Cardiac

Question 1

Causes of Cong Heart Diseases

Answer 1

• Down Syndrome: Endocardial cushion defect _{^{(ASD & VASD)}}
  
  • _{^{​​ASD present in adults w/same as VSD}}
• Turner syndrome: Coarction of aorta _{^{<strong>(narrow lumen)</strong>}}
  
  • _{^{<strong>​Pre-ductal stenosis</strong>}}
• Rubella: patent ductus arteriosus or VSD
• _{PDA <strong>(machine like murmur)</strong> w/premature infants w/RDS}
• High altitude: Patent ductus arteriosus
• Familial: Tetralogy of Fallot

Question 2

Left-Right Shunt

Answer 2

• Non-cyanotic baby
• Causes:
  
  • Atrial septal defects
  • Vent septal defect (MOST COMMON)-Close spontaneously in children
  • Patent or presistent ductus arteriosus
• Atrial septal defect = Secundum is involved _{^{<u>(grows from upper wall of atrium &amp; right of primary secundum)</u>}}
• High O2 saturation in right chambers & Pulmonary artery
• Assoc w/CHF & pulmonary hypertension
• High blood vol in rt vent = High blood sent to pulm vessels = Pulm hypertension
• Rt vent hypertrophy = Rt vent pressure greater than Lt heart pressure = Reversal of shunt _{^{(Eisenmenger’s complex-Cyanosis)}}

Question 3

VSD

Answer 3

• L to R shunt
• Pressure is same in BOTH vents
• Pressure hypertrophy in right
• Volume Hypertrophy in left
• Clinical due to large defects:
• Pulmonary hypertension & CHF
• Reversal of shunt & cyanosis & severe clubbing of fingers = Eisenmenger’s _{^{<strong><u>(boot shaped heart w/RVH)</u></strong>}}
• Risk of infective endocarditis
• Murmur type:
• Holo-systolic=Tricuspid insuff
• Wide split between A2 & P2 in S2 = delayed closure of pulmonic valve in right bundle branch
• Diamond shape = crescendo/decrecendo

Question 4

Patent Ductus Arteriosus

Answer 4

• Ductus arteriosis _{^{(connects pulm artery-descending aorta)}} remains open after birth
• Due to HIGH PGE2 (helps dialate cervix in labor)
• High risk: Premature birth & rubella infection
• High pressure left-right shunt (Aorta to PA)
• ID by contin machinery murmur due to continous flow from aorta to PA
• Complications:
• Pulm hypertension w/reversal of shunt & cyanosis–>CHF

Question 5

Right to left (Tetralogy)

Answer 5

• Clinical: Early cyanosis @ birth
• Most common
  
  • VSD
  • Dextraposed aortic root override VSD
  • Rt vent outflow obstruction (pulm stenosis)
  • Right Vent hypertropy
• Severity depends on pulm stenosis (cyanosis)
• Blush skin during episodes of crying/feeding - central cyanosis
• Enlarged/Boot shaped heart=RVH
• Pt survives due to to PDA
• Clinical:
• Infective endocarditis w/large vegetations cause sudden death
• Reduced pulm perfusion=Pulm vascular atrophy (pulm stenosis=Sudden death)

Question 6

Right to left

Answer 6

• Transp of great arteries:
• Aorta arises from the right vent (anterior)
• Pulm artery arises from left vent (post)
  
  • _{^{<em><strong>Keep shunts open w/prostaglandins</strong></em>}}
• Cyanosis @ birth
• Pts die w/in 1st 30 days w/o surgery
• No change in Blood O2 conc even with O2 therapy
• Calcific valvular degeneration
• Truncus Arteriosis:
• No septum between aorta & pulm artery = Common trunk
• Major complication = Pulm hypertension
• Low blood O2 sat that does NOT improve

Question 7

Cong. Obstructive Lesions

Answer 7

• Coarctation of aorta:
• More common amongst males
• Associated w/PDA, VSD, ASD
• Manifestation of Turner
• Def: Obstruction/Narrowing of aorta
• Location: pre or post ductal arteriosis
• Pre = Infantile (post)
  
  • de-o2 blood from right vent/Pulm trunk goes to aorta via PDA
  • Cyanosis of lower limbs
  • Hypertension in Upper limbs ONLY
• Post = Adult (post)
  
  • Fibrotic DA
  • NO cyanosis
  • HT in upper due to excess flow = opening of collateral blood vessels _{(<em><strong>Rib nothcing-</strong></em>Internal mammary & intercostals)}

Question 8

CHF General

Answer 8

• Reduced Cardiac output to meet demand = Forward failure
• ** ** = damming of blood back in venous system
• 90% associated w/Left vent hypertrophy
  
  • Re-expression of embryonic/fetal type of protein ^{<strong>(B-myosin)</strong>} in heart muscle
  • Reduced cap density (reduced O2)-Heart failure cells
• Overall=Cardiac muscle fails lack of O2 & presence of fetal myosin
• Progresses from underlying cond:
• HT or cor-pulmonale
• Valv disease
• Multiple MI

Question 9

CHF Morphology/Clinical

Answer 9

• Concentric Hypertrophy:
• Pressure overload = Hypertension
• Narrow chamber & Thick wall
• Eccentric Hypertrophy:
• Volume Overload = Regurg
• Dilated chamber & Thick wall
• Clinical:
• Long progressive
• Exercise intolerance - Dyspenea
• Fluid retention=swelling
• Jugular vein + Facial distention
• Gallop rythms of S3

Question 10

Left Vent Failure

Answer 10

• 2 types:
• Systolic dysfunction _{^{(MI or HTN)}}
• Diastolic dysfunction _{^{(Amyloidosis)}}
• Caused by:
• _{^{Ischemic HD}}
• _^HTN
• _{^{Aortic/Mitral valve disease}}
• _^Amyloidosis
• _{^{Increase BV = Pulm congestion = <em><strong>Pulm HTN</strong></em>}}
• _{^{Pul edema + <em><strong>Heart failure cells</strong></em> + Increase in hydrostatic pressure = <u><em><strong>Dyspnea</strong></em></u>}}
• Presentation:
• Orthopnea ^{(sleep with several pillows)}
• Pulm edema ^{(Pink, low protein=Transudate)}
• Rales
• S3 gallop ^{<strong>(vent filling early diastole)</strong>}
• Hypoxic encephalopathy ^{(-O2 all organs)}

Question 11

IHD (Angina)

Answer 11

• Acute coronary Syndrome (3 types)
• Imbalance between myocardial demand & blood supply
• Common in middle age males & post-menopausal women
• 75% narrowing
• Partial block fixed by artherosclerosis
• Spasm due increase in TXA2
• Stable=Transient reversible pain w/exertion or stress
• pain relieved w/Vasodialators-Nitro=Reduce in Venous return
• Prinzmetal: Occurs @ rest & stems from coronary artery spasm With or w/o obstruction ^{<strong>(rise in ST)</strong>}
• Unstable: acute plaque change w/o 100% occulsion-Crecendo increase pain
  
  • _{^{Pain w/less exertion, more frequent, longer time & <em><strong>HIGH risk for MI</strong></em>}}

Question 12

Biochem of Angina & MI

Answer 12

• C-reactive protein (CRP)-Marker to predict MI in pts w/Angina
  
  • _{^{Marker to <em><strong>predict risk of new infarcts </strong></em>in pts who recover from infarcts}}
  • _{^{Inflammation stimulated by <em><strong>IL-6 = CRP</strong></em>}}
• MI = Pain more than 30 min due to increase in _{^{<em><strong>lactic acid</strong></em>}}
  
  • _{^{<em><strong>Shock </strong></em>due to acute LVF - Pulm edema}}
• Myoglobin RISE immediate ^{(toxic for kidney)}
• *CK-MB* ^{(phosphorlate enzyme)}
• 2-4 hr elevation, Peak @ 18-20hrs, Normal @ 2-3 days
  
  • Normal ratio of 1:2 = 1.2 when larger than 1.5 possible MI
• Troponin I/T 2-4 hr elevation, peak @ 16-20hrs, Normal 7-10 days
• LDH show after 1 day peak @ 3-6 days (old MI)
  
  • LDH flip LDH1>LDH2 =MI

Question 13

Pathogenesis of MI

Answer 13

• 100% occulsive intracoronary thrombus:
  
  • Complications of atheroma _{^{(Rupture of plaque)}}
  • Prolonged coronary artery spasm (smoking/cocaine)
  • Emboli-left atrium w/atrial fibrillation
  • vegetative endocarditis
  • Paradoxical emboli w/ASD
• Sub-endocardial MI-less than 50% of wall thickness
  
  • MI begins in this area (less perfused area of myocardium)
  • EKG ST depression
• Transmural MI-Necrosis extend external & involve myocardium
  
  • Common-24 hours to develop=St Elevation

Question 14

Sites of Occulsion of MI

Answer 14

• LAD (Lft ant. dec)=40-50%
  
  • Lt. Vent-Anterior & apical
  • Ant 2/3 of inter-vent septum
• RCA (Rt. coronary)=30-40%
  
  • Lt. vent-Post wall
  • IVS post 1/3
• LCX (Lt. Circumflex)=15-20%
  
  • Lt. vent lateral wall
• Occulsion of coronary artery - Necrosis goes from inside to out
• Atheroscleorotic plaque rupture:
  
  • Acute coronary thrombosis is superimposed on atherosclerotic plaque w/focal disruption of cap
  • Massive plaque rupture w/superimposed thrombus

Question 15

Morphology of MI

Answer 15

1. 0-30min = Hydropic changes ^{_{<u>(accumulation of water=degradation of cell)</u>}}, relaxation of myofibrils w/Glycogen loss & mitochondrial swelling
2. 18-24 hours = Pallor of myocardium
3. 3-7 days = Hyperemic border w/central yellowing
4. 10-21 days = maximally yellow & soft w/vascular margins
5. 7 weeks = white fibrosis (scarring)

• First line med = anti-arrythmic (betablocker)

Question 16

Microscopic Changes due to MI

Answer 16

• 1-3 hours - Few wavy fibers @ margin of MI
• _{^{Contraction bands irregular darker pink wavy across fibers<em><strong>(Ca+2 influx)</strong></em>}}
• 4-12 hours - Loss of cross striations & edema
• 12-23 hours - Coag necrosis, marginal contraction band necrosis
• 1-3 days - accumulation of PMNs & coag necrosis
  
  • _^Neutrophils
• 4-7 days - macrophage & mononuclear infiltration
• 10-21 days - Prominent granulation tissue ^{(loose collagen & abundant capillaries)}
• 7-8 weeks - Fibrosis healing ^(collagen) pale scar

Question 17

Complications of MI

Answer 17

• Arrythmias!!! - lead to death occur immediately or w/in hour from onset
• Vent fibrillation: Most common cause of SUDDEN DEATH in early MI
• Acute fibrinous pericarditis: Second or third day
  
  • Late = Dressler syndrome Auto Ab
  • Histo: Dark-roughened epicardial surface over infarct w/friction rub
• Mural thrombi & thrombo embolism (1week)^:
  
  • Infarct brain, kidney, GI
• Cardiogenic shock (multi-organ failure)
• Vent aneurysms = LATE complication
  
  • SV & EF reduced=^weakness

Question 18

Cardiac Rupture Syndromes

Answer 18

• Rupture of Lt. Vent free wall & tamponade:
  
  • Occurs @ 3-7 days after MI
  • Sudden drop in BP =Shock
  • Blood in pericardial sac = Cardiac tamponade
  • Large shadow
• Papillary muscle rupture & mitral incompetence:
  
  • 3-7 days after MI = Pansystolic murmur _{^{(Regurg or VSD)}}
• common mitral insuff-Pt in left lateral lie down position radiates to axillae
• Rupture of septum VSD:
  
  • 3-7 days after MI
  • Pansystolic murmur
  • Prolaspe murmur @ S1-S2

Question 19

Clinical Presentation of MI

Answer 19

• Severe crushing substernal pain due to lactic acid accumulation in damaged cardiac cells
• Pain radiate to:
• Neck/Jaw
• Epigastric
• Shoulder
• Left arm
• Diabetics occansionaly do not feel pain of MI
• Classic EKG:
• ST elevation
• T wave **inversion **
• Q wave transmural infarct (fibrosis)
• SCD = Lethal Arrhythmia common cause IHD
  
  • Aortic stenosis or MV prol

Question 20

Inhalation

Answer 20

• Drop in intrathoracic pressure
• Increases capacity of pulm circ
• Prolonging ejection time = Closure of pulm valve (carvallo’s maneuver)
  
  • Detects murmurs from Rt Heart
  • + carvallo’s sign=increase in intensity of Tricuspid regurg murmur w/inspiration
  • Ex. Abrupt standing/Sqautting

Question 21

Valsalva maneuver

Answer 21

• Detects hypertrophic obstructive cardiomyopathy
• Standing and maneuver = decrease venous return - decrease left vent filling
  
  • Summary: Increase in loudness of murmur hypertrophic cardiomyo
  • outflow obstruction increased by decreasing preload
• Left heart aortic obstruction easier to eject during inhalation murmur less pronounced- mumur worse in standing

Question 22

Hypertensive Heart Disease (general)

Answer 22

• Hypertrophy of left vent (over 2cm thick w/small chamber)
• Concentric hypertrophy = decrease in vent compliance due to pressure overload
• Imaging = Shift to left
• EKG: widened QRS/T angle & LEFT shift on QRS axis
• Secondary causes of Left Vent hypertrophy:
  
  • HT
  • Aortic valve stenosis
  • Aortic valvular regurg

Question 23

Cor Pulmonale

Answer 23

• Pulm hypertensive heart disease
• Associated w/disease of Rt heart due to intrisic lung disease
• If caused by an exsisting or old heart disease then it is NOT cor-pulmonale
• Acute: massive pulm embolism (saddle) due hypercoag states w/NO change in Rt. Vent
• No lung shadow
• Sudden onset of dyspnea/Pain
• Cause DVT
• Chronic: Obstructive pulm disease-COPD OR Multiple pulm embolism w/RT vent hypertrophy (Bootshaped)
• Narrowing of pulm vessels(re-canalized vessel/fibrous web)
• Jugular vein distention
• Hepto-spelomegaly-Edema

Question 24

Valvular Heart Disease

Answer 24

• Mitral valve disease:
• Cause Rheumatic Heart Disease = Stenosis
• Mitral Regurg/Insufficiency:
  
  • _{^{Prolapse (marfan syndrome-female) w/mid-systolic click}}
  • _^Rheumatic
  • _{^{Rupture of papillary}}
  • _{^{Rupture of <u>chordae tendineae</u>}}
• Aortic valve disease:
  
  • Stenois-
  • Rheumatic HD
  • Senile calcific aortic stenosis ^{(in older pts)}
• Aortic regurg-
  
  • _{^{Rheumatic heart disease}}
  • _{^{Infective endocarditis}}
  • _{^{<em><strong>Syphilitic</strong></em> aortitis}}
  • _{^{Degenerative aortic dilation <strong>(aging</strong>) HTN}}

Question 25

Rheumatic Fever & Heart Disease

Answer 25

• Disease=Group A beta Hemolytic strep _{<strong>^{(ex. Sore throat in child)}</strong>}
• Develop Ab from infection=Destroys heart & involves Joints/skin rash
• Acute: Rheumatic carditis w/fever
• Chronic: Heart valvular deformities _{^{<strong>(manifests years later)</strong>}} NO fever
• Diagnosis:
• ASO ^{<strong>(anti-strep O)</strong>} titer ELEVATED
• Morphology:_{^{<u><strong>Cross rxn w/Ab</strong></u>}}
• Small Vegetations mitral valve
• Myocardial **Aschoff body **_{^{<strong>(inflammed/granulomatos-macrophages)</strong>}}
• Fibrinous pericarditis (bread & butter)
  
  • Chest pain (type 2 HS)
  • Friction rubs w/distant sounds
  • St elevation

Question 26

Jones Criteria (acute)

Answer 26

• Used in diagnosis of Acute RF:
• Migratory polyarthritis-*No chronic deformity *
• Pancarditis ^{(inflammation @ all lvls)}-**Fibrinous exudate on epicardial **
• Subcutaneous nodule (elbow)-non-tender w/leukocytic infiltrate w/aschoff-anitschow
• Skin rash (erythemia marginatum)
• Sydenham chorea (uncoordinated move)
• Minor:
  
  • Fever
  • Increase in **cRP & SAA **
• Rheumatic aortic stenosis-Commissural fusion
• Vegetations are non-infectous & can cause systemic issue due to detachment

Question 27

Chronic RHD

Answer 27

• Mitral valve more common than aortic (acute)
• Stenosis common then regurg BUT BOTH can be present
• Mitral stenosis (morph):
• Thick, rigid - “Fish Mouth”
• Lft Atrium enlarged = Mural thrombi ^{(sitck to large vessels w/lines of Zahn)}** **LEADS to systemic embolism
• Increase in Lft Atrial press leads to pulm congestion w/hemorrahge = Rt heart fail
• 20 mmHg pressure in severe stenosis
• Mid-Diastolic rumbling murmur
• Complications of stenosis:
  
  • _^CHF
  • _{^{<em><strong>Arrhythmia </strong></em>(atrial fib)}}
  • _{^{Thromboembolism (strokes)}}
  • _{^{<em><strong>Infective endocarditis</strong></em> (vegetations)}}
  • _{^{<em><strong>Hemoptysis </strong></em>(coughing blood)}}

Question 28

Valvular Disease (Aortic Stenosis)

Answer 28

• Dystrophic calcification (Happens in Necrotic tissue)
  
  • Due to age
  • In Bicuspid or aortic
• Increased pressure gradient across ca+2 valve = Lft vent pressure is greater than 200mmHg
• Calcification of bicsupid seen in 45X
• Histo: nodular masses NO fusion
• Mumur heard @ isovolumetric contration phase of systole
• Clinical:
• HYPOperfusion to brain (syncope)
• Angina/CHF
• LOUD systolic murmur-radiates to carotid ^{(diamond shape = crescendo/decres)}
• Reduced stroke vol
• Left vent hypertrophy w/NORMAL BP

Question 29

Valvular Disease (Aortic/Mitral Regurg)

Answer 29

• Aortic Regurg:
• Retraction of leaflets towards aortic wall from fibrosis
• Severe left vent hypertrophy & dilatation (Cor Bovinum = Vol overload)
• Wide pulse pressure
• BP = 160/50 mmHg
• Murmur = Diastolic/decrescendo (Austin Flint rumble)
• Mitral Regurg:
• Due to mitral insuff
• Holosystolic/Pansystolic murmur
• Found in:
  
  • Post MI
  • RHD
  • NOT in Mitral prolaspe

Question 30

Valvular Disease (MVP)

Answer 30

• Mitral valve prolaspe
• Isolated mitral regurg
• Assoc = Marfan syndrome
• Common in women
• Accumulation of loose myxoid ^{(degenertive of coonective tissue)} = Loss of elastic prop w/in leaflets
• Morphology:
• Floppy valve
• Chordae tendinae are thin & elongated
• Murmur = Late systolic w/Mid systolic CLICK ^{<strong>(Heard FIRST)</strong>}
• Clinical:
• **Asymptomatic **
• Possible arrhythmia & Infective endocard

Question 31

Non-Bacterial (Marantic) Endocarditis

Answer 31

• Malignancies = Adenocarcinoma _{^{(neoplasia of epi w/glandular origin)}} are 50% of all cases or TB
• Also known as Marantic endocarditis for pts w/debility or wasting
• Found in hypercoag states
• Sterile Vegetations can embolize
• Sterile/Non-destructive-Small 1 to 5mm in multiple or single regions along line of closure of leaflets/cusps
• Thrombi made of Platelets from carcinoma _^(hypercoag)
• Libman-Sack: Sterile vegetations in SLE
  
  • Occurs on Both surfaces of Mitral & Aortic

Question 32

Infective Endocarditis

Answer 32

• Infection of edocardium (heart valves) by microbio agent = Formation of LARGE vegetations
• RIsk groups:
• Heart defects
• Prosthetic devices ^{(Staph Epidermis)}
• IV drug abusers _^(HIV)
• RHD
• Diabetes
• Acute IE: Normal valve
  
  • Caused by Staph aureas
• Sub-Acute IE: Previously damaged
  
  • Strep Viridans _{^{(splinter hemorr)}}
  • Small vegetations _^(murmur)
• Cong defect/Abnormal valve=Alpha hemolytic viridans strep
• IV abuser = Staph aureus _{^{(tricuspid valve)}}

Question 33

IE: Morphology & Clinical

Answer 33

• HACEK organisms:
• Hemophilus
• Actinonacillus
• Cardio bacterium
• Eikenella
• Kingella
• Formation of large vegetations reddish/tan
• Mitral valve most common **w/ring abscess **
• Clinical:
• Fever/chill
• Splenomegaly & clubbing ^{(splinter hemo)}
• Diastolic murmur ^{(due to vegetations)}
• Emboli (due to rogue vegetations):
• *Janeway lesions_ *****^{(palms & soles)}_
• Micro abscess infarction in eye, brain…
• Petechial lesion on palate
• Roth’s spots ^{<strong>(hemorrhage)</strong>}

Question 34

Cardiomyopathy (Dilated)

Answer 34

• Dilated (congestive):Interstitial fibrosis w/collagen deposit
• Most common @ any age
• Left vent ejection less than 40%
• Flabby, hypo-contracting, ALL chambers
• Mural thrombis @ apex of left vent
• Progressive CHF
• Due to:
• Alcohol ^{(more blood in periphery=+VR)}
• Genetic
  
  • Mutations in dystrophin gene X^{(muscular dystrophy)}
• Coxsackievirus B (ssRNA)
• Doxorubicin (chemo)
• Cocaine
• Chronic anemia
• Thiamin Def B1-_{^{Also hemo mamilary body of brain (wet beri-beri)}}

Question 35

Cardiomyopathy (Hypertrophic)

Answer 35

• Genetic MOST common
• Thickened myocardium w/o any cause
• Left Vent & IVS thickened
  
  • I_{^{VS bulges into left vent outflow tract-Obstruction-DEATH}}
• Abnormal diastolic filling due to:
  
  • _{^{stiff wall}}
  • _{^{Vent outflow obstruction}}
• Genetic: Autosomal dominant B-myosin heavy chain mutation
• Histo: Myofiber disarray w/Prominent nuclei
• _{^{<em><strong>Increased </strong></em>connective tissue (Hypertrophy)-<strong>Predisposed to arrthymia</strong>}}
• Clinical (family history):
  
  • _{^{<em><strong>Systolic ejection murmur-</strong></em>decreased lying down}}
  • _{^{Common <em><strong>death in young athletes</strong></em>}}

Question 36

Cardiomyopathy (Restrictive)

Answer 36

• Decrease in vent compliance=impaired vent filling during diastole _{^{<u><strong>(same as constrictive)</strong></u>}}
• Due to inflitrative process:
• Endocardial fibrolastosis _{^{(death in infants)}}
• Eosinophilic endocardial fibrosis _{^{(Loeffler’s syndrome)-<u>Allergic rxns &amp; parasites</u>}}
• Amyloidosis (insol proteins)
  
  • _{^{Pink amorphous extracell deposits w/<em><strong>Congored</strong></em>}}
  • _{^{<strong><em>Transthyretin </em><u>(transp Retinol &amp; Thyroxine)</u><em> Misfolding causes Amylodosis</em></strong>}}
  • _{^{Seen in old people}}
• Hemochrommatosis (iron overload)
  
  • _{^{Prussian blue stain}}
• Radiation Injury (fibrosis-scarring)

Question 37

Myocarditis (causes)

Answer 37

• Inflammatory processes of myocardium
• Viruses myocarditis:
• Coxsackievirus A/B (ssRNA)
• Echovirus
• Cytomegalovirus (herpes)
• HIV & Influenza
• Parasites:
• Trypanosoma Cruzi (Chagas)-Mega colon/esophagus
• Trichonosis
• Bacterial:
• Lyme Disease (Borrelia)
• Diphtheria (gram+)
• Fungi: Candida
• Drug Injury:
• Doxorubicin (chemo) w/hercepctin treat breat cancer

Question 38

Bacterial & Viral Myocarditis

Answer 38

• Bacterial:
• Absceses gross appearance
• Histo: Small micro abscesses & bacterial colonies
• Diphtheria=w/exudates in tonsils
• Viral is MOST common:
• Patchy intersitial lymphocytic infiltrates
• Myocyte injury
• Starry sky appearance

Question 39

Hypersensitivity Myocarditis

Answer 39

• _Caused by: _
• SLE
• Methyldopa
• Drug sensitivity
• Transplant rejection
• Morphology:
• Interstitial infiltrates in perivascular
• Made of lymphocytes, macrophages, & HIGH proportion of eosinophils
• Chagas Disease: in cardiac muscle caused by trypanosoma cruzi
• associated w/achalasia cardia ^{(narrowing of lower esophagus)}
• Fatigue, dyspnea, palpitations, precordial discomfort & fever
• Low ejection fraction
• Years later can be diagnosed w/dilated cardiomyopathy

Question 40

Carcinoid heart disease

Answer 40

• Caused by carcinoid tumor & turns into carcinoid syndrome _{^{(Rt heart common)}}
• Produce serotonin (flushing & dry cough)
  
  • _{^{5 hydroxy acid VMA}}
• Secondary cause = restrictive cardiomyopathy “TIPS”
• T = Tricuspid
• I = Insuff
• P = pulm
• S = Stenosis
• Histo: Fibrotic lesion in Rt vent & Tricupid valve w/intimal thickening
  
  • _{^{Movat stain underlying elastic tissue <em><strong>Black & acid mucopolysac Blue-green</strong></em>}}