10/23 - Pathology of the Heart Flashcards
what is a mechanical organ that generates pulsatile blood? when does it begin?
heart - 3 weeks after fertilization
proper development of heart depends on what
network of transcription factors regulated by several signaling pathways
many inherited defects of heart involve what genes
genes that encode transcription factors
what are abnormalities of heart or greater vessels that are present at birth
congenital heart disease
when does congenital heart disease arise
Most arise from faulty embryogenesis during gestational week 3 to 8, when major CV structures form and begin to function
what are anomalies of CHD compatible with live birth
- septal defects
- stenotic lesions
- outflow tract abnormalities
what CHD is ‘hole in heart’
septal defect (ASD or VSD)
what CHD occurs either at level of valves or entire cardiac chamber (hypoplastic left heart syndrome)
stenotic lesions
what CHD has inappropriate routing of greater vessels from ventricles
outflow tract anomalies
CHD incidence
VSD and ASD detected in 5% of live births (most close spontaneously in first year)
T/F: surgical interventions fail to restore complete normalcy or complications arise from prosthetic materials and devices in CHD
TRUE
CHD etiology (how does this happen)
- Environmental exposure (congenital rubella exposure)
- Nutritional factors (folate supplementation reduces risk)
- Therapeutic drugs
- Gestational DM
- Genetic factors
modifiable CHD risk factors
- dietary deficiency
- substance abuse
- obesity and diabetes
- air pollution
non-modifiable CHD risk factors
- medications (e.g., anti seizure or anti depressants)
- infections (e.g., rubella)
- rheumatological disorders (e.g., SLE)
- race and genetics
what are the two major categories of CHD structural anomalies
- shunts
- obstruction
what is an abnormal communication between chambers of heart of blood vessels of heart
shunts
what happens with a CHD shunt
Abnormal channels allow blood to flow down pressure gradients from left (systemic) side to the right side (pulmonary) side of circulation or vice versa
what happens in left to right shunt
- Pressure higher in left side of heart than in right side of heart
- No cyanosis initially
- Cyanosis develops when shunt reverses following development of pulmonary hypertension
what happens in right to left shunt
- Pressure higher in right side of heart than in the left side of the heart
- Cyanosis initially since blood is shunted away from lungs (reduced oxygenation)
when do you get cyanosis
right to left shunt
what is the most common congenital cardiac malformation first diagnosed in adults
atrial septal defect
when is there no symptoms of atrial septal defect in childhood
flow is left to right
T/F: pulmonary HT may reverse shunt and produce cyanosis
TRUE
what is the most common congenital heart disease (CHD) diagnosed at birth
ventricular septal defect (VSD)
*most are small and close spontaneously
are atrial septal defects (ASD) more OR less common in adults
MORE common
when does patent ductus arteriosus normally close?
- normally closes shortly after birth (1-2 days)
- usually identified early on and corrected with medication or surgery
what happens if patent ductus arteriosus is not corrected
shunt reverses due to pulmonary hypertension and cyanosis develops
what are congenital defects causing right to left shunt
- Tetralogy of Fallot
- Transposition of great arteries
*both give cyanosis since right to left shunt
what happens in right to left shutns
blood diverted from pulmonary circulation to systemic circulation thus reducing oxygenation
when is cyanosis characteristic
at or near birth
features of Tetraloy of Fallot
- pulmonary artery stenosis
- right ventricular hypertrophy
- overriding aorta
- ventriculoseptal defect
- may have patent ductus which helps oxygenate the blood (some babies)
know word for word PROVe(P)
what is a congenital heart defect where aorta is positioned directly over ventricular septal defect instead of over left ventricle
overriding aorta
what is a birth defect of heart in which the two main arteries carrying blood out of the heart, the pulmonary artery and aorta are switched in position (transposed)
transposition of great arteries
what is the second leading cause of congenitol cyanosis
transposition of great arteries
what congenital diseases are left to right
VSD (Ventricular septal defects)
ASD (Atrial septal defects)
PDA (Patent (persistent) ductus arteriosus)
what congenital diseases are right to left
Tetralogy of Fallot
Transposition of great arteries
what is main clinical sign of transposition of great arteries
cyanosis
what is CHD causing obstructive lesions
coarctation of aorta
what is abnormal narrowing of aortic lumen
coarctation of aorta
what does coarctation of aorta result in
- Higher BP in arms than legs
- Weak pulses in the lower extremities with signs and symptoms of intermittent claudication (ischemic leg pain)
- Enlarged heart
- Dissection or rupture of aorta, which can befatal
9/10 with untreated coarctation don’t survive to what age
50 years
what does ischemic heart disease (IHD) result from
- Atherosclerotic lesions in the epicardial coronary artery
- Coronary artery emboli
- Coronary vessel inflammation
- Coronary vascular spasm
atherosclerotic lesions in epicardial coronary artery leads to what
leading to myocardial ischemia (an imbalance between myocardial supply (perfusion) and cardiac demands for oxygenation)
ischemic heart disease could also be called what? why?
coronary artery disease (since it is the #1 cause of ischemic heart disease)
what is #1 cause of ischemic heart disease
plaques in coronary artery (atherosclerotic lesions in epicardial coronary artery)
what are consequences of IHD
- angina pectoris (ischemia is not severe to cause infarction but can pose infarction risk)
- chronic IHD w/ heart failure
- myocardial infarction (MI) (ischedmia can cause frank cardiac necrosis)
- sudden cardiac death
what is temporary chest pain or discomfort caused by inability of diseased coronary arteries to deliver sufficient oxygen-laden blood to heart muscles
angina pectoris
angina pectoris is a sign of what
increased risk of heart attack
what can trigger angina pectoris
- emotional stress
- physical exercise
- being exposed to very hot or cold temperatures
- smoking
- eating a heavy meal
symptoms of ___ include:
Pressure or pain in the center of the chest that may radiate to the shoulder, arm, back, neck, and jaws
angina pectoris
what patients have sensations of having indigestion or gas
angina pectoris
types of angina pectoris
- stable angina
- prinzmetal
- unstable angina
where does angina pectoris pain radiate
center -> shoulder -> arm -> back -> neck -> jaws
stable angina pectoris is associated with what?
fixed atherosclerotic narrowing of one or more coronary arteries
stable angina pectoris symptoms
discomfort in chest descibed as deep, poorly localized pressure, squeezing or burning sensation (like indigestion) but unusually as pain
what causes stable angina pectoris
physical activity, emotional excitement, or physiological stress
how to relieve stable angina pectoris pain
rest and/or nitroglycerin or calcium channel blockers
what is pain in Prinzmetal angina pectoris
anginal pain occuring at rest or awakening patient from sleep
what is prinzmetal angina pectoris associated with
Usually associated with coronary artery
spasm often adjacent to a site of
atherosclerotic plaque
mechanism that causes prinzmetal angina pectoris
poorly understood
what is unstable angina pectoris
increased frequency of angina episodes
what precipitates unstable angina pectoris
progressively less exertion (less emotional trauma like not eating as much)
what is unstable angina pectoris pain described as
intense pain
what is a more intense pain that last longer than “stable angina”? how long does it last?
unstable angina pectoris >20 minutes
what is induced by acute plaque change w/ superimposed partial thrombosis or vasospasm or both
unstable angina pectoris
treatment of angina pectoris
nicroglycerin (oral medication classified as vasodilater)
when do patients take nitroglycerin
10 mintues before begin doing activity that will trigger symptoms (of angina pectoris)
what is irreversible necrosis of heart muscle (secondary to prolonged ischemia)
myocardial infarction
etiology of myocardial infarction
associated with coronary artery disease
common symptoms of myocardial infarction
- chest discomfort
- shortness of breath
- discomfort in the upper body
when does myocardial NECROSIS begin after infarction?
Myocardial necrosis begins within 20-30 minutes of infarction and reaching full size within 3 - 6 hours
where does myocardial infarction begin then extend toward?
begin: subendocardium
extend toward: epicardium
what can limit size of infarct during myocardial infarction
thrombolytic agents (tissue plasminogen activator t-PA) may limit size of infarct during time frame
what are thrombolytic drugs
- eminase
- retavase
- streptase activase
is ASPIRIN thromoblytic? explain
NO! but may limit clot size- antiplatelet adhesion drug
what are clinical complications of acute MI
- sudden death
- cardiogenic shock
- cardiac arrythmias
- cardiac tamponade due to cardiac rupture
what are anatomic complications of MI?
- Valve insufficiency due to infarcted papillary muscle
- Ventricular aneurysms
- Mural thrombus giving rise to systemic arterial emboli
- Cardiac tamponade due to rupture of the infarcted area of the heart
what results due to infarcted papillary muscles (doors are bad)
valve insufficiency
what giver rise to systemic arterial emoboli?
mural thrombus (thrombus in wall of heart)
what results due to the rupture of infarcted area of heart
cardiac tamponade
myocardial infarction treatmetn
- reperfusion therapy
- nitrates
- beta-blockers
- lipid-lowering treatment (statins)
- antithrombotic therapy
what is indicated in all patients with symptoms of ischemia of less than 12 hours duration
reperfusion therapy
what are the more effect nitrates? what does it do?
IV nitrates more effective than sublingual nitrates (giving rise to nitric oxygen, which caused vasocilation - nitroglycerin)
what doe beta blockers do? example?
Beta-blockers (reduces myocardial workload, and thus oxygen demand,, via reduction in heart rate and BP) (olol’s- atenolol, bisoprolol)
most common cause of sudden cardiac death
ischemic heart disease (sudden death may be initial manifestation of ischemic heart disease
what are other causes of sudden cardiac death
(1 = ischemic heart disease)
2. Arrhythmias not caused by ischemia
3. Acute cor pulmonale due to massive pulmonary artery thromboembolism
what are abonormalities in myocardial conduction that are sustained or sporadic (paroxysmal)
arrythmias
how are aberrant rhythmias initiated
Aberrant rhythms can be initiated anywhere in the conduction system (from SA down to the level of an individual myocyte)
in structurally normal heart, what causes arrythmias
mutations in ion channels that cause aberrant repolarization and depolarization
what is a consequence of increase demands placed on heart by HT
pressure overload and ventricular hypertrophy
what causes hypertensive heart disease? leads to what?
chronically elevated BP; leading cause of illness and death
classic example of HT heart disease
left ventricular hypertrophy (LVH)
progression from HT to LVH is important step on pathway toward what
heart failure
is HT heart disease chronic or acute?
EITHER OR
sign and symptoms of HT Heart Disease
- Shortness of breath with activity or when lying down
- Persistent cough or wheezing with white or pink blood-tinged mucus
- Rapid or irregular heartbeat
- Fatigue and weakness
- Reduced ability to exercise
- Swelling in the legs, ankles and feet
- Swelling of the belly area (abdomen)
- Rapid weight gain
HT heart disease treatment
Individuals are treated with drug therapy that typically includes diuretics and beta-blockers
patients with HT heart disease are advised to do what
- Reduce salt and alcohol in the diet
- Abstain from smoking
- Lose weight
- Exercise regularly
what is most prevalent heart valve disorder in developed countries
calcific aortic stenosis
what is characterized by:
Progressive fibro-calcific remodeling and thickening of the aortic valve leaflets that evolve over years to cause severe obstruction to cardiac outflow; age-related degeneration
calcific aortic stenosis
what does calcific aortic stenosis result in
LEFT ventricular hypertrophy and decreased aortic outflow leads to myocardial ischemia
when do patients with calcific aortic stenosis die
within 3-4 years unless treated
what are new calcific aortic stenosis treatment options
balloon valvuloplasty
transcatheter valve replacement
what causes mitral regurgitation (Back flow)
mitral valve prolapse
is mitral valve prolapse common? are most cases sporadic?
common (3-5% of population)!
most cases are sporadic!
what syndrome could see mitral valve prolapse
Marfan syndrome
people with mitral valve prolapse are prone to what
infective endocarditis, arrythmias and emobli from left atrium
T/F: antibiotic prohylaxis is needed prior to dental procedures unless other factors present
FALSE!!! no longer recommended!
what causes acute, multisystem, immunologically-mediated inflammatory disease usually following group A streptococcal pharyngitis after an interval of a few weeks
rheumatic fever causing valve disease
is pharyngitis severity related to risk of developing rheumatic fever?
no - not related
long term consequence of rheumatic fever is related to what
induction of permanent cardiac damage
rheumatic carditis typically occurs as what
pancarditis - involves pericardium, myocardium, and endocardium
what is an infection caused by bacteria that enter the bloodstream and settle in the heart lining, a heart valve or a blood vessel
infective endocarditis
is infective endocarditis common?
It is uncommon, but people with some heart conditions have a greater risk of developing it
what is an infection of cardiac valves of mural surfaces of endocardium?
infective endocarditis
