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USMLE Step 1 > January 2020 > Flashcards

January 2020 Flashcards

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USMLE® Step 1 flashcards
1
Q

Positive predictive value: definition

A

Percentage of people that actually have the disease out of all positive test results (ie probability that a patient actually has the disease given a positive test result).

PPV = TP / (TP + FP)

TP = true positive
FP = false positive
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2
Q

Sensitivity

A

Sensitivity is the likelihood a patient with the disease will test positive.

Sensitivity = TP/(TP + FN)

TP = true positive
FN = false negative
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3
Q

Specificity

A

Specificity is the likelihood a patient without a disease will test negative.

Specificity = TN/ (TN+FP)

TN = true negative
FP = false positive
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4
Q

Young patient presenting w/ vague, nonspecific mono-like symptoms (fever, lymphadenopathy, wt loss, sore throat, myalgias, diarrhea, headache) should be evaluated for what, with what?

A
  • Check for HIV w/ detailed sexual hx and IV drug use

- test w/ fourth-generation HIV test and HIV viral load.

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5
Q

Treatment options for latent TB infection

A
  • isoniazid + rifapentine weekly x3 months under direct observation (not for HIV pts)
  • Isoniazid monotherapy x6-9 months
  • Rifampin x4 months

add pyridoxine to prevent neuropathies in pts taking isoniazid w/ following conditions: diabetes, uremia, alcoholism, malnutrition, HIV, pregnancy, or epilepsy

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6
Q

What is latent TB infection (LTBI)?

A

Patients w/ >/= 10mm induration of tuberculin skin test who don’t have CXR abnormalities and no symptoms (eg no wt loss, night sweats, chronic cough)

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7
Q

Is latent TB infection (LTBI) infectious?

A

No. LTBI is no infectious.

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8
Q

Should latent TB infection (LTBI) be treated?

A

Lifetime risk of advancement 5-10%, so typically only offer treatment to:

  • pts at higher risk of developing active TB (eg immunosuppressed)
  • pts who live or work in high-risk congregate settings (eg prisons or health care personnel)
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9
Q

What happens if a healthcare worker has latent TB infection?

A

They may continue to work without restrictions (even if refuse treatment) and don’t need precautions (eg N95 mask)

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10
Q

Can pts exposed to TB several years prior have false-negative initial tuberculin skin testing?

A

YES.

Recommendation is repeat testing in 1-3 weeks if initial test neg.

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11
Q

When are pts treated for active TB considered non infectious?

A

After 3 consecutive acid-fast bacilli sputum smears negative

*Samples taken 8-24-hour intervals w/ 1 or more early-morning samples

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12
Q

Signs + symptoms of lupus nephritis

A

LEE
Proteinuria
Renal dysfunction
Urinalysis with active sedimentation (eg hematuria, red blood cell casts)

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13
Q

How is lupus nephritis classified?

A

6 classes and NEED a renal biopsy prior to treatment to determine class

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14
Q

What guides treatment for lupus nephritis?

A

Disease classification, which is determined on pathology by renal biopsy

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15
Q

Class 1 Lupus nephritis subtype: histology and clinical features

A

histo: Minimal mesangial
Clin: usually asymptomatic

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16
Q

Class 2 lupus nephritic subtype: histology and clinical features

A

Histo: mesangial proliferative

Clin:

  • microscopic hematuria, proteinuria
  • favorable prognosis
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17
Q

Class III lupus nephritis subtype: histology and clinical features

A

Histo: focal

Clin:

  • hematuria, proteinuria (possible nephrotic syndrome)
  • possible HTN, decr GFR
  • variable prognosis
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18
Q

Class IV lupus nephritis subtype: histology and clinical features

A

Histo: diffuse

Clin:

  • most common
  • similar to focal lupus nephritis (hematuria, proteinuria, possible nephrotic syndrome, possible HTN, decr GFR)
  • POOR prognosis
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19
Q

Class V lupus nephritis: histology and clinical features

A

Histo: membranous

Clin:

  • nephrotic syndrome
  • ?poor prognosis?
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20
Q

Class VI lupus nephritis: histology and clinical features

A

Histo: advanced sclerosing

Clin:

  • progressive CKD w/ bland urinary sediment
  • immunosuppressive therapy not recommended
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21
Q

How should classes I & II lupus nephritis be treated?

A

Typically mild, don’t need treatment unless disease progresses

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22
Q

How should classes III & IV lupus nephritis be treated?

A

Immunosuppression w/ glucocorticoids and either cyclophosphamide or mycophenolate mofetil

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23
Q

How to treat class V lupus nephritis?

A

May require immunosuppression if there are proliferative lesions or nephrotic syndrome

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24
Q

How to treat class VI lupus nephritis?

A

No immunosuppression bc this is advanced sclerosing disease. Renal transplant…?

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25
Q

What to monitor in SLE patients w/ renal involvement?

A

Anti-double stranded DNA and complement levels

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26
Q

What do complement levels look like in SLE pt with renal involvement?

A

Decreased during active disease bc immune complement deposition w/in glomerulus induces complement fixation —> decreased levels

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27
Q

What are anti-smith antibodies highly specific for?

A

SLE

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28
Q

What are anti-smith antibodies useful for?

A

Identifying pts at risk of developing renal involvement of SLE, however, NOT good for monitoring renal disease progression (remain elevated/don’t change w/ active disease)

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29
Q

Relative risk reduction: formula

A

RRR = risk in unexposed - risk in exposed) / (risk in unexposed)

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30
Q

Relative risk reduction: alternative formula

A

RRR = 1 - RR

RR = relative risk

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31
Q

Relative risk: formula

A

RR = risk of disease in exposed group / risk of disease in unexposed group

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32
Q

How to use relative risk to compare risk for disease at different levels of an intervention or risk factor?

A

RR <1.0 -> decr risk in group in numerator
RR = 1.0 -> no diff in risk bt groups
RR >1.0 -> incr risk in group in numerator

RR = risk disease in exposed grp/ risk disease in unexposed grp

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33
Q

Definition of neonatal polycythemia

A

Hematocrit >65% in term infant

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34
Q

Causes of neonatal polycythemia

A
  • increased erythropoiesis from intrauterine hypoxia (maternal diabetes, smoking, HTN, IUGR)
  • erythrocyte transfusion (delayed cord clamping, twin-twin transfusion)
  • genetic / metabolic disease (hypo or hyperthyroid, genetic trisomy 13, 18, 21)
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35
Q

Clinical presentation of neonatal polycythemia

A
  • asymptomatic (most common)
  • ruddy skin
  • hypoglycemia, hyperbilirubinemia
  • respiratory distress, cyanosis, apnea
  • irritability, jitteriness
  • abd dissension
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36
Q

Treatment for neonatal polycythemia

A

IVF
Glucose
Partial exchange transfusion

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37
Q

Are neonatal hematocrit levels from capillary sample (heel prick) reliable?

A

No.

If heel sticks shows polycythemia, must repeat with venous sample.

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38
Q

What does hyperviscosity cause in neonates?

A

Complications:
Hypoperfusion
Tissue hypoxia

Clinically:
Lethargy
Irritability
Drowsiness
Abd distension
Poor feeding
Hypotonia
Metabolic derangements — hypoglycemia, hyperbilirubinemia
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39
Q

Initial treatment of neonatal polycythemia

A

Hydration

Correction of hypoglycemia

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40
Q

Alternate management of neonatal polycythemia

A

Partial exchange transfusion

— > withdraw blood from infant and infuse w normal saline

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41
Q

Glucose-6-phosphate deficiency epidemiology

A

X-linked

Asian, African, or Middle Eastern descent

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42
Q

Manifestations of G6PD

A

Neonatal unconjugated hyperbilirubinemia — jaundice & anemia day of life 2-3

Acute hemolytic episode — secondary to oxidative stress (eg fava beans, sulfa drugs); jaundice, pallor, dark urine, abdominal/back pain

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43
Q

Laboratory findings of G6PD

A

Hemolytic anemia

Bite cells with Heinz bodies on peripheral smear

Low glucose-6-phosphate deficiency assay (may be normal during attack)

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44
Q

What helps differentiate between G6PD and hemolytic anemia of the neonate?

A

Timing of jaundice onset.

Hemolytic anemia (typically infant w A or B blood type born to type O mother) presents in first 24 hrs of life; G6PD generally presents day 2-3 of life

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45
Q

How does breast milk jaundice present?

A

Indirect hyperbilirubinemia over first few weeks of life

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46
Q

Why does breast milk jaundice happen?

A

Increased enterohepatic circulation

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47
Q

Physiologic jaundice

A

Happens in almost every newborn because of:

  • increased RBC count w/ a shorter RBC life span
  • decreased hepatic bilirubin clearance
  • increased enterohepatic circulation

*NOT associated w/ anemia.

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48
Q

Acute mitral regurgitation: etiology

A

Ruptured mitral chordae tendineae from:

  • mitral valve prolapse
  • infective endocarditis
  • rheumatic heart disease
  • trauma

Papillary muscle rupture due to MI or trauma

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49
Q

Acute mitral regurgitation: clinical features

A
  • rapid onset of pulmonary edema
  • biventricular heart failure
  • hypotension, cardiogenic shock
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50
Q

Acute mitral regurgitation: physical exam

A
  • Diaphoresis, cool extremities
  • Jugular venous distension, pulmonary crackles
  • Hyperdynamic cardiac impulse
  • Apical decrescendo systolic murmur (often absent)
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51
Q

Acute mitral regurgitation: management

A
  • Bedside echocardiogram

- Emergent surgical intervention

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52
Q

Who is at risk for mitral chordae tendineae rupture?

A

Patients with mitral valve prolapse, esp when it’s related to an underlying connective tissue disorder (Ehlers-Danlos syndrome, Marfan syndrome).

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53
Q

What happens to cardiac pressures in acute mitral regurgitation?

A

Patients w acute, severe MR have early equalization of left atrial and left ventricular pressures, and up to 50% (esp w/ ischemic MR) may have no audible murmur (silent MR).

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54
Q

Skin features of Ehlers-Danlos

A
  • Transparent and hyperextensible
  • Easy bruising, poor healing
  • Velvety with atrophy and scaring
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55
Q

Skin features of Marfan Syndrome

A

No features other than striae

56
Q

Musculoskeletal features of Ehlers-Danlos syndrome

A
  • Joint hypermobility
  • Pectus excavated
  • Scoliosis
  • High, arched palate
57
Q

Cardiac features of Ehlers-Danlos Syndrome

A

Mitral valve prolapse ( can lead to acute mitral regurgitation)

58
Q

Associated with Ehlers-Danlos

A

Abdominal and inguinal hernias

Uterine prolapse

59
Q

Genetics of Ehlers-Danlos syndrome

A

COL5A1 and COL5A2 mutation

Autosomal dominant

60
Q

Musculoskeletal features of Marfan Syndrome

A

Joint hypermobility
Pectus excavatum or carinatum
Scoliosis
Tall w/ long extremities

61
Q

Cardiac features of Marfan Syndrome

A

Progressive aortic root dilation

Mitral valve prolapse

62
Q

Other associations with Marfan Syndrome

A

Lens and retinal detachment

Spontaneous pneumothorax

63
Q

Genetics of Marfan Syndrome

A

FBN1 mutation

Autosomal dominant

64
Q

Empiric treatment of CAP: Outpatient

A

Macrolide or doxycycline (healthy)

Fluoroquinolone or beta lactam + macrolide (comorbidities)

65
Q

Empiric treatment of CAP: Inpatient (non-ICU)

A

Fluoroquinolone

Beta lactam + macrolide (IV)

66
Q

Empiric treatment of CAP: ICU

A

Beta-lactam + macrolide (IV)

Beta-lactam + fluoroquinolone (IV)

67
Q

What two scales determine appropriate clinical setting for treatment of CAP?

A

CURB-65 and pneumonia severity index

68
Q

What does metformin do additionally that is helpful?

A

Decreases triglycerides, increases HDL and improves nonalcoholic steatohepatitis (NASH)

69
Q

How can analgesic-induced nephropathy present?

A
  • florid nephrotic range proteinuria

- acute interstitial nephritis

70
Q

What do NSAIDs do to kidneys?

A

Reversible decline in GFR due to inhibition of vasodilatory prostaglandin production

71
Q

What would kidney biopsy of NSAID-induced acute interstitial nephritis look like?

A

Minimal changes and a typical interstitial inflammatory pattern

72
Q

Absolute risk reduction

A

ARR obtained by subtracting risk of relapses in a treatment group from that of the placebo group

73
Q

Number needed to treat

A

NNT = 1/ARR

ARR = absolute risk reduction

74
Q

Two steps for screening for gestational diabetes melitus

A

1) glucose challenge test (GCT)

2) if GCT failed, do 3-hour glucose tolerance test (GTT)

75
Q

Are HgA1C levels sensitive for screening pregnant women?

A

No, bc physiologic increase in RBC mass and cell turnover lowers HgA1C

76
Q

Target blood glucose levels during pregnancy

A

Fasting = 95mg/dL (5.3 mmol/L)
1-hr postprandial = 140 mg/dL (7.8 mmol/L)
2-hour postprandial = 120 mg/dL (6.7 mmol/L)

77
Q

Treatment for gestational diabetes

A

1st line: exercise and dietary modification
2nd line: insulin, metformin, maybe glyburide (although glyburide associated w higher risk of neonatal hypoglycemia than insulin)

78
Q

How can analgesic-induced nephropathy present?

A
  • florid nephrotic range proteinuria

- acute interstitial nephritis

79
Q

What do NSAIDs do to kidneys?

A

Reversible decline in GFR due to inhibition of vasodilatory prostaglandin production

80
Q

What would kidney biopsy of NSAID-induced acute interstitial nephritis look like?

A

Minimal changes and a typical interstitial inflammatory pattern

81
Q

Absolute risk reduction

A

ARR obtained by subtracting risk of relapses in a treatment group from that of the placebo group

82
Q

Number needed to treat

A

NNT = 1/ARR

ARR = absolute risk reduction

83
Q

Two steps for screening for gestational diabetes melitus

A

1) glucose challenge test (GCT)

2) if GCT failed, do 3-hour glucose tolerance test (GTT)

84
Q

Are HgA1C levels sensitive for screening pregnant women?

A

No, bc physiologic increase in RBC mass and cell turnover lowers HgA1C

85
Q

Target blood glucose levels during pregnancy

A

Fasting = 95mg/dL (5.3 mmol/L)
1-hr postprandial = 140 mg/dL (7.8 mmol/L)
2-hour postprandial = 120 mg/dL (6.7 mmol/L)

86
Q

Treatment for gestational diabetes

A

1st line: exercise and dietary modification
2nd line: insulin, metformin, maybe glyburide (although glyburide associated w higher risk of neonatal hypoglycemia than insulin)

87
Q

Can patients refuse to receive medical information?

A

Yes. Included in the ethical principle of autonomy is the right to receive or refuse to receive medical information.
*excludes genetic testing for newborn babies or children for treatable conditions

88
Q

What are the effects of radiation-induced cardiotoxicity?

A
  1. Myocardial ischemia and/or infarction
  2. Restrictive cardiomyopathy with diastolic dysfunction
  3. Constrictive pericarditis
  4. Valvular abnormalities (mitral or aortic stenosis/regurgitation)
  5. Conduction defects (sick sinus syndrome or variable degrees of heart block)
89
Q

What are side effects of the anthracycline class of drugs?

A

Causes a dose-dependent decline in the ejection fraction, leading to dilated cardiomyopathy.

90
Q

When does breastfeeding failure jaundice begin?

A

First week of life

91
Q

What is the pathophysiology of breastfeeding failure jaundice?

A

Lactation failure resulting in:

  • decreased bilirubin elimination
  • increased enterohepatic circulation
92
Q

What are the clinical features of breastfeeding failure jaundice?

A
  • suboptimal breastfeeding

- signs of dehydration

93
Q

What is the timing of breast milk jaundice?

A

Starts at age 3-5 days; peaks at 2 weeks

94
Q

What is the pathophysiology of breast milk jaundice?

A

High levels of beta-glucuronidase in breast milk deconjugate intestinal bilirubin & increase enterohepatic circulation

95
Q

What are clinical features of breast milk jaundice?

A
  • adequate breastfeeding

- normal elimination

96
Q

What should babies with breast milk jaundice do for nutrition?

A

Continue breastfeeding exclusively, assuming the neonate is gaining weight and has a normal exam, and the mother’s breast milk supply is adequate.

97
Q

What should be performed for neonate with conjugated hyperbilirubinemia?

A

If direct bilirubin is elevated (>20% of total bilirubin), ultrasound of biliary tree should be performed to evaluate for biliary atresia.

98
Q

When should breast milk jaundice resolve?

A

Spontaneous resolution by age 3 months.

99
Q

What separates the upper and lower GI tract?

A

Ligament of Treitz

100
Q

What signs are suggestive of upper GI bleed?

A

Hemodynamics compromise, orthostasis, BUN to Cr ratio >20:1

101
Q

Bright red blood per rectum is nearly always due to _______ GI bleed.

A

lower

102
Q

What signs are more common in upper GI bleed?

A

Hematemesis and melena

103
Q

In a patient with hematochezia who is hemodynamically stable, perform a ________ first.

A

Colonoscopy

104
Q

In a patient with hematochezia who is hemodynamically unstable or suspected upper GI bleed…

A

1) Resuscitate
2) +/- Surgery/IR consult
3) EGD

105
Q

If source is not found in a hemodynamically unstable patient after EGD….

A

Perform angiography

106
Q

If source of GI bleed after EGD and colonoscopy not found, what do you do?

A

obscure GI bleed evaluation

Eg capsule endoscopy, repeat EGD/colonoscopy

107
Q

What is a secondary / obscure CT scan that could be (but rarely is) used to detect GI bleed?

A

Arterial-phase contrast-enhanced CT with negative oral contrast

108
Q

What medication is used to treat bleeding esophageal varices?

A

Octreotide

109
Q

Hazard ratio: definition

A

Likelihood of an event occurring in a treatment group relative to the control group

HR <1.0 indicates an event is less likely to occur in a treatment group than the control group

110
Q

Diverticular bleeding: etiology

A

Arterial erosion due to conflicting mucosal outcropping

111
Q

Diverticula bleeding: Clinical presentation

A

Painless hematochezia in patients age >40

Bleeding often self-limited but can recur

112
Q

Diverticular bleeding: diagnosis

A

Colonoscopy or tagged red blood cell scan

113
Q

Diverticular bleeding: treatment

A
  • Intravenous volume replacement
  • endoscopic therapy or angiographic embolization
  • colonic resection for persistent bleeding
114
Q

What causes colonic diverticulosis?

A

Outpouching of the colon wall at points of weakness where the vasa recta penetrate the circular muscle layer of the colon.

115
Q

Infectious mononucleosis: etiology

A

Epstein-Barr virus most common

116
Q

Infectious mononucleosis: clinical features

A 
Fever
Tonsillitis/pharyngitis +/- exudates
Posterior or diffuse cervical lymphadenopathy
Significant fatigue
\+/- hepatosplenomegaly 
\+/- rash after amoxicillin
117
Q

Infectious mononucleosis: diagnostic findings

A

Positive heterophile antibody (Monospot) test (25% false-negative rate during 1st week of illness)
Atypical lymphocytosis
Transient hepatitis

118
Q

Infectious mononucleosis: management

A

Avoid sports for >/= 3 weeks (contact sports >/= 4 weeks) due to risk of splenic rupture

119
Q

What is the primary means of treatment for infectious mononucleosis?

A

Supportive care - eg rest, adequate hydration, nutrition, avoidance of strenuous activity.
No sports for >/= 3 weeks, no contact sports >/= 4 weeks.
Can give acetaminophen or NSAIDS for symptomatic relief (do not shorten duration of illness)

120
Q

When are corticosteroids warranted in the treatment of infectious mononucleosis?

A

Rare cases when airway obstruction appears imminent

Warning signs:
SOB while recumbent
Tachypnea
Inability to swallow

Also, possibly in immunocompromised patients

121
Q

What happens to a patient’s chronic cough after they quit smoking?

A

Initial temporarily increase in cough during first few weeks after cessation; ultimately chronic cough improves.

122
Q

Who experiences more benefit in pulmonary function after smoking cessation?

A

Younger quitters (vs older quitters)

123
Q

What does smoking do to bones?

A

Accelerates osteoporosis

Cessation can reverse loss of bone density and decrease the excess risk of fracture but benefits may not be apparent in first 10 yrs after quitting

124
Q

Is nicotine withdrawal worse, the same, or better in old vs young?

A

Same

Peak in first few days, improve over course of the next few weeks

125
Q

What does smoking cessation do for mortality?

A

Cessation at age 60 or older has been shown to lower the risk of all-cause mortality and cardiovascular events

Benefit seen within 5 years of quitting

Gain even greater for those who quit at a younger age

126
Q

Benefits of smoking cessation

A

Reduction in mortality
Reduced risk of cardiac events
Reduced risk of osteoporosis
Less decline in lung function over time in comparison to current smokers

127
Q

What are symptoms of vertebrobasilar insufficiency?

A

Vertigo
Dizziness
Diplopia
Numbness

128
Q

Risk factors for vertebrobasilar insufficiency

A 
DM
HTN
Hypercholesterolemia
Arrhythmia
CAD
Circulatory problems
Hx of smoking cigarettes
129
Q

Symptoms of labyrinthitis

A 
Vertigo
Tinnitus
Nausea
Loss of balance
Often follows a viral illness
Can also be cause by bacterial inf, allergies, benign tumors, and certain meds
130
Q

What is benign proximal vertigo (BPV)?

A

Abnormal feeling of motion triggered by certain provocative positions

Most often attributed to calcium debris w/in posterior semicircular canal

Nystagmus commonly seen

131
Q

What are panic attacks?

A

Discreet periods of intense fear or discomfort

Sx include:
Palpitations
Seating
Trembling
SOB
Choking sensation
CP
Nausea
Dizziness
Paresthesias
A fear of dying or losing control
132
Q

Cataplexy: define

A

Sudden, temporary loss of muscle tone that can result in collapse.

Often caused by intense emotions, including laughter.

133
Q

What are keloids?

A

Benign fibrous growths that develop in scar tissue secondary to an overproduction of extracellular matrix and dermal fibroblasts.

134
Q

Preferred treatment of most keloids?

A

Intralesional glucocorticoids preferred treatment — Up to 70% patients respond

Silicone sheeting can reduce symptoms (pain or itching) associated w/ keloids or reduce formation, but data poor and not understood

135
Q

How to treat pregnant women w/ TB?

A

3-drug therapy:
Isoniazid (INH) + Rifampin (RIF) + Ethambutol for 2 months followed by INH and RIF for an additional 7 months

All 3 meds do cross placenta but not assoc w/ fetal toxicity

Don’t give pyrazinamide bc uncertain teratogenicity, not very effective

also need to give pregnant women pyridoxine (vitamin B6) supplementation to prevent INH-induced neurotoxicity.

USMLE Step 1 (2 decks)

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