saturation: Normal
    • Total O2 content (both dissolved and O2 attached to Hb): ↓
  102. Describe the findings in Polycythemia with respect to Hb concentration, PaO2 (dissolved O2), % Saturation, Total O2 content (both dissolved and O2 attached to Hb).
    • Hb concentration: ↑
    • PaO2 (dissolved O2): Normal
    • % Saturation: Normal
    • Total O2 content(both dissolved and O2 attached to Hb): ↑
  103. Which non-glucose monosacchardie is metabolized the fastest?
    • Fructose. 
    • It bypasses phosphofructokinase-1, the rate limiting enzyme of glycolysis. 
    • Other sugars (e.g glucose, galactose, mannose enter glycolysis prior to PKF-1 and are metabolized more slowly.
  104. What are Nissl bodies?
    • A neurons Rough endoplasmic reticulum.
    • They synthesize peptide neurotransmitters for secretion.
  105. What kind of transport does kinesin participate in?
    • Anterograde transport- moves intracellular vesicles and organelles toward the plus (rapidly growing) ends of microtubules. 
    • Anterograde transport is usually directed away from the nucleus, down the axon, toward the nerve terminal.
  106. This type of microtubule motor protein participates in Anterograde transport.
    • Kinesin (- -> +)
    • Moves vesicles and organelles toward the plus (rapidly growing) ends microtubules.
    • Away from nucleus -> Down axon -> Nerve terminal.
  107. This microtubule motor protein transports this way: - -> +
    • Kinesin 
    • Anterograde transport.
  108. This microtubule motor protein transports this way: + -> -
    • Dyenin 
    • Retrograde transport
  109. What kind of transport does Dyenin participate in?
    • Retrograde transport.
    • Moves organelles toward the nucleus (+ -> -)
  110. What type of movement does Dyenin function in?
    Ciliary and flagellar movement
  111. What are the lengths of Microtubules, Intermediate filaments and Microfilaments in diameter?
    • Microtubules- 23 nm
    • Intermediate filaments- 8-10 nm
    • Microfilaments- 6 nm
  112. What are the MEN1 tumors?
    • Parathydoid
    • Pancreas
    • Pituitary
  113. What are the MEN2A tumors?
    • Parathyroid
    • Pheochromocytoma
    • Medullary carcinoma of the thyroid
  114. What are the MEN2B tumors?
    • Pheochromocytoma
    • Medullary carcinoma of the thyroid
    • Neuromas
  115. MEN2A and 2B are associated with a mutation in which gene?
    RET gene (codes for receptor tyrosine kinase)
  116. RET oncogene is associated with which tumors? What is its gene product?
    • MEN2A: Parathyroid, pheochromocytoma, medullary carcinoma of the thyroid
    • MEN2B: Pheochromocytoma, medullary carcinoma of the thyroid, neuromas.
    • (codes for receptor tyrosine kinase)
  117. Where do parafollicular cells arise from?
    4th/ 5th pharyngeal pouches
  118. What forms the adrenal cortex?
    Mesoderm/ mesothelial cells
  119. What forms the adrenal medulla?
    Neural crest cells
  120. What are the effects of the gene product associated with von Hippel-Lindau disease?
    Inhibits hypoxia inducible factor 1a which increases the formation of vascular endothelial growth factor and erythropoetin.
  121. What causes Fragile X syndrome?
    An increased number of CGG trinucleotide repeats leads to HYPERMETHYLATION of cytosine bases and subsequent gene inactivation (FMR1 gene).

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