Section 1
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Chronic ischemic heart disease
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Mar 1, 2020
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Section 1
(50 cards)
Chronic ischemic heart disease
Heart failure in MI patients 1. hypertrophic and dilated heart 2. scars from previous infarcts 3. fibrous thickening of endocardium 4. Myocytolysis → vacuolization of subendocardium
1-3 Days after MI
Yellow/ tan center neutrophillia risk of pericarditis
Reperfusion injury
Myocyte hypercontractility → elevated Calcium Lots of free radicals Contraction band necrosis (hypereosinophilia)
Clinical presentation of MI
crushing upper left limb and chest pain dyspnea weak, rapid pulse diaphoresis
Myocardial rupture after MI
Heart is weakened 3-7 after MI free wall rupture → cardiac tamponade septal rupture → VSD
2 weeks after MI
Granulation tissue neovascularization
Other causes of ischemic heart disease besides artherosclerosis
1. Anemia 2. Shock 3. Hypertrophy 4. Vasculitis 5. Aortic dissection
Rheumatic fever
Type 2 hypersensitivity to M protein of Strep bacteria strep infection is absent elevated ASO titers, Anti DNAase titers and ESR
Changes in right heart failure
liver congestion jugular veinous distention splenic enlargement edema
Occlusion of left circumflex coronary artery
lateral LV wall
1 Day after MI
Coagulative necrosis and wavy fibers
Aortic stenosis clinical presentation
Less blood systemically - angina - syncope - congestive heart failure ejection systolic murmur → radiates to neck during S1
Causes of Mitral regurgitation
prolapse rheumatic fever endocarditis dilated cardiomyopathy myocarditis
Stable angina
gets worse with stress/ physical activity 75% of coronary artery is stenosed crushing chest pain due to adenosine and bradykinin → reversible cell injury
Cardiac enzymes of MI
troponins (I&T) - rise in 12 hours drop after 2 weeks CK-MB - rise in 12 hours and drop after 4 days (reinfarction)
Ischemic complications of MI
more infraction reinfarction angina of previously healthy muscle
Systemic hypertensive heart disease
LV hypertrophy → heart failure hypertension causes up regulation of actin and myocin in cardiomyocytes → hypertrophy (not hyperplasia)
Ventricular aneurism after MI
large transmural infarcted tissue heals fully bulges during systole leads to 1. arrythmia 2. mural thrombus
Concentric hypertrophy of heart
caused by aortic stenosis/ hypertension → pressure overload 1. sarcomeres added in parallel 2. Wall gets thicker 3. Lumen gets smaller
2 months after MI
granulaton tissue replaced with dense collagenous scar remaining muscle is hypertrophied
Systolic dysfunction of heart vs systolic dysfunction of heart
Heart cannot contract properly vs heart cannot relax and fill
Precipitation of MI
90% → acute thrombosis: collaterals cannot open 10% time - vasospasm - mural thrombus emboli - congenital vascular disease - hypercoagulable state
High output vs low output heart failure
high output = increased tissue demands low output = heart doesn't pump enough blood
Clinical presentation of mitral stenosis
dyspnea due to congestion of pulmonary vessels Low pitched diastolic murmur crepations in lung
Risk factors for MI
Men before 80, afterwards it levels out - smoking - hyperlipidemia - hypertension - smoking - diabetes
MI contractile dysfunction
progressive heart failure → 20-30% necrosis cardiogenic shock → 40% necrosis
Changes in left heart failure
Left ventricle hypertrophy/ dilation lack of perfused tissues - hypoxic encephalopathy - tubular necrosis brown induration of lungs - macrophages filled with hemosiderin (heart failure cells)
Arrythmia caused by MI
Conduction disturbance electrolyte imbalance Ischemia → sudden cardiac death
Aortic regurgitation clinical presentation
bounding pulse early diastolic murmur laterally displaced apex beat → LV hypertrophy
Acute plaque changes (Unstable plaque)
plaque cannot stand mechanical forces - exposed core (collagen + lipids) - thrombus formation incomplete occlusion → angina complete occlusion → MI
Chronic cor pulmonale
a chronic respiratory illness leads to narrow and distorted pulmonary vessels increased right heart burder → dilation and hypertrophy
Changes in acute rheumatic fever
Myocardium - achoff bodies (t-cells and plasma cells) with anitschkow macrophages Endocardium - thick valves - focal fibrinoid necrosis at tip of valves Pericarditis Artheritis Erythmea Skin nodes
Subendocardial MI
inner 1/3 of heart ST depression prolonged hypertension artherosclerosis → less serious
MI and papillary muscle dysfunction
ruptures after MI valvular incompetence 1. Mitral 2. Tricuspid
Post MI pericarditis
neutrophils attack → 2-3 days post MI dresslers syndrome → autoimmune reaction to pericardium 14 days after MI
Acute cor pulmonale
pulmonary embolism causes immediate right heart failure heart is dilated but no hypertrophy
Occlusion of left anterior descending coronary artery
infarct of anterior LV and septa
Causes of mitral stenosis
Rheumatic fever
Mural thrombus
complication of MI systemic embolistation - stroke - kidneys - mesentry
Eccentric hypertrophy of heart
Aortic regurgitation → volume overload 1. sarcomeres added in series 2. heart dilates
Causes of aortic regurgitation
rheumatic fever degenerative aortic dilation syphillic aneurism marfan syndrome
Unstable angina
episodes get worse and worse plaque gets distupted → precursor to MI
Transmural MI
all layers of the heart ST elevation due to acute plaque changes and cocaine use
7-10 Days after MI
macrophages break down necrotic tissue hyperemic boarder greatest risk of rupture
Causes of aortic stenosis
rheumatic fever calcific aortic stenosis
Causes of acute vasoconstriction that lead to plaque rupture
1. Thromboxane (from platelets) 2. Endothelial dysfunction → balance of Nitric Oxide and Endothelin 3. elevated sympathetic tone 4. smoking
Occlusion of right coronary artery
posterior LV wall and septa
Prinzmental angina
happens randomly due to vasospasm Elevated ST → Transmural ischemia
Left vs right sided heart failure
Pulmonary vs systemic symptoms
Clinical presentation of mitral regurgitation
dyspnea palpitations pansystolic murmur → radiates to axilla
Section 2
(50 cards)
Hypertrophic cardiomyopathy
always genetic Beta myosin heavy chain Myosin binding protein C Cardiac troponin T
Complications of mitral prolapse
mitral regurgitation infective endocarditis arrythmia thromboemboli
Ventricular septal defect
trisomy 13, 18, 21 close after 1-2 years can lead to - pulmonary hypertension - congestive heart failure pansystolic murmur due to L→R shunting
Causes of autoimmune myocarditis
Lupus polymyositis Drugs→ Methyl dopa, sulfonamides eosinophilic infiltrate
causes of restrictive cardiomyopathy
1. endomyocardial fibrosis → whole heart, africa and tropics 2. Loaefllers endomyocarditis → fibrosis + mural thrombi (caused by major basic protein from eosinophils) 3. radiation amyloidosis 5. hemochromatosis
Clinical presentation of Myocarditis
acute MI-like chest pain children and young adults diagnose with PCR or serology
Risk factors for dilated cardiomyopathy
alcohol → cytotoxic myocarditis → coxakie virus Thiamine deficiency chronic anemia Chemotherapy
Eisenmenger complex
reversal of shunt to R→L in VSD 1. pulmonary hypertension 2. right ventrical hypertrophy 3. pRV > pLV
Subacute endocarditis
changing murmur weight loss splenomegaly
Morphology of subacute endocarditis
less friable no ring abscess granulation tissue calcification
Transposition of great arteries
aorta and pulmonary vessels are swapped kept working via shunts cyanosis
Truncus arteriosis
pulmonary vessels and aorta don't seperate during embryogenesis cyanotic
Changes in dilated cardiomyopathy
all chambers dilated equally mural thrombosis → stasis large myocytes with large nuclei interstitial fibrosis
causative organisms of native valve endocarditis
S. viridans S. aureus → IV drug users S. bovis → colon cancer HACEK
Teratology of fallot
1. pulmonary stenosis → degree of symptoms 2. ventricular septal defect 3. overriding aorta 4. right ventricular hypertrophy
Morphology of Hypertrophic cardiomyopathy
thick walls and no dilation narrow lumen scarring myocyte dissaray
Clinical presentation of acute rheumatic fever
A - artheritis C - carditis C - chorea N - skin nodes E - erythema
Pulmonary vasularity
pleothoric → wide blood vessels (left→right shunt) Oligemic → narrow blood vessels (right → left shunt)
Complications of Patent ductus arteriosis
Pulmonary hypertension cyanosis of lower limb → only branches of descending aorta
Libman sachs endocarditis
lupus endocarditis anywhere on any valve can cause ischemia in coronary arteries
Dilated cardiomyopathy
usually idiopathic genetic mutations 1. cytoskeletal proteins 2. X-linked dystrophin gene 3. proteins of oxidative phosphorylation
Morphology of acute endocarditis
large friable vegetations ring abscess → infiltrate myocardium rupture of valve, chordae tendinae or leaflets
Giant cell myocarditis
caused by lupus and thyrotoxicosis adults 30-50 causes CHF and arrythmia
Viral myocarditis
coxackie virus is directly cytotoxic cell mediated immune reaction CD8+ T cells dilated flabby heart patchy and pale with mottling → small areas of stasis and fibrosis
Parasitic myocarditis
trichinosis → most common chagas disease (trypnosoma cruzi) → endemic to south america Toxoplasmosis → immune compromised from cats
Patent ductus arteriosis
more common in females associated with rubella machine-like murmur close with indomethacin keep open with prostaglandin
fungal myocarditis
immunocompromised mixed inflammation PMNs Macrophages Plasma Cells
Clinical presentation of restrictive cardiomyopathy
diastolic dysfunction → exertional dyspnea → fatigue → chest pains
Tricuspid atresia
tricuspid valve is occluded Hypoplastic RV Needs ASD and VSD to be kept open cynotic from birth
Complications of calcific aortic stenosis
angina → LV hypertrophy syncope → poor brain perfusion death due to CHF and arrhythmia
Clinical presentation of hypertrophic cardiomyopathy
Exertional dyspnea myocardial infaction harsh ejection systolic murmur healthy young person → sudden cardiac death
Clinical presentation of tetralogy of fallow
present at 6 months dyspnea cyanosis → elevated EPO → polycythemia (thrombosis) squatting infective endocarditis associated with down syndrome
Non-bacterial thrombotic endocarditis
cancer patients in hyper coagulable state small fibrinous nodules along line of closure thrombus that isn't attached well
Mitral prolapse
woman 20-40 (marfans syndrome) softened mitral valve cusps balloons into atrium during systole → mid-systolic click thinning fibrosa of valve myxamateous degeneration → excess loose basophillic ground substance
Total anomalous pulmonary venous connections
pulmonary veins drain into coronary sinus ASD helps shunt blood
Chronic rheumatic fever
irregular fibrous thickening of mitral and/ or aortic valve leaflet calcification fusion of commisures of mitral valve → fish mouth appearance
causative organisms of prosthetic valve endocarditis
early (2 months) → staph epidermidis later → normal agents
Clinical presentation of dilated cardiomyopathy
ineffective contraction → 25% ejection fraction heart failure → needs transplant
Clinical presentation of rheumatic heart disease
1. valvulitis 2. heart hypertrophy 3. CHF 4. Arrhythmia 5. Endocarditis
Restrictive cardiomyopathy
Systolic and distolic dysfunction still walls that cant pump properly
Bio prosthetic valve complications
- perforation - calcification → stenosis - infective endocarditis - leaky valve
Morphological changes in restrictive cardiomyopathy
cavities are not dilated thick and hard yocardium variable patchy fibrosis
Acute endocarditis
fever new murmur septicemia
Complications of mechanical heart valves
thromboembolism need life long anticoagulation endocarditis hemolysis paravalvular leaks
Peripartum dilated cardimyopathy
happens during late pregnancy and labour mural thrombosis hypertrophic myocytes with large nuclei and interstitial fibrosis caused by - volume overload - Hypertension - nutritional disturbances
Risk factors of infective endocarditis
pre-existing heart disease prosthetic valve IV drug use Bacteremia
Arrhythmogenic Right ventricular cardiomyopathy
autosomal dominant defect in desmosomal adhesion proteins associated with Naxos syndrome → hyperkeratosis of palms and soles dilated thin right ventricle → right sided heart failure and arrythmia heart tissue is replaced with fat and fibrosis
Atrial septal defect
usually diagnosed in adults increased pulmonary vasularity 1. pulmonary hypertension 2. paradoxycal embolism → stoke from DVT
Calcific aortic stenosis
old age wear and tear of aortic valve - previous rheumatic fever/ bicuspid valve rigid and calcified valves on both sides left ventricle hypertrophy
Complications of endocarditis
1. bacteremia 2. heart tissue destruction 3. embolisation 4. Bacterial antigen-antibody immune complex → rothspot →Janeway lesions
Section 3
(50 cards)
Diagnosis of wegeners granulomatosis
c-anca bilateral nodes in lungs with cavitary lesions sinusitis renal failure
P-ANCA
- microscopic polyarteritis - churg-strauss
complications of hypertension
artherosclerosis LV hypertrophy MI nephrosclerosis retinopathy CNS → infarct or hemorrhage
Fibrinopurulent pericarditis
from bacterial pericarditis → neutrophilia
Pathogenesis of secondary hypertension
elevated blood volume → Na retention due to elevated RAAS and ADH Pheochromocytoma → elevated sympathetic tone
Types of secondary hypertension
1. Renal disease → elevate RAAS 2. Endocrine 3. Vascular → aortic regurgitation, narrowed blood vessels 4. Neurogenic → elevated intercranial pressure
Morphology of kawasaki's disease
from mild changes to intima only → segmental necrosis in all layers acute change→ coronary artery aneurism
Fibrinous pericarditis
bread and butter appearance → irregular and shaggy causes - uremia - rheumatic fever - MI - Virus
Microscopic polyarteritis hypersensitivity
all small vessels → arterioles, capillaries, small veinules segmental fibrinoid necrosis and focal transmural lesions due to strep infection or penecillin allergy (not immune complex mediated)
Clinical presentation of Polyarteritis nodosa
1. Kidney → no hematuria 2. Heart 3. Liver 4. GIT
Primary vs secondary hypertension
Primary → idiopathic (shitty lifestyle) Secondary → organ/ endocrine dysfunction
Cardiac tamponade
1. weak pulse 2. jugular veinous distention 3. Muffled heart sounds
Hyaline arterosclerosis
proteins leak into vessel walls due to hypertension appear pink and glassy loss of structural details more ECM produced
Fibrinous and hemorrhagic pericarditis
from malignancy
Clinical presentation of acute pericarditis
atypical chest pain → worse when lead back, better when lean forward high pithed friction rub chronic fibrosis → constrictive pericarditis cardiac tamponade
Most common presentations of atherosclerosis
coronary heart disease → MI, CHF, angina Abdominal aorta aneurism Cerebral vascular disease → stroke, TIA Peripheral vascular disease → claudication, gangrene
Wegeners granulomatosis
40 year old man 1. Upper and lower RT granulomas 2. Small and medium vessel granuloma 3. focal renal necrosis → hematuria
Morphology of wegeners granulomatosis
ulcerative lesions → nose, pharynx palate lung → diffuse nodular focal necrosis with cavities granulomas with giant cells → undergo fibrosis
Role of lipids in artherosclerosis
cytotoxic to endothelial cells → free radical injury oxidized lipids are ingested by macrophages and make the macrophages immobile
Postductal coarctation of Aorta
Bounding upper limb pulse weak lower limb pulse rip notching → engorged intercostal anteries due to collaterals Intermittent claudation → ischemic exercise pain in lower limb
Mechanism of atherosclerosis
Cause of injury Branch points Hypercholestremia Endothelial injury → endothelial activation - increased permeability - adhesion molecules expressed - leukocyte adhesion
Role of macrophages in artherosclerosis
foam cells engulf oxidized lipids → release free radicals acute inflammation → Il-1, TNF-A smooth muscle proliferation → convert fatty streak to fibrofatty atheroma
Kawasaki's disease
effects all artery size → often coronary young children → especially japn autoantibodies to endothelial cells
Takayasu arteritis
effects large vessels woman younger than 40 blindness neurological defects no palpable pulse
C-ANCA
wegener granulomatosis
Types of pericardial effusion
1. serous → Fluid - CHF - Hypoalbuminemia (low oncotic pressure) 2. serosanguinous - BV rupture from trauma or malignancy 3. chylous - blocked thoracic lymphatic duct - buildup of fat 4. Hemopericardium - aortic dissection - MI - trauma
Coarctation of Aorta
narrowed aorta associated with - turner's syndrome - bicuspid aorta - VSD - PDA - ASD
Appearance of polyarteritis nodosa
string-of-pearls acute → transmural inflammation, fibrinoid necrosis of inner half of vessel wall chronic → inflammation replaced by fibrosis
Artherosclerotic plaque
extracellular and intracellular lipids fibrosis smooth muscle proliferation thickened intima thinned out media neovascularizations
Giant cell temporal arteritis
large artery vasculitis head → temporal, vertebral, opthalmic seen in 50 years +
Morphology of artherosclerosis
fatty dots → isolated foam cells fatty streaks → foam cells and extracellular lipids (everyone has them)
Appearance of giant cell temporal arteritis
focal nodular thickening granuloma in intima and inner media giant cells fragmented internal elastic lamina neutrophils in adventitia
Clinical presentation of microscopic polyarteritis
p-anca - hemoptysis - hematuria - melena - purpura
Polyarteritis nodosa
young adults exposed to Hep b effects small and medium vessels everywhere leads to weakened arterial walls and narrowed lumen
Clinical appearance of Kawasaki's disease
high fever for 5 days cervical lymphadenopathy conjunctival/ oral rash edema of hand/ feet desquamifying skin rash
Morphology of takayasu arteritis
irregular thickening narrow lumen granulomatous patchy necrosis of media collagenous fibrosis
Buerger's disease
young male vasculitis cigarette smoke → cytopathic reynauld's phenomenon pain that doesn't improve with rest segmental microlesions → neutrophils
Malignant hypertension
BP 210/120 necrotizing arteriolitis organ failure
Unstable plaque
thinned out fibrous caps more free radicals shoulder is more susceptible can be made loose by hemorrhage of neovascularization
Causes of Pericarditis
MI Uremia → toxic to heart (from kidney failure) rheumatic fever lupus → focal inflammation
Monkenberg arteriorsclerosis
asymptomatic calcification after the age of 50
Appearance of cardiac myxoma
red fleshy pedunculated mass attached by very small stalk multinuclead stellate cells suspended in a loose ground substance → mucopolysaccharide rich strom
Risk factors for Ateriosclerosis
Hyperlipidemia → with other diseases, very early and severe Hypertension → dose response curve Cigarette smoke Diabetes → elevated cholesterol (bad fat metabolism) Plasma homocysteine Lipoprotein A → altered LDL, not caused by hyperlipidemia
Preductal coarctation of the aorta
R → L shunt - lower limb cyanosis → reversal of PDA - congestive heart failure - weak femoral pulse
Tumors that metastasize to the heart
melanoma lung lymphoma breast cancer
Hyperplastic arteriosclerosis
due to acute severe hypertension concentric laminated thickening of ateriolar walls necrotizing arteriolitis → malignant hypertension
Cardiac myxoma
benign primary tumor females 30-60 usually left atrium → calcify (seen on x-ray) can embolize or block AV valve
Lesions of artherosclerosis
1. Calcification 2. Rupture → thrombus or cholesterol embolism 3. hemorrhage → ruptured new vessels 4. aneurism → thinned out vessel walls
Diagnosis of Temporal giant cell arteritis
elevated ESR patchy lesions in temporal artery → elastic trichrome associated with polymyalgia rheumatica → giant cell artheritis in woman over 50 (shoulder)
Caseous pericarditis
TB
Section 4
(13 cards)