Cardiovascular- pathology (2) Flashcards
Dilated cardiomyopathy
- etiology
Most common cardiomyopathy (90% of cases).
Often idiopathic or familial.
Other etiologies ABCCCD:
chronic Alcohol abuse, wet Beriberi, Coxsackie B viral myocarditis, chronic Cocaine use, Chagas disease, Doxorubicin toxicity, hemochromatosis, sarcoidosis,
thyrotoxicosis, peripartum cardiomyopathy.
Dilated cardiomyopathy
- Findings
- Treatment
HF, S3, systolic regurgitant murmur, dilated heart on echocardiogram, balloon appearance of heart on CXR.
Na+ restriction, ACE inhibitors, β-blockers, diuretics, digoxin, ICD, heart transplant.
Takotsubo cardiomyopathy:
broken heart syndrome—ventricular apical ballooning likely due to increased sympathetic stimulation (eg,
stressful situations).
Hypertrophic obstructive cardiomyopathy
- etiology
60–70% of cases are familial, autosomal dominant (most commonly due to mutations in genes encoding sarcomeric proteins, such as myosin binding protein C and β-myosin heavy chain).
Other causes of concentric LV hypertrophy: chronic HTN, Friedreich ataxia.
Marked ventricular concentric hypertrophy
Hypertrophic obstructive cardiomyopathy
- Findings
- Treatment
S4, systolic murmur. May see mitral regurgitation due to impaired mitral valve closure. Causes syncope during exercise and may lead to sudden death.
cessation of high-intensity athletics, use of β-blocker or non-dihydropyridine Ca2+ channel blockers (eg, verapamil). ICD if patient is high risk.
Restrictive/infiltrative cardiomyopathy
- Etiology
“Puppy LEASH”
Postradiation fibrosis, Löffler endocarditis, Endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children), Amyloidosis, Sarcoidosis, Hemochromatosis (although dilated cardiomyopathy is more common).
Löffler endocarditis
associated with hypereosinophilic syndrome; histology shows eosinophilic infiltrates in myocardiu
Heart failure
- Symptoms
dyspnea, orthopnea, fatigue; signs include S3 heart sound, rales, jugular venous distention (JVD), pitting edema.
Right HF most often results from left HF. Cor pulmonale refers to isolated right HF due to pulmonary cause.
Heart failure
- Diastolic dysfunction
- Systolic dysfunction
preserved EF, normal EDV; low compliance (high EDP) often 2° to myocardial hypertrophy.
reduced EF, high EDV; decrease contractility often 2° to ischemia/MI or dilated cardiomyopathy.
Heart failure
- Treatment
ACE inhibitors or angiotensin II receptor blockers, β blockers (except in acute decompensated HF), and spironolactone decrease mortality.
Thiazide or loop diuretics are used mainly for symptomatic relief.
Hydralazine with nitrate therapy improves both symptoms and mortality in select patients.
Left heart failure triad
right heart failure triad
Orthopnea, Paroxysmal nocturnal dyspnea, Pulmonary edema.
Hepatomegaly (nutmeg liver), Jugular venous distention, Peripheral edema
Shock
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Bacterial endocarditis
- Acute
- Subacute
S aureus (high virulence). Large vegetations on previously normal valves. Rapid onset
viridans streptococci (low virulence). Smaller vegetations on congenitally abnormal or diseased valves. Sequela of dental procedures. Gradual onset.
Bacterial endocarditis
- Signs and symptoms
Bacteria FROM JANE Fever Roth spots Osler nodes Murmur Janeway lesions Anemia Nail-bed hemorrhage Emboli
Bacterial endocarditis
- If culture ⊝
- Most frecuent valve affected
- Tricuspid valve endocarditis
- in colon cancer
- on prostetic valves
most likely Coxiella burnetti, Bartonella spp, HACEK (Haemophilus, Aggregatibacter [formerly Actinobacillus],
Cardiobacterium, Eikenella, Kingella)
Mitral
Is associated with IV drug abuse. Associated with S aureus, Pseudomonas, and Candida.
S bovis (gallolyticus)
S epidermidis
nonbacterial (marantic/thrombotic) endocarditis
2° to malignancy, hypercoagulable state, or lupus.
Rheumatic fever
- etiology
- sequelae
A consequence of pharyngeal infection with group A β-hemolytic streptococci.
Late sequelae include rheumatic heart disease,
which affects heart valves—mitral > aortic»_space; tricuspid.
*Early lesion is mitral valve regurgitation; late lesion is mitral stenosis.
Rheumatic fever
- Characteristics
- diagnosis
- Treatment
Associated with Aschoff bodies (granuloma with giant cells), Anitschkow cells (enlarged macrophages with ovoid, wavy, rod-like nucleus), antistreptolysin O (ASO) titers.
Antibodies to M protein cross-react with self antigens
(molecular mimicry).
Treatment/prophylaxis: penicillin.
Rheumatic fever
- major criteria
J♥NES (major criteria):
Joint (migratory polyarthritis) ♥ (carditis) Nodules in skin (subcutaneous) Erythema marginatum (evanescent rash with ring margin) Sydenham chorea
Acute pericarditis
- clinical characteristics
presents with sharp pain, aggravated by inspiration, and relieved by sitting up and leaning forward. Often complicated by pericardial effusion.
Presents with friction rub. ECG changes include widespread ST-segment elevation and/or PR depression.
Acute pericarditis
- Etiology
Causes include idiopathic (most common; presumed viral), confirmed infection (eg, coxsackievirus B), neoplasia, autoimmune (eg, SLE, rheumatoid arthritis), uremia, cardiovascular (acute STEMI or Dressler syndrome), radiation therapy.
Myocarditis
- Clinical features
- Complications
Major cause of SCD in adults < 40 years old.
Presentation highly variable, can include dyspnea, chest pain, fever, arrhythmias (persistent tachycardia out of proportion to fever is characteristic).
Complications include sudden death (SCD), arrhythmias, heart block, dilated cardiomyopathy, HF, mural thrombus with systemic emboli.
Myocarditis
- etiology
Multiple causes:
Viral (eg, adenovirus, coxsackie B, parvovirus B19, HIV, HHV-6); lymphocytic infiltrate with focal necrosis highly indicative of viral myocarditis.
Parasitic (eg, Trypanosoma cruzi, Toxoplasma gondii)
Bacterial (eg, Borrelia burgdorferi, Mycoplasma pneumoniae)
Toxins (eg, carbon monoxide, black widow venom)
Rheumatic fever
Drugs (eg, doxorubicin, cocaine)
Autoimmune (eg, Kawasaki disease, sarcoidosis, SLE, polymyositis/dermatomyositis)
Cardiac tamponade
Findings: Beck triad (hypotension, distended neck veins, distant heart sounds), high HR, pulsus paradoxus. ECG shows low-voltage QRS and electrical alternans.
Pulsus paradoxus
decrease in amplitude of systolic BP by > 10 mm Hg during inspiration.
Seen in cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, croup.
Syphilitic heart
disease
3° syphilis disrupts the vasa vasorum of the aorta with consequent atrophy of vessel wall and dilatation of aorta and valve ring.
May see calcification of aortic root, ascending aortic arch, and thoracic aorta. Leads to “tree bark” appearance of aorta.
Vasculitides
- Large-vessel vasculitis
- Medium-vessel vasculitis
- Small-vessel vasculitis
Giant cell (temporal) arteritis, Takayasu arteritis
Polyarteritis nodosa, Kawasaki disease (mucocutaneous
lymph node syndrome), Buerger disease (thromboangiitis obliterans)
Granulomatosis with polyangiitis (Wegener), Microscopic
polyangiitis, Behçet syndrome, Eosinophilic granulomatosis with polyangiitis (Churg- Strauss), Immunoglobulin A vasculitis
Vasculitides
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Cardiac tumors
Most common heart tumor is a metastasis (eg, melanoma).
Myxomas, Rhabdomyomas
Myxomas
Most common 1° cardiac tumor in adults. 90% occur in the atria (mostly left atrium).
Usually described as a “ball valve” obstruction in the left atrium (associated with multiple syncopal episodes). May auscultate early diastolic “tumor plop” sound.
Histology: gelatinous material, myxoma cells immersed in glycosaminoglycans.
Rhabdomyomas
Most frequent 1° cardiac tumor in children (associated with tuberous sclerosis).
Histology: hamartomatous growths.
Kussmaul sign
Increase in JVP on inspiration instead of a normal decrease.
May be seen with constrictive pericarditis, restrictive cardiomyopathies, right atrial or ventricular tumors.
Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu)
Inherited disorder of blood vessels. Findings: blanching lesions (telangiectasias) on skin and mucous membranes, recurrent epistaxis, skin discolorations, arteriovenous malformations (AVMs), GI bleeding, hematuria.
