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Cardio II: Exam 2 > Heart Pathology > Flashcards

Heart Pathology Flashcards

1
Q

foramen ovale

A

Foramen Ovale formation: Septum primum seperates the atria with ostrium primum hole. As Septum primum continues to grow, the ostium primum gets smaller. Programmed cell death results in formation of a second hole in septum primum called ostium secundum. A second wall of tissue called septum secundum grows over the ostrium secundum in the RA but is kept open due to the high pressure in the right atrium. When the pressure drops at birth, this flap is slammed shut from higher pressure in left atria, and eventually fuses.

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2
Q

LAD

A
  • Left anterior descending artery (LAD): supplies most of apex of heart: most commonly infarcted (40-50%)
    o anterior wall of left ventricle near apex
    o anterior 2/3 of ventricular septum
    o apex of heart
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3
Q

LCX

A

Left circumflex artery (LCX) – (15-20% of infarcts)

o lateral wall of left ventricle, except for apex

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4
Q

RCA

A
  • Right coronary Artery (RCA) – (30-40% of infarct)
    o inferior/posterior wall of left ventricle
    o posterior portion of ventricular septum
    o inferior/posterior right ventricular free wall
    o most often causes arrhythmias
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5
Q

CHF

A

= heart is unable to pump blood at a rate sufficient to meet the metabolic demands of the tissues or can do son only at an elevated filling pressure
• due to insufficient pump rate to meet demands
• due to pump only being able to meet demands with elevated filling pressure

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6
Q

cardiomegally

A

Normal: Male 300-350 gm; Female 250-300 gm

  • 350-600 gm: Pulmonary HTN, IHD
  • 400-800 gm: Systemic HTN, aortic stenosis, mitral regurgitation, dilated cardiomyopathy
  • 600-1000 gm: Aortic regurgitation, hypertrophic cardiomyopathy
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7
Q

“Concentric Hypertrophy”

A
  • Pressure overload hypertrophy: “Concentric Hypertrophy” - results in new sarcomeres assembled in parallel, expanding the cross-sectional area of myocytes and causing concentric increase in wall thickness
    • left ventricle: due to systemic HTN or aortic stenosis
    • right ventricle: cor pulmonale
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8
Q

“Eccentric Hypertorphy

A
  • Volume-overload hypertrophy: “Eccentric Hypertorphy” new sarcomeres are assembled in series w/in existing sarcomeres leading to ventricular dilation
    • see an overall cardiac mm. mass increased even though dilation may cause chamber wall to look thinner
    • seen in valve disorders and congenital heart disease
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9
Q

left sided heart failure

A

• accumulation of fluid within the lungs and pleural cavities, pleural effusions
• Chronic: slowly progressive failure which may over time develop sufficient severity to cause right sided heart failure
• Acute: Rapidly progressing fatal course – often see massive pulmonary edema and “pink frothy fluid coming out of mouth”, due to macrophages ingestion of the lungs of fluid and RBCs
• Most commonly caused by:
- Ischemic heart disease
- Hypertensive heart disease
- Aortic and mitral valvular disease
- Primary nonischemic myocardial disease (cardiomyopathy)
• “Systolic Failure” = insuff. ejection fraction, pump failure
• “Diastolic Failure” = Stiff left ventricle, that can’t fully fill during diastole → decreased CO

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10
Q

path of LSHF?

A

• Cardiomegaly: hypertrophy and/or chamber dilation
o ischemic heart disease: see chamber dilation
o left sided valvular disease: mostly see LV hypertrophy
• Secondary enlargement of Left Atrium
o assoc. w/ A Fib
o High incidence of mural thrombosis due to stasis and turbulence → systemic emboli
• Tachycardia
• Third Heart Sound (S3 gallup): occurs in diastolic filling due to decreased compliance of ventricular wall – blood from atria shoots into ventricle and hits the wall making this sound. This is normal in children, but watch out for in adults that never had before
• Mitral regurgitation: heart systolic murmur – due to dilation of walls, valves no longer properly seal
Extra-Cardiac Effects:
• Pulmonary Congestion and Edema:
o hear pulmonary basilar crackles (rales) and possible pleural effusions
o “flash pulmonary edema” due to rapid onset
o Siderophages: “Heart Failure Cells” – seen in long term, macrophages in lungs that have engulfed RBCs
o Dyspnea: SOB
o Orthopnea: dyspnea when laying down
o Paroxysmal Nocturnal Dyspnea: random, severe dyspnea attacks at night
• Renal Problems:
o decreased CO → hypoperfusion of kidney → activation of RAAS → fluid retention and expansion of vascular volume (further damage to heart) → decrease in blood flow to kidney →azotemia
o “pre-renal azotemia” = inability of kidney to excrete nitrogenous waste products
• Brain: hypoxic ncephalopathy

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11
Q

S3

A

LSHF

• Third Heart Sound (S3 gallup): occurs in diastolic filling due to decreased compliance of ventricular wall – blood from atria shoots into ventricle and hits the wall making this sound. This is normal in children, but watch out for in adults that never had before

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12
Q

siderophages

A

heart failure cells, seen in LSHF

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13
Q

RSHF

A

MOST COMMONLY CAUSED BY LEFT HEART FAILURE!
• peripheral edema: see accumulation of fluid in all other body sites and body cavities, liver and spleen
• left heart failure → increased pulmonary pressure → increased workload on RV → right side failure
• Cor Pulmonale = Heart disease that is secondary to lung disease
- pure/isolated right sided failure
- uncommon
- cardiac hypertrophy and filation are confined to RA and ventricle
Extracardiac Effects:
o Pitting Edema: accumulation of edema fluid in subcutaneous tissues = “anasarca” (massive generalized edema)
o Congestive Hepatomegaly: increased pressure in IVC → increased pressure in hepatic vv → congestion in hepatic sinusoids → centrilobular necrosis (due to ischemia and congestions)
o “Cardiac Cirrhosis” see increased fibrous tissue in centrilobular zone
o “nutmeg liver” appearance
o Congestive Splenomegally: usually mild with only doubling in size
o Ascites: massive peritoneal effusions
o Pleural and Pericardial Cavity Effusions (transudates)

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14
Q

natriuretic peptides

A

Peptides → cause vasodilation, natriuresis and diuresis
- ANP: produced by atrial myocytes due to atrial distension
- BNP: due to ventricular mycotes: used for determination of CHF!
o if BNP 500 then it is mostly likely CHF
- CNP: due to endothelial cells b/c of shear stress

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15
Q

congenital heart diseases

A

Congenital Heart Disease:

  • ** defects occur: week 3-8 gestation ***
  • Most common: bicuspid aortic valve, ventricular septal defect, atrial septal defect (most common ddx in adulthood), pulmonary stenosis, patent ductus arteriosus, tetraology of fallot….

Where does problem in great vessels stem from? Neural crest defect

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16
Q

NKX2-5 transcription factor and TBX5

A

NKX2-5 transcription factor:

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17
Q

TBX1 tx factor: del 22q11.2

A

DiGeorge Syndrome = Cardiac outflow tract defects
o “Catch-22” = Cardiac abnormalities, abnormal facies, thymic aplasia, cleft palate, hypocalcemia
o Cardiac outflow defects = persistent truncus arteriosus, aortic arch interruption/coarctation
o see T cell deficiency from thymus problems

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18
Q

JAG1, NOTCH2:

A

tetralogy of fallot

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19
Q

Fibrillin protein mutation:

A

Marfan’s Syndrome: Aortic aneurysm and valve abnormalities

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20
Q

left to right shunts

A

: ASD, VSD, PDA, AVSD
o ** pink babies ** see increased pulmonary blood flow with no initial cyanosis
• chronically elevated volume and pressure in the right side of heart→ results in right ventricular hypertrophy
• muscular pulmonary aa. develop medial hypertrophy and vasoconstriction to normalize distal pressure
• Esenmenger syndrome: (shunt reversal): increased right heart pressure → irreversible pulmonary HTN → right to left shut and shunt reversal → cyanosis

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21
Q

Esenmenger syndrome

A

(shunt reversal): increased right heart pressure → irreversible pulmonary HTN → right to left shut and shunt reversal → cyanosis

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22
Q

VSD

A

Ventricular Septal Defect (VSD)
• most common!
• 90% involves membranous septum (high up)
• 10% involves muscular septum (low)
• large defects result in murmur, pulmonary HTN
Clinical:
• most assoc. with other cardiac anomalies, only 20%are isolated
• smaller lesions can be well tolerated for many years – will close spontaneously
• large lesions lead to irreversible pulmonary vascular disease→ shunt reversal, cyanosis, death

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23
Q

ASD

A
  • Three Major Types:
    1. Secundum (90%): involves fossa ovalis, found near the center (Note: patent foramen ovale is not ASD)
    2. Primum (5%) – adjacent to AV valve
    3. Sinus Venosus- near superior vena cava
    • ASD’s are well tolerated and may be symptomatic, 10% of untreated develop pulmonary HTN
    • May hear murmur from increased flow across pulmonary valve
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24
Q

PDA

A

Patent (Persistent) Ductus Arteriosus: (PDA)
• Ductus usually closes 1-2 days due to: increased O2, decreased pulmonary resistance, decreased Prostaglandin E2
• 90% are isolated defects
• Narrow ductus defect is asymptomatic
• harsh machine-like murmur
• if chronic, can develop pulmonary HTN, due to back flow into right side of heart → cyanosis
• can get paradoxical embolisms
• Treatment: NSAID to close, or prostaglandin E to keep open until surgery
• ** note: prior to closure, must ensure that there are no other defects!

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25
Q

AVSD

A

Atrioventricular Septal Defect (AVSD):
• partial = ASD and cleft anterior mitral leaflet with mitral insufficiency
• complete = large combined AV valve with all 4 chambers communicating

  • MOST common defect in Down syndrome >1/3 patients have AVSD***
    • 40-60% of children with Trisomy 21 have CHD: AVSD>VSD>ASD>PDA>TF
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26
Q

right to left shungs

A

TF, TPGA, persistent truncus arteriosus, tricuspid atresia
• ** see hypoxia and cyanosis** = hypoxic from day 1
• pulmonary circulation is bypassed and poorly O2 venous blood shunts directly into systemic arterial supply, decreased amout of blood going to lungs to be oxygenated
• paradoxical embolism: emboli from peripheral vv. can bypass lung and enter systemic circulation
• “clubbing” of tips of fingers and toes: “hypertrophic osteoarthropathy”
• polycythemia due to hypoxia

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27
Q

tetrology of fallot

A

**Tetrology of Fallot:
1) Ventricular Septal Defect (VSD)
2) Subpulmonic (+/- pulmonic valve) stenosis = obstruction of right ventricular outflow tract
• subpulmonic stenosis protects lung from increased pressure, and pulmonary arteries may be hypoplastic
3) Aorta overrides the VSD – heart is laying down on its side
4) Right ventricular hypertrophy
• note: marked right ventricular hypertrophy: “boot-shaped” heart, results in blood to be shunted from right side to left side
• if subpulmonic stenosis is balanced with left ventricular pressure, then it behaves like a VSD and lungs are perfused = pink tetralogy of Fallot
• as child grows, the subpulmonic stenosis does not increase in size, making it progressively worse

What determines if baby is cyanotic or pink? the degree of stenosis in the outflow tract

  • too much stenosis, have right to left shunting à blue cyanotic baby
  • not too much stenosis, don’t have the right to left shunting à pink baby
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28
Q

TGA

A

Transposition of the Great Arteries:
• defect with truncal and aorta pulmonary septae
• results in separation of pulmonary and systemic circulations, incompatible with life unless pt. has VSD, patent foramen ovale or patent ductus arteriosus
• Patient is stable with VSD (35%), but PDA or patent foramen ovale can close
• if PDA infuse with prostaglandin E and perform atrial septostomy followed by surgical correction

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29
Q

coarctation of aorta

A

Coarcation of the Aorta: (coarcation = narrowing/constriction)
• more common in males
• Infantile form (With PDA): symptomatic in early childhood – see hypoplasia of aorta prior to patent ductus arteriosus (cyanosis of inferior body and weak femoral pulses)
• Adult form (Without PDA): ridge-like fold opposite ligamentum arteriosus, closed ductus arteriosus → encroachment of aortic lumen (HTN in upper extremities, low pressure and pulses in lower extremities)
o disease may go unrecognized until adult life
o 50% of cases accomp. by bicuspid aortic valve, ASD, VSD, mitral regurg, berry aneurysms
• Coarctation of aorta, postductal adult type
o Murmurs are often present with coarctations
o may develop collateral circulation b/w pre-coarctation and post-coarctation arteries through enlarged intercostal and internal mamm. aa.: results in “notching” visible erosions on radiographs in undersurface of ribs
o Kidneys will sense low pressure → turn on RAAS
o high pressure in head, low pressure in extremities

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30
Q

aortic stenosis/atresia

A

(80% isolated congenital finding)
• Valvular aortic stenosis – have hypoplastic, dysplastic, or abnormal number of cusps (if severe get hypoplastic left heart syndrome)
• Subaortic stenosis – ring or collar below cusps: hear prominent systolic murmur and sometimes a thrill
• Supravalvular aortic stenosis – elastin gene mutation with aortic dysplasia (thickening)
• Williams–Beuren syndrome -deletion of about 28 genes from chromosome 7 with ELN gene (elastin) haploinsufficiency, hypercalcemia, glucose intolerance, facial and cognitive defects.

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31
Q

stable angina

A

Typical) Angina: increases in myocardial O2 demand that outstrip ability of stenosed coronary arteries to increase O2 delivery; not usually associated with plaque disruption
• stenosis is often > 75%, no plaque disruption or assoc. thrombus, no cellular necrosis
• occurs during emotional excitement, stress or physical activity
• most common form, usually relieved by sublinqual nitroglycerine

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32
Q

unstable angina

A
  1. Unstable (Crescendo, Pre-infarction) angina: caused by acute plaque disruption that results in thrombosis and vasoconstriction and leads to severe but transient reductions in coronary blood flow
    • variable stenosis with plaque disruption and nonocclusive thromboemboli present
    • see pattern of increasingly frequent, prolonged, severe angina that does not occur at high levels of activity
    • may be relieved by rest or sublingual nitroglycerine
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33
Q

MI

A

often result of acute plaque change that induces an abrupt thrombotic occlusion, resulting in myocardial ischemia
• Transmural MI: stenosis, with plaque disruption leading to complete block due to thrombus
• Subendocardial MI: variable stenosis with partial blockage

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34
Q

SCD

A

Unexpected death from cardiac causes early after onset of symptoms (1 to 24 hours) or sudden death from cardiac cause without antecedent acute symptoms
• usually due to lethal arrhythmia or ventricular fib
• see non-ischemic SCD in younger people (most commonly due to hypertrophic cardiomyopathy)

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35
Q

CRP

A

C Reactive Protein = non-specific measure of chronic inflammation- when elevated its indicative of risk for coronary heart disease
Other types of Angina:

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36
Q

Prinzmetal variant Angina:

A

episodic myocardial ischemia usually caused by sustained coronary artery vasospasm
• relieved by rest, nitroglycerine or CCB’s

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37
Q
  • Takotsubo cardiomyopathy:
A

dilated cardiomyopathy secondary to emotional or physical stress with normal angiogram

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38
Q

channelopathies

A

: Disorders of K+, Na+, or Ca++ channel structure or accessory proteins involved in channel function
• **Mostly autosomal dominant
• ex: Long QT syndrome, Short QT syndrome, Brugada syndrome

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39
Q

Chronic IHD

A

Chronic Ischemic Heart Disease: Ischemic Cardiomyopathy
• Fairly severe atherosclerosis → ischemic myocytes and necrosis → build scars → CHF
• onset of congestive heart failure in patients who have had past myocardial infarcts (MIs) or angina
• Cardiomegaly with left ventricular hypertrophy & dilatation
• Evidence of previous healed MIs or ischemia (areas of myocardial fibrosis)
• Develop arrhythmias, congestive heart failure and MIs

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40
Q

transmural infarct

A
  • Transmural Infarction: Ischemic necrosis involves >50% of the ventricular wall thickness
    • Commonly associated with acute plaque change with thrombosis
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41
Q

subendocardial infarct

A

: area of ischemic necrosis is limited to the inner 1/3 and thus is <50%

  • May occur as a result of acute plaque change and thrombosis
  • May result from prolonged and severe reduction in systemic blood pressure ,as encountered in shock
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42
Q

pathogenesis of MI

A

• Initial sudden change in plaque
• Immediate formation of initial platelet plug over plaque
• Vasospasm from platelet adhesion (vasoactive substances from platelets)
• Propagation of platelet plug into stable clot via extrinsic clotting system
• Within minutes, clot occludes lumen of the involved vessel (thrombosis with coronary occlusion)
Note: adrenergic stimulation can induce MI: peak incidence at 6am-noon
Note: subendocardium is first infarcted

43
Q

timing of MI

A
  • Seconds: ATP depletion due to decreased glycolysis
  • 2 minutes: loss of contraction
  • 20-40 minutes: irreversible cell injury – necrosis
  • > 1 hr: microvacular injury
  • 6 hours = complete unsalvageable necrosis
44
Q

morphology of MI

A
  • 0-1/2 hr: no gross features, no LM changes
  • ½ -4 hr: no gross features, see variable waviness of fibers in LM
  • 4-12 hr: usually see no gross features (maybe dark mottling); LM shows early coagulation necrosis, edema, hemorrhage
  • 12-24 hours: grossly see dark mottling, LM shows early neutrophilic infiltrate
  • 1-3 days: mottling with yellow tan infarct, see large infiltrate of neutrophils
  • 3-7 days: see central yellow-tan softening; LM shows dying neutrophils, early phagocytosis of macrophages
  • 7-10 days: see early formation of fibrovascular granulation tissue at margins
  • 10-14 days: see red-gray depressed infarct grossly; granulation tissue w/ new blood vessels and collagen
  • 2-8 week: see gray white scar, LM shows collagen deposition
  • > 2 mos: see dense collagenous scar
45
Q

clinical features of MI

A
  • Severe substernal chest pain with radiation of pain down left arm, neck, jaw, epigastrium
  • Weak, rapid pulse
  • Sweating profusely (diaphoretic)
  • Nausea
  • Dyspnea (difficulty breathing) secondary to pulmonary congestion and edema
46
Q

myoglobin

A 
\: can be due to any muscular stress…
•	elevated 1-4 hours after AMI
•	peaks in 6 hours
•	returns to baseline after 18-24 hours
•	best for reading MI’s <6 hours
47
Q

CK-MB

A
  • elevated 3-12 hours after AMI
  • peaks in 10-24 hours
  • returns to baseline after 48-72 hours
48
Q

CTnI/CTNT

A

most specific, though not good for recurrent MI
• elevated 3-12 hours after
• peaks 10-24 hours after Ami
• returns to baseline after 5-10 days, thus best for determining if there was an MI in past week

49
Q

reperfusion injury

A

Pathologic changes due to Reperfusion:
• Reperfusion-induced arrhythmias
• Myocardial hemorrhage with contraction bands
• Irreversible myocardial damage in addition to that caused by the initial episode of ischemia (reperfusion injury)
• Microvascular injury with endothelial swelling (no-reflow)
• Reversible “Myocardial stunning” (prolonged ischemic dysfunction) with heart failure for days

50
Q

cardiac tamponade

A

can occur after myocardial rupture due to MI

Free wall (usually anterior) → cardiac tamponade: Cardiac tamponade is pressure on the heart that occurs when blood or fluid builds up in the space between the heart muscle (myocardium) and the outer covering sac of the heart (pericardium).

51
Q

Systemic (left sided) hypertensive heart disease:

A

Criteria for Diagnosis:
• Left ventricular hypertrophy (usually concentric) in the absence of other cardiovascular pathology that may have induce it.
• A history or pathologic evidence of systemic hypertension (BP > 140/90 mm Hg)
• May present clinically with CHF or atrial arrhythmias

52
Q

Pulmonary (Right-sided) Hypertensive Heart Disease:

A 
Cor Pulmonale results from pulmonary disorders that cause chronic severe pulmonary hypertension.
Occurs with: 
•	Pulmonary Parenchyma Disorders
•	Chronic Obstructive Pulmonary Disease (COPD)
•	Diffuse Interstitial Lung Disease
•	Pulmonary Vessel Disorders
•	Recurrent Pulmonary Embolism
•	Primary Pulmonary Hypertension
•	Chest Movement Disorders
•	Kyphoscoliosis
53
Q

aortic stenosis

A

Calcification of anatomically normal and congenitally bicuspid aortic valves (more common in US)

54
Q

aortic insufficiency

A

: Dilatation of the ascending aorta due to hypertension and aging

55
Q

mitral stenosis

A

Rheumatic heart disease (more common worldwide)

56
Q

mitral insufficiency

A

Myxomatous degeneration (mitral valve prolapse)

57
Q

senile calcific aortic stenosis

A

(Senile) Calcific Aortic Stenosis:
• most common of all valvular abnormalities
• see nodular masses of Ca2+ heaped within the sinuses of valsalva
Clinical features:
• seen in ages 60-80 (7th to 9th)
• pressure hypertrophy results from flow obstruction and patient develops left ventricular concentric hypertrophy
• Left ventricular cardiac mass ischemia → CHF, syncope or angina pectoris

58
Q

Calcific Stenosis of Congenitally Bicuspid Aortic Valve

A
  • Congenital bicuspid aortic valve occurs in ~ 2% population
  • Two cusps frequently not equal size: larger cusp may have a raphe” (seam) – result of incomplete separation during development
  • Bicuspid valves more susceptible to progressive degenerative calcification; develop significant calcification earlier
  • Develop clinical symptoms and signs of cardiac dysfunction earlier, 5th and 6th decades (7th to 9th decades with tricuspid aortic valves)
59
Q

Mitral Annular Calcification:

A

“looks like a ring around the heart”
• Occurs in three types of patients
– Women over 60 years of age
– Individuals with myxomatous mitral valves
– Patients with elevated left ventricular pressure - e.g., hypertension
• Generally does not affect valvular function
• Occasionally associated with arrythmias
• Most diagnosed because: Large calcium deposits are incidentally detected on radiography done for other reasons

60
Q

MVP

A

Myxomatous Degeneration of Mitral Valve = Mitral Valve Prolapse
• One or both mitral valve leaflets are “floppy” and prolapse into the left atrium during systole (midsystolic click +/- regurgitant murmur)
• Affects ~2-3% adults in US, most often young women (7F:1M)
• Seen in Marfan syndrome (fibrillin-1/elastic fibers)
• Vast majority patients clinically asymptomatic, but small subset (3%) may develop one of four serious complications (infective endocarditis, mitral insuffic, stroke, arrhythmias, atypical chest pain)
Pathology:
• Intercordal ballooning of mitral valve leaflets
• Affected leaflets are enlarge, thick and rubbery
Secondary changes:
• dilation of annulus, fibrosis of valve leaflets and endocardial surfaces of atrium and ventricle (jet lesions); thrombi on atrial surfaces of mitral leaflets, and focal calcification at base of posterior leaflet

61
Q

Acute Rheumatic fever

A
  1. Group A streptococcal infection that is not treated
  2. Acute rheumatic fever: acute systemic autoimmune disease with ASO Abs - thought to be hypersensitivity reaction to M protein cross-reacting with tissue glycoproteins)
    • Migratory polyarthritis of large joints (swollen, painful joints)
    • Acute carditis with cardiac enlargement and diminished function
    • Subcutaneous nodules
    • Erythema marginatum of skin
    • Sydenham chorea (involuntary, purposeless movements of extremities)
    • Occurs 10 days – 6 weeks after clinical episode of Strep infection
    • Jones Criteria” Evidence of group A strep + 2 major systemic finding
    • patient should receive long term antiobitic prophylaxis
62
Q

vegetations, aschoff bodies, endocarditis, pericardial rub

A

acute rheumatic fever

Aschoff body - Collection of large activated histiocytes
Anitschkow cells – “mononuclear”
Aschoff cells - multinucleated forms
caterpillar” cells - unique linear chromatin pattern

63
Q

mitral valve stenosis

A

chronic rheumatic heart disease

64
Q

rheumatoid arthritis and fibrinous pericarditis

A

rheumatoid heart disease

65
Q

RHD

A

Chronic rheumatic heart disease (RHD): longer term sequellae of ARG
• affects mitral and aortic valve mostly
• 99% of all mitral stenosis is caused by RHD
Note: Cardiac involvement is present in 20-40 cases of rheumatoid arthritis, usually fibrinous pericarditis!

66
Q

criteria for ddx of endocarditis?

A

major: + blood cutures, EKG finding, murmur thats new (get 3 blood cultures in 24 hours)
minor: fever, lesions, IV drug use, jaeway lesions, rothspots, petechial

67
Q

janeway lesions

A

new lesions on palms and soles –> infective endocarditits

68
Q

olser nodes

A

noldues on fingers –> IE

69
Q

roth spots

A

retinal hemorrhages w/ pale centers –> IE

70
Q

petechial hemorrhage under hails

A

IE

71
Q

infective endocarditis

A
  • see vegetations on leaflets –> vegetations can break and become septic emboli
  • • usually involves the left valves (except in IV drug users)
    • S. viridans (50-60%)>S. aureus (20-30%)>HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
    • #1 in artificial valves is S. epidermidis
72
Q

1 infection in artificial valves

A

S. epidermidis

73
Q

acute bacterial endocarditis

A

: Staph Aureus
• rapidly progressive destruction of cardiac valves
• usually due to S. aureus (IV drug abusers)
• 50% of pt. die w/in days or weeks of onset of sx

74
Q

subacute bacterial endocarditis

A

Streptococcus viridans
• endocarditis of native but previously damaged valves
• involved valve is usually deformed of abnormal (RHD, mitral valve prolapse #1)
• most pt. recover with Antibiotic therapy

75
Q

small warty verrucae along lines of closure of valve leaflets

A

RHD

76
Q

large irregular masses on valve cusps that can extend into chordae

A

IE

77
Q

NBTE

A

hypercoagulable state –> non bacterial thrombotic endocarditis
- may produce systemic emboli

78
Q

small, bland vegetations usually attached to line of closure

A

NBTE

79
Q

medium sized vegetations on either side of valve leaflets

A

Libman- Sacks Disease (Endocarditis of SLE):
• small (1-4 mm) sterile, pink vegetations with warty appearance
• located on undersurfaces of AV valves, valvular endocardium, chordae tendinae, ventricular or atrium
• may be due to immune complex deposition with inflammation

will also see malar rash, and murmur

80
Q

carcinoid tumors

A

Carcinoid Heart Disease:
- carcinoid syndrome = systemic disorder marked by flushing, diarrhea, dermatitis, bronchoconstriction caused by release of bioactive compounds like serotonin from carcinoid tumors (serotonin, kallikrein, bradykinin, histamine, prostaglandin) –> irritate heart

  • Fibrous intimal thickening of the endocardial surfaces of the right side of the heart, particularly right ventricle, and the tricuspid and pulmonic valves
  • Histo: see glistening white intimal plaquelike thickenings

tumor in gut –> affects right heart

tumor in lungs –> affects left heart

81
Q

problems w/ artifical valves

A
  • thromboembolism is major consideration with mechanical valves
  • structural deterioration is main problem of bioprosthesis
  • infective endocarditis is potentially serious complication of any valve replacement
  • pt. needs to be on coumadin/warfarin b/c are in high coagulable state
82
Q

cardiomyopathies

A

“heart muscle disease”

  • Cardiomyopathy = heart disease resulting from primary abnormality in the myocardium (including inflammatory, immunologic disorders, muscular dystrophies and genetic disorders of myocardium)
83
Q

dilated cardiomyopathy

A

large flabby heart, hypocontracting

• DCM → poor heart contraction → slowly progressive end stage disease
• familial in 30-50% of cases
• can be due to myocarditis (Cocksakie B), alcohol abuse, peripartum cardiomyopathy, iron overload, supraphysiologic stress, autosomal dominant inheritance
• LVEF: <25% pt. will soon die
Most common indication for cardiac transplantation
Histology:
• see markedly increased size, large and flabby mass with dilation of all chambers. Mural thrombi are common and see coronary arteries free of narrowing with normal valves

84
Q

defects in cytoskeletal proteins; anchoring proteins

A

DCM

85
Q

defects in myocytes, they are unorganized and problems with contractile proteins

A

hypertrophic cardiomyopathy

86
Q

hypertrophic cardiomyopathy

A

= marked thickened left ventricle, hypercontracting
• poorly compliant left ventricle → abnormal diastolic filling and ventricular outflow obstruction
• heart is thick-walled, heavy, hypercontracting
• see massive myocardial hypertrophy without ventricular dilation
• assymetric septal hypertrophy: Disproportionate thickening of left ventricular septum in comparison to LV free wall
• ventricular cavity may be compressed into “banana-like” shape
• see myofiber disarray and haphazard disarray of myocytes
• LVEF 50-80%: impairment of compliance and diastolic function: mimics HHD, aortic stenosis
• mostly dominant mutations involving proteins of the sarcomere (mutations of Beta-myosin heavy chain on Ch 14)
Clinical:
• stable and nonprogressive course: pt. often live until 7th/8th decade
• Majority of patients have reduced stroke volume due to impaired diastolic filling
• exertional dyspnea,
• harsh systolic ejection murmur,
• can lead to A fib and sudden death
• *** one of most common causes of SCD in young athletes **
Histology:
• Marked myocyte hypertrophy, haphazard myofiber disarray
• interstitial and replacement fibrosis in myocardium

87
Q

SCD in someone active?

A

think hypertrophic cardiomyopathy

88
Q

What are differences b/w hypertrophic vs. Dilated cardiomyopathy?

A
  • In HCM the ventricle is firms, small, thick walled, hypercontracting, diastolic dysfunction, shows exertional dyspnea and mutations exist in sarcomere proteins
  • In DCM the ventricle is dilated and flabby, hypocontracting, systolic dysfunction, leads to CHF, and dysfunction exists in cytoskeletal proteins
  • Both HCM and DCM can lead to heart failure, sudden death, A fib, and stroke
89
Q

Restrictive cardiomyopathy?

A

= mild increase in cardiac mass without increase in volume of left ventricle
• characterized by decrease in ventricular compliance → impaired ventricular filling during diastole
• ventricles are normal sized or slightly enlarged, but not dilated – and systolic function usually unaffected
• myocardium is firm and noncompliant
• LVEF: 45 to 90%, impaired compliance (diastole), caused by amyloidosis, induced fibrosis: mimics pericardial constriction
Heart findings:
• ventricles are normal size or slightly enlarged
• ventricular chambers are normal size
• Biatrial enlargement is common
Associated Disorders:
• Amyloidosis
• Endomyocardial fibrosis: - endocardial and subendocardial fibrosis with mural thrombi, occurs in African children/young adults and in other tropical areas (most common worldwide)
• Loeffler endomyocarditis - endomyocardial fibrosis with large mural thrombi that occurs worldwide and is associated with eosinophilic leukemia [some have platelet derived growth factor receptor abnormalities (Rx tyrosine kinase inhibitor imatinib) or may be secondary to basic protein release]
• Endocardial fibroelastosis - multifactorial left ventricular endocardial fibrosis that usually occurs in first 2 years of life

90
Q

Arrythmogenic Right Ventricular Cardiomyopathy

A

(Right ventricular Dysplasia): subtype of DCM

  • see mm. replaced by fat and collagen
  • See right sided heart failiure and rhythm disturbances (V-tach)
  • one of the causes of unexpected death found in 2-5% of deaths of young people
  • results in right ventricle (and sometimes left ventricle) being severely thinned with decreased myocytes and replacement with adipocytes and interstitial fibrous tissue
  • Most due to autosomal dominant mutations: Plakoglobin and desmoplakin genes
  • Naxos syndrome: – palmoplantar keratoderma with arrhythmogenic right ventricular cardiomyopathy and woolly hair (recessive plakoglobin mutation)
  • Carvajal syndrome - palmoplantar keratoderma with left ventricular cardiomyopathy and woolly hair (recessive desmoplakin mutation)

*** make ddx by looking at right ventricle, its all fat!

91
Q

mutations in plakoglobin and desmoplakin genes

A

Arrythmogenic Right Ventricular Cardiomyopathy (Right ventricular Dysplasia):

92
Q

Amyloidosis:

A

interstitial deposition of amyloid protein resulting in restrictive cardiomyopathy which may be complicated by arrhtymias

transtheritin protein deposit most common

93
Q

Systemic Senile (Cardiac) Amyloidosis

A
  • Amyloidosis primarily in heart: Occurs in “aged” patients (>60 yrs.)
  • May be localized to both ventricular and atrial myocardium - or limited to atria (isolated atrial amyloidosis)
  • Far more common cause of cardiac amyloidosis than primary systemic amyloidosis
  • Much better prognosis and milder clinical course
  • Amyloid composed of transthyretin product
  • More common in African-Americans (transthyretin mutation)
94
Q

myocarditis

A

inflammatory process due to infectious microorganisms → myocardial injury

Major Causes Myocarditis in US
• Viral: Coxsackieviruses A and B and other enteroviruses account for vast majority of cases - see lymphatic invasion
• Lyme Disease (Borrelia burgorferi): Occurs in 5% patients with clinically symptomatic Lyme disease (AV block)
• Hypersensitivity (eosinophilic) myocarditis – see esoinophils!
• Trichinosis (Trichinella spiralis and others): helminth acquired from eating infected undercooked meat from bears, pigs, boars, deer, warlus, dogs, cats, cougar, horses, wolves, foxes, mice, rats, humans and other animals.

95
Q

chagas disease

A

Major Cause of myocarditis South America: Chagas Disease (Trypanosoma cruzi) : a parasitic disease that affects 50% of patients in endemic areas of parasite. In Brazil, Chagas Disease is a more common cause of cardiac disease than ischemic heart disease

= cardiomyopathy and hx of travel

96
Q

round mononuclear cells

A

lymphocytes or macrophages = viral infection

97
Q

lobated w/ two lobes

A

eos = allergic txn

98
Q

4 lobes

A

neutrophil

99
Q

most common cardiac tumor?

A

metastatic malignancy

100
Q

myxoma

A

cardiac tumor made of mucoid material - often in left atria and fossa ovalis

  • can cause fever and malaise
101
Q

most common cardiac tumor in children?

A

benign

• Rhabdomyoma (#1 in children and 50% associated with tuberous sclerosis/ TSC1 and TSC2 genes)

102
Q

pericardial effusions

A
  • Serous: CHF, hypoalbuminemia - pale yellow, transparent
  • Serosanguinous: Malignancy, trauma, ruptured MI, aortic dissection
  • Sanguinous: Hemopericardium (aortic/cardiac rupture) - just blood
  • Purulent: Infection - neutrophils, yellowish green
  • Chylous: Lymphatic obstruction - white, look for malignancies!
  • Malignant (neoplastic): associated with malignant cells
103
Q

1 systemic cause of pericarditis?

A

uremia - renal faiure, looks like a shaggy heart

104
Q

types of pericarditis?

A
  • Serous: RF*, SLE**, scleroderma, tumors, uremia, Dressler syndrome (immune reaction post myocardial/pericardial injury)
  • Fibrinous/serofibrinous: Myocardial infarct, Dressler syndrome, uremia, radiation RF, SLE, trauma, cardiac surgery
  • Purulent/supperative: Infections
  • Constrictive: pericardium is rigid, thickened, scarred, and less elastic than normal
  • Hemorrhagic: Neoplasia, bacteria, TB***, bleeding diathesis, cardiac surgery
  • Casseous: TB or fungus
  • Adhesive: fibrous or fibroelastic scar, if severe is called concretio cordis and may calcify
  • Malignant (neoplastic): associated with malignant cells

Cardio II: Exam 2 (7 decks)

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