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
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
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
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
- Fibrinous pericarditis (neutrophils attaching the dead heart will leak out into pericardium)
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
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
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
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
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
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
- Percutaneous coronary intervention (PCI) = catheter
- If NSTEMI:
- PCI only (no fibrinolytics)
11
Q
Long-term managment of MI
A
- Aspirin and/or Clopidogrel
- Beta blockers
- ACEI / ARBs
- Potassium sparing diuretics
- Statins
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
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
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)
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
16
Q
Describe the defect in restrictive cardiomyopathy
A
- Deposition in myocardium disrupts diastolic function
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
18
Q
What is Loffler syndrome
A
- Myocardial fibrosis with an eosinophilic infiltrate that causes restrictive cardiomyopathy
19
Q
Hemochromatosis most often results in what cardiomyopathy?
A
Dilated
20
Q
What valve is most often involved in infective endocarditis
A
Mitral
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)
22
Q
What eye findngs are seen in bacterial endocarditis
A
- Roth spots (retinal hemorrhages with clear central necrosis)
23
Q
Most common bacterial causes of infective endocarditis
A
Staph aureus
Strep viridans
Enterococci
Staph epidermidis
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
25
What type of valves are affected with Strep viridans and is it acute or subacute
* 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
Describe the pathogenesis of Rheumatic fever
* Molecular mimicry between antibodies against M protein and self-antigens
* Type II HSR (not a direct effect of bacteria)
27
Diagnostic criteria of rheumatic fever
* 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
Describe effect of acute vs. chronic rheumatic disease on the heart
* Valves affected:
* Mitral \> aortic \> tricuspid
* Early disease
* Mitral regurgitation (due to small vegetations)
* Late disease
* Mitral stenosis (due to valve scarring – “fish mouth”)
29
What will be seen on histology of rheumatic fever
* Aschoff bodies (granuloma with giant cells)
* Anitschkow cells (HIstiocytes with slender, wavy nuclei (“caterpillar nuclei”) within Aschoff bodies
30
What disorder presents as sharp chest pain, aggravated by inspiration, and relieved by sitting up and leaning forward
Pericarditis
31
What will you see on ECG of pericarditis
Diffuse ST elevation in all EKG leads (rather than specific to certain leads)
32
What physical exam finding may be seen in pericarditis
* Kussmaul sign = JVD with inspiration (instead of normal decreased JVD)
* Constrictive pericarditis \> Cardiac tamponade
33
What is the classic presentation of cardiac tamponade
* Beck triad:
* Hypotension
* Increased venous pressure, JVD
* Distant heart sounds
* Increased heart rate
* Pulsus paradoxus
34
What is pulsus paradoxus
* 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
What will be seen on ECG in cardiac tamponade
* ECG will show electrical alternans
* Alternating amplitude (big, small, big, small) of QRS complex
36
What are the pathologic CV findings in syphilis
* 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
What is the most common heart tumor
Metastatic
38
Most common primary heart tumor in adults
Myxoma
39
Classic location, presentation, and heart sound of cardiac myxoma
* 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
What are the tumors assoicated with tuberous sclerosis
* Tuberous sclerosis = Rhabdomyoma, Astrocytoma, Angiomyolipoma
41
Most common primary cardiac tumor in children
Rhabdomyoma
42
What are the large-vessel vasculitides
Giant cell (temporal)
Takayasu
43
What are the medium-vessel vasculitides
(THINK: put a COW on a PAN in order to cook a MEDIUM BURGER)
Polyarteritis nodosa (PAN), Kawasaki, Buerger
44
What are the small-vessel vasculitides
Granulomatosis with polyangiitis (Wegener)
Microscopic polyangiitis
Churg-Strauss (Eosinophilic granulomatosis with polyangiitis)
Henoch-Schonlein Purpura
45
What vasculitis is associated with polymyalgia rheumatica
Giant cell
46
Feared complication of Giant cell arteritis
Blindness (due to ophthalmic a. involvment)
47
Treatment of giant cell arteritis
Corticosteroids
48
What vasculitis is associated with Hepatitis B
Polyarteritis nodosa
49
Common organs involved in polyarteritis nodosa
* Involves multiple organs, _sparing the lungs_
* Presentation:
* HTN – renal artery involvement
* Abd pain – mesenteric artery
* Neuro and skin
50
Imaging and treatment of polyarteritis nodosa
* Imaging:
* String-of-pearl appearance (multiple renal microanuerysms)
* Treatment:
* Corticosteroids – fatal if not treated
51
Common presentation of Kawasaki disease
* 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
Treatment of Kawasaki disease
* Aspirin (to prevent thrombosis of coronary arteries)
* IVIG
53
What vasculitis presents with pulseless disease
Takayasu - involves branches of aortic arch
54
Histology and treatment of Takayasu
* Biopsy:
* Granulomas
* Treatment:
* Corticosteroids
55
Cause, presentation, and treatment of Buerger disease
* Necrotizing vasculitis of the digits
* Highly associated with smoking
* Presentation:
* Ulceration, gangrene, and autoamputation of fingers and toes
* Raynaud phenomenon
* Treatment:
* Smoking cessation
56
Organs involved in microscopic polyangiitis
* Involves lung and kidney – NO nasopharyngeal involvement
* LRI = hemoptysis, cough, dyspnea
* Renal = hematuria, red cell casts
* Causes pauci-immune crescentic glomerulonephritis
57
Which vasculitides are associated with c-ANCA and p-ANCA
c-ANCA = Wegener's
p-ANCA = Microscopic polyangiitis, Churg-Strauss
58
Presentation, histology, and treatment of Granulomatosis with polyangiits
* 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
Common presentation of Eosinophilic granulomatosis with polyangiitis
* 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
Presentation of Henoch-Schonlein purpura
* 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
Treatment of Henoch-Schonlein purpura
* Disease is self-limited
* Steroids if severe
