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Dedicated - Step 2 > 13 > Flashcards

13 Flashcards

1
Q

DDx - obstructive pattern (FEV1/FVC <70%) + divide by low, normal, and increased DLCO

A

Low: emphysema
Normal: chronic bronchitis, asthma
Increased: asthma

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2
Q

DDx - restrictive pattern (FEV1/FVC >70% predicted, FVC <80% predicted) + divided by low, normal, and increased DLCO

A

Low: ILD, sarcoidosis, asbestosis, heart failure
Normal: MSK deformity, neuromuscular disease
Increased: morbid obesity

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3
Q

DDx - normal spirometry with low DLCO

A

Anemia
PE
Pulmonary HTN

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4
Q

DDx - normal spirometry with increased DLCO

A

Pulmonary hemorrhage

Polycythemia

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5
Q

Define chronic bronchitis.

A

Productive cough for 3+ months over 2 consecutive years

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6
Q

What is bronchiectasis?

A

Disease of abnormal bronchial widening in the setting of recurrent infection and inflammation

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7
Q

Drug of choice for stabilizing bony metastatic lesions to prevent hypercalcemia of malignancy and pathologic fractures?

A

Bisphosphonates

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8
Q

___ injury can occur from blunt force injury but typically results in immediate coma. It is usually diagnose dwith ___.

A

Diffuse axonal; MRI

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9
Q

___ presents with rapidly progressive dementia, myoclonus, mood symptoms, and hypersomnia. How is it diagnosed?

A

Creutzfeldt-Jakob disease; high levels of 14-3-3 protein in the CSF

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10
Q

Other diagnostic findings in CJD?

A

Periodic sharp wave complexes on EEG
Caudate nucleus/putamen findings
Spongiform changes and neuronal loss without inflammation (path)

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11
Q

High anti-Hu Ab titers are seen in ___, a syndrome associated with ___.

A

Paraneoplastic encephalomyelitis; small cell lung cancer

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12
Q

Pathologic cause of nephrogenic DI?

A

Impaired renal RESPONSE to ADH

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13
Q

Infants born to women with ___ are at risk for thyrotoxicosis due to passage of maternal TSH receptor Ab across the placenta. How do these infants present?

A

Graves’ disease

Warm, moist skin, tachycardia, poor feeding, irritability, poor weight gain, low birth weight or preterm birth

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14
Q

Rx neonatal thyrotoxicosis?

A

Methimazole + beta-blocker to prevent AE on the developing nervous system; will self-resolve as the Ab clears from the infant’s circulation

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15
Q

Management of blunt abdominal trauma leading to suspected abruptio placentae?

A
  1. Aggressive fluid resuscitation with crystalloids + place patient in LLD position if the spine is stable to displace the uterus off the aortocaval vessels and maximize CO
  2. Emergency transfusion if fluid resuscitation is unresponsive or if bleeding is persistent (CBC should be repeated after IVF)
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16
Q

What is the Kleihauer-Betke test used for?

A

To determine the necessary dose of Rh(D) anti-D Ig after delivery of an Rh-positive fetus to an Rh-negative mother

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17
Q

Hypomagnesemia can lead to refractory hypokalemia - why?

A

Intracellular Mg2+ is thought to inhibit potassium secretion by renal outer medullary potassium (ROMK) channels in the collecting tubules

Therefore, low intracellular Mg results in excessive renal K loss and refractory hypokalemia

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18
Q

Define fetal tachycardia

A

> 160/min

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19
Q

Cause of a sinusoidal fetal heart tracing?

A

Fetal anemia

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20
Q

What is an early deceleration? What causes them?

A

Shallow decrease in the fetal HR that is a mirror image with the uterine contraction

Autonomic response to alterations in intracranial pressure caused by fetal head compression during contractions

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21
Q

What is a late deceleration and what causes it?

A

Smooth and subtle drops in fetal heart rate that occur after contractions due to transient fetal hypoxia caused by placental hypoperfusion during contractions

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22
Q

What are variable decelerations and what causes them?

A

Abrupt drops in the fetal heart rate of varying length and duration; compression of the umbilical cord causing transient fetal hypertension that triggers a parasympathetic response and slows the HR

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23
Q

Clinical features of intrahepatic cholestasis of pregnancy?

A

3rd Trimester
Generalized pruritis worse on the hands and feet
No associated rash
RUQ pain

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24
Q

Lab abnormalities seen in intrahepatic cholestasis of pregnancy?

A

Increased total bile acids (>10)
Increased transaminases
+/- increased total and direct bilirubin

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25
Q

Obstetric risks of intrahepatic cholestasis of pregnancy?

A

Intrauterine fetal demise (>100 bile acids)
Preterm delivery
Meconium-stained amniotic fluid
Neonatal RDS

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26
Q

Management of intrahepatic cholestasis of pregnancy?

A

Delivery at 37 weeks gestation
Frequent monitoring
Ursodeoxycholic acid
Antihistamines

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27
Q

Features of Turner syndrome?

A

Webbed neck
Horseshoe kidney
Nail dysplasia
Congenital lymphedema

Narrow high-arched palate
Low hairline
Broad chest with widely spaced nipples
Cubitus valgus
Short stature
Coarctation of the aorta
Bicuspid aortic valve
Streak ovaries, amenorrhea, infertility
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28
Q

How does congenital lymphedema present?

A

Non-pitting carpal and pedal edema

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29
Q

Severe obstruction of lymphatic vessels can result in ___ of the neck.

A

Cystic hygroma

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30
Q

What causes NONPITTING edema?

A

High protein content of interstitial fluid

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31
Q

Beta-hCG levels become undetectable ___ after delivery.

A

2-4 weeks

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32
Q

Presentation of rotator cuff impingement or tendinopathy

A

Pain with abduction and external rotation
Subacromial tenderness
Normal range of motion with positive impingement tests (eg, Neer, Hawkins)

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33
Q

Presentation of rotator cuff tear

A

Similar to above, but weakness with external rotation and age >40

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34
Q

Presentation of adhesive capsulitis (frozen shoulder)

A

Decreased PASSIVE AND ACTIVE ROM

Stiffness +/- pain

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35
Q

Presentation of biceps tendinopathy/rupture

A

ANTERIOR shoulder pain
Pain with lifting, carrying, or overhead reaching
Weakness less common

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36
Q

Presentation of glenohumeral OA

A

Uncommon, usually caused by trauma
Gradual onset of anterior or deep shoulder pain
Decreased active and passive abduction and external rotation

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37
Q

What is the key pathogenic factor in the development of DM2 and associated abnormalities?

A

INSULIN RESISTANCE

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38
Q

Next step in work-up of hemarthrosis after minor trauma?

A

Coagulation studies (suspicious for a bleeding disorder)

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39
Q

Coag studies in hemophilia?

A

Prolonged PTT
Normal PT
Normal platelet count
Absent or decreased factor 8 (hemophilia A) or 9 (hemophilia B) activity

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40
Q

Rx hemophilia A and B

A

Factor replacement

Desmopressin for mild A

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41
Q

The receiver operating characteristic curve of a quantitative diagnostic test demonstrates the trade-off between sensitivity and specificity of a test at various cutoff points. How does changing the cutoff point affect the sensitivity and specificity?

A

Increasing the true-positive rate (increases sensitivity) also increases the false-positive rate (decreases specificity)

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42
Q

Presentation of hereditary angioedema?

A

Recurrent episodes of edema (face, limbs, genitalia, bowel, larynx, etc.) WITHOUT associated pruritis or urticaria

Laryngeal edema
Colicky abdominal pain, vomiting, diarrhea

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43
Q

Cause of heredtiary angioedema?

A

Deficiency or dysfunction of C1 inhibitor -> excessive bradykinin

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44
Q

Dx hereditary angioedema

A

Low C4 level

Low C1 inhibitor protein or function

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45
Q

Management of hereditary angioedema?

A

C1 inhibitor concentrate

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46
Q

Pathogenic mechanism of immune hemolytic anemia (for example)?

A

Antibody-mediated (type II) hypersensitivity

IgG/M react with cell-bound Ag -> complement activation and cell destruction

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47
Q

Pathogenic mechanism of tuberculin skin test and allergic contact dermatitis?

A

Cell-mediated (type IV) hypersensitivity

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48
Q

Pathogenic mechanism of anaphylaxis?

A

IgE-mediated (type I) hypersensitivity -> mast cell and basophil degranulation

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49
Q

Pathogenic mechanism of serum sickness?

A

Immune complex-mediated (type III) hypersensitivity

Ab complexes activate complement wherever IC deposit

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50
Q

What is unique about a STEMI in the inferior leads (and what are these leads)?

A

II, III aVF, RCA occlusion

50% chance of involving the R ventricle

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51
Q

Management of RV MI?

A

Leads to impaired RV filling and creates high sensitivity to intravascular volume depletion

AVOID nitrates (venous dilation -> decreased preload -> profound hypotension), diuretics (volume depletion), opiates (venous dilation)
GIVE BOLUS with IV saline to increase preload
Otherwise - standard STEMI management
-Inotropes (dopamine, dobutamine) if persistent hypotension

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52
Q

Which antibiotic can exacerbate MG and why?

A

FQs

Block neuromuscular transmission

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53
Q

How does the body compensate for chronic hypercapnia?

A

Increasing renal bicarbonate retention; creating a compensatory metabolic alkalosis

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54
Q

Main cause of hypercapnia in COPD?

A

Increased dead space ventilation

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55
Q

Cause of positive Trendelenburg sign?

A

Weakness or paralysis of the gluteus medius and minimus muscles, which are innervated by the superior gluteal nerve

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56
Q

Features of primary sclerosing cholangitis?

A

Fatigue and pruritis
Majority asymptomatic at diagnosis
90% have underlying IBD (mainly UC)

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57
Q

Complications of PSC?

A 
Intrahepatic or extrahepatic biliary stricture
Cholangitis and cholelithiasis
Cholangiocarcinoma
Cholestasis
Colon cancer
58
Q

Distinguish PBC from PSC?

A

PBC - middle-age women, no association with UC, +serum antimitochondrial Ab

59
Q

Cause of TRALI?

A

Donor anti-leukocyte Ab

60
Q

What is a primary hypotension reaction to blood transfusion?

A

Transient hypotension often in patients taking ACEIs that occurs within minutes of transfusion and is caused by bradykinin in blood products

61
Q

What are the HIV-associated neurocognitive disorders and how do they present?

A

Impaired memory and attention/concentration, personality and behavior changes, motor symptoms (eg, ataxia, slowed movement)

Asymptomatic neurocognitive impairment
Mild neurocognitive disorder
HIV-associated dementia

62
Q

Distinguish PML from HIV dementia.

A

PML - AMS, motor deficits, ataxia, vision abnormalities, FOCAL ASYMMETRIC lesions on MRI

63
Q

CHA2DS2-VASc Score?

A 
CHF
HTN
Age 75+ (+2)
DM
Stroke/TIA/thromboembolism (+2)
Vascular disease
Age 65-74 (+1)
Sex category (F)
64
Q

Anticoagulation in NONVALVULAR AF based on CHA2DS2-VAsc

A

0 -> none
1 -> none or aspirin or oral anticoagulants
2+ -> oral anticoagulants

65
Q

Secondary amyloidosis is a complication of a chronic inflammatory condition (eg, chronic infection, IBD, RA) resulting in extracellular tissue deposition of fibrils into tissues and organs. Patients can develop multi-organ dysfunction (eg, kidneys, liver, GI tract). Treatment?

A

Treat the underlying inflammatory disease

Colchicine for prevention and treatmen

66
Q

Define SGA?

A

<10th percentile for gestational age at birth

67
Q

Complications of SGA infants?

A 
Hypoxia
Polycythemia
Hypoglycemia
Hypothermia
Hypocalcemia
68
Q

How is PEA of asystole managed?

A

CPR and vasopressor therapy (eg, epinephrine or vasopressin)
+assess for reversible causes

NO role for defibrillation or synchronized cardioversion

69
Q

Reversible causes of asystole/pulseless electrical activity?

A 
Hypovolemia
Hypoxemia
Hydrogen ions (acidosis)
Hypo/hyperkalemia
Hypothermia
Tension pneumothorax
Tamponade (cardiac)
Toxins (narcotics, benzos)
Thrombosis (pulmonary or coronary)
Trauma
70
Q

Indications for imaging in low back pain (X-ray)?

A

Osteoporosis/compression fracture
Suspected malignancy
Ankylosing spondylitis (eg, insidious onset, nocturnal pain, better with movement)

71
Q

Indications for imaging in low back pain (MRI)?

A

Sensory/motor deficits
Cauda equina syndrome
Suspected epidural abscess/infection (eg, fever IVDU, concurrent infection, hemodialysis)

72
Q

Red flag features prompting consideration for imaging in low back pain?

A 
Sudden onset of pain associated with midline spine tenderness
Hx cancer or recent infection
Constitutional symptoms
Trauma
Significant/progressive neuro defects
73
Q

What can increase sensitivity of XR in patients with low back pain?

A

ESR/CRP

74
Q

Fever and sore throat in any patient taking antithyroid drugs suggests ___. What should be done?

A

Agranulocytosis

STOP the drugs and check the WBC count. If agranulocytosis has occurred, give broad-spectrum ABX +/- granulocyte colony stimulating factors

75
Q

Long-term medical therapy in patients with an NSTEMI?

A
  1. Dual antiplatelet therapy (aspirin and P2y12 receptor blocker aka clopidogrel etc)
  2. Beta blockers
  3. ACEIs or ARBs
  4. Statins
  5. Aldosterone agonists if LVEF of 40 or less with heart failrue symptoms or DM
76
Q

Who else gets dual antiplatelet therapy?

A

Drug-eluting stent (minimum 12 months)

77
Q

Outcome of radioiodine therapy for Graves disease?

A

Resolution of hyperthyroidism in 6-18 weeks

Gradually leads to permanent hypothyroidism in most patients

Can acutely worsen Graves ophthalmopathy

78
Q

Features of digitalis toxicity?

A

Increased atopy + increased vagal tone (and thus decreased conduction through the AV node) -> atrial tachycardia + AV block

79
Q

Presentation of patients with MASSIVE PE?

A

Low arterial perfusion (hypotension, syncope), acute dyspnea, pleuritic chest pain, tachycardia

Thrombus increases pulmonary vascular resistance and RV pressure -> RV hypokinesis and dilation and hypotension

80
Q

Language delay without an attempt to compensate through non-verbal means?

A

ASD

81
Q

Absence of joint attention (ie, spontaneous attempt to share interests with others by eye gazing and pointing at objects)

A

ASD

82
Q

What is the primary predisposing factor for vulvulus in children?

A

Malrotation of the midgut during early fetal development

83
Q

The evaluation of clinically stable neonates with bilious emesis begins with what?

A
  1. Cessation of enteral feeds, NG tube decompression, IV fluids
  2. XR to r/o pneumoperitoneum
84
Q

If there is no evidence of free air and the bowel gas pattern is not suggestive of duodenal atresia (double bubble) or distal obstruction (dilated loops of bowel), then ___ should be performed.

A

Upper GI series

85
Q

Dx malrotation vs. volvulus based on upper GI series (aka barium swallow)

A

Malrotation: Ligament of Treitz on the R side of the abdomen

Volvulus: corkscrew pattern

86
Q

What are the 3 major types of fetal heart rate decelerations seen on tracing?

A
  1. Early
  2. Late
  3. Variable
87
Q

Describe the relationship of early decelerations to contraction.

A

Symmetric to contraction
Nadir of deceleration corresponds to peak of contraction
Gradual (30+ seconds from onset to nadir)

88
Q

Etiology of early decelerations?

A

Fetal head compression

89
Q

Describe the relationship of late decelerations to contraction.

A

Delayed compared to contraction
Nadir of deceleration occurs after peak of contraction
Gradual (30+ seconds from onset to nadir)

90
Q

Etiology of late decelerations?

A

Uteroplacental insufficiency

91
Q

Describe the relationship of variable decelerations to contractions.

A

Can be but not necessarily associated with contractions
Abrupt (<30 seconds from onset to nadir)
Decrease over 15+ seconds/minute, duration 15+ seconds, but <2 minutes

92
Q

Etiology of variable decelerations?

A

Cord compression
Oligohydramnios
Cord prolapse

93
Q

Normal baseline FHR?

A

110-160

94
Q

Define moderate variability?

A

Average amplitude of 6-25/min

95
Q

Why are variable decelerations common after ROM/decreases in amniotic fluid volume?

A

Umbilical cord compression

96
Q

When do variable decelerations due to umbilical cord compression require intervention?

A

Intermittent (decelerations with <50% of contractions) are well-tolerated, no intervention

50+% of contractions can result in lack of fetal placental blood flow -> maternal repositioning, then amnioinfusion

97
Q

Category I tracing?

A 
ALL:
-Baseline 110-160
-Moderate variability (6-25/min)
-No late/variable decelerations
\+/- early decelerations
\+/- accelerations
98
Q

Category III tracing?

A

1+ of the following:
-Absent variability + recurrent late decelerations
-Absent variability + recurrent variable decelerations
-Absent variability + bradycardia
Sinusoidal pattern

99
Q

What is the purpose of fetal scalp stimulation?

A

Evaluate fetal acidosis in patients who have no accelerations on FHR monitoring

CONTRAINDICATED in patients with decelerations

100
Q

Which opioids do not show up on standard UDS?

A

Standard UDS measure morphine (breakdown product of all natural non-synthetics)

Not on UDS: semi-synthetic (hydrocodone, hydromorphone, oxycodone, etc.) and synthetic: (eg, fentanyl, meperidine, methadone, tramadol)

101
Q

What testing can be used to very false-positive and possible false-negative results obtained on initial UDS.

A

Gas chromatography/mass spectometry

102
Q

Presentation - severe microcephaly, thin cerebral cortices, multiple intracranial calcifications, neuro and ocular abnormalities, ventriculomegaly

A

Congenital Zika syndrome

103
Q

Presentation - generalized erythema, superficial flaccid blisters, epidermal shedding with light pressure in infants and young children

A

Staphylococcal scalded skin syndrome

104
Q

Rx Staphylococcal scalded skin syndrome?

A 
Antistaphylococcal antibiotic (eg, nafcillin, vancomycin)
Wound care
105
Q

Presentation - well-demarcated, warm, tender area of erythema, +/- constitutional symptoms

A

Erysipelas (bacterial infection of the dermis)

106
Q

Fine pink sandpaper-like rash following an episode of pharyngitis in children, prominent in flexural areas, often desquamates

A

Scarlet fever (GAS)

107
Q

“Sail sign” on X-ray?

A

Thymus

108
Q

Presentation - abdominal pain, jaundice, palpable mass in chidlren <10 y/o

A

Biliary cyst (dilation of the biliary tree)

109
Q

Managementof biliary cyst?

A

Surgical resection to relieve the obstruction and reduce the risk of malignancy

110
Q

Maternal management of HCV in pregnancy?

A

Avoid ribavirin (teratogen)
No indication for barrier protection in serodiscordant monogamous couples
Hepatitis A and B vaccination

111
Q

Prevention of vertical transmission of HCV in pregnancy?

A

Strongly associated with maternal viral load
C/S not protective
Avoid scalp electrodes
Encourage breastfeeding unless maternal blood is present

112
Q

___ occurs in 25% of patients with severe factor 8 deficiency. When should it be considered?

A

Inhibitor development (recognition of the infused factor as foreign, forming antibodies); bleeding refractory to replacement therapy or with increased bleeding frequency

113
Q

Most common AE of inhaled corticosteroid therapy?

A

Oropharyngeal thrush

114
Q

Most common cause of a non-reactive non-stress test (eg, no accelerations)?

A

Quiet fetal sleep cycle (up to 40 minutes)

115
Q

Define a reactive stress test.

A

Baseline of 110-160/min
Moderate variability (6-25/min)
2+ accelerations in 20 minutes each peaking 15+ minutes about baseline and lasting 15+ seconds

116
Q

Acute unilateral motor weakness WITHOUT sensory deficits or higher cortical dysfunction is suggestive of what type of stroke? Common cause?

A

Lacunar stroke affecting the posterior limb of the internal capsule; chronic hypertension

117
Q

Rapidly growing volcano-like nodule with a central keratotic plug

A

Keratoacanthoma

118
Q

Presentation - early adolescence to young adulthood - herald patch (erythematous annular lesion on the trunk) that may increase in size and develop scaling around the edge; within a week, clusters of smaller, erythematous oval lesions appear on the trunk, typically distributed obliquely along the lines of tension +/- pruritis +/- viral produrome

A

Pityriasis rosea

119
Q

Management of pityriasis rosea?

A

Supportive (self-limited)

120
Q

Clinical findings of milk-alkali syndrome?

A

Symptomatic hypercalcemia (N/V, constipation, polyuria, polydipsia, neuropsych symptoms)
Metabolic alkalosis
AKI

121
Q

Rx milk-alkali syndrome?

A

D/C of causative agent

Isotonic saline followed by furosemide

122
Q

Dx Wilson disease?

A

Decreased ceruloplasmin
Increased urinary copper excretion
Kayser-Flesicher rings
Increased copper content on liver biopsy

123
Q

In a patient with suspected infective endocarditis, what is the most appropriate next step?

A

Serial blood cultures from separate venipuncture sites over a specified period prior to initiating antibiotic therapy

Then TTE or TEE

124
Q

Presentation of organophosphate poisoning?

A

Inhibition of AChEsterase -> cholinergic excess -> bradycardia, miosis, rhonchi, muscle fasciculations, salivatino, lacrimation, urination, defecation

125
Q

Reverse organophosphate poisoning?

A

Atropine

126
Q

Rx hepatic encephalopathy?

A

Identify the underlying precipitant and lower serum ammonia with non-absorbable disaccharides (lactulose, lactilol, etc.)

127
Q

New-onset SOB, fevers, dry cough, bilateral mid- and lower-lung reticular opacities, possible maculopapular rash, recent UTI

A

Acute nitrofurantoin-induced pulmonary injury (acute hypersensitivity pneumonitis in the short-term, 3-9 days after medication initiation)

Note - long-term use can lead ot ILD

128
Q

Most common cause of healthcare-associated infective endocarditis?

A

Staphoylococcal

129
Q

Most common cause of community-acquired infective endocarditis?

A

Streptococcal

130
Q

Infective endocarditis after a dental procedure

A

Viridans group streptococci

131
Q

Cause of acute anterolateral STEMI?

A

Left anterior descending artery occlusion

132
Q

Causes of thyrotoxicosis with normal or increased radioactive iodine uptake?

A

Graves disease
Toxic multinodular goiter
Toxic nodule

133
Q

Causes of thyrotoxicosis with decreased RAIU?

A 
Painless thyroiditis
Subacute thyroiditis
Amiodarone-induced thyroiditis
Excessive dose of levothyroxine
Struma ovarii
Iodine-induced
Extensive thyroid cancer mets
134
Q

Presentation - unilateral head and neck pain, transient vision loss, ipsilateral partial Horner syndrome (ptosis + miosis without anhidrosis), signs of cerebral ischemia

A

Carotid artery dissection (suspect in the setting of trauma, can be spontaneous, HTN, smoking, connective tissue disease, OCs contribute)

135
Q

Dx carotid artery dissection?

A

Neurovascular imaging (CTA, etc.)

136
Q

Rx carotid artery dissection?

A

Thrombolysis (if within 4.5 hours of symptom onset)

Antiplatelet therapy +/- anticoagulation

137
Q

3 most common causes of aortic stenosis in the general population?

A

Senile calcific aortic stenosis
Bicuspid aortic valve
Rheumatic heart disease

138
Q

Most common cause of aortic stenosis in patients under 70 y/o?

A

Bicuspid aortic valve

139
Q

Distinguish HCM murmur from AS.

A

HCM is best appreciated in the LLSB and does not typically radiate tot he carotids

140
Q

Rx acute bacterial prostatitis?

A

6 weeks TMP-SMX or FQ

Dedicated - Step 2 (22 decks)

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