Cardiac Pathology I&II - Zaloga Flashcards
1
Q
intercalated discs
A
-gap junctions that join cardiomyocytes forming a syncytium for communication b/w cells
2
Q
conduction system
A
- myocytes used to conduct electrical impulses
- maintain rhythm and rate –> arrythmia if altered
3
Q
blood supply of the heart
A
- myocardium vulnerable to ischemia –> needs constant O2 supply (metabolically active)
- blood flows through coronary arteries during DIASTOLE
4
Q
cardiac pathophysiology
A
- pump failure - inadequate CO
- flow obstruction - lesions obstructing flow or or preventing valve opening
- regurge - overloads affected atria or ventricles
- shunted flow - cardiovascular defects b/w blood vessels (ex. PDA)
- cardiac conduction disorders - inefficient myocardial contractions
- rupture of heart or major vessels
5
Q
heart failure aka CHF
A
- progressive, poor prognosis**
- unable to provide adequate perfusion to tissues due to decreased CO (forward failure)
- low CO –> increase venous pool congestion (backward failure)
- changes in workload (pressure/volume overload)–> ventricular remodeling –> thin wall, dilated, hypertrophy (variable)
- overstretch heart –> less actin/myosin overlap –> decrease contraction*
- systolic dysfunction –> decreased ejection fraction
- no chamber expansion with stiff ventricle –> diastolic dysfunction (decreased filling)
- hypertrophic myocytes –> enlarged “boxcar” nuclei and associated with interstitial fibrosis
6
Q
what is an independent risk factor for sudden death?
A
- cardiomegaly**
- can predispose you to cardiac dysrhythmias
7
Q
how does cardiac hypertrophy progress to heart failure?
A
- pressure-overload hypertrophy –> sarcomeres assebled in parallel
- volume-overload hypertrophy –> sarcomeres assembled in series
-increasing cardiac workload and O2 demand with hypertrophy, but NO increase in blood supply to myocytes –> ischemia –> cardiac death/failure
8
Q
left sided heart failure
A
- usually due to ischemia*, systemic HTN, or mitral/aortic valve problems
- lung problems** –> pulmonary congestion/edema
- systemic hypoperfusion –> renal and brain dysfunction
- secondary dilation of LA –> Afib and stasis of blood (thrombi)
- Afib –> exacerbate CHF and diminish renal perfusion –> + RAAS exacerbating pulmonary edema**
- hemosiderin laden macrophages (heart failure cells)**
- Kerley B lines** from lung interstitial edema
9
Q
right sided heart failure
A
- usually due to left sided heart failure* (pulmonary HTN)*
- peripheral edema and organ congestion –> affect extremities and visceral organs**
- hepatic and portal vein congestion –> congestive hepatomegaly (nutmeg liver)** and splenomegaly
- venous congestion –> pitting edema, ascites, pleural effusions
10
Q
most common congenital heart diseases
A
-VSD and ASD 50% of cases
11
Q
genetic abnormalities in congenital heart disease
A
- tuner syndrome (monosomy X)
- trisomy 21 (most common) –> down syndrome**
- VSD –> GATA4, TBX5, NKX2-5 gene mutations
- bicuspid aortic valve –> NOTCH1
- tetralogy of fallot –> JAG1 and NOTCH2
- marfan –> fibrillin mutation
- DiGeorge –> chromosome 22q11.2 deletion and TBX1 TF –> neural crest migration (heart, cleft palate, abnormal face)
12
Q
left to right shunts (most common)
A
- lead to reversal of flow (Eisenmenger syndrome)**
- elevate pressure/volume in pulmonary circulation
- ASD
- murmur present
- secundum ASD most common (primum affects AV valves and VSD)
- sinus venous defects where IVC and SVC attach - patent foramen ovale (PFO)
- close by age 2 by septum primum and secundum - VSD (most common)
- 90% membranous VSD
- higher pressure on left side - patent ductus arteriosus (PDA)
- closes 1-2 days due to declining PG2 forming ligamentum arteriosum
- continuous harsh murmur
- no cyanosis initially –> want closure to prevent reversal of flow
- can give PGE2 to keep the duct open in someone with pulmonary or systemic outflow obstruction**
13
Q
right to left shunts
A
- lead to cyanosis and hypoxemia (bypass pulmonary circulation)
- venous emboli enter systemic circulation directly
- clubbing and polycythemia
- tetralogy of fallot (most common)**
- large VSD, overriding aorta, pulmonary stenosis, RV hypertrophy**
- boot shaped heart*
- pressure on right side increases - transposition of great arteries (TGA)
- aorta from RV, pulmonary artery from LV
- deoxygenated blood into systemic circulation
- need shunt –> give PGE2 for PDA - tricuspid atresia
- complete tricuspid occlusion –> RV hypoplasia
- maintain circulation with right to left shunting
- cyanosis
14
Q
Eisenmenger syndrome
A
reversal of blood flow due to pulmonary HTN –> becomes a right to left shunt
15
Q
obstructive diseases
A
- coarctation of the aorta
- constriction of aorta around PDA
- infantile (associated with PDA) –> coarctation distal to aortic arch and proximal to PDA –> lower extremity cyanosis**
- adult (not associated with PDA) –> coarctation distal to aortic arch –> HTN in upper extremities, hypotension and weak pulses in lower extremitites** - aortic stenosis/atresia
- severe –> obstructed LV flow causes hypoplasia of LV and ascending aorta (hypoplastic left heart syndrome)
- PDA duct closure is lethal
16
Q
ischemic heart disease (IHD)
A
- myocardial ischemia (imbalance b/w supply and demand)
- can lead to CHF
- usually from atherosclerotic lesions in coronary arteries (CAD if >75% obstruction)
- may be due to chronic vascular occlusion or acute plaque change (abrupt occlusion of vessel)
can see acute coronary syndrome with downstream myocardial ischemia
- stable angina –> no plaque disruption
- unstable angina –> has plaque disruption
- MI
- sudden cardiac death (ventricular arrythmia)
17
Q
angina pectoris
A
-recurrent chest discomfort from myocardial ischemia
- stable –> brought on by exertion, relieved with rest
- unstable –> brought on by exertion or rest –> incomplete occlusion is high risk for MI
- Prinzmetal –> coronary artery spasm not related to physical activity
18
Q
MI
A
- necrosis of cardiac tissue from prolonged ischemia
- acute plaque change –> microthrombi –> tissue factor and coagulation –> complete occlusion of coronary artery
- diabetic neuropathy patients asymptomatic of chest pain, nausea, dyspnea
risk factors: age, atherosclerosis, post-menopause
19
Q
progression of ischemic necrosis after coronary artery occlusion
A
- subendocardium 1st –> myocardium –> epicardium
- transmural branches reach subendocardium last
- transmural ischemia within 6 hr.
20
Q
distribution of myocardial necrosis
A
- occlusion of epicardial vessels –> transmural infarct if untreated (usually involves LV)
- transmural infarct aka ST elevation MI (STEMI)
- subendocardial infarct aka non ST elevation MI (NSTEMI)
- LAD most commonly infarcted (anterior wall of LV near apex)
- multifocal microinfarction –> affect small transmural vessels
21
Q
myocardial ischemia
A
- stop aerobic metabolism and ATP production –> build up of metabolites and lose contractility
- disruption of sarcolemma membrane 1st sign of myocyte necrosis –> proteins leak into blood
- irreversible injury in 20-40 min.
22
Q
cardiac biomarkers in MI
A
- tropinin I and tropinin T most sensitive* (peak in 5-14 days)
- CK-MB (peak in 24 hr. and back to normal in 3 days)
all elevated in 3-12 hours
23
Q
morphologic changes in heart in acute MI
A
-4-24 hr. –> dark mottling and coagulation necrosis
-1-3 days –> yellow pallor, neutrophil infiltrate
-4-7 days –> yellow pallor, macrophage infiltrate to clean up neutrophils
1-3 weeks –> red gray infarcted borders, formation of granulation tissue
-months –> scar formation
24
Q
acute MI
A
- necrosis of cardiac myocytes
- myocardial hemorrhage with cardiac rupture
25
Q
reperfusion
A
- better salvage with early reperfusion –> restores flow and removes the infarct
- can sometimes trigger arrythmias and induce damage (Ca2+ overload, oxidative stress, activate complement)
- abnormalities may persist in stunned myocardium (prolonged failure) even though they are being perfused
26
Q
chronic ischemic heart disease
A
- acute plaque change –> coronary artery thrombosis and myocardial ischemia
- heart muscle replaced with fibrous connective tissue
- leads to progressive CHF –> cardiomegaly with LV hypertrophy
27
Q
sudden cardiac death (SCD)
A
- unexpected death from cardiac issues
- acute ischemia from CAD is common cause**
- usually due to fatal ventricular arrythmias**
- may see coronary artery atherosclerosis, previous scars, and myocyte vacuolization
28
Q
hypertensive heart diseases (HHD)
A
- increase heart demands/work load
- high pressure induce myocyte hypertrophy (“box car” nuclei) and interstitial fibrosis –> wall thickness/stiffness
1. systemic HTN –> pressure overload and LV hypertrophy with LA dilation - induce Afib or progressive CHF
2. pulmonary HTN –> pressure overload and RV hypertrophy with LA dilation - due to lung disorders (emphysema, HTN, etc.)
29
Q
major functional valvular lesions
A
- Aortic stenosis: Calcification and sclerosis from “wear and tear”
- Aortic insufficiency: Dilation of ascending aorta, often due to hypertension
- Mitral stenosis: Rheumatic heart disease
- Mitral insufficiency: Myxomatous degeneration (mitral valve prolapse)
valvular insufficiency –> volume overload
valvular stenosis –> pressure overload –> hypertrophy
30
Q
mitral valve prolapse (MVP)
A
- myxomatous degeneration of the mitral valve
- floppy leaflets that prolapse and balloon into RA
- causes: marfan syndrome or secondary to regurgitation
- mid systolic clicks murmur
- can lead to infective endocarditis, mitral insufficiency, arrythmia, SCD
- see spongiosa thickening with deposition of collagen/fibrosis
31
Q
rheumatic fever (RF) and rheumatic heart disease (RHD)
A
- inflammatory disease from host immune response to GAS pharyngitis**
- see pancarditis and polyarthritis*
- inflammatory lesions called Aschoff bodies (plasma cell lymphocyte) with Anitschkow cells (activated macs)*
- cause mitral stenosis** –> buttonhole stenosis and LA dilatation
32
Q
infective endocarditis (IE)
A
-microbial infection (usually bacterial) of heart valves or endocardium –> cause vegetations on heart valves (thrombotic debris of organisms)
- acute IE –> caused by staph aureus; infection of previously NORMAL valve**
- IV drug users
- splinter hemorrhage, janeway lesions (tender), osler nodes (nontender), roth spots**
- glomerulonephritis - subacute IE –> caused by strep viridans (low virulence); infection of once DAMAGED valve**
- increased risk with cardiac and vascular abnormalities
-prosthetic valve endocarditis caused by staph epidermidis
33
Q
cardiomyopathies
A
- intrinsic diseases of myocardium with mechanical or electrical dysfunction
- usually genetic and lead to CHF or arrythmias
- dilated cardiomyopathy (most common)–> systolic dysfunction**
- restrictive and hypertrophic cardiomyopathy –> diastolic dysfunction**
34
Q
dilated cardiomyopathy
A
- causes: myocarditis, toxins (ex. EtOH), pregnancy, Fe overload, persistent tachycardia, catecholamines, contraction band necrosis, mutations in dystrophin
- myocarditis from secondary infection of Coxsackie A and B viruses** –> immune rxn that affects myocytes
- dilation of atria and ventricles –> decreased contraction (systolic dysfunction) –> lower ejection fraction
35
Q
restrictive cardiomyopathy
A
- stiff, non-compliant myocardium from deposition of amyloid, interstitial fibrosis from radiation, or endomyocardial scarring
- apple green birefringents on Congo red stain is diagnostic for amyloidosis (accumulation of protein fibrils)*
- Loeffler endomyocarditis –> eosinophil infiltrate releasing toxic substance on subendocardium causing necrosis and scarring*
- impaired ventricular filling during diastole
36
Q
hypertrophic cardiomyopathy
A
- usually genetic; autosomal dominant mutations of B-myosin heavy chain**
- also mutations in troponin T, tropomyosin, myosin binding protein C
- caused by obstructed outflow of aortic valve –> systolic ejection murmur
- poor compliance of LV (less filling) due to thick wall –> diastolic dysfunction –> decreased SV
- also asymmetric septal hypertrophy from thickening of ventricular septum
37
Q
Arrhythmogenic right ventricular cardiomyopathy (ARVC)
A
- inherited disease of myocardium causing RV failure/tachycardia/fibrillation or sudden death
- loss of myocytes replaced with connective tissue (fibrosis) and fat
38
Q
most common cause of myocarditis**
A
- coxsackie A and B virus**
- can develop dilated cardiomyopathy
39
Q
pericardial diseases
A
-cause fluid accumulation, inflammation, fibrous constriction
- pericardial effusion - accumulate fluid in parietal pericardium either slowly or suddenly (hemopericardium)
- fatal cardiac tamponade with sudden effusion - acute pericarditis
- serous pericarditis –> noninfectious inflammatory disease; rare fibrous adhesions
- fibrinous and serofibrinous –> serous fluid with fibrinous exudate (more intense inflammation with serofibrinous) - purulent or suppurative pericarditis
- active infection from lobar pneumonia or blood –> acute inflammatory rxn
- cloudy fluid with pus
- have scarring and fibrosis that limits diastole –> constrictive pericarditis (restrictive pericarditis mimick) - hemorrhagic pericarditis
- exudate composed of blood caused by spread of malignant neoplasm
40
Q
what is the most common tumor of the heart?
A
- Myxoma**
- arises from primitive multipotent mesenchymal cells*
- 90% arise in left atria near fossa ovalis
- ball valve obstruction (obstruct mitral valve or form thrombus in lungs)
