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UWORLD missed questions > missed questions 1 > Flashcards

missed questions 1 Flashcards

1
Q

what nerve traverses the cribriform plate?

A

I

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2
Q

what nerves and vessels traverse the optic canal

A

II, ophthalmic a, central retinal v.

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3
Q

what nerves and vessels traverse the SOF?

A

III, IV, V1, VI

ophthalmic v.

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4
Q

what nerve traverses the foramen rotundum?

A

V2

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5
Q

what nerve traverses the foramen ovale?

A

V3

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6
Q

what vessels traverse the foramen spinosum?

A

middle meningeal a. & v.

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7
Q

what nerves traverse the internal acoustic meatus

A

VII, VIII

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8
Q

what nerves and vessel traverse the jugular foramen?

A

IX, X, XI

jugular v.

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9
Q

what nerve traverses the hypoglossal canal?

A

XII

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10
Q

what nerve and vessel traverse the foramen magnum?

A

XI
brainstem
vertebral a.

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11
Q

what is the consequence of a lesion to the upper trunk of the brachial plexus? What nerves are affected?

A

Erb palsy (waiter’s tip)

Musculocutaneous, axiallary, radial, median

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12
Q

what is the consequence of a lesion to the lower trunk of the brachial plexus? What nerves are affected?

A

Claw hand (Klumpke palsy, all fingers flexed)

Axillary, radial, median, ulnar

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13
Q

What is the consequence of a lesion to the posterior cord of the brachial plexus? What nerves are affected?

A

Wrist drop

axillary, radial

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14
Q

What is the consequence of a lesion to the long thoracic nerve? What are the nerve roots?

A

Winged scapula

C5, 6, 7

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15
Q

What is the consequence of a lesion to the axillary nerve?

A

Deltoid muscle impairment

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16
Q

What is the consequence of a lesion to the radial nerve?

A

Wrist drop (“Saturday night palsy”)

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17
Q

What is the consequence of a lesion to the musculocutaneous nerve?

A

Elbow flexion impairment, loss of sensation on lateral forearm

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18
Q

What is the consequence of a lesion to the median nerve?

A

Pope’s blessing (inability to make a fist with thumb, second and third digit)

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19
Q

What is the consequence of a lesion to the ulnar nerve?

A

Ulnar claw (inability to extend the fourth and fifth digits)

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20
Q

What neoplasms can cause secondary dermatomyositis?

A

COLL = colorectal, ovarian, Non Hodgkin lymphoma, lung

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21
Q

What is the most common pineal mass and in what demographic is this most prevalent?

A

germinoma, young boys

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22
Q

What are examples of merocrine glands?

A

salivary, eccrine sweat glands, apocrine sweat glands

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23
Q

What are examples of apocrine glands?

A

mammary glands

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24
Q

what are examples of holocrine glands?

A

Sebaceous glands, meibomian glands

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25
Q

In CO poisoning, how are dissolved O2 (PO2), % Hb saturation (O2 binding capacity), and total O2 content affected?

A

PO2 is normal, % sat is decreased but may appear normal on testing, O2 content is decreased

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26
Q

In anemia, how are PO2, %sat, and O2 content affected? What disorder mimics anemia?

A

PO2 is normal, %sat is normal, and O2 is decreased. Methemoglobinemia mimics anemia because the metHb can not bind O2.

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27
Q

what type of collagen is in scar tissue?

A

Type I

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28
Q

what is the pathophysiology of emphysema?

A

macrophages and neutrophils secrete proteases that destroy alveoli

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29
Q

How are the leads in a biventricular pacemaker placed?

A

RA

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30
Q

describe Hib’s virulence factor

A

PRP (polyribosylribitol phosphate) in the capsule binds factor H, which degrades C3b and prevents opsonization

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31
Q

describe clostridium perfringens virulence factor

A

lecithinase (toxin A) lyses cell membranes and causes gas gangrene

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32
Q

describe streptococcus virulence factor

A

M protein binds factor H, which degrades C3b and prevents opsonization

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33
Q

describe staph aureus virulence factor

A

Protein A binds the Fc portion of Ig

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34
Q

describe mycobacterium tuberculusis virulence factor

A

trehalose dimycolate in the cell wall prevents macrophage killing and promotes formation of granulomas

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35
Q

what is the difference between schizophrenia, schizophreniform disorder, and schizoaffective disorder?

A

schizophrenia > 6 months

schizophreniform < 6 months

schizoaffective = schizophrenia + major depressive disorder or manic episode + delusions or hallucinations in the absence of mood sx for > 2 weeks

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36
Q

what are neurophysins?

A

the Uber drivers of hormones that travel in neurons from the HT –> PP (ADH, oxytocin)

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37
Q

what cells have highly developed smooth endoplasmic reticulum?

A

cells that synthesize steroids

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38
Q

what are cholesteatomas? are they made of cholesterol?

A

growths in the middle ear that may be congenital or secondary to infection, trauma, or surgery. They are NOT MADE OF CHOLESTEROL, they are composed of squamous cell debris.

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39
Q

what is the formula for resistance in a vessel?

A

R = nL / r4

40
Q

what are the findings in POTTER sequence?

A 
pulmonary hypoplasia
oligohydramnios
twisted face (flat face, low-set ears)
twisted skin (wrinkly skin)
extremities (club feet)
renal agenesis
41
Q

what spinal tracts are affected in B12 deficiency?

A

dorsal columns and lateral corticospinal tract

42
Q

What changes occur in the axon and in the neuronal body when an axon becomes severed due to trauma?

A

axon –> Wallerian degeneration (swelling and irregularity, eventual digestion by Schwann cells and macrophages, occurs up to the closest node of Ranvier)

neuronal body –> axonal reaction (edema, peripheral displacement of the nucleus and Nissl substance)

43
Q

what are two consensus sequences of the promoter region?

A

CAAT box, TATA box

44
Q

what is the start codon and what are the stop codons?

A 
start = AUG
stop = UAA, UAG, UGA
45
Q

what are the crescents composed of in rapidly progressive glomerulonephritis

A

glomerular parietal cells, monocytes, macrophages, fibrin

46
Q

what are the different insulin types?

A

Long acting:

  • NPH (2x/day)
  • glargine, detemir (1x/day)

short-acting:

  • regular (peak 2-5 hours, IV)
  • lispro, aspart, glulisine (peak 0.5-3 hours, best for postprandial hyperglycemia)
47
Q

how does rat poison work? What is the antidote?

A

“superwarfarin,” give fresh frozen plasma

48
Q

How are Langhans giant cells formed in the setting of mycobacterium tuberculosis infection?

A

Macrophages phagocytose and present to Th1 cells. The Th1 cells stimulate macrophages and endow them with the ability to kill intracellular mycoplasma organisms. Activated macrophages form Langhans giant cells.

49
Q

Are Langhans giant cells a specific finding for mycobacterium tuberculosis infection?

A

No, they are a nonsepecific finding in granulomatous conditions.

50
Q

Are Langhans giant cells the same as Langerhans cells?

51
Q

What are symptoms associated with thaimine (B1) deficiency?

A

Wernicke-Korsakoff syndrome (confusion, ataxia, oculomotor abnormalities, memory deficits)

dry beriberi (peripheral neuropahty)

wet beriberi (cardiac involvement)

52
Q

What are the symptoms of niacin (B3) deficiency?

53
Q

what are the symptoms of pyridoxine (B6) deficiency?

A

cheilosis, stomatitis, glossitis

54
Q

what are the symptoms of folate (B9) deficiency?

A

megaloblastic anemia, NTDs

55
Q

what are the symptoms of cobalamin (B12) deficiency?

A

megaloblastic anemia with neurologic deficits

56
Q

what are the symptoms of vitamin C deficiency?

57
Q

What type of receptor is the opioid receptor?

58
Q

What is the effect of opiate binding to receptors on the presynaptic and postsynaptic membranes?

A

presynaptic–> block Ca2+ influx

postsynaptic –> open K+ channels causing membrane hyperpolarization and potassium efflux

59
Q

what genes are associated with pheochromocytoma?

60
Q

what is the MOA of ribavirin in the treatment of HepC?

A

ribavirin is a nuceloside antimetabolite drug that interferes with duplication of viral genetic material. It also directly inhibits HCV RNA polymerase

61
Q

are pigmented gall stones associated with hereditary spherocytosis?

62
Q

what are the first and second generation antihistamines?

A

first generation = hydroxyzine, promethazine, chlorpheniramine, diphenhydramine

second generation = loratadine, cetirizine

63
Q

what is the MOA of fibrates?

A

activate ppar-a, deading to decreased hepatic VLDL and increased LPL activity, used to decrease TG levels

64
Q

what is the MOA of ezetimibe?

A

selectively blocks intestinal cholesterol absoprtion

65
Q

what is the MOA of bile acid-binding resins (eg cholestyramine)

A

increase fecal loss of cholesterol derivatives by binding bile acids in the intestine and disrupting enterohepatic bile acid circulation

66
Q

what is the MOA of PCSK9 inhibitors?

A

monoclonal antibodies that reduce LDL receptor degradation in the liver (affect mainly cholesterol not TGs)

67
Q

what is the MOA of statins?

A

inhibit HMG-CoA reductase, decreasing hepatic cholesterol synthesis (moderate affect on TGs)

68
Q

is neuroblastoma a brain cancer?

A

NO! It is a cancer of the adrenal medulla typically presenting in children < 2

69
Q

what findings are seen on light microscopy of a liver biopsy in Reye’s syndrome?

A

microvesicular steatosis (small fat vacuoles in the cytoplasm of hepatocytes)

70
Q

what are the signs of congenital hypothyroidism?

A

none at first (have maternal T4), after about 2 months, nonpitting edema, umbilical hernia, protruding tongue, large anterior fontanelle

71
Q

what cytokine is critical for fibroblast migration, proliferation, and connective tissue synthesis?

72
Q

what malignancy has a t(11;14) translocation

A

Mantle cell lymphoma (results in activation of the cyclin D gene)

73
Q

what is prophylaxis for MAC in HIV patients with CD4 < 50 cells and how does it present?

A

azithromycin, presents with fever, weight loss, and diarrhea. anemia, HSM, elevated alk phos and LDH are also common.

74
Q

how does theophylline treat COPD?

A

it is an adenosine receptor antagonist and PDE inhibitor that causes bronchodilation by increasing intracellular cyclic AMP levels (similar to B-adrenergic agonists)

75
Q

what are the steps of leukocyte passage into inflamed tissues?

A
  1. margination
  2. rolling (L-selectin, E-selectin/P-selectin)
  3. activation
  4. tight adhesion and crawling (Mac-1, LFA-1/CD 18, ICAM-1)
  5. transmigration (PECAM-1)
76
Q

dermatitis herpetiformis is associated with what GI disorder?

A

celiac disease

77
Q

what is the distinct histopathologic finding in chronic Hepatitis B infection?

A

accumulation of hep B surface antigen within hepatocytes, resulting in the appearance of a finely granular, diffusely homogeneous, pale eosinophilic cytoplasm (“ground glass” hepatocytes)

78
Q

what are the derivatives of the 1st, 2nd, 3rd, 4th, and 6th aortic arches?

A 
1 = maxillary a.
2 = hyoid a., stapedial a.
3 = common carotid a., internal carotid a.
4 = (L) aortic arch, (R) R subclavian a.
6 = proximal pulmonary a.'s, (L) ductus arteriosus
79
Q

what drugs can cause DRESS?

A

seizure drugs (phenytoin), sulfonamides, allopurinol

80
Q

what is the effect of prostaglandins in the eye?

A

increase outflow of aqueous humor

81
Q

what is the most common cause of spontaneous lobar hemorrhage in adults >60?

A

amyloid angiopathy (B-amyloid deposition in walls of small to medium-sized cerebral arteries)

82
Q

Auer rods are associated with which hematologic malignancy and stain for _____?

A

AML, peroxidase

83
Q

what hematologic malignancy stains positive for terminal deoxynucleotidyl transferase (TdT)

84
Q

hairy cell leukemia stains positive for what?

A

tartrate resistant acid phosphatase (TRAP)

85
Q

platelet-derived growth factor receptor mutations play a role in which hematologic malignancy?

86
Q

how does vitamin E deficiency present?

A

neuromuscular disease + hemolytic anemia

87
Q

what is the cause of Mallory-Weiss tears?

A

rapid increase in intraabdominal and intraluminal gastric pressure (such as occurs during vomiting)

88
Q

In albinism, are melanocytes present in the skin? What about in vitiligo?

A

YES, but they do not make melanin. In vitiligo, there is an absence of melanocytes.

89
Q

what does a PAS stain highlight?

A

PAS oxidizes carbon-carbon bonds, so it is really good at highlighting polysaccharides in fungal cell walls, mucosubstances secreted by epithelia, and basement membranes.

90
Q

what intracellular pathway is activated by growth factor?

91
Q

What antibiotics are used for MRSA, what are their MOAs and what are their side effects?

A

vancomycin - blocks polymerization by binding D-alanyl-D-alanine - red man syndrome, nephrotoxicity

daptomycin - depolarizes cell membrane by creating transmembrane channels - elevated CPK, myopathy

linezolid - binds 50s, inhibits initiation of translation - thrombocytopenia, optic neuritis, serotonin syndrome

92
Q

what antihypertensive can cause peripheral edema

A

calcium channel blockers

93
Q

what is the inheritance pattern of G6PD deficiency?

A

X-linked recessive

94
Q

cataracts, frontal balding, and gonadal atrophy?

A

myotonic dystrophy, autosomal dominant (CTG repeat expansion)

95
Q

what is the sequence of colorectal adenoma to carcinoma?

A
  1. normal mucosa to small adenomatous polyp = APC mutation
  2. increase in size of adenoma = KRAS mutation
  3. malignant transformation = P35 mutation
96
Q

muddy brown casts are pathognomonic for which renal pathology?

A

acute tubular necrosis, affecting the PCT and the medulla in response to ischemic injury

97
Q

which cell type is responsible for the intense inflammatory response seen in patients with gout?

A

neutrophils

UWORLD missed questions (1 decks)

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