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Dedicated - Step 2 > 11 > Flashcards

11 Flashcards

1
Q

What causes GVHD?

A

Recognition of host major and minor HLA-antigens by donor T-cells and consequent cell-mediated immune response

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2
Q

Organs typically affected in GVHD + symptoms?

A

Skin (maculopapular rash involving palms, soles, and face), intestine (blood + diarrhea), liver (abnormal LFTs, jaundice)

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3
Q

What mediates graft rejection?

A

Activation of host T-cells

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4
Q

GnRH, FSH, and estrogen findings in hypothalamic hypogonadism?

A

All decreased

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5
Q

GnRH, FSH, and estrogen findings in primary ovarian insufficiency?

A

GnRH and FSH increased

Estrogen decreased

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6
Q

GnRH, FSH, and estrogen findings in PCOS?

A

GnRH: increased
FSH: normal
Estrogen: increased

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7
Q

GnRH, FSH, and estrogen findings in exogenous estrogen use?

A

GnRH and FSH decreased

Estrogen increased

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8
Q

Management of preterm prelabor rupture of membranes?

A

If <34 weeks -> expectant management with prophlyactic latency ABX, steroids, and inpatient monitoring

If <34 weeks + complications develop -> deliver + IAI Rx, steroids, Mg if <32 weeks

If 34 to <37 weeks: deliver, GBS PPx, +/- steroids

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9
Q

What is amnioinfusion used for?

A

Variable fetal HR decelerations in labor

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10
Q

When are tocolytics indicated in PPROM?

A

Never - they are contrindicated because contractions often indicate a complication requiring delivery or intervention

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11
Q

Management of dyspareunia due to hypoestrogenism in the setting of postpartum breastfeeding?

A

Non-hormonal lubricants and moisturizers

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12
Q

Presentation - hematuria, renovascular congestion (enlarged kidney on imaging), flank pain, possible elevated ADH and/or AKI

A

Renal vein thrombosis

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13
Q

Common causes/risk factors of renal vein thrombosis?

A

Hypercoagulability: nephrotic syndrome, malignancy, OCPs
Volume depletion (infants)
Trauma

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14
Q

Dx renal vein thrombosis

A

CTA or MRA

Renal venography

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15
Q

Rx renal vein thrombosis

A

Anticoagulation

Thrombolysis/ectomy if AKI present

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16
Q

There is significant overlap between presentation of renal infarction and acute RVT - distinguish between them.

A

Infarct - cardioembolic disease -> incomplete infarction -> wedge-shaped area of ischemia, often report abdominal pain + flank pain

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17
Q

Nearly all patients with CF develop ___. Most male patients develop ___. ~20% develop sensorineural hearing loss - why?

A

Sinopulmonary disease; infertility (only 20% of females have fertility problems)

Frequent treatment with aminoglycosides for GN infections

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18
Q

When comparing iron studies in the 3 main microcytic anemias (iron deficiency, thalassemia, and anemia of chronic disease), what are the key distinguishing findings?

A

[MCV: decreased in all three; may be normal in chronic disease or very decreased in thalassemia]

Iron: INCREASED in thalassemia; decreased in the other 2

TIBC: INCREASED in iron deficiency; decreased in the other two

Ferritin: DECREASED in iron deficiency; increased (both) or normal (chronic) in the other two

Transferrin saturation: VERY INCREASED in thalassemia, decreased (both) or normal (chronic) in the other two

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19
Q

Transferrin saturation = ?

A

Iron/TIBC

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20
Q

Key findings in iron studies suggesting iron deficiency anemia?

A

Decreased ferritin

Increased TIBC

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21
Q

Key findings in iron studies suggesting thalassemia?

A

Increased iron

Very increased transferrin

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22
Q

Key findings in iron studies suggesting anemia of chronic disease?

A

Decreased iron + decreased TIBC

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23
Q

Rx hereditary spherocytosis?

A

Splenectomy

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24
Q

Rx anemia of chronic disease?

A

Rx underlying condition (Fe supplementation is not helpful, because the problem involves USING iron rather than a deficiency of iron)

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25
Q

Presentation - micrognathia, microcephaly, prominent occiput, low-set ears, rocker-bottom feet, overlapping fingers, absent palmar creases, heart and renal defects

A

Trisomy 18 (Edward syndrome)

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26
Q

Holosystolic murmur best heard at the LLSB

A

VSD

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27
Q

What causes the fixed split S2 heard in ASD?

A

Delayed closure of the pulmonic valve

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28
Q

Truncus arteriosus is associated with what syndrome?

A

DiGeroge

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29
Q

Acute rheumatic fever is a complication of untreated S. pyogenes pharyngitis. List 5 major clinical features.

A
  1. Carditis
  2. Chorea
  3. Erythema marginatum
  4. Subcutaneous nodules
  5. Migratory arthritis

Minor - fever, arthralgias, elevated ESR/CRP, prolonged PR interval

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30
Q

Late cardiac sequelae of acute rheumatic fever?

A

Mitral regurgitation/stenosis

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31
Q

Diagnostic criteria for acute rheumatic fever?

A

2 major
1 major + 2 minor
Anything with chorea or carditis present

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32
Q

Why do we give patients penicillin when they have GAS pharyngitis?

A

TO PREVENT ARF

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33
Q

Follow-up management of patients with ARF?

A

Prophylactic long-acting IM benzathine PNC G for several years

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34
Q

Most common virus causing peri/myocarditis

A

Coxsackievirus

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35
Q

List 6 ECG findings suggesting an arrhythmias as the cause of syncope.

A
  1. Inappropriate sinus bradycardia
  2. SA block
  3. Sinus pauses
  4. AV block
  5. Non-sustained ventricular arrhythmias
  6. Short or prolonged QTc interval

NOT isolated premature ventricular beats

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36
Q

___ is due to polymorphic ventricular tachycardia in the setting of a prolonged QT interval.

A

Torsades de pointes

37
Q

What crystals cause gout and how are they identified?

A

Monosodium urate crystals: needle shaped, negatively birefringent (YELLOW when PARALLEL, BLUE when PERPENDICULAR)

38
Q

True or false - the presence of synovial crystals rules out septic arthritis.

A

False - they can be present between flares - look for other signs of septic arthritis

39
Q

What crystals cause pseudogout and how do they appear?

A

Calcium pyrophosphate crystals - smaller, rhomboid, weakly positive birefringent (opposite gout)

40
Q

Synovial fluid findings in gout?

A

Leukocytosis (2000-100,000 with >50% neutrophils)

41
Q

Presentation - normal internal genitalia, external virilization, undetectable serum estrogen, polycystic ovaries in an adolescent female patient

A

Aromatase deficiency

42
Q

How does aromatase deficiency first manifest?

A

In utero -> placenta cannot convert androgens into estrogens -> transient masculinization of Mom that resolves after delivery

43
Q

Presentation - females with ambiguous external genitalia, normal internal female reproductive organs, electrolyte abnormalities

A

Classic congenital adrenal hyperplasia

44
Q

Presentation - females with primary amenorrhea and virilization at puberty, normal genitalia at birth

A

Non-classic late-onset CAH

45
Q

Features of Kallman syndrome?

A

X-linked
Hypogonadotropic hypogonadism + anosmia
Delayed puberty, LH and FSH low or absent

46
Q

What is McCune-Albright syndrome?

A

Cafe au lait spots
Polyostotic fibrous dysplasia
Autonomous endocrine hyperfunction -> gonandotropin-independent precocious puberty

47
Q

Rx ethylene glycol poisoning?

A

Fomepizole (competitive inhibitor of alcohol dehydrogenase)

Sodium bicarbonate
Hemodialysis

48
Q

What is methylene blue used for?

A

Rx methemoglobinemia (ingestion of dapsone or anesthetics)

49
Q

Antidote for cyanide poisoning?

A

Sodium thiosulfate

50
Q

Calcium oxalate deposition in the kidneys + hypocalcemia?

A

Ethylene glycol ingestion

51
Q

Lifestyle changes to decrease risk for gout?

A 
Dairy product intake
Vitamin C (>1500 mg/day)
Coffee intake (6+ cups/day)
52
Q

Etiology of allergic conjunctivitis?

A

IgE-mediated acute hypersensitivity to environmental allergens

53
Q

Exercise recommendations for healthy women with uncomplicated pregnancies?

A

Moderate-intensity exercise for 20-30 minutes on most or all days of the week + avoid contact sports and activities with high fall risks. Also don’t scuba dive or do hot yoga.

54
Q

Contraindications to exercise in pregnancy?

A

Risk of preterm delivery
Preeclampsia
Severe caridopulmonary disease

55
Q

Pathophysiology of ARDS?

A

Lung injury -> fluid and cytokine leakage into alveoli -> impaired gas exchange, decreased lung compliance, and pulmonary HTN

56
Q

Management of ARDS?

A

MV (eg, low TV, high PEEP, permissive hypercapnia)

57
Q

Dx ARDS?

A

New/worsening respiratory distress within 1 week of insult
Bilateral lung opacities (pulmonary edema) NOT due to CHF/fluid overload
Hypoxemia with PaO2/FiO2 ratio of 300 mm Hg or less

58
Q

Patients with upper GI bleeding often have an elevated BUN and BUN/Cr ratio - why?

A
  1. Increased urea production from intestinal breakdown of Hgb
  2. Increased urea reabsorption from hypovolemia
59
Q

The aldosterone/renin ratio is elevated in ___.

A

Primary hyperaldosteronism

60
Q

___ toxicity is a severe adverse effect of long-term amiodarone use and can occur months to several years after the initiation of therapy.

A

Pulmonary

61
Q

Presentation of interstitial pneumonitis due to amiodarone toxicity?

A

Progressive dyspnea, non-productive cough, new reticular or ground-glass opacities on chest XR

62
Q

What is amiodarone used for?

A

(Class III antiarrhythmic)

Management of ventricular arrhythmias in patients with CAD and ischemic cardiomyopathy

63
Q

Loop diuretics cause what 2 electrolyte abnormalities, which can cause what EKG abnormality?

A

Hypokalemia; hypomagnesemia

Ventricular tachycardia

64
Q

___ is a potassium sparing diuretic with proven mortality benefit in patients with severe CHF.

A

Spironolactone

65
Q

Both Crohn disease and UC have multiple extraintestinal manifestations - list 4.

A
  1. Arthritis - axial or peripheral
  2. Eye (uveitis, episcleritis, etc.)
  3. Skin (pyoderma gangreonsum, etc.)
  4. Hepatobiliary (PSC, etc.)
66
Q

4 major causes of HF with preserved LVEF.

A
  1. LV diastolic dysfunction (HTN w/concentric LVH, restrictive, hypertrophic)
  2. Valvular heart disease (AS/AR/MS/MR)
  3. Pericardial disease (constrictive pericarditis, tamponade)
  4. Systemic disorders -> high-output failure (thyrotoxicosis, severe anemia, large AV fistula)
67
Q

Manage HFpEF?

A

Control BP and HR
Address concurrent conditions (AF, MI)
Rx volume overload with diuretics
Exercise training/cardiac rehab

68
Q

2 general causes of diastolic dysfunction?

A

Impaired myocardial relaxation
Increased LV wall stiffness (decreased compliance)

Both of these cause LV end-diastolic pressure -> back-up

69
Q

Type of selection bias - study population differs from target population due to non-random selection methods

A

Ascertainment (sampling) bias

70
Q

Type of selection bias - disease studied using only hospital-based patients may lead to results not applicable to target population

A

Berkson bias

71
Q

Type of selection bias - exposures that happen long before disease assessment can cause study to miss diseased participants that die early or recover

A

Prevalence (Neyman) bias

72
Q

Type of observational bias - subjects with negative outcomes are more likely to report certain exposures than controls, common in retrospective studies

A

Recall bias

73
Q

Type of observational bias - subjects over- or under-report exposure history due to perceived social stigma

A

Reporting bias

74
Q

Type of observational bias - risk factor itself causes increased monitoring in exposed group relative to unexposed group, which increases probability of identifying a disease

A

Surveillance (detection) bias

75
Q

3 strongest predictors of AAA expansion and rupture?

A
  1. Large aneurysm diameter
  2. Rapid rate of expansion
  3. Current cigarette smoking
76
Q

Current indications for operative or endovascular repair of AAA?

A

Size >5.5 cm
Rapid rate of expansion (>0.5 cm in 6 months or >1 cm/year)
Symptoms regardless of size

77
Q

Presentation - 46XY, phenotypically female at birth with female external and male internal genitalia + virilization at puberty

A

5-alpha-reductase deficiency

78
Q

Pathogenesis of 5-alpha-reductase deficiency?

A

Testes produce T -> male internal genitalia
T converted to DHT via 5-alpha-reductase; DHT -> male external genitalia and prostate
Without 5-alpha-reductase, no external genitalia

79
Q

Dx 5-alpha-reductase deficiency?

A

Elevated T/DHT ratio

80
Q

Pathogenesis of androgen insensitivity syndrome?

A

Defect androgen receptor -> prevents virilization during embroygenesis

Testosterone resistance -> absent male external genitalia

81
Q

Distinguish between 5-alpha-reductase deficiency and androgen insensitivity syndrome

A

5-alpha-reductase: NO breast development (T binds receptor and inhibits proliferation)

AIS: ++Breast development (defective androgen receptor unable to inhibit breast tissue proliferation)

82
Q

Bilateral labial masses

A

Undescended testes

83
Q

Features of Takayasu arteritis?

A

Female, Asian, age 10-40
Constitutional symptoms
ARTERIO-OCCLUSIVE (claudication, ulcers, etc.) in upper extremities
Arthralgias/myalgias

BP discrepancies
Pulse deficits
Arterial bruits

84
Q

Dx and Rx Takayasu arteritis

A

Elevated ESR/CRP
CXR with aortic dilation and widened mediastinum
CT/MRI: wall thickening and narrowing of lumen of large arteries

Rx - systemic glucocorticoids

85
Q

Fundoscopy - blood and thunder appearance, cotton wool spots, disc swelling, hemorrhages, venous dilation

A

Central retinal vein occlusion

86
Q

Unlike sensitivity and specificity, PPV and NPV depend on the ___ of the disease in the population being tested.

A

Prevalence

87
Q

A change in a test cutoff point that causes an increase in the number of false positives and true positives will have what effect on PPV?

A

Decrease

88
Q

PPV = ?

A

TP/(TP + FP) = (a/a+b)

High PPV -> positive test more likely to be true

Dedicated - Step 2 (22 decks)

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