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Review / Wrong Answers > DIT review - Cardiology 7 > Flashcards

DIT review - Cardiology 7 Flashcards

1
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
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2
Q

What will you see < 4 hours after an MI:

  • Grossly
  • 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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3
Q

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

  • Grossly
  • Microscopically
  • Complications
A
  • Gross changes
    • Dark discoloration
  • Microscopic changes:
    • Coagulative necrosis (nucleus removed from dead cells)
    • Contraction bands
  • Complications:
    • Arrhythmia
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4
Q

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

  • Grossly
  • Microscopically
  • Complications
A
  • Gross changes
    • Hyperemia
  • Microscopic changes:
    • Neutrophils
  • Complications
    • Fibrinous pericarditis (neutrophils attaching the dead heart will leak out into pericardium)
      • Presents as chest pain with friction rub
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5
Q

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

  • Grossly
  • 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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6
Q

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

  • Grossly
  • 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
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7
Q

What will you see months after an MI:

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

What leads will you see ST elevation in infarcts of the following:

  • Anteroseptal infarct (LAD)
  • Anteroapical (distal LAD)
  • Anterolateral (LAD or LCX)
  • Lateral (LCX)
  • Inferior (RCA)
  • Posterior (PDA)
A
  • Anteroseptal infarct (LAD) = V1-V2
  • Anteroapical (distal LAD) = V3-V4
  • Anterolateral (LAD or LCX) = V5-V6
  • Lateral (LCX) = I, aVL
  • Inferior (RCA) = II, III, aVF
  • Posterior (PDA) = V7-V9
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9
Q

Describe treatment of MI before you know if it’s a STEMI or NSTEMI

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
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10
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)
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11
Q

Long-term managment of MI

A
  • Aspirin and/or Clopidogrel
  • Beta blockers
  • ACEI / ARBs
  • Potassium sparing diuretics
  • Statins
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12
Q

What are the morphologic heart changes you see in hypertrophic cardiomyopathy

A
  • 60-70% are familial, autosomal dominant
  • Heart changes:
    • Ventricular hypertrophy marked with myofibrillar disarray and fibrosis
    • Hypertrophy of the interventricular septum can compress the mitral valve, causing outflow obstruction
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13
Q

What heart sound is heard with hypertrophic cardiomyopathy, and what makes the sound louder/softer

A
  • S4 systolic murmur (recall: S4 = stiffened ventricle)
    • Murmur louder with Valsalva and softer with squatting
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14
Q

What are the heart sounds heard in dilated cardiomyopathy

A
  • Most common cardiomyopathy
  • Causes systolic dysfunction
  • Findings:
    • S3 heart sound (recall S3 = ventricular failure/volume overload)
    • Apical impulse displace laterally (due to enlarged heart)
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15
Q

Causes of dilated cardiomyopathy

A
  • 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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16
Q

Describe the defect in restrictive cardiomyopathy

A
  • Deposition in myocardium disrupts diastolic function
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17
Q

Causes of restrictive cardiomyopathy

A
  • Sarcoidosis
  • Amyloidosis
  • Loffler syndrome
  • Hemochromatosis
  • Post-radiation fibrosis
  • Endocardial fibroelastosis – thick fibroelastic tissue in endocardium of young children
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18
Q

What is Loffler syndrome

A
  • Myocardial fibrosis with an eosinophilic infiltrate that causes restrictive cardiomyopathy
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19
Q

Hemochromatosis most often results in what cardiomyopathy?

A

Dilated

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20
Q

What valve is most often involved in infective endocarditis

A

Mitral

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21
Q

Compare Osler nodes and Janeway lesions

A

Both seen in infective endocarditis

  • Osler nodes (painful red nodules on finger and toe pads)
  • Janeway lesions (painless erythematous macules on palms and soles)
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22
Q

What eye findngs are seen in bacterial endocarditis

A
  • Roth spots (retinal hemorrhages with clear central necrosis)
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23
Q

Most common bacterial causes of infective endocarditis

A

Staph aureus

Strep viridans

Enterococci

Staph epidermidis

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24
Q

What type of valves are affected with Staph aureus and is it acute or subacute

A
  • 30% of all cases
  • Causes acute endocarditis
  • Large vegetations on previously normal valves
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25
Q

What type of valves are affected with Strep viridans and is it acute or subacute

A
  • 20-30% of all cases
  • Subacute
  • Smaller vegetations on valves that were already abnormal
  • Sequela of dental procedures (give prophylaxis on patients with abnormal valves)
26
Q

Describe the pathogenesis of Rheumatic fever

A
  • Molecular mimicry between antibodies against M protein and self-antigens
  • Type II HSR (not a direct effect of bacteria)
27
Q

Diagnostic criteria of rheumatic fever

A
  • Elevated anti-streptolysin O (ASO) titer + major or minor criteria
  • Major criteria = JONES criteria
    • J = Joints (polyarthrtisi)
    • O = <3 (pancarditis – valvular damage, myocarditis, pericarditis)
    • N = Nodules in skin (subcutaneous)
    • E = Erythema marginatum (rash with thick red borders)
    • S = Syndenham chorea (rapid involuntarily movements especially of face, tongue, and upper extremities)
28
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”)
29
Q

What will be seen on histology of rheumatic fever

A
  • Aschoff bodies (granuloma with giant cells)
  • Anitschkow cells (HIstiocytes with slender, wavy nuclei (“caterpillar nuclei”) within Aschoff bodies
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 will you see on ECG of pericarditis

A

Diffuse ST elevation in all EKG leads (rather than specific to certain leads)

32
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
33
Q

What is the classic presentation of cardiac tamponade

A
  • Beck triad:
    • Hypotension
    • Increased venous pressure, JVD
    • Distant heart sounds
  • Increased heart rate
  • Pulsus paradoxus
34
Q

What is pulsus paradoxus

A
  • Decrease in amplitude of systolic BP by > 10 mm Hg during inspiration
    • Usually when you inspire this decreases intrathoracic pressure and causes the ventricular septum to deviate to the L, causing a smaller LV and a normal but slight decrease in BP
    • In pulsus paradoxus, there will be an exaggerated decrease in BP
  • Seen in cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, croup
  • Occurs in cardiac tamponade > constrictive pericarditis (vs. Kussmaul sign)
35
Q

What will be seen on ECG in cardiac tamponade

A
  • ECG will show electrical alternans
    • Alternating amplitude (big, small, big, small) of QRS complex
36
Q

What are the pathologic CV findings in syphilis

A
  • Causes disruption of the vasa vasorum of the aorta
    • Dilated of aorta and valve ring
      • Aortic regurgitation
      • Aortic aneurysm
    • Calcification of the aorta
      • “Tree bark” appearance
37
Q

What is the most common heart tumor

A

Metastatic

38
Q

Most common primary heart tumor in adults

A

Myxoma

39
Q

Classic location, presentation, and heart sound of cardiac myxoma

A
  • 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
40
Q

What are the tumors assoicated with tuberous sclerosis

A
  • Tuberous sclerosis = Rhabdomyoma, Astrocytoma, Angiomyolipoma
41
Q

Most common primary cardiac tumor in children

A

Rhabdomyoma

42
Q

What are the large-vessel vasculitides

A

Giant cell (temporal)

Takayasu

43
Q

What are the medium-vessel vasculitides

A

(THINK: put a COW on a PAN in order to cook a MEDIUM BURGER)

Polyarteritis nodosa (PAN), Kawasaki, Buerger

44
Q

What are the small-vessel vasculitides

A

Granulomatosis with polyangiitis (Wegener)

Microscopic polyangiitis

Churg-Strauss (Eosinophilic granulomatosis with polyangiitis)

Henoch-Schonlein Purpura

45
Q

What vasculitis is associated with polymyalgia rheumatica

A

Giant cell

46
Q

Feared complication of Giant cell arteritis

A

Blindness (due to ophthalmic a. involvment)

47
Q

Treatment of giant cell arteritis

A

Corticosteroids

48
Q

What vasculitis is associated with Hepatitis B

A

Polyarteritis nodosa

49
Q

Common organs involved in polyarteritis nodosa

A
  • Involves multiple organs, sparing the lungs
  • Presentation:
    • HTN – renal artery involvement
    • Abd pain – mesenteric artery
    • Neuro and skin
50
Q

Imaging and treatment of polyarteritis nodosa

A
  • Imaging:
    • String-of-pearl appearance (multiple renal microanuerysms)
  • Treatment:
    • Corticosteroids – fatal if not treated
51
Q

Common presentation of Kawasaki disease

A
  • Asian children < 4 y/o
  • Presentation
    • Viral-like symptoms – fever, conjunctivitis, cervical lymphadenopathy
    • Strawberry tongue
    • Rash on hands and feet
    • May develop coronary artery aneurysm:
      • Thrombosis with myocardial infarction
52
Q

Treatment of Kawasaki disease

A
  • Aspirin (to prevent thrombosis of coronary arteries)
  • IVIG
53
Q

What vasculitis presents with pulseless disease

A

Takayasu - involves branches of aortic arch

54
Q

Histology and treatment of Takayasu

A
  • Biopsy:
    • Granulomas
  • Treatment:
    • Corticosteroids
55
Q

Cause, presentation, and treatment of Buerger disease

A
  • Necrotizing vasculitis of the digits
  • Highly associated with smoking
  • Presentation:
    • Ulceration, gangrene, and autoamputation of fingers and toes
    • Raynaud phenomenon
  • Treatment:
    • Smoking cessation
56
Q

Organs involved in microscopic polyangiitis

A
  • Involves lung and kidney – NO nasopharyngeal involvement
    • LRI = hemoptysis, cough, dyspnea
    • Renal = hematuria, red cell casts
      • Causes pauci-immune crescentic glomerulonephritis
57
Q

Which vasculitides are associated with c-ANCA and p-ANCA

A

c-ANCA = Wegener’s

p-ANCA = Microscopic polyangiitis, Churg-Strauss

58
Q

Presentation, histology, and treatment of Granulomatosis with polyangiits

A
  • Wegener Granulomatosis aka Granulomatosis with polyangiitis
    • Necrotizing granulomatous vasculitis involving nasopharynx, lungs, and kidney
      • URI = perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis
      • LRI = hemoptysis, cough, dyspnea
      • Renal = hematuria, red cell casts
        • Causes pauci-immune crescentic glomerulonephritis
    • Antibody:
      • c-ANCA
    • Biopsy:
      • Granulomas
    • Treatment:
      • Cyclophosphamide
59
Q

Common presentation of Eosinophilic granulomatosis with polyangiitis

A
  • Churg-Strauss syndrome aka Eosinophilic granulomatosis with polyangiitis
    • Necrotizing granulomatous vasculitis with eosinophils
    • Especially involves lungs and heart
      • Asthma
      • Sinusitis, skin nodules or purpura, peripheral neuropathy
    • Antibody:
      • p-ANCA
    • Biopsy:
      • Granulomas
60
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)
61
Q

Treatment of Henoch-Schonlein purpura

A
  • Disease is self-limited
  • Steroids if severe

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