heart

Question 1

Extracted Text

Answer 1

Q

Question 2

the heart: Normal Pathology (not on test)

Answer 2

-Heart Failure: Left, Right
-Heart Disease
-Congenital: ASD, VSD, PDA, Tetralogy of Fallot
-Ischemic: Angina, Infarction, Chronic Ischemia, Sudden Death
-Hypertensive Heart Disease
-Valvular: AS, MVP, Rheumatic, Infective endocarditis, Non-Infective
-Cardiomyopathy: Dilated, Hypertrophic, Restrictive, Myocarditis
-Pericardium: Effusions, Pericarditis
-Tumors: Primary, Metastatic

Question 3

valves (not on test)

Answer 3

-AV:
-tricuspid
-mitral
-SL:
-pulmonic
-aortic

Question 4

cardiac pump problems

Answer 4

-Failure of the pump –MC problem
-Cardiac muscle contracts weakly and chambers cannot empty properly— (systolic dysfunction)
-Myocardium cannot relax enough to allow ventricular filling – (diastolic dysfunction)
-Obstruction to flow - Lesions that prevent valve opening (e.g., calcific aortic valve stenosis) or cause increased ventricular chamber pressures (e.g., systemic hypertension) can overwork myocardium (has to pump against obstruction)
-Regurgitant flow- Valve pathology that allows backward flow of blood results in increased volume workload; may overwhelm pumping capacity of affected chambers
-Shunted flow - Defects (congenital or acquired) that divert blood inappropriately from one chamber to another, leading to pressure and volume overloads
-Disorders of cardiac conduction - Uncoordinated cardiac impulses or blocked conduction pathways can cause arrhythmias that slow contractions or prevent effective pumping
-Rupture of the heart or major vessel - Loss of circulatory continuity (e.g., a gunshot wound through the thoracic aorta) may lead to massive blood loss, hypotensive shock, and death

Question 5

CHF (normal- not on test)

Answer 5

-Heart cannot pump blood adequately to meet metabolic demands of peripheral tissues
-Fluid overload, abrupt valvular dysfunction, or myocardial infarction, can cause sudden CHF
-Initially, compensatory mechanisms try to maintain arterial pressure and organ perfusion:
-!!!!Frank-Starling mechanism: Increased filling volumes dilate the heart, increasing actin-myosin cross-bridge formation, and enhancing contractility and stroke volume
-Activation of neurohumoral systems: aid heart function and/or regulate filling volumes and pressures
-Release of norepinephrine by adrenergic nerves of the autonomic nervous system: elevates heart rate, augments myocardial contractility and increases vascular resistance
-Activation of the renin-angiotensin-aldosterone system: promotes water and salt retention (augmenting circulatory volume) and increases vascular tone
-Release of atrial natriuretic peptide: counterbalances the renin-angiotensin-aldosterone system by diuresis and vascular smooth muscle relaxation
-Myocardial adaptations
-Ventricular remodeling: general term for collective molecular, cellular, and structural changes that occur in response to injury or altered ventricular loading

Question 6

CHF causes

Answer 6

-Heart failure can result from progressive deterioration of myocardial contractile function (systolic dysfunction)—reflected as a decrease in ejection fraction (EF = percentage of blood volume ejected from ventricle during systole; normal approximately 45% to 65%)
-Reduction in EF can occur with:
-ischemic injury
-inadequate adaptation to pressure or volume overload due to hypertension or valvular disease
-ventricular dilation
-Heart failure may result from inability of heart chamber to expand and fill sufficiently during diastole (diastolic dysfunction), due to left ventricular hypertrophy, myocardial fibrosis, constrictive pericarditis, or amyloid deposition

Question 7

cardiac hypertrophy: patho and progression to HF

Answer 7

-Sustained increase in mechanical work of either ventricle due to pressure overload, volume overload, or trophic signals (e.g., activation of β-adrenergic receptors) causes increase in !myocyte size (hypertrophy)!
-Pressure-overload hypertrophy (e.g., hypertension or aortic stenosis): new sarcomeres predominantly assembled in parallel to long axes of cells, expanding cross-sectional area of myocytes in ventricles- results in concentric wall thickness increase
-Volume-overload hypertrophy (e.g., valvular regurgitation): new sarcomeres assembled in series within existing sarcomeres, leading primarily to ventricular dilation
-Hypertrophied heart vulnerable to ischemia:
-Larger myocytes need more blood
-Larger heart has increased metabolism needs because of increased mass, heart rate, contractility – increase oxygen consumption

Question 8

LEFT sided HF: Causes

Answer 8

-Most often caused by:
-IHD (ischemic heart disease)
-Hypertension
-Aortic and mitral valvular diseases
-Primary myocardial diseases
-Clinical and morphologic effects of left-sided CHF: consequence of passive congestion (blood backing up in the pulmonary circulation), stasis of blood in the left-sided chambers, and inadequate perfusion of downstream tissues leading to organ dysfunction
-Left-sided heart failure divided into systolic and diastolic failure:
-Systolic failure - insufficient ejection fraction (pump failure)
-Diastolic failure - left ventricle abnormally stiff and cannot relax during diastole; hypertension most common cause

Question 9

left sided HF

Answer 9

-Left ventricle usually hypertrophied, often dilated -> not increase in cells but increase in size
-Enlarged heart (cardiomegaly, CXR), tachycardia, a third heart sound due to volume overload (S3), or a fourth heart sound (S4) due to increased myocardial stiffness
-Lungs: Pulmonary congestion and edema (heavy, wet lungs) – micro will show “heart failure cells”; Initially, cough and dyspnea may occur with exertion; with progression - orthopnea or paroxysmal nocturnal dyspnea, dyspnea at rest
-tachy- heart has to work harder
-Auscultation: fine rales at lung bases (edematous pulmonary alveoli snap open during inspiration)
-Moderate CHF: reduced ejection fraction leads to decreased renal perfusion, activating renin-angiotensin-aldosterone system leading to salt and water retention; if renal hypoperfusion severe, may cause prerenal azotemia (excess nitrogen compounds in blood, may lead to renal failure)
-Very severe CHF, cerebral hypoperfusion can lead to hypoxic encephalopathy: irritability, loss of attention span, and restlessness; can progress to stupor and coma

Question 10

LEFT heart failure main symptoms

Answer 10

-Dyspnea
-Orthopnea
-PND (Paroxysmal Nocturnal Dyspnea)‏
-Blood tinged sputum
-Cyanosis

Question 11

right sided heart failure causes

Answer 11

-MC caused by left-sided heart failure (any increase in pressure in the pulmonary circulation from left-sided failure burdens right side of the heart)
-Causes of right-sided heart failure include all the causes for left-sided heart failure.; isolated right-sided heart failure not as common - typically occurs in patients with lung diseases (cor pulmonale)
-Cor pulmonale can also be secondary to primary pulmonary hypertension, recurrent pulmonary thromboembolism, or conditions that cause pulmonary vasoconstriction (obstructive sleep apnea, altitude sickness)
-Pulmonary congestion minimal; engorgement of systemic and portal venous systems pronounced

Question 12

right sided HF

Answer 12

-Congestion of hepatic and portal vessels lead to changes in liver, spleen, and gastrointestinal tract:
-Liver increased in size and weight (congestive hepatomegaly) caused by passive congestion; Grossly: congested red-brown pericentral zones, with relatively normal-colored tan periportal regions, produce characteristic “nutmeg liver”
-Portal venous hypertension causes enlargement of spleen with platelet sequestration (congestive splenomegaly)
-Systemic venous congestion can lead to fluid accumulation (effusions) in the pleural, pericardial, or peritoneal spaces (ascites)
-Hallmark of right sided heart failure: Edema of peripheral and dependent portions of the body, especially foot/ankle (pedal) and pretibial edema
-Renal congestion more marked with right-sided heart failure = more fluid retention and peripheral edema, azotemia
-Hypoxia of CNS can also produce deficits of mental function

Question 13

right heart failure symptoms

Answer 13

-FATIGUE
-“Dependent” edema
-JVD
-Hepatomegaly (congestion)‏
-ASCITES, PLEURAL EFFUSION
-GI
-Cyanosis
-Increased peripheral venous pressure (CVP)‏

Question 14

CHF labs

Answer 14

-Usually patients have both right and left sided heart failure
-Serum levels of BNP used to assess CHF (BNP released by ventricular cardiomyocytes during increased wall stress)
-Echocardiography helpful: measure ejection fraction, wall motion, valvular function, and possible mural thrombosis
-Treatment initially focused on correcting any underlying cause (e.g., valvular defect or inadequate cardiac perfusion)
-Also salt restriction, diuretics (reduce volume overload), inotropes (increase myocardial contractility), adrenergic blockers or ACE inhibitors (reduce afterload)

Question 15

congenital heart disease

Answer 15

-Cause unknown in almost 90% of cases; most probably interaction of environment and multiple genes (multifactorial)
-Three categories:
* Left-to-right shunt
* Right-to-left shunt
* Obstruction
-Shunt = abnormal communication between chambers or blood vessels

Question 16

CHD, L to R

Answer 16

-Left-to-right shunts (all have “D”s in their names) increase pulmonary blood flow but NOT initially associated with cyanosis; may develop pulmonary hypertension
-Atrial Septal Defect - Usually asymptomatic until adulthood; increase only right ventricular and pulmonary outflow volumes; usually don NOT show symptoms before 30 years
-Ventricular septal defect - Most common CHD defect; only 30% are isolated; often with TETRALOGY of FALLOT
-50% of small muscular VSDs close spontaneously
-large defects usually cause significant left-to-right shunting, leading to early right ventricular hypertrophy and pulmonary hypertension
-Patent Ductus Arteriosus -During intrauterine life, allows blood flow from pulmonary artery to aorta, bypassing unoxygenated lungs; usually ductus closes within 1 to 2 days of birth (because of increased arterial oxygenation, decreased pulmonary vascular resistance, and declining local levels of prostaglandin E2
-PDAs account for about 7% of cases of CHD; 90% isolated: Characteristic, continuous, harsh “machinery-like” murmur
-Isolated PDA should be closed early; therapy includes prostaglandin synthesis inhibitors and possibly surgical interventions

Question 17

congenital HD R to L shunts

Answer 17

-When blood from right side of circulation flows directly into the left side (right-to-left shunt), hypoxemia and cyanosis result (because pulmonary circulation is bypassed and poorly oxygenated venous blood shunts directly into systemic arterial supply)
-Right-to-left shunts: ( all have “T”s in their names)
-tetralogy of Fallot (TOF)!!!
-dont need to know the rest:
-transposition of the great arteries (TGA),
-persistent truncus arteriosus
-tricuspid atresia
-total anomalous pulmonary venous connection

Question 18

R -> L shunts

Answer 18

-TETRALOGY of FALLOT most COMMON
-(1) VSD
-(2) obstruction of right ventricular outflow tract (subpulmonic stenosis),
-(3) an aorta that overrides the VSD
-(4) right ventricular hypertrophy
-Heart usually enlarged, classically “boot-shaped” because of marked right ventricular hypertrophy
-VSD usually large with aortic valve at superior border, overriding the defect and both ventricular chambers
-The obstruction to right ventricular outflow most often due to narrowing of the infundibulum (subpulmonic stenosis)
-Depending on severity of the subpulmonic stenosis, untreated TOF can be tolerated into adulthood; 10% of unoperated individuals are alive at 20 years of age
-!!!With more severe right ventricular outflow obstruction, right-sided pressures approach or exceed left-sided pressures, and right-to-left shunting develops, producing cyanosis (classic TOF)

Question 19

VSD

Answer 19

The aorta is positioned directly over a ventricular septal defect (VSD), instead of over the left ventricle. Result - the aorta receives some blood from the right ventricle, causing mixing of oxygenated and deoxygenated blood, reducing amount of oxygen delivered to the tissues

Question 20

ischemic heart disease

Answer 20

-Single largest cause of mortality worldwide
-90% of IHD patients have ATHEROSCLEROSIS
-Angina Pectoris: Stable, Unstable
-Myocardial Infarction ‏
-Chronic IHD CHF
-Sudden Cardiac Death (SCD)‏
-“Acute” Coronary Syndromes:
-UNSTABLE ANGINA
-Acute myocardial infarction
-SCD (Sudden Cardiac Death)

Question 21

acute plaque change

Answer 21

-Rupture/Refissuring
-Erosion/Ulceration, exposing ECM
-Acute Hemorrhage
-Please note - Plaques do NOT have to be severely stenotic to cause acute changes, i.e., 50% of AMI results from thromboses of plaques showing LESS THAN 50% stenosis
-but stable angina requires 75% stenosis

Question 22

coronary artery patho in ischemic heart disease

Answer 22

dont need severe stenosis for an MI

Question 23

angina pectoris

Answer 23

-Chest pain
-Paroxysmal (sudden)‏
-Recurrent
-15 sec -> 15 min.
-Reduced perfusion, but NO infarction!
-THREE TYPES
-STABLE: relieved by rest or nitro
-PRINZMETAL: SPASM is main feature, responds to nitro
-UNSTABLE (crescendo, PRE-infarction, Q-wave angina): pattern of increasingly frequent, prolonged (>20 min), or severe angina, usually occurring at rest -> associated with plaque disruption and superimposed partial thrombosis

Question 24

sequence leading to most MIs

Answer 24

-!!!An atheromatous plaque is eroded or suddenly disrupted by endothelial injury, intraplaque hemorrhage, or mechanical forces, exposing subendothelial collagen and necrotic plaque contents to the blood
-Platelets adhere, aggregate, are activate: releasing thromboxane A 2 , adenosine diphosphate (ADP), and serotonin—causing further platelet aggregation and vasospasm
-Activation of coagulation by tissue factor and other mechanisms adds to growing thrombus
-Within minutes, thrombus completely occludes the coronary artery lumen

Question 25

MI

Answer 25

-Transmural vs. Subendocardial (inner 1/3)‏
-SAME risk factors as atherosclerosis
-Most are TRANSMURAL, and MOST are caused by coronary artery occlusion
-In the 10% of transmural MIs NOT associated with atherosclerosis:
-Vasospasm
-Emboli
-UNexplained

Question 26

timing of gross and microscopic findings

Answer 26

dont need to know

Question 27

AMI dx

Answer 27

-SYMPTOMS – chest pain radiating to left axilla/arm, dyspnea, diaphoresis; women and diabetics may have atypical symptoms
-EKG
-CK-MB
-Troponin
-C-reactive protein predicts risk of AMI in angina patients

Question 28

lab enzymes

Answer 28

coagulation necrosis
CHARACTERIZED BY THE LOSS OF THE NUCLEUS
-TEST QUESTION
-A WEEK LATER AFTER MI -> AND YOU LOOK AT TISSUE -> GRANULATION TISSUE- A BUNCH OF MACROPHAGES, COLLAGEN, & NEW VESSELS
-TEST QUESTION
-if CK-MB is low it doesnt rule out MI -> must do troponins

Question 29

reperfusion

Answer 29

-Goal in acute MI – save myocardium; restore tissue perfusion (via thrombolysis, angioplasty, CABG)
-Late restoration of blood flow can be associated with arrhythmias, can cause reperfusion injury: Although reperfusion can save reversibly injured cells, it also alters the morphology of irreversibly injured cells
-Some factors that contribute to reperfusion injury:
-Mitochondrial dysfunction: Ischemia alters mitochondrial membrane permeability, leads to swelling and rupture of outer membrane
-Myocyte hypercontracture: During ischemia, intracellular levels of calcium are increased because of impaired calcium cycling and sarcolemmal damage; after reperfusion, contraction of myofibrils is augmented and uncontrolled, causing cytoskeletal damage and cell death
-Free radicals including superoxide anion (O2), hydrogen peroxide (HO2 ), hydroxyl radicals (OH), etc. produced within minutes of reperfusion: damage myocytes by altering membrane proteins

Question 30

complications of MI

Answer 30

-Wall motion abnormalities
-Arrhythmias (usually within first 24 hours)!!!!- MC
-Rupture (4-5 days) – cardiac tamponade
-Pericarditis
-Dressler syndrome (autoimmune pericarditis 2 weeks – 2 months post MI)
-RV infarction
-Infarct extension
-Mural thrombus
-Ventricular aneurysm
-Papillary muscle dysfunction (regurgitation)
-CHF

Question 31

hypertensive heart disease

Answer 31

-Consequence of increased demands placed on heart by hypertension, causing pressure overload and ventricular hypertrophy
-Hypertension creates a greater pressure load on the heart to cause left ventricular hypertrophy
-Micro shows INCREASED FIBER (MYOCYTE) THICKNESS
INCREASED nuclear size (boxcar nucleus)
-Hypertrophic adaptive response of the heart, which can progress:
-Myocardial dysfunction
-Cardiac dilatation
-CHF
-Sudden death

Question 32

valvular heart disease

Answer 32

-Opening problems: Stenosis
-Closing problems: Regurgitation or Incompetence

Question 33

calcific aortic stenosis

Answer 33

-MC; result of age-associated “wear and tear” of either anatomically normal valves or congenitally bicuspid valves (approximately 1% of population)
-Aortic stenosis of previously normal valves (degenerative calcific aortic stenosis): seventh to ninth decades of life; stenotic bicuspid valves one to two decades earlier
-Most likely results from recurrent chronic injury due to hyperlipidemia, hypertension, inflammation
-Morphology - mounded calcified masses on the outflow surfaces of the cusps that ultimately prevent cuspal opening
-!!Functional valve area is decreased by large nodular calcific deposits that can eventually cause outflow obstruction; subjects left ventricular myocardium to progressively increasing pressure overload

Question 34

aortic stenosis

Answer 34

-Obstruction to left ventricular outflow leads to gradual narrowing of valve orifice and an increasing pressure gradient across calcified valve
-!!Left ventricular pressures rises, producing concentric left ventricular (pressure overload) hypertrophy
-Hypertrophied myocardium tends to be ischemic (diminished microcirculatory perfusion); angina pectoris may occur; eventually, cardiac decompensation and CHF
-If untreated, most patients with aortic stenosis will die within 5 years of developing angina, within 3 years of developing syncope, and within 2 years of CHF onset
-!!Treatment requires surgical valve replacement

Question 35

mitral annular calcification

Answer 35

-Degenerative calcific deposits in the mitral valve usually develop in the fibrous annulus
-Irregular, stony hard, occasionally ulcerated nodules at base of the leaflets
-Usually does not affect valvular function; however, rarely can lead to:
-* Regurgitation by interfering with physiologic contraction of the valve ring
-* Stenosis by impairing opening of the mitral leaflets
-* Arrhythmias and occasionally sudden death by penetration of calcium deposits deep enough to impinge on AV conduction system
-Increases with age, more common in women and individuals with mitral valve prolapse

Question 36

mitral valve prolapse (MVP) aka myxomatoid degeneration of the mitral valve

Answer 36

-One or both mitral valve leaflets are “floppy” and protrude into left atrium during systole
-2% to 3% of adults in US, more common in women; mostly incidental finding, but may lead to serious complications in small minority
-parachute valve
-Cause not really known
-Uncommonly, associated with heritable disorders of connective tissue including Marfan syndrome
-!!Ballooning (hooding) of mitral leaflets; affected leaflets often enlarged, redundant, thick, and rubbery; associated tendinous cords may be elongated, thinned, or even ruptured, and the annulus may be dilated

Question 37

MVP: clinical features

Answer 37

-Usually asymptomatic
-Mid-systolic “click” (caused by abrupt tension on redundant valve leaflets and chordae tendineae as valve tries to close)
-May or may not be associated regurgitant murmur
-Diagnosis confirmed by echocardiography
-Minority of patients - occasional chest pain, dyspnea
-3% may develop Infective endocarditis, mitral insufficiency, arrythmias, stroke or other systemic infarct (from embolism of leaflet thrombi), sudden death

Question 38

rheumatic heart disease- just know ab pain carditis and joint pain

Answer 38

-Rheumatic fever: acute, immunologically mediated, multisystem inflammatory disease usually occuring a few weeks after group A streptococcal pharyngitis
-Acute rheumatic carditis in active RF may progress over time to chronic rheumatic heart disease (RHD)
-RHD (chronic) characterized by deforming fibrotic valvular disease, esp. of the mitral valve
-Incidence and mortality rate of RF and RHD have declined

Question 39

acute rheumatic fever

Answer 39

-Acute RF results from host immune responses to group A streptococcal antigens that cross-react with host proteins (2- to 3-week delay in symptoms: time needed to generate an immune response)
-Damage to heart tissue may be caused by combo of Ab- and T cell–mediated reactions
-Around 3% of infected patients develop acute rheumatic fever
-Chronic fibrotic lesions result from healing and scarring associated with resolution of the acute inflammation
-Mostly children between 5 - 15 years of age
-Manifestations include:
-Migratory polyarthritis (large joints)
-Pancarditis (myocarditis, pericarditis, or endocarditis) -> all three layers
-Subcutaneous nodules (typically on extensor surfaces of extremities)
-Erythema marginatum, irregular circinate skin rash
-Sydenham chorea, a neurologic disorder with involuntary rapid movements

Question 40

rheumatic fever dx criteria (Dont need to know jones)

Answer 40

-Revised Jones criteria:
-evidence of a preceding group A streptococcal infection, and
-presence of two major manifestations, or one major and two minor manifestations (nonspecific include fever, arthralgia, or elevated blood levels of acute-phase reactants)
-Strep cultures usually negative by time of illness; though Abs to streptolysin O and DNaseB present in serum
-Approximately 1% die of fulminant RF involvement of the heart

Question 41

acute RF clinical features

Answer 41

-Migratory Polyarthritis
-Pancarditis
-Subcutaneous nodules
-Erythema marginatum
-Sydenham chorea
-joint pain
-Heart (micro) shows Aschoff bodies (with plump activated macrophages called Anitschkow cells (aka “caterpillar cells”)
-Diffuse inflammation and Aschoff bodies may be found in all layers of heart - (pancarditis)

Question 42

chronic rheumatic heart disease

Answer 42

-Clinical manifestations appear years/decades after initial episode of RF: cardiac murmurs, cardiac hypertrophy and dilation, and heart failure
-Mitral valve: leaflet thickening, commissural fusion and shortening, and thickening and fusion of tendinous cords; calcification and fibrous bridging across valvular commissures create “fish mouth” stenosis!!!!!!!!
-MC CAUSE OF MITRAL STENOSIS IS CHRONIC RHEUMATIC HEART DISEASE !!!

Question 43

infectious endocarditis

Answer 43

-Microbial infection of heart valves; leads to formation of vegetations (thrombotic debris and organisms) often with destruction of underlying cardiac tissues; Most infections bacterial
-Acute IE usually caused by infection of previously normal heart valve by a highly virulent organism (e.g., Staphylococcus aureus ) that rapidly produces destructive lesions; Staph. aureus usually in IE among IV drug users
-S. aureus commonly found on skin can infect either healthy or deformed valves; responsible for 20% to 30% of cases
Subacute IE usually caused by organisms with lower virulence (e.g., viridans streptococci, usu oral cavity) that cause insidious infections of deformed valves with less destruction
-Other bacterial causes: enterococci and the HACEK group (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella , and Kingella ), commensals in oral cavity
-Disposing factor for endocarditis: bacteremia (or fungemia) from other infection, dental or surgical procedure, contaminated needle in IV drug abusers

Question 44

endocarditis criteria- DONT NEED TO KNOW

Answer 44

-Diagnosis by these guidelines, Modified Duke Criteria, requires either pathologic or clinical criteria; if clinical criteria are used, 2 major, 1 major + 3 minor, or 5 minor criteria are required for definitive diagnosis.
-Osler’s “nodes” (raised), small, tender subcutaneous nodules, develop in the pulp of digits, last for hours to days
-Janeway lesions: small erythematous or hemorrhagic, macular, non-tender lesions on palms and soles, result of septic embolic events

Question 45

infectious endocarditis

Answer 45

-Vegetations on heart valves: friable, bulky, potentially destructive lesions containing fibrin, inflammatory cells, and bacteria; may be single or multiple, may involve more than one valve; can sometimes erode into underlying myocardium and produce an abscess (ring abscess)
-Vegetations of subacute endocarditis associated with less valvular destruction (v. acute IE)
-Acute endocarditis: rapid onset of fever, chills, weakness, and lassitude; in older adults only manifestations may be nonspecific fatigue, weight loss, and flulike syndrome
-Sepsis, arrhythmias (suggesting invasion into underlying myocardium and conduction system), and systemic embolization associated with poor prognosis
-If not treated, acute IE generally fatal
-Treatment: long-term (6 weeks or more) antibiotic therapy and/or valve replacement; reduces mortality
-For infections involving low-virulence organisms (e.g., S. viridans ), cure rate is 98%

Question 46

nonbacterial thrombotic endocarditis (NBTE)

Answer 46

-AKA marantic endocarditis
-Deposition of small (1 to 5 mm) sterile thrombi on leaflets of cardiac valves; micro shows bland thrombi, loosely attached to underlying valve; vegetations are nondestructive, do not elicit any inflammatory reaction
-Often in debilitated patients with cancer or sepsis
-Usually occurs on previously normal valves
-Hypercoagulable states predisposition:
-chronic DIC
-increased estrogen
-underlying malignancy (esp. mucinous adenocarcinomas secondary to procoagulant effects of tumor-derived mucin factor- can cause migratory thrombophlebitis aka Trousseau syndrome)
-indwelling catheters

Question 47

vegetations

Answer 47

-INFECTIVE >5mm
-NON-Infective <5mm
-dont need to memorize^
-Vegetations:
-1) rheumatoid = small, at chordae tendinae junction
-2) infectious = big (>5 mm)
-3) NBTE = non-bacterial thrombotic endocarditis (<5 mm)
-4) lupus (Libman-Saks) = BOTH sides

Question 48

cardiomyopathies

Answer 48

-DILATED (DCM)
-Systolic dysfunction
-HYPERTROPHIC (HCM)
-Diastolic dysfunction
-RESTRICTIVE (RCM)
-Diastolic dysfunction

Question 49

dilated cardiomyopathy

Answer 49

-Adults
-Progressively declining LVEF
-LVEF ~ prognosis
-3 Main causes
-Myocarditis
-Alcohol
-Adriamycin- chemo agent
-cocksackies - viral ;.
-Heart changes:
-4 chamber dilatation
-irregular hypertrophy
-Interstitial Fibrosis

Question 50

hypertrophic cardiomyopathy

Answer 50

-Also called IHSS, (Idiopathic Hypertrophic Subaortic Stenosis)
-GENETIC defects involving:
-Beta-myosin heavy chain
-Troponin T
-Alpha-tropomyosin
-Myosin binding protein C
-PATHOLOGY: Massive hypertrophy, Asymmetric septum, DISARRAY of myocytes, INTERSTITIAL fibrosis
-CLINICAL: ↓chamber volume, ↓SV, ↓ diastolic filling
-Sudden death in young athletes can occur
-Disproportionate ventricular septal hypertrophy involving basal and midventricular regions

Question 51

restrictive cardiomyopathy

Answer 51

-↓ ventricular compliance
-May be caused by amyloid, radiation fibrosis, sarcoidosis, etc.
-Chiefly affects DIASTOLE
-NORMAL chamber size and wall thickness
-THREE similar diseases affecting predominantly the SUBENDOCARDIAL area:
-Endomyocardial Fibrosis (African children)
-Loeffler Endomyocarditis (eosinophilic leukemia)
-Endocardial Fibroelastosis (infants)

Question 52

myocarditis

Answer 52

-INFLAMMATION of MYOCARDIUM
-Mainly microbial
-COXACKIE A & B, CMV, HIV
-Trypanosoma cruzi (Chagas dis.), 80%
-Trichinosis
-Toxoplasmosis
-Lyme disease (5%)
-Diphtheria
-IMMUNE: Post-viral, rheumatic, SLE, drug hypersensitivity->alpha-methyl dopa, sulfas

Question 53

myocarditis: viral

Answer 53

-MC cause in US: viral infections ; Coxsackie viruses A and B and other enteroviruses account for most cases
-Less common causes: cytomegalovirus, HIV, and influenza
-Depending on pathogen and host, viruses potentially cause myocardial injury either as a direct cytopathic effect, or by eliciting a destructive immune response
-Myocardial injury produces inflammatory cytokines which can also cause myocardial dysfunction out of proportion to degree of actual myocyte damage

Question 54

other causes of myocarditis

Answer 54

-Protozoan Trypanosoma cruzi (Chagas disease - endemic in some regions of South America
-Trichinosis (Trichinella spiralis): most common helminthic disease associated with myocarditis
-Parasitic diseases, including toxoplasmosis
-Lyme disease caused by spirochete Borrelia burgdorferi (5% of patients affected): self-limited conduction system disorder
-In diphtheritic myocarditis, myocardial injury results from diphtheria toxin release by Corynebacterium
-AIDS-associated myocarditis may reflect inflammation and myocyte damage without clear etiologic agent, or myocarditis attributable directly to HIV or an opportunistic pathogen
-Noninfectious causes of myocarditis: immunologically mediated (hypersensitivity myocarditis) or idiopathic conditions with distinctive morphology (giant cell myocarditis) probably of immunologic origin
-Some chemotherapy may occasionally lead to fatal lymphocytic myocarditis

Question 55

pericardium

Answer 55

-Normally 30-50 ml clear serous fluid
-Visceral (epicardium)
-Parietal (Fibrous pericardium)
-PERICARDIAL EFFUSIONS TAMPONADE
-Ruptured MI
-Traumatic perforation
-Infective endocarditis
-Ruptured aortic dissection

Question 56

pericarditis

Answer 56

-SEROUS: Rheum. Fever (RF), SLE, scleroderma, tumors, uremia
-FIBRINOUS: MI (Dressler), uremia, radiation, RF, SLE, s/p open heart surgery
-PURULENT: infective, bacterial
-HEMORRHAGIC: Malignancy, TB
-CASEOUS: TB
-CHRONIC: (ADHESIVE, CONSTRICTIVE)
-The “bread and butter” pericarditis is classically and most often described in uremia or pericardial infections. What is the exudate? Ans: Fibrin
“Bread and butter” pericarditis = fibrinous pericarditis.

Question 57

cardiac tumors

Answer 57

-Primary cardiac tumors uncommon, most benign
-Five most common: no malignant potential, account for almost 90% of all primary heart tumors: myxomas, fibromas, lipomas, papillary fibroelastomas, and rhabdomyomas.
-Myxomas: most common primary tumor of the adult heart (benign)
-About 90% in the atria, left/right ratio 4:1
-Major clinical manifestations due to valvular “ball-valve” obstruction, embolization, or syndrome of constitutional symptoms, such as fever and malaise (tumor may produce cytokine IL-6)
-Surgical removal usually curative
-Rhabdomyomas: most frequent primary tumor of the pediatric heart (benign)
-50% of cases associated with tuberous sclerosis, with mutations in the tuberous sclerosis complex TSC1 or TSC2 tumor suppressor genes
-Primary malignant cardiac tumors: very rare, usually an angiosarcoma

Question 58

metastatic tumor to heart

Answer 58

-Occur in approximately 5% of patients dying of cancer
-Most frequent are lung and breast carcinomas, melanomas, leukemias, and lymphomas
-Clinical symptoms: symptomatic pericardial effusions or a mass-effect restricting cardiac filling
-Lung carcinoma or malignant lymphoma can infiltrate mediastinum, causing encasement, compression, or invasion of the superior vena cava with resultant obstruction to blood coming from head and upper extremities (superior vena cava syndrome)
-Renal cell carcinoma often invades the renal vein; can grow as a continuous column of tumor up the inferior vena cava lumen and into the right atrium, blocking venous return to the heart
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