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Pathology 2-Systemic > Cardiac > Flashcards

Cardiac Flashcards

(40 cards)

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1
Q

Causes of Cong Heart Diseases

A
  • 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
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2
Q

Left-Right Shunt

A
  • 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)
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3
Q

VSD

A
  • 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
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4
Q

Patent Ductus Arteriosus

A
  • 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
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5
Q

Right to left (Tetralogy)

A
  • 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)
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6
Q

Right to left

A
  • 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
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7
Q

Cong. Obstructive Lesions

A
  • 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)
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8
Q

CHF General

A
  • 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
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9
Q

CHF Morphology/Clinical

A
  • 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
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10
Q

Left Vent Failure

A
  • 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)
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11
Q

IHD (Angina)

A
  • 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>
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12
Q

Biochem of Angina & MI

A
  • 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
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13
Q

Pathogenesis of MI

A
  • 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
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14
Q

Sites of Occulsion of MI

A
  • 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
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15
Q

Morphology of MI

A
  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)
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16
Q

Microscopic Changes due to MI

A
  • 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
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17
Q

Complications of MI

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A
  • 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
18
Q

Cardiac Rupture Syndromes

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A
  • 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
19
Q

Clinical Presentation of MI

Study These Flashcards
A
  • 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
20
Q

Inhalation

Study These Flashcards
A
  • 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
21
Q

Valsalva maneuver

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A
  • 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
22
Q

Hypertensive Heart Disease (general)

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A
  • 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
23
Q

Cor Pulmonale

Study These Flashcards
A
  • 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
24
Q

Valvular Heart Disease

Study These Flashcards
A
  • 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
25
Rheumatic Fever & Heart Disease
* Disease=***Group A beta Hemolytic strep*** (ex. Sore throat in child) * ***Develop Ab from infection***=Destroys heart & involves Joints/skin rash * **_Acute:_** Rheumatic carditis ***w/fever*** * **_Chronic:_** Heart valvular deformities (manifests years later) ***NO fever*** * **_Diagnosis_**: * ASO (anti-strep O) titer ELEVATED * **_Morphology:_**Cross rxn w/Ab  * **_Small_** Vegetations mitral valve * Myocardial ***Aschoff body ***(inflammed/granulomatos-macrophages) * **_Fibrinous pericarditis_** ***(bread & butter)*** * Chest pain **(type 2 HS)** * ***Friction rubs*** w/distant sounds * ***St elevation***
26
Jones Criteria (acute)
* **_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/l***eukocytic 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***
27
Chronic RHD
* ***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 * Arrhythmia (atrial fib) * Thromboembolism (strokes) * Infective endocarditis (vegetations) * Hemoptysis (coughing blood)
28
Valvular Disease (Aortic Stenosis)
* 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***
29
Valvular Disease (Aortic/Mitral Regurg)
* **_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
30
Valvular Disease (MVP)
* 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*** _(Heard FIRST)_ * **_Clinical:_** * ***Asymptomatic *** * ***Possible*** arrhythmia & Infective endocard
31
Non-Bacterial (Marantic) Endocarditis
* 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
32
Infective Endocarditis
* 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)_***
33
IE: Morphology & Clinical
* **_HACEK organisms:_** * **H**emophilus * **A**ctinonacillus * **C**ardio bacterium * **E**ikenella * **K**ingella * 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 (hemorrhage)
34
Cardiomyopathy (Dilated)
* **_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)**
35
Cardiomyopathy (Hypertrophic)
* ***Genetic MOST common*** * Thickened myocardium w/o any cause * Left Vent & IVS thickened * ***IVS 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*** * Increased connective tissue (Hypertrophy)-Predisposed to arrthymia * **_Clinical (family history):_** * Systolic ejection murmur-decreased lying down * Common death in young athletes
36
Cardiomyopathy (Restrictive)
* ***Decrease in vent compliance***=impaired vent filling during diastole (same as constrictive) * **_Due to inflitrative process:_** * Endocardial fibrolastosis **(death in infants)** * Eosinophilic endocardial fibrosis ***(Loeffler's syndrome)-***Allergic rxns & parasites * ***Amyloidosis*** (insol proteins) * Pink amorphous extracell deposits w/Congored * Transthyretin (transp Retinol & Thyroxine) Misfolding causes Amylodosis * Seen in old people * Hemochrommatosis (iron overload) * Prussian blue stain * Radiation Injury (fibrosis-scarring)
37
Myocarditis (causes)
* 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
38
Bacterial & Viral Myocarditis
* **_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
39
Hypersensitivity Myocarditis
* **_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 t***rypanosoma 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***
40
Carcinoid heart disease
* 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 Black & acid mucopolysac Blue-green

Pathology 2-Systemic (15 decks)

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