Step 1 - Cardio (Path)

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Hypertension

BP >140/90
-Risk factor: inc. age, obesity, diabetes, smoking, genetics, black>white>Asian
-90% is essential HTN and related to inc. CO or inc TPR
-10% is secondary to renal disease
-Malignant HTN: severe and rapidly progressing
-Predisposes to atherosclerosis, LVH, stroke, CHF, renal failure, retinopathy, and aortic dissection

Signs of hyperlipidemia

1. Atheromas
-Plaques in blood vessel walls
2. Xanthomas
-Plaques or nodules composed of lipid-laden histiocytes in the skin, esp. eyelids (xanthelasma)
3. Tendinous xanthoma
-Lipid deposit in tendon, esp. Achilles
4. Corneal arcus
-Lipid deposit in cornea, nonspecific (arcus senilis)

Monckeberg's medial calcification

Calcification in the media of the arteries, esp. radial or ulnar
-Usually benign
-"Pipestem" arteries
-Does not obstruct blood flow
-Intima not involved

Arteriolosclerosis

1. Hyaline arteriolosclerosis: essential HTN, diabetes mellitus
-Homogenous deposition of eosinophilic hyaline material in the intima and media of small arteries and arterioles
2. Hyperplastic arteriolosclerosis: malignant HTN
-Homogenous concentric thickening of arteriolar walls ("onion skinning")

Atherosclerosis

Fibrous plaques and atheromas form in intima of arteries
-Risk factors: smoking, HTN, DM, hyperlipidemia, fam Hx
-Can lead to aneurysms (esp. abdominal aorta), ischemia, peripheral vascular disease, thrombus, or emboli
-Plaque rupture is due to collagen degradation by macrophage metalloproteinases
-Location: abdominal aorta > coronary artery > popliteal artery > carotid artery
-Sx: angina, claudication; may be asymptomatic

Pathogenesis of atherosclerosis

1. Endothelial cell injury -> recruitment of platelets and inflammatory cells as well as deposition of modified LDL in the intima
2. Inflammation recruits macrophages to scavenge LDL -> foam cells and fatty streak formation
3. Macrophages produce pro-inflammatory cytokines, PDGF, and VEGF -> recruit smooth muscle cells to repair inflamed tissue
4. SMCs proliferate in the endothelium and secrete collagen and metalloproteinases -> creation of fibrous cap
5. Eventually lesion is too large to support cell activity, causing apoptosis and necrosis -> creation of necrotic core

Aortic dissection

Longitudinal intraluminal tear forming a false lumen
-HTN is number one risk factor for development of intimal tears!!!
-Also caused by cystic medial necrosis in Marfan's syndrome
-Tearing chest pain radiating to the back
-CXR: mediastinal widening
-False lumen occupies most of the descending aorta
-May result in aortic rupture (most commonly due to MVA injury at the isthmus)

Stable/unstable angina

ST depression on ECG
1. Stable angina
-Mostly secondary to atherosclerosis
-Retrosternal chest pain with exertion
2. Unstable angina
-Thrombosis but no necrosis
-Worsening chest pain at rest or with minimal exertion

Prinzmetal's angina

Angina that occurs at REST
-Secondary to coronary artery vasospasm
-ST elevation on ECG

Coronary steal syndrome

Vasodilators (adenosine, dipyridamole) can aggravate ischemia by shunting blood from an area of critical stenosis to an area of higher perfusion

Myocardial infarction

Coronary artery occlusion: LAD>RCA>circumflex
-Loss of contractility and lactate accumulation due to myocyte necrosis begins within 60 seconds of total ischemia
-Sx: diaphoresis, nausea, vomiting, severe retrosternal pain, pain in left arm and/or jaw, shortness of breath, fatigue, adrenergic symptoms
-Hibernating myocardium: chronic but reversible loss of contractile function (there is sufficient ATP to prevent total loss of function)

Evolution of MI: first day

Risk for arrhythmia
1. 0-4 hours: no visible change
2. 4-12 hours: early coagulative necrosis, edema, wavy fibers, hemorrhage
3. 12-24 hours: coagulation necrosis, contraction bands, release of necrotic cell content into blood, beginning of neutrophil emigration

Evolution of MI: 2-4 days

Risk for arrhythmia
-Tissue surrounding infarct shows acute inflammation
-Neutrophil emigration
-Muscle shows extensive coagulative necrosis -> possible early-onset pericarditis over necrotic myocardium (sharp, pleuritic chest pain)

Evolution of MI: 5-10 days

Risk for free wall rupture, tamponade, papillary muscle rupture, interventricular septal rupture
-Macrophages phagocytose dead tissue and degrade important structural components
-Ingrowth of granulation tissue at the margins

Evolution of MI: 7 weeks

Risk for ventricular aneurysm
-Contracted scar complete

Diagnosis of MI

1. ECG: gold standard in first 6 hours
-ST elevation = transmural infarct
-ST depression = subendocardial infarct
-Pathologic Q-waves = transmural infarct
2. Cardiac troponin I: rises after 4 hours and is elevated for 7-10 days
3. CK-MB: rises at 4-6 hours, peaks at 24 hours, gradually decreases after 2-3 days
4. AST: found in cardiac, liver and skeletal muscle cells (less specific)

Transmural infarcts

-Increased necrosis
-Affects entire wall
-ST elevation on ECG
-Pathologic Q-waves

Subendocardial infarcts

-Due to ischemic necrosis of <50 of ventricle wall
-Subendocardium especially vulnerable to ischemia
-Due to fewer collaterals, higher pressure
-ST depression on ECG

ECG diagnosis of MI

Anterior wall (LAD) = V1-V4
Anterolateral (LCX) = V4-V6
Lateral wall (LCX) = I, aVL
Inferior wall (RCA) = II, III, aVF

MI complications

1. Cardiac arrhythmia
2. LV failure and pulmonary edema (CHF)
3. Cardiogenic shock
4. Ruptures
5. Aneurysm formation
6. Post-infarction fibrinous pericarditis
7. Dressler's syndrome

Myocardial ruptures

1. Ventricular free wall rupture -> cardiac tamponade
2. Papillary muscle rupture -> severe mitral regurgitation
3. Interventricular septal rupture -> ventricular septal defect (VSD)

Dressler's syndrome

Autoimmune phenomenon resulting in late-onset fibrinous pericarditis
-Occurs several weeks post-MI
-Heart cells Ags are exposed that normally aren't -> body forms Abs against tissue

Dilated cardiomyopathy

Most common cardiomyopathy (90%)
-Etiologies: alcohol abuse, wet beriberi, Coxsackie B virus myocarditis, chronic cocaine use, Chagas' disease, doxorubicin toxicity, hemochromatosis, peripartum cardiomyopathy
-Causes systolic dysfunction (volume overload) -> eccentric hypertrophy (sarcomeres in series)
-Findings: S3, dilated heart on U/S, balloon appearance on CXR

Hypertrophic cardiomyopathy

1. Etiology
-Cause of sudden death in young athletes
-50% of cases are familial, AD mutations in cardiac sarcomere proteins
-Associated with Friedreich's ataxia
2. Pathogenesis
-Hypertrophied IV septum is too close to mitral valve leaflet -> outflow tract obstruction (worsened by standing, Valsalva -> dec. venous return)
-Diastolic dysfunction (pressure overload) -> concentric hypertrophy (sarcomeres in parallel)
3. Findings
-Disoriented, tangled, hypertrophied myocardial fibers
-Normal sized heart, S4, apical impulses, systolic murmur, syncopal episodes

Restrictive cardiomyopathy

Thickening/stiffening of the ventricular myocardium
1. Causes:
-Idiopathic
-Amyloidosis, sarcoidosis, hemochromatosis (deposition in myocardial tissue)
-Radiation exposure
-Endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young kids)
-Loffler's syndrome (endomyocardial fibrosis w/prominent eosinophilic infiltrate)
2. Complications
-Inc. risk for ventricular arrhythmias
-Diastolic dysfunction (pressure overload)

Congestive heart failure (CHF)

1. Left heart failure
-Pulmonary edema, paroxysmal nocturnal dyspnea (pulmonary venous distention, hemosiderin-laden macrophages)
-Orthopnea (inc. venous return exacerbates pulmonary venous congestion)
2. Right heart failure
-Nutmeg liver (inc. central venous pressure -> inc. resistance to portal vein flow)
-Ankle, sacral edema (inc. venous pressure -> fluid transudation)
-JVD (inc. venous pressure)

Findings of bacterial endocarditis

"Bacteria FROM JANE":
-Fever (most common)
-Roth's spots (round white spots on retina surrounded by hemorrhage)
-Osler's nodes (PAINFUL raised lesions on finger or toe pads)
-Murmur (valvular damage)
-Janeway lesions (PAINLESS erythematous lesions on palms or soles due to microemboli)
-Anemia
-Nail-bed hemorrhage (splinter hemorrhages)
-Emboli

Acute bacterial endocarditis

Due to S. aureus (high virulence), S. epidermidis (prosthetic valves), S. bovis (colon cancer)
-Large vegetations on previously normal valves
-Rapid onset

Subacute bacterial endocarditis

Due to viridans Streptococci (low virulence)
-Smaller vegetations on congenitally abnormal or diseased valves
-Sequela of dental procedures
-More insidious onset

Tricuspid valve endocarditis

S. aureus, Pseudomonas, Candida
-Associated with IV drug users ("don't tri drugs")

Marantic (thrombotic) endocarditis

Nonbacterial causes secondary to malignancy or hypercoagulable state

Libman-Sacks endocarditis

Manifestation of SLE
-Sterile immune complexes deposit on the valves
-Most often benign
-Can be associated with mitral regurgitation and less commonly with mitral stenosis
-SLE may cause an acute coronary syndrome at a young age even with normal coronary arteries

Rheumatic heart disease

Consequence of S. pyogenes pharyngeal infx
1. Pathophysiology
-Antibody-mediated (type II) hypersensitivity against bacterial M protein (NOT direct effect of the bacteria)
-Due to molecular mimicry between bacterial cells and human cardiac, CNS, & cutaneous tissue
2. Findings
-Aschoff bodies (granuloma w/giant cells), Anitschkow's cells (activated histiocytes), elevated ASO titers
-Late sequelae: mitral prolapse/regurgitation (early) -> mitral stenosis (late)

Rheumatic heart disease findings

FEVERSS:
-Fever
-Erythema marginatum
-Valvular damage (vegetation, fibrosis)
-ESR increases
-Red-hot joints (migratory polyarthritis)
-Subcutaneous nodules
-Syndenham's chorea

Pericarditis

1. Acute pericarditis: acute inflammation of the visceral and parietal pericardium
-Causes: idiopathic, Coxsackie infx, trauma, uremia, MI, rheumatoid arthritis, SLE
-Findings: chest pain that increases with inspiration and is relieved by sitting up, pericardial friction rub
-Inflammation creates fibrinous exudate -> pericardium becomes dull, opaque, and "sandy"
2. Constrictive pericarditis
-Cause: tuberculosis, radiation therapy, or previous open heart surgery
-Findings: Kussmaul's sign, JVD, pericardial knock (heart beats against calcified pericardium)

Cardiac tamponade

Compression of heart by fluid in pericardium -> dec. CO, equilibration of diastolic pressures in all 4 chambers
-Due to serious viral pericarditis or acute pericardial effusion
-Findings: hypotension, inc. CVP (JVD is present), distant heart sounds, tachycardia
-Pulsus paradoxus (Kussmaul's sign): exaggerated dec. in amplitude of pulse during inspiration (IV septum pushes against LV -> impaired filling); absent Korotkoff sounds on inspiration

Syphilitic heart disease

Tertiary syphilis obliterates the vasa vasorum of the aorta -> dilation of the aorta and valve ring (mediastinal widening)
-May result in aneurysm of the ascending aorta or aortic arch and aortic valve incompetence
-May see calcification of the aortic root and ascending aortic arch ("tree bark" appearance)

Cardiac tumors

1. Cardiac myxomas
-90% are atrial myxomas -> impairment of ventricular filling
-Findings: diastolic murmur that varies with the patient's position, Kussmaul's sign
2. Rhabdomyomas: tuberous sclerosis

Marfan's syndrome

AD mutation in fibrillin-1 gene -> defective CT in skeleton, heart, and eyes
1. Findings:
-Tall w/long extremities
-Pectus excavatum
-Hyperextensive joints
-Long tapering fingers and toes
-Scoliosis/kyphosis
2. Complications
-Cystic medial necrosis of aorta -> dissecting aortic aneurysms (most common cause of death)
-Floppy mitral valve -> mitral valve prolapse

Varicose veins

Dilated, tortuous superficial veins due to chronically inc. venous pressure
-Most commonly caused by incompetent venous valves
-Predisposes to poor wound healing, varicose ulcers, and stasis dermatitis

Raynaud's disease

Dec. blood flow to the skin due to arteriolar vasospasm in response to cold temperature or emotional stress
-Primary: Raynaud's disease
-Secondary: Raynaud's phenomenon (mixed CT disorders, SLE, CREST syndrome)
-Rx: avoid cold exposure, Ca-channel blockers

Wegener's granulomatosis

Small vessel vasculitis; C-ANCA associated (PR3 proteinase)
1. Triad:
-Focal necrotizing vasculitis
-Necrotizing granulomas in the lung and upper airway
-Necrotizing RPGN
2. Sx: hemoptysis, hematuria, nasal ulcers, chronic sinusitis, otitis media, mastoiditis, cough, dyspnea
-Findings: large nodular densities on CXR, hematuria w/red cell casts
3. Tx: cyclophosphamide and corticosteroids

Microscopic polyangiitis

Small vessel vasculitis; P-ANCA associated (myeloperoxidase)
1. Major clinical manifestation: RPGN
-Pulmonary involvement: pulmonary capillaritis, diffuse alveolar hemorrhage -> dyspnea, cough, pleuritic pain, hemoptysis
2. Differences from polyarteritis nodosa
-Lesions are of the same age
-Affects small caliber vessels
-Involves the lung
-P-ANCA positivity

Churg-Strauss syndrome

Small vessel vasculitis; P-ANCA associated (myeloperoxidase)
1. Classic triad:
-Asthma, allergic rhinitis, nasal polyps
-Peripheral eosinophilia
-Vasculitis
2. Sx: mononeuritis multiplex (e.g. wrist-foot drop), myocardial eosinophilic infiltrates, palpable purpura
3. Tx: corticosteroids, cyclophosphamide

Henoch-Schonlein purpura

Small vessel vasculitis; immune complex-mediated
-Most common form of childhood systemic vasculitis (<10 y.o.); often preceded by URI
-Necrotizing lesions (of the same age) w/IgA & C3 deposition in capillaries and venules
-Palpable purpura on arms, legs, and buttocks
-Sx: arthralgias, intestinal hemorrhage, abdominal pain, melena, renal involvement (IgA nephropathy)
-Tx: steroids (renal involvement)

Buerger's disease (thromboangiitis obliterans)

Medium vessel vasculitis
-Occurs in young, heavily-smoking males
-Hypersensitivity to tobacco extracts -> segmental vasculitis that extends into contiguous nerves and veins
-Sx: intermittent claudication in hand/foot/calf, cold sensitivity (Raynaud's phenomenon), severe distal pain at rest
-Complications: limb ischemia, ulceration/gangrene of toes/feet/fingers
-Tx: stop smoking!

Kawasaki's disease

Medium vessel vasculitis
-Children < 4 y.o.; associated with Asian ethnicity
-T-cell mediated hypersensitivity -> endothelial cell auto-Ab formation -> acute, self-limiting vasculitis
-Sx: persistently high fever, conjunctivitis, strawberry tongue, lymphadenitis, desquamative rash
-Inc. risk of coronary artery ectasia and aneurysms
-Tx: aspirin, IVIG

Polyarteritis nodosa

Medium vessel vasculitis
-Middle-aged individuals
-Transmural inflammation of arterial wall w/fibrinoid necrosis
-Affects the heart, kidneys, GI tract, and liver; spares the lungs (vs. microscopic polyangiitis)
-30% of cases are associated with HBV infection
-Lesions are of different ages (vs. microscopic polyangiitis)
-Sx: constitutional, cutaneous nodules, mononeuritis multiplex, hematuria (if kidneys involved)
-Tx: corticosteroids, cyclophosphamide

Takayasu's arteritis

Large vessel vasculitis ("pulseless disease")
-Young Asian women <50 y.o.
-Granulomatous thickening of subclavian arteries -> diminished peripheral pulses
-Sx: Fever, Arthritis, Night sweats, MYalgia, SKIN nodules, Ocular disturbances, Weak pulses in upper extremities ("FAN MY SKIN On Wednesday")
-Dx: giant cells, inflammation across all 3 arterial layers, inc. ESR
-Tx: steroids, cytotoxic agents

Temporal (giant cell) arteritis

Large vessel vasculitis (most common)
-Older individuals
-Granulomatous inflammation of the media of extracranial arteries (temporal, ophthalmic)
-Sx: headache, jaw claudication, polymyalgia rheumatica (shoulder or hip pain/stiffness)
-Involvement of ophthalmic artery -> blindness
-Dx: temporal artery biopsy, giant cells, inc. ESR
-Tx: high-dose steroids

Sturge-Weber disease

Congenital vascular malformation disorder that affects capillary-sized blood vessels
-Mech: proliferation of brain arteries -> angiomas -> AV malformations
-Sx: port-wine stains on face, ipsilateral leptomeningeal angiomatosis (intracerebral AVMs), seizures, early-onset glaucoma

Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)

Inherited blood vessel disorder
-Telangiectasias
-Recurrent epistaxis
-Skin discoloration
-Arterio-venous malformations (AVMs)

Vascular tumors

1. Strawberry hemangioma (children): initially grows with child, then spontaneously regresses
2. Cherry hemangioma (elderly): does NOT regress
3. Pyogenic granuloma: can ulcerate and bleed, associated with trauma and pregnancy
4. Cystic hygroma: Turner's syndrome
5. Glomus tumor: painful red-blue tumor of smooth muscle cells under fingernails (participate in temperature regulation)
6. Bacillary angiomatosis: capillary skin papules in AIDS patients, caused by Bartonella henselae infx
7. Liver angiosarcoma: associated with vinyl chloride, arsenic, and Thorotrast exposure
8. Lymphangiosarcoma: associated with persistent lymphedema post-mastectomy

Mitral regurgitation

Holosystolic, high-pitched "blowing murmur"
-Loudest at apex, radiates toward axilla, LV S3 gallop
-Enhanced by maneuvers that increase TPR (squatting, hand grip) or LA return (expiration)
-Due to ischemic heart disease, mitral valve prolapse, LV dilation, rheumatic fever
-Hemodynamics: increased V-wave

Tricuspid regurgitation

Holosystolic, high-pitched "blowing murmur"
-Loudest at tricuspid area, radiates to right sternal border
-Enhanced by maneuvers that increase RA return (inspiration)
-Due to RV dilation, endocarditis (IV drug users), rheumatic fever

Ventricular septal defect

Holosystolic, harsh-sounding murmur
-Loudest at tricuspid area, accentuated by hand grip

Aortic stenosis

Crescendo-decrescendo systolic ejection murmur following ejection click (abrupt halting of valve leaflets)
-LV pressure>aortic pressure during systole, radiates to carotids/apex
-Pulses weak compared to heart sounds
-Can lead to syncope
-Chronic AS: acute AFib can cause systemic hypotension and acute pulmonary edema
-Often due to age-related calcification of aortic valve or bicuspid aortic valve

Mitral valve prolapse

Late systolic crescendo murmur with midsystolic click (sudden tensing of chordae tendineae)
-Loudest at S2, usually benign
-May predispose to infective endocarditis
-Caused by myxomatous degeneration, rheumatic fever, or chordae rupture
-Enhanced by maneuvers that increase TPR (squatting, hand grip)

Aortic regurgitation

Immediate high-pitched "blowing" diastolic murmur
-Widened pulse pressure if chronic
-Bounding pulses and head bobbing
-Often due to aortic root dilation, bicuspid aortic valve, or rheumatic fever
-Vasodilators decrease the intensity of the murmur

Mitral stenosis

Delayed rumbling late diastolic murmur following opening snap (tensing of chordae tendineae)
-LA>>LV pressure during diastole
-Often occurs secondary to rheumatic fever
-Chronic MS -> LA dilation
-Severity of disease determined by S2-to-opening snap time interval: tensing of leaflets occurs earlier as the disease becomes more severe
-Enhanced by maneuvers that increase LA return (expiration)

Wolff-Parkinson-White syndrome

Ventricular pre-excitation syndrome
-Accessory conduction pathway from atria to ventricle (Bundle of Kent) bypasses the AV node -> ventricles begin to partially depolarize earlier
-ECG: delta wave, shortened PR interval, widened QRS complex
-May cause re-entry current -> supraventricular tachycardia

Atrial fibrillation

Chaotic and erratic baseline (irregularly irregular rhythm) with no discrete P waves in between irregularly spaced QRS complexes
-Triggered by alcohol binge drinking, increased sympathetic tone, or pericarditis
-Can cause atrial stasis -> embolic stroke
-Tx: beta-blocker or Ca-channel blocker
-Prophylaxis against thromboembolism: warfarin

Atrial flutter

Rapid succession of identical, back-to-back atrial depolarization waves
-"Saw-tooth" appearance of flutter waves
-Attempt to convert to sinus rhythm
-Tx: class IA, IC, III anti-arrhythmics

Torsades de pointes

Ventricular tachycardia characterized by shifting sinusoidal waveforms on ECG
-Can progress to VFib
-Anything that prolongs the QT interval can predispose to TdP

Congenital long QT syndromes

1. Jervell Lange-Nielsen syndrome: long QT + severe congenital sensorineural deafness
2. Roman-Ward syndrome: long QT w/o deafness

Ventricular fibrillation

Completely erratic rhythm with no identifiable waves
-Fatal arrhythmia without immediate CPR and defibrillation

1st degree AV block

PR interval is prolonged, asymptomatic

2nd degree AV block: Mobitz Type I (Wenckebach)

Progressive PR interval delay, then dropped beats

2nd degree AV block: Mobitz Type II

Dropped beats that aren't preceded by change in PR interval

3rd degree AV block

Atria and ventricles beat independently of each other (P waves have no relation to QRS complexes)
-May be caused by Lyme disease

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