CV Pathology Flashcards
What are 5 congenital defects that lead to a right to left shunt? What is the presentation of a right to left shunt (congenital)? Treatment?
Early cyanosis; blue babies; diagnosed prenatally or become evident soon after
Surgical correction or maintenance of PDA
5 T’s
Truncus arteriosus (1 vessel) Transposition of great vessels (2 switched vessels) Tricuspid atresia (Tri=3) Tetralogy of Fallot (4) TAPVR (5 letters)
What is the pathophys of persistent truncus arteriosus? What usually accompanies it? Pathophys of transposition? What makes it compatible with life? Treatment? Anatomy of tricuspid atresia? What makes it compatible? What causes tetralogy of fallot? What are the 4 anatomical features? Pathophys/symptoms? What does squatting do? How? Treatment? What is TAPVR? What is it associated with?
PERSISTENT
Failure of aoricopulmonary septum to form
VSD
TRANSPOSITION OF GREAT VESSELS
Aorta leaves RV and pulmonary trunk leaves LV
Failure of AP septum to spiral
Must have mixing of blood (VSD, PDA, or PFO)
Surgical intervention within months to prevnt death
TRICUSPID ATRESIA
Absence of tricuspid vavle and hypoplastic RV
Requires both ASD and VSD
TETRALOGY OF FALLOT
The infundibular septum is moved more over the right atria (anterior) so the pulmonary opening is small and aorta opening is large. It’s also moved superior which causes a VSD
PROV Pulmonary infundibular stenosis RVH (boot shaped heart on CXR) Overriding aorta VSD
Pulmonary stenosis forces right to left flow across VSD leading to early cyanotic tet spells and RVH.
Squatting incr. SVR which decr. right to left shunt which incr. cyanosis
Early surgical correction
TAPVR-total anomalous pulmonary venous return
Pulmonary veins drain in right heart
ASD and sometimes PDA allow for right to left shunting which maintains CO
What are 3 left to right shunts? How do they present? Order of commonness?
Late cyanosis-blue kids
VSD, ASD, PDA
When does vsd present? What can large lesions lead to? What is heard on auscultation in ASD? What are the symptoms? What does PDA lead to? What is heard on auscultation? What happens if its uncorrected?
VSD
Can present after weeks after birth or always be asymptomatic.
LV overload and HF
ASD
Loud S1 and wide fixed split S2
No symtoms to HF
PDA
Decr. lugn resistance leads to left to right shunt leads to progressive RVH and/or LVH and HF
Continuous machine like murmur
Can lead to late cyanosis in lower extremities
What is the pathophys of eisenmenger syndrome? Symptoms? What are coarctation of the aorta? What is it associated with? symptoms?
left to right shunt leads to incr. pulmonary blood flow leading to remodeling of vasc. leading to pulm. artery hypertension.
RVH occurs to compensate and the shunt becomes right to left
late cyanosis, clubbing, and polycythemia
COARCTATION
aortic narrowing near insertion of ductus arteriosus
bicuspid aortic valve, turners
hypertension in upper extremiteis and weak, delayed pulse in lower
Collateral arteries erode ribs (notched appearance on x ray)
What cardiac defects are associated with fetal alcohol syndrome, congenital rubella, DS, infant of diabetic mother, marfan syndrome, prenatal lithium, turners, williams, and 22q11 syndromes?
fetal alcohol syndrome: VSD, PDA, ASD, TOF
congenital rubella: SEPTAL DEFECTS, PDA, pulm. artery stenosis
DS: AV septal defect (endocardial cushion defect), VSD, ASD
infant of diabetic mother: Transposition
marfan syndrome: MVP, thoracic aortic aneurysm and dissection, aortic regurgitation
prenatal lithium: ebstein anomaly
turners: Coarc, bicuspid
williams: supravalvular aortic stenosis
22q11 syndromes: truncus, TOF
What is the definition of hypertension? Risk factors? What is primary hypertension? Relations? Percentage of cases? Secondary? Assocations? What is hypertensive urgency? What is a hypertensive emergency? Symptoms? What does hypertension presdispose to? What is the pathology of fibromuscular dysplasia and hypertensive nephropathy?
Persistent systolic >140 or diastolic >90
Incr. age, obesity, diabetes, inactivity, excess salt, excess alcohol, family history, black>white>asian
90% is primary (Incr. CO or TPR)
10% secondary (fibromuscular dysplasia (beads on a string of renal artery), primary hyperaldosteronism, etc.)
Severe (>180/>120) hypertension without end organ damage
Severe hypertension with end ordgan damage (papilledema, encephalopathy, stroke, retinal hemorrhages and exudates, MI, HF, aortic dissection, kidney injury, MAHA, eclampsia)
CAD, LVH, HF, a fib, aortic dissection, aortic aneurysm, stroke, chronic kidney disease (hypertensive nephropathy–renal artery hyalinosis), retinopathy
What are xanthomas? Where do they occur? What are tendinous xanthomas? What is corneal arcus? What causes them?
Hyperlipidemia
Plaques or nodules composed of lipidl aden histiocytes in skin (eyelids=xanthelasma)
Lipid deposit in tendon,especially achilles
liipid deposit in cornea
Describe arteriosclerosis. Describe the two types of arteriolosclerosis. Describe monckeberg arteriosclerosis.
Artery hardening with thickening of wall and loss of elasticity
Small arteries and arterioles
Hyaline: thickening of vessel walls in essential hypertension or diabetes
Hyperplastic: onion skinning in severe hypertension
Medial calcific sclerosis
Medium sized arteries
calcification of elastic lamina leading to vascular stiffening w/o obstruction.
Does not obstruct blood flow
What is atherosclerosis? What are some modifiable and non modifiable risk factors? Describe the pathophys. Complications? Common locations? Symptoms?
Elastic and large and medium sized muscular arteries: arteriosclerosis caused by build up of plaques.
Modifiable: smoking, hypertension, hyperlipid, diabetes
non: age, family history, gender,
Endothelial cell dysfuntion macrophage and LDL accumulation Foam cell formation Fatty streaks Smooth muscle cell migration (PDGF and FGF) Smooth cell proliferation EC matrix deposition Fibrous plaque Complex atheromas
Aneurysm, thrombosis, embolism, Periph. vac. disease, ischemia, infarcts
Abdom aorta>coronary>popliteal>carotid
Angina, claudication
What is an aortic aneurysm? symtpoms? What do symptoms mean? What is an abdom aortic aneur associated with? Risk Factors? How does it present? What is a thoracic aortiic aneurysm associated with? Risk factors?
Localized pathologic dilatation of aorta
Abdominal or back pain=sign of leak, imminent rupture, dissection
Atherosclerosis (tobacco, incr. age, male, family history)
palpable pulsatile mass
Cystic medial degeneration
Hyperension, bicuspid aortic, marfans, tertiary syphilis
What is an aortic dissection? Assocations? Presentation? CXR findings? Results?
Longitudinal intimal tear forming false lumen
hypertension, bicuspid aortic, marfans
Tearing chest pain of sudden onset, radiates to back
unequal BP in arms
CXR: mediastinal widening
rupture, pericardial tamponade, and death
What is angina? What causes the 3 different types? Triggers? What makes the better? Treatment? Lab findings? Symptoms?
Chest pain due to ischemic myocardium de to coronary artery narrowing or spasm. No necrosis
Stable: Pain during exertion, ST depression on ECG, resolves with rest of Nitroglycerin
Variant (prinzmetal): at rest due to spasm. transient ST elevation. Tobacco, cocaine, and triptans, unknown.
CA channel blockers, nitrates and smoking cessation
Unstable: thrombosis wit incomplete occlusion. May or may not have ST depression and T wave inversion. No biomarkers. Is an increase in frequency or intensity of the angina or when pain occurs at rest.
What is coronary steal syndrome? Describe the pathophys. What is this principle used for?
Distal to coronary artery stenosis, vessels are maximally dilated. Therefore, when a vasodilator is given, they can dilate anymore, so the unstenosed vessels dilate making the stenosed area more ischemic
Pharmacological stress tests
What is sudden cardiac death? Cause? associations? What is chronic ischemic heart disease?
Death from cardiac causes under 1 hour of onset of symptoms.
Arrhythmia (v fib)
CAD, cardiomyopathy, hereditary ion channelopathies
Progressive onset of HF over many years due to chronic ischemic yocardial damage
What is order of most commonly occluded coronary arteries? What are the sytmpoms of MI? What is the gross pathology and microscopic pathology at 0-4 hr, 4-24 hr, 1-3 days, 3-14 days, and 2 weeks to several months?
LAD>RCA>circumflex
diaphoresis, N/V, retrosternal pain, pain in left arm and jaw, SOB, fatigue
0-4
G: none
M: none
4-24
G: dark mottling, pale with tetrazolium stain
M: early coag necrosis, necrotic contents into blood; edema, hemorrhage, wave fibers, neutrophils appear, reperfusion injury? (contraction bands)
1-3 days
G: hyperemia
M: extensive coag necrosis. Tissue surrounding infarct shows acute inflammation with neutrophils
3-14 days
G: hyperemic border; central yellow brown softening-maximally yellow and soft by 10 days
M: Macrophages, then granulation tissue at margins
2 weeks to several months
G: recanalized artery, gray-white
M: contracted scar complete
What is the gold standard for MI diagnosis in first 6 hours? What changes occur? what is the timeline for cardiac troponin? What is it useful for? What is the timeline for CK-MB? Waht is it useful for? Why?
ECG in first 6 hours
STEMI (transmural infarct)=ST elevation
NSTEMI (subendocardial infarct)=ST depression
hyperacute T waves, T wave inversion
New LBBB
pathologic Q waves or poor R wave progression=evolving or old transmural (STEMI) infarct
Troponin I=rises after 4 hours and is incr. 7-10 days; more specific than toher markers
CK-MB=6-12 hours. Diagnosing reinfarction after acute MI b/ levels return to normal after 48 hours.
What leads will have ST elevations or path. q waves in an infarct in the anteroseptal location? anteroapical? anterolateral? Lateral? Inferior? Which CAs are affected?
anteroseptal location? V1-V2 (LAD) anteroapical? V3-V4 (distal LAD) anterolateral? V5-V6 (LAD or LCX) Lateral? I, aVL (LCX) Inferior? II, III, aVF (RCA)
What are some complications of an MI? When do they occur and why are they problematic?
arrhythmia; first few days
Post infarction fibrinous pericarditis: friction rub (1-3 days)
LV failure and pulmonary Edema
Cardiogenic shock
Ventricular free wall rupture leading to cardiac tamponade and papillary muscle rupture leading to severe mitral regurg and IV septum rupture leading to VSD (3-14 days post MI)
ventricular pseudoaneurysm formation (contained free wall rupture)=decr. CO, risk of arrhythmia, embolus from mural thrombus (3-14 days)
true ventricular aneurysm: outward bulge during contraction; associated with fibrosis (2 weeks to several months)
Dressler syndrome-autoimmune phenomenon leading to fibrinous pericarditis (several weeks post MI)
How is unstable angina/NSTEMI treated? What else is done for STEMI?
anticoag, antiplatelets, beta blockers, ACE I, NO and morphine (symptom control)
Reperfusion therapy most important (percutaneous coronary intervention preferred over fibrinolysis)
What is the most often etiology of a dilated cardiomyopathy? What are some other etiologies? What are some findings? Treatment? What kind of dysfunciton ensues? Gross/microscopic path?
Idiopathic of familial
ABCCCCCDD
Alcohol abuse wet Beri beri Coxsackie B virus myocarditis chronic Cocaine use Chagas hemoChromatosis peripartum Cardiomyopathy Doxorubicin toxicity sarcoiDosis
HF, S3, systolic regurgitant murmur, dilated heart on echo, balloon appearance on CXR
Na restriction, ACEI, beta blockers, diuretics, digoxin, ICD, heart transplant
Systolic dysfunction
sarcomeres added in series (eccentric hypertrophy (longer wall not thicker wall))
What are 60-70% of hypertrophic cardiomyopathy caused by (specificallly)? Association? Symptoms? Findings? Treatment? Dysfunction? Gross/micro path? What is obstructive hypertrophic cardiomyopathy?
familial, autosomal dominant (beta myosin heavy chain)
Friedrichs ataxia
Syncope durig exercise and sudden death in yougn athletes
S4, systolic murmur, maybe mitral regurg
Cessation of high intensity exercise, beta blocker or verapamil. ICD.
Diastolic dysfunction
Ventricular hypertrophy (myofibrillar disarray and fibrosis)
HOCM: septal hypertrophy and systolic anterior motion of mitral valve–>outflow obstruction—>dyspnea/syncope
What are some major causes of restrictive/infiltrative cardiomyopathy? dysfunction? What can be seen on ECG?
sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastosis (young children), loffler syndrome (fibrosis with a prominent eosinophilic infiltrate), hemochromatosis.
diastolic dysfunction
Low voltage ECG
What is heart failure? Symptoms? Signs? compare/contrast systolic/diastolic function and how they effect EF, EDV, and contractility/compliance (causes). What most often causes right HF? 2nd leading cause? What treatments decr. mortality? Help symptoms? improve symptoms and decr. motrality in some patients?
cardiac pump dysfunction—>congestion and low perfusion
dyspnea, orthopnea, fatigue
rales, JVD, pitting edema
Systolic: reduced EF, Incr. EDV, Decr. contractility due to ischemia/MI or dilated CM
Diastolic: preserved EF, normal EDV, decr. compliance due to myocardial hypertrophy.
Right HF from left HF, then from cor pulmonale
ACEI and ARBs, Beta blockers (except in acute decompensated HF) and spironolactone decr. mortality
Thiazide or loop diuretics for symptoms
hydralazine with nitrate therapy improve symptoms and mortality in some patients.
