Path - Heart Flashcards
What cells are almost exclusively on oxidative phosphorylation?
cardiac myocytes
Why is the myocardium vulnerable to ischemia?
It has a limited amt of blood supply to the heart (only 4 vessels).
- left mainstem coronary artery
- left circumflex
- left anterior descending branch (LAD)
- right coronary artery
3 Major Pathologic changes of valves?
- dmg to collagen that weakens leaflets –> mitral valve prolapse
- nodular calcification beginning in interstitial cells –> calcific aortic stenosis
- fibrotic thickening –> rheumatic heart disease
What happens in Congestive Heart Failure? How does the body try to resolve this?
- In CHF, heart is unable to pump blood at rate sufficient to metabolic demands of the tissues.
- Several physiologic mechanisms maintain arterial pressure and organ perfusion such as myocardial hypertrophy
What is the pathophysiology & progression to heart failure?
Pressure (systemic hypertension) or volume overload (aortic stenosis) → increase in mechanical work → myocyte adaptation → increase in size (hypertrophy) of myocyte → increase in size and weight of the heart
*aortic stenosis = opening of the aortic valve is narrowed
Myocyte hypertrophy not accompanied by a proportional increase in capillary numbers → weak blood supply for hypertrophied heart while oxygen consumption is elevated. What does this eventually lead to?
- More vulnerability of hypertrophied heart to ischemia-related decompensation, which leads to cardiac failure
What are 3 causes of cardiac hypertrophy?
- hypertension - pressure overload
- valvular disease - pressure &/or volume overload
- myocardial infarction - regional dysfunction w/ volume overload
What are the causes and consequences of LEFT-SIDED HEART FAILURE?
- Causes:
1. Ischemic heart disease
2. Hypertension
3. Aortic and mitral valvular diseases
4. Primary myocardial diseases - Consequences:
1. Passive congestion (blood back up in the pulmonary circulation)
2. Stasis of blood in the left-sided chambers
3. Inadequate perfusion of downstream tissues
What is the morphology of LEFT-SIDED HEART FAILURE in the HEART and LUNG?
What is special about cardiac muscle cells & neural cells?
They are permanent cells, so they never divide. However, it is possible to stimulate cardiac stem cells to undergo regen.
What are heart failure cells?
mac’s w/ injected RBCs (hemociderin laden)
What is cor pulmonale?
isolated right-sided heart failure–infrequent occurrence; blood will pool in systemic system
What is the morphology of right-sided heart failure in the liver?
- congestion of hepatic & portal vessels
2. congestive hepatomegaly
What is one of the most prevalent birth defects (incidence of up to 5%)? And what is a major cause of this disease
congenital cardiovascular malformations
Causes:
- GENETIC - sporadic genetic abnormalities (major cause); down syndrome (mut in TFs: NKX2.5, GATA4)
- ENVIRONMENTAL- alone or w/ genetic factors (congenital rubella infection, gestational diabetes, teratogen exposure, nutritional factors–folate supplements reduce risk)
- IDIOPATHIC - aka we don’t know–unknown cause(s)!!
What are the 3 groups Congenital Heart Disease (CHD) can be classified as?
- malformations causing left-to-right shunt (*most common CHD)
- malformations causing right-to-left shunt
- malformation causing an obstruction
Describe the fetal circulation.
- Lungs are not in use, so the fetal heart gets O2 from placenta.
- Foramen Ovale gets blood from placenta and is a valve betw the R&L side of the heart–communication.
- Ductus arteriosis - blood from pulm. a. to the aorta (deoxy blood bc not as much blood needed in fetus), but some of the blood still goes to lung to give the tissue some O2.
What is Eisenmenger syndrome?
when a left-to-right shunt CHD becomes a right-to-left shunt (this is an inevitable event unless treated)
What is arterial septal defect?
- type of left-to-right shunt
- abnormal, fixed openings in atrial septum
- tx: ASD closure
What is patent foramen ovale (PFO)?
- type of left-to-right shunt
- failure to close foramen ovale (usu closes at age 2)
- do NOT confuse w/ ASD
What is a ventricular septal defect (VSD)?
- type of left-to-right shunt (*most common)
- incomplete closure of ventricular septum
What is a patent ductus arteriosus (PDA)?
- connects aorta & pulm. a.
- essential in fetal circ.; can be induced to remain open (PG E1 analogs)
- tx: NSAIDS, indomethacin
Describe right-to-left shunt in general. What is an example of this type of shunt?
- R-to-L = cyanotic CHD
- hypoxemia/cyanosis –> clubbing of fingers (hypertrophic osteoarthritis), polycythemia
- paradoxical embolism (prone to embolism bc blood is thicker)
- Ex: Tetralogy of Fallot (TOF) - enlarged boot-shaped heart, blue tongue, 4 defects
What are the 4 defects seen in Tetralogy of Fallot (TOF)?
- overriding aorta (abnormal position)
- subpulmonary stenosis (narrowing of artery)
- ventricular septal defect (deoxy mixes w/ oxy blood)
- right ventricular hypertrophy (R-to-L shunt)
What is obstructive congenital disease?
- abnormal narrowing of chambers, valves, or BVs
- atresia = complete obstruction
- ex. coarctation of aorta, aortic valvular stenosis, pulmonary valvar stenosis
- 2 types: w/ PDA, w/o PDA
What is ischemic heart disease (IHD)?
- resulting from myocardial ischemia, an imbalance betw myocardial perfusion & cardiac demand for oxy blood
- result = cardiac hypoxia
- 90% of cases: atherosclerotic lesions in coronary aa. –> IHD
- varying degrees of acute plaque change, thrombosis, & vasospasm
- consequences: angina pectoris (chest pain due to ischemia), myocardial infarction, sudden cardiac death
What are the 3 types of angina pectoris?
- stable angina (most common)
- unstable angina
- prinzmetal angina
Stable angina?
- produced by physical activity, emotional stress, or heavy meal
- relieved by rest or vasodilators (nitroglycerine, Ca chnl blockers [inc perfusion])
Unstable angina?
prolonged/severe angina; unpredictable even at rest; mostly caused by disruption of atherosclerotic plaque
Prinzmetal angina?
uncommon form of episodic myocardial ischemia caused by coronary artery spasm, unrelated to physical activity; responds to vasodilators
What is the #1 cause of death in US?
myocardial infarction (MI)
What are the early changes after onset of severe myocardial ischemia?
Loss of ATP & accumulation of lactate; first 30 min = reversible changes (swelling of cell = reversible)
- will eventually lead to irreversible injury when cytoplasmic memb is not intact
KNOW the sequence of events in the progression of myocardial ischemic injury.
- ATP depletion
- Loss of contractility in cardiomyocytes
- ATP reduction (due to anaerobic production)
- Reversible cell injury (if within 30 mins)
- Irreversible cell injury
- Microvascular injury
What are the patterns of infarction & what are the differences between the two?
Transmural infarct - involving the entire thickness of the left ventricular wall from endocardium to epicardium
Subendocardial infarct - multifocal areas of necrosis confined to the inner 1/3-1/2 of the left ventricular wall.
What is used to detect & diagnose someone w/ myocardial infarction?
cardiac-specific troponins T & I (cTnT & cTnl) & CK-MB
What is Rheumatic fever (RF) & what is its progression?
RF = acute inflamm disease following group A streptococcal pharyngitis
- becomes acute rhematic carditis (ARC)
- if chronic = rheumatic heart disease (RHD) w/ valvular abnormalities –> mitral valve (stenosis)
What are Aschoff bodies?
focal inflammatory lesions consisting of foci of T lymphocytes, , occasional plasma cells, & plump activated mac’s called Anitschkow cells
what is infective endocarditis (IE)?
a microbial infection of heart valves or mural endocardium leading to formation of vegetations; acute & subacute forms
Describe acute infective endocarditis (IE).
infection of a previously normal valve by highly virulent organism; rapidly necrotizing & destructive lesions; difficult ot cure; death w/i days to weeks
Describe subacute infective endocarditis (IE).
organisms w/ lower virulence; infections of deformed valves; less destructive; cure can be achieved w/ ABs
What are the clinical features of Infective Endocarditis?
- fever/chills, new or changing murmur, vascular lesions, including petechiae, “splinter” hemorrhages under nails & *Janeway lesions (small erythematous, non-tender or nodular lesion on soles or palms–caused by septic emboli)
- modified “Duke criteria” for diagnosis
What is the morphology of Infective Endocarditis (IE)?
- vegetations = classic
- friable, bulky, potentionaly destructive
- aortic & mitral valves, most common sites
- prone to embolization
So what are the 4 major forms of vegetative endocarditis?
- rheumatic heart disease (RHD): small, warty vegetations along the lines of closure of valve leaflets
- infective endocarditis (IF): large, irregular mass on valve
- nonbacterial thrombotic endocarditis (NBTE): small, bland vegetations at line of closure
- Libman-Sacks endocarditis (LSE): small/medium-sized vegetations on either or both sides of the valve leaflets
Who needs AB prophylaxis one hour before dental procedures or operations on the mouth?
Only recommended for pts w/ high risk of infective endocarditis:
- Artificial heart valve
- Heart valve repaired w/ artificial material
- History of endocarditis
- Heart transplant w/ abnormal heart valve function
- Certain types of congenital heart defects
What congenital heart defects that require antibiotic prophylaxis?
- cyanotic congenital heart disease that has not been fully repaired
- congenital heart defect repaired w/ artificial material or a device for first six months after repair procedure
- repaired congenital heart disease w/ residual defects
What are the most common causes of myocarditis in the US?
viral infections
What is a cardiomyopathy?
any dysfunction of myocardium; associated w/ mechanical or electrical dysfunction
What are the 3 morphologic patterns of cardiomyopathies?
- dilated (systolic dysfunction)
- hypertrophic
- restrictive
* last 2 are diastolic dysfunction
What causes dilated cardiomyopathy?
- supraphysiologic stress & excess catecholamine (cardiotoxicity–Ca overload in myocyte or focal vasoconstriction)
- cocaine, dopamine
- DEFECT IN: force generation, force transmission, &/or myocyte signaling
what is hypertrophic cardiomyopathy?
“hunned per cent” genetic disorder–autosomal dominant; mutations in proteins of sarcomere; abnormal diastolic filling
- DEFECT IN: energy transfer from mito to sarcomere &/or direct sarcomeric dysfunction
