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Review / Wrong Answers > 6/18 UWorld > Flashcards

6/18 UWorld Flashcards

1
Q

Intoxication of what drug causes:

Violent behavior, dissociation, hallucinations, amnesia, nystagmus, ataxia

A

PCP = Hallucinogen

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2
Q

Intoxication of what drug causes:

Visual hallucinations, euphoria, dysphoria/panic, tachycardia/HTN

A

LSD - Hallucinogen

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3
Q

Intoxication of what drug causes:

Euphoria, agitation/psychosis, chest pain, seizures, tachycardia/HTN, mydriasis

A

Cocaine - stimulant

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4
Q

Intoxication of what drug causes:

Increased appetite, euphoria, dysphoria/panic, slow reflexes, impaired time perception, dry mouth, conjunctival injection

A

Marijuana = psychoactive

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5
Q

Intoxication of what drug causes:

Violent behavior, psychosis, diaphoresis, tachycardia/HTN, choreiform movements, tooth decay

A

Methamphetamine = stimulant

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6
Q

Intoxication of what drug causes:

Euphoria, depressed mental status, miosis, respiratory depression, constipation

A

Heroin = opioid

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7
Q

Withdrawal of what drug causes:

· Tremors, agitation, anxiety, delirium, psychosis

· Seizures, tachycardia, palpitations

A

Alcohol

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8
Q

Withdrawal of what drug causes:

Increased appetite, hypersomnia, intense psychomotor retardation, severe depression (“crash”)

A

Stimulants (cocaine / methamphetamine)

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9
Q

Withdrawal of what drug causes:

· Nausea, vomiting, abdominal cramping, muscle aches

· Dilated pupils, yawing, piloerection, lacrimation, hyperactive bowel sounds

A

Heroin = opioid

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10
Q

Why is there only minimal/rare risk of pulmonary infarction following a PE

A

Collateral circulation

Clot occludes the pulmonary artery, but the bronchial artery can continue to supply nutrients

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11
Q

Describe the effect of Class I anti-arrhythmics on EKG

A
  • Class I antiarrhythmics widen the QRS complex on EKG (due to decreased AP conduction velocity)
  • Because drug effect is stronger on channels with more depolarization (rapid heart rate), QRS will be even WIDER in patients with tachycardia
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12
Q

D

A
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13
Q

From what embryological derivative does the pituitary form? (endo, meso, or ectoderm)

A
  • Ectoderm
    • Anterior pituitary = surface ectoderm
    • Posterior = neural tube
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14
Q

What is Rathke’s pough

A

Surface ectoderm where anterior pituitary sprouted from mouth

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15
Q

What are the differences in Troponin I and CK-MB seen after an MI

A
  • Troponin I
    • Rises after 4 hours
    • Peaks at 24 hours
    • Is elevated for 7-10 days
    • Most specific to cardiac myocytes
  • CK-MB
    • Rises after 6-12 hours
    • Peaks at 16-24 hours
    • Return to normal after 48 hours
    • Useful in diagnosing reinfarction following acute MI
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16
Q

What will you see < 4 hours after MI:

  • Gross
  • Microscopically
  • Complications
A
  • Gross changes:
    • None
  • Microscopic changes:
    • None
  • Complications:
    • Cardiogenic shock (cannot provide blood to organs)
    • Congestive heart failure (decreased ejection fraction)
    • Arrhythmias
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17
Q

What will you see 4-24 hours after an MI:

  • Gross
  • Microscopically
  • Complications
A
  • Gross changes
    • Dark discoloration
  • Microscopic changes:
    • Coagulative necrosis (nucleus removed from dead cells)
    • Contraction bands (due to reperfusion injury from hypercontraction)
    • Wavy fibers with narrow, elongated myocytes
  • Complications:
    • Arrhythmia
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18
Q

What will you see 1-3 days after an MI:

  • Gross
  • Microscopically
  • Complications
A
  • Gross changes:
    • Yellow pallor (due to WBC)
  • Microscopic changes
    • Macrophages
  • Complications
    • Rupture of ventricular free wall can lead to cardiac tamponade
    • Rupture of interventricular septum
    • Rupture of papillary muscle (fed by R coronary artery) leading to mitral insufficiency
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19
Q

What will you see 4-7 days after an MI:

  • Gross
  • Microscopically
  • Complications
A
  • Gross changes:
    • Yellow pallor (due to WBC)
  • Microscopic changes
    • Macrophages
  • Complications
    • Rupture of ventricular free wall can lead to cardiac tamponade
    • Rupture of interventricular septum
    • Rupture of papillary muscle (fed by R coronary artery) leading to mitral insufficiency
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20
Q

What will you see 1-3 weeks after an MI:

  • Gross
  • Microscopically
  • Complications
A
  • Gross changes:
    • Red border emerges as blood vessel from normal tissue grow into necrotic tissue to form granulation tissue
  • Microscopic changes:
    • Granulation tissue with fibroblasts, collage, and blood vessels
  • Complications:
    • Arrhythmias
21
Q

What will you see months after an MI:

  • Gross
  • Microscopically
  • Complication
A
  • Gross changes
    • White scar
  • Microscopic changes:
    • Fibrosis
  • Complications
    • Aneurysm (scar is not as strong as myocardium)
    • Mural thrombus and embolism (secondary to aneurysm)
    • Dressler syndrome (antibodies against pericardium) occurring 6-8 weeks after infarction
      • Chest pain, pericardial friction, and persistent fever
22
Q

Treatment of MI before you know if it is an NSTEMI or STEMI

A
  • ABCs (airway, breathing, circulation)
  • MONA:
    • Morphine (IV) – to relieve chest pain
    • O2 supplemental (only if hypoxia present)
    • Nitroglycerin (venodilator decreases preload)
    • Aspirin – to decrease clotting
  • Beta-blockers (Metoprolol)
    • If no signs of heart failure or severe asthma
  • Statins (Atorvastastin)
    • Preferably before cath lab
  • Antiplatelet therapy (Clopidogrel or Ticagrelor)
    • To all patients
  • Anticoagulant therapy to all patients
    • Unfractionated heparin to patients undergoing catheterization
    • Enoxaparin for patients not managed with catheterization
  • Potassium and magnesium to decrease risk of arrhythmia
    • Only if there are abnormalities
23
Q

Treatment of STEMI vs. NSTEMI

A
  • If STEMI:
    • Percutaneous coronary intervention (PCI) = catheter
      • If significant CAD on the catheter, then the patient may receive stenting or coronary artery bypass graft
    • If PCI unavailable, treat with fibrinolysis within 90-120 minutes
      • Avoid fibrinolysis with a NSTEMI
  • If NSTEMI:
    • PCI only (no fibrinolytics)
24
Q

Describe eccentric vs. concentric cardiac hypertrophy

A

Eccentric = sarcomeres added in series = dilated cardiomyopathy

Concentric = sarcomeres added in parallel = hypertrophic cardiomyopathy

25
Q

What is Loffler syndrome

A

Myocardial fibrosis with eosinophilic infiltrate that causes restrictive cardiomyopathy

26
Q

Hemochromatosis most often results in what cardiomyopathy?

A

Dilated

27
Q

What are Roth spots?

A

Round white spots on retina, surrounded by hemorrhage

Seen in bacterial endocarditis

28
Q

Compare Osler nodes and Janeway lesions

A

Both seen in infective endocarditis

  • Osler nodes (painful red nodules on finger and toe pads) - B
  • Janeway lesions (painless erythematous macules on palms and soles) - C
29
Q

Describe effect of acute vs. chronic rheumatic disease on the heart

A
  • Valves affected:
    • Mitral > aortic > tricuspid
  • Early disease
    • Mitral regurgitation (due to small vegetations)
  • Late disease
    • Mitral stenosis (due to valve scarring – “fish mouth”)
30
Q

What disorder presents as sharp chest pain, aggravated by inspiration, and relieved by sitting up and leaning forward

A

Pericarditis

31
Q

What physical exam finding may be seen in pericarditis

A
  • Kussmaul sign = JVD with inspiration (instead of normal decreased JVD)
    • Constrictive pericarditis > Cardiac tamponade
32
Q

What is Beck triad seen in cardiac tamponade

A
  • Hypotension
  • Increased venous pressure, JVD
  • Distant heart sounds
33
Q

What will be seen on EKG in cardiac tamponade

A
  • ECG will show electrical alternans
    • Alternating amplitude (big, small, big, small) of QRS complex
    • Due to swinging movement of the heart in large effusion
34
Q

Classic presentation, location, and heart sound associated with cardiac myxoma

A
  • Most common primary heart tumor in adults
  • 90% occur in left atria
  • Presents as a ball within the atria which can obstruct the mitral valve
    • Decreased filling of ventricle = decreased output during systole = syncopal episode
  • Tumor may flop over into LV during diastole
    • Early diastolic “tumor plop” sound
35
Q

Tumors associated with tuberous sclerosis

A

Rhabdomyoma, Astrocytoma, Angiomyolipoma

36
Q

What vasculitis is associated with polymyalgia rheumatica

A

Giant cell

37
Q

What vasculitis is associated with hepatitis B

A

Polyarteritis nodosa

38
Q

Presentation of Takayasu

A
  • < 50 y/o Asian females
  • Branches of aortic arch
  • Presentation:
    • Pulseless disease (weak UE pulses)
    • Visual and neuro symptoms
  • Biopsy:
    • Granulomas
39
Q

Cause of Polyarteritis nodosa

A
  • Type III HSR
  • Transmural inflammation of the arterial wall with fibrinoid necrosis
40
Q

Presentation and treatment of Kawasaki

A
  • Presentation
    • Viral-like symptoms – fever, conjunctivitis, cervical lymphadenopathy
    • Strawberry tongue
    • Rash on hands and feet
    • May develop coronary artery aneurysm:
      • Thrombosis with myocardial infarction
  • Treatment:
    • Aspirin (to prevent thrombosis of coronary a.)
    • IVIG
41
Q

Common organs affected/presentation of Polyarteritis nodosa

A
  • Presentation:
    • HTN – renal artery involvement
    • Abd pain – mesenteric artery
    • Neuro and skin
42
Q

Classic imaging of polyarteritis nodosa

A
  • String-of-pearl appearance
43
Q

Cause, presentation, and treatment of Buerger disease

A
  • Segmental thrombosing vasculitis
  • Necrotizing vasculitis of the digits
  • Highly associated with smoking
  • Presentation:
    • Ulceration, gangrene, and autoamputation of fingers and toes
    • Raynaud phenomenon
  • Treatment:
    • Smoking cessation
44
Q

Presentation of Eosinophilic granulomatosis with polyangiitis

A

Aka Churg Strauss

  • Necrotizing granulomatous vasculitis with eosinophils
  • Especially involves lungs and heart
    • Asthma
    • Sinusitis, skin nodules or purpura, peripheral neuropathy
    • Can also involve heart, GI kidneys (pauci-immune glomerulonephritis)
  • Antibody:
    • p-ANCA
  • Biopsy:
    • Granulomas
45
Q

Presentation of Henoch-Schonlein purpura

A
  • Due to IgA immune complex deposition
    • Follows URI infections
  • Presentation:
    • Palpable purpura on buttocks and legs
    • Arthralgias
    • GI pain and bleeding
    • Hematuria – IgA nephropathy (aka Berger disease)
46
Q

What vitamin deficiency causes Beriberi

A

Vitamin B1 (Think: Ber1 Ber1)

47
Q

What is wet beriberi vs. dry beriberi

A

Dry = polyneuritis, symmetrical muscle wasting

Wet = high-output cardiac failure (dilated cardiomyopathy), edema

48
Q

Causes of dilated cardiomyopathy

A
  • Idiopathic/familial
  • Chronic myocardial ischemia
  • Hemochromatosis
  • Anthracyclines (Doxrubicin and Daunorubicin) – chemotherapy
  • Chronic cocaine use
  • Chronic alcohol use
  • Wet beriberi (Thiamine B1 deficiency)
  • Chagas disease (trypanosoma cruzi)
  • Coxsackie B viral myocarditis

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