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CPR 2 Exam 1 > Hillard Cardiac Pathology Part 2 > Flashcards

Hillard Cardiac Pathology Part 2 Flashcards

1
Q

What is the most common structural birth defect?

A

Congenital heart defect, specifically VSD

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2
Q

What causes congenital heart disease?

A
  • most common due to sporadic genetic mutations
  • fetal alcohol syndrome
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3
Q

Describe left to right shunts and the symptoms.

A
  • High pressure left heart or aorta (ox blood) moves to the lower pressure right heart or pulmonary trunk
  • Initially asymptomatic, not cyanotic
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4
Q

Describe right to left shunts.

A
  • Blood bypasses pulmonary circulation
  • Typically symptomatic and cyanotic
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5
Q

What are the three L to R shunts?

A
  • ASD
  • VSD
  • PDA
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6
Q

What is the main type of ASD?

A
  • Ostium Secundum (insufficient formation of septum secundum)
    • 90% of all ASD’s are this and located in the center of the atrial septum
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7
Q

Clinical features of ASD? Prognosis?

A
  • usually asymptomatic until adulthood
  • hear systolic ejection murmur
  • Mortality is low and small defects spontaneously close
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8
Q

What are the majority of VSDs? Clinical features? Prognosis?

A
  • 80-90% are membranous VSD
  • Asymptomatic until adulthood
  • Holosystolic murmur
  • ~50-70% small VSDs close spontaneously
  • Prognosis depend on presence of other heart defects, those that have symptoms as kids are probably associated with other cardiac anomalies
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9
Q

What is PDA?

A
  • Ductus arteriosus fails to close when infants have increased pulmonary vascualr pressure
  • Sx include hypoxia and other heart defects such as VSD
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10
Q

Clinical features of PDA? (what is heard, symptoms, when do you close vs keep open)

A
  • Typically asymptomatic
  • Hear harsh machinery like murmmur peaks during systole but throughout diastole as well
  • Initally L to R shunt so no cyanosis
  • Isolated PDA should be closed with Indomethacin
  • Preservation of patency with prostaglandin E1 can be life saving with certain congeintal malformations
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11
Q

What is Eisenmenger syndrome?

A
  • Occurs in long term L to R shunt results in:
    • Increased pulmonary blood flow
    • Endothelial dysfunction and pulmonary vascular remodeling ( irreversible)
    • Increases backflow pressure (so we have increase in Pulmonary vascular resistance, blood doesn’t like to go in anymore)
    • Results in inverted shunt, now it is right to left
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12
Q

What are the threee R to L shunts? Cyanotic or not?

A
  • Tetralogy of fallot
  • Transposition of great arteries
  • Tricuspid atresia
  • Cyanosis at birth
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13
Q

What are the symptoms in general of R to L shunts?

A
  • “blue baby” cyanosis
  • Clubbing of fingers (long term)
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14
Q

What are the 4 features of tetralogy of fallot?

A
  • VSD
  • R. vent hypertrophy
  • Subpulmonic stenosis (severity of this abnormality contributes to severity of overall disease)
  • Overriding aorta (aorta is located in center of heart over the VSD)
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15
Q

What is the most common Cyanotic congenital heart defect?

A

Tetralogy of fallot

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16
Q

Clinical characteristics of tetralogy of fallot?

A
  • Infants are cyanotic from birth in most cases
  • VSD causes holosystolic murmur
  • Squatting to increase systemic pressure
  • Tet spell=cyanosis syncope during emotional distress, exercise
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17
Q

What is a case of preserving a PDA?

A

Transposition of great arteries to allow mixing of blood

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18
Q

Describe transposition of great arteries

A
  • Aorta and pulmonary artery are switched
  • Incompatible with life unless shunt is present allowing for mixing of blood
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19
Q

Describe tricuspid atresia.

A
  • Complete absence of triscupid valve
  • Oxygenation maintained by ASD/PFFO and VSD
  • Severe immediate cyanosis after birth
  • High mortality- need surgery
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20
Q

Congenital obstructive cardiac conditions?

A
  • Coarctation of aorta
  • Congenital aortic and pulmonary stenosis/atresia
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21
Q

Coarctation of aorta?

A
  • Focal narrowing of aorta
  • Infantile form: coarctation with PDA
  • Adult form coarctation without PDA
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22
Q

Epidemiology of Coarctation of aorta?

A
  • More common in males 2x
  • Females assoc with turner syndrome
  • Bicuspid aortic valve
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23
Q

Describe the adult form of coarctation of aorta?

A
  • upper body htn
  • Lower body hypotension, weak pulses, arteiral insufficiency
  • Long standing rib notching
    • due to collateral intercostal vessels oxygenating causing a pressure erosion
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24
Q

Infantile form of coarctation of aorta?

A
  • Presents with cyanosis at birth on lower half of body only
  • Severity depends on narrowing
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25
Q

What is congenital aortic stenosis/atresia?

A
  • mild stenosis or sub aortic stenosis causing left ventricular hypertrophy
    • hypertrophy of ventricle causes larger muscle amount but no increase in vasculature
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26
Q

What is a paradoxical emobolism? Where would an embolism normally go?

A
  • Emboli arising in the venous system passes through a PFO and travels into arterial system causing a stroke
  • Normally go to lungs only
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27
Q

What is a PFO?

A
  • 80% close permanently by 2 years
  • 20% can remain open if the right side pressure is increased
    • Temporary increase in pressure can produce brief periods of R to L shunting
      • valsalva
      • Bowel movement
      • Cough/sneeze
    • Resulting in possible paradoxical emboli
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28
Q

3 Most common congenital heart defects with down syndrome?

A
  • Atrioventricular> Ventricular> atrial
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29
Q

What is marfan syndrome? What cardiac risks do they have?

A
  • Fibrillin 1 mutation, excessive TFG-B causing increase in MMP’s which degrade elastin
  • talll thin build, flexible joints, pectus excavatum, long arms/legs/fingeers
  • Increase risk of aortic aneurysm and aortic dissection
  • mitral or aortic valve prolapse
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30
Q

What is DiGeorge? What are the associated cardiac anomalies?

A
  • CATCH-22
    • cardiac anomalies, abnormal facies, thymic aplasia, cleft palate, hypocalcemia, deletion 22q11
  • Conotruncal heart abnormalities tetralogy of fallot, transposition arteries, ASD VSD
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31
Q

What cardiac anomaly is turner syndrome associated with?

A
  • Coarctation of aorta
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32
Q

What is the hypertensive heart disease criteria?

A
  • Concentric left ventricular hypertrophy
  • Other evidence of htn
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33
Q

How does hypertensive heart disease impact diastolic function and what can that lead to?

A
  • Dysfunction of diastole (cant relax), left atrial enlargement, atrial fibriliation
  • can lead to CHF and atrial fib can lead to thrombus
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34
Q

How does hypertensive heart disease impact systole?

A
  • Systolic dysfunction, due to increase oxygen demand without vasculature to handle it leads to congestive heat failure
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35
Q

Describe the mechanism of right sided hypertensive disease? (Cor pulmonale)

A
  • isolated right sided pulmonary hypertensive disease
  • diseases of pulmonary parenchyma, vessels, or chest movement can increase the pulmonary pressure by constricting pulmonary small vessels
    • this leads to increased resistance so high pressure in the pulmonary artery and therefore right side of heart
    • eventually induces right side heart failure
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36
Q

What is the most common valve abnormality? Prevelance, risk factors?

A
  • Calcific aortic stenosis
  • increase with age around 60-80 yo
  • “wear and tear” assoc. with chronic htn hyperlipidemia
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37
Q

What is a bicuspid aortic valve? What can it lead to?

A
  • accelerated course of calcific aortic stenosis showing symptoms 1-2 decades earlier
  • May become incompetent leading to aortic valve prolapse
38
Q

What can a bicuspid aortic valve predispose an individual to?

A
  • Infective endocarditis
39
Q

How does a calcific aortic stenosis change the cardiac system and what are the signs and sx?

A
  • Increases LV pressure leading to concentric left ventricular hypertrophy
  • Signs and sx:
    • systolic murmur, syncope, angina, CHF
40
Q

Prognosis of aortic stenosis with angina, syncope and CHF?

A
  • Angina die w/n 5 yrs
  • die w/n 3 years with syncope
  • Die w/n 2 years with CHF onset
41
Q

What are mitral annular calcifications?

A
  • calcific deposits in the fibrous annulus (base of leaflets)
  • Females >60yo
  • Can cause arrhythmia
  • Can lead to infective endocarditis
42
Q

What is MVP? Prevelance? Causes?

A
  • Valve leaflets prolapse back into left atrium during systole
  • F:M 7:1
  • Caused by marfan syndrome or complication of MI or rheumatic fever
43
Q

Clinical findings of MVP?

A
  • Mid systolic click but asymptomatic
  • However chronic MVP can lead to dyspnea
  • Complications include:
    • infective endocarditis
    • Arrhythmia
  • Find:
    • Leaflets thick and rubbery (myxomatous degeneration)
    • Interchordal ballooning (hooding) of leaflets
44
Q

Rheumatic fever signs and symptoms?

A
  • Fever
  • Migratory polyarthritis
  • Pancarditis
  • Subcutaneous nodules
  • Erythema marginatum
  • Syndham chorea
45
Q

Rheumatic fever: Acute Rheumatic heart disease

A
  • Pericarditis myocarditis and or endocarditis
  • Valvulitis with vegetation
  • MacCallum plaques
  • Aschoff bodies with Anitschkow cells (acute rheumatic heart disease indicator)
46
Q

What valves are affected with rheumatic heart disease?

A
  • Mitral>aortic>tricuspid
47
Q

Describe chronic rheumatic heart disease

A
  • Valvular leaflet thickening short chordae tendinae, fusion, regurgitation
  • Valvular stenosis Mitral>Aortic>Tricuspid
48
Q

What causes infective endocarditis?

A
  • infectious organism, inflammation,fibribnous debris
  • Occur on abnormal or prosthetic valves
  • Vast majority are bacterial
49
Q

Risk factors for infective endocarditis?

A
  • IV drug use
  • piercings, males
  • Poor dentition, invasive dental procedures
50
Q

Preexisting conditions with infective endocarditis?

A
  • Valvular disease such as rheumatic heart disease, MVP, calcific stenosis
  • Prosthetic heart valve
51
Q

Acute endocarditis symptoms?

A
  • Rapid development of fever, chills, weakness
  • diagnose pathologically by histology or clinically by duke criteria
52
Q

Symptoms of subacute endocarditis?

A
  • Low grade fever <101
  • Fatigue
53
Q

Minor Duke Criteria for endocarditis?

A
  • Subungual splinter hemorrhages
  • Janeway lesions (not painful)
  • Osler nodes (painful)
  • Roth spots
54
Q

With infective endocarditis is staph aureus acute or subacute, early or late prosthetic valve infection, risk factos and unique features?

55
Q

With S. viridans describe infective endocarditis type, infection of valves, risks and unique feautres.

56
Q

With enterococci describe infective endocarditis type, infection of valves, risks and unique feautres.

A

Subacute and NO and nothing for risks and features

57
Q

with S. epidermidis describe infective endocarditis type, infection of valves, risks and unique feautres.

58
Q

with HACEK group describe infective endocarditis type, infection of valves, risks and unique feautres.

59
Q

Nonbacterial thrombotic endocarditis?

A
  • valvular thrombi form made of platelet rich fibrin clots
  • Due to hypercoagulable conditions
    • cancers, Antiphospholipid syndrome, lupus and sepsis are causes
60
Q

What is carcinoid heart disease?

A
  • Bioactive compounds (serotonin) secreted by carcinoid tumors induces plaque like endocardial valvular htickening and carcinoid syndrome
61
Q

What are s&s of carcinoid syndrome?

A
  • flushing
  • diarrhea
  • dermatitis
  • Bronchoconstriction
  • occurs when metz to the liver
62
Q

Reference for murmurs

63
Q

What is cardiomyopathy?

A
  • “heart muscle disease”
  • structurally and functionally abnormal with mechanical and or electrical dysfunction in absence of coronary artery disease, htn, valvular disease, congenital heart
64
Q

Describe type of dysfunction, cardiac abnormality and a unique feature in dilated cardiomyopathy

65
Q

Describe type of dysfunction, cardiac abnormality and a unique feature in hypertrophic cardiomyopathy.

66
Q

Describe type of dysfunction, cardiac abnormality and a unique feature in restrictive cardiomyopathy

67
Q

What causes dilated cardiomyopathy?

A
  • Familial TTN gene Titin mutation in 20% of the 30-50% of familial cases, AD
  • Peripartum cardiomyopathy
  • Alcohol
  • Doxorubicin and daunorubicin
  • Iron overload
  • Takotsubo cardiomyopathy (catecholamine overload “broken heart syndrome”)
68
Q

clinical features of dilated cardiomyopathy?

(age it presents, systolic or diastolic, what is dilated, what are the causes?)

A
  • manifest between 20 and 50 yo
  • Progressive dilation of ALL four chambers
  • Systolic dysfunction
  • Causes:
    • Genetic 30-50% (titin mutation)
    • Peripartum
    • alcohol
    • doxorubicin/danorubicin,
    • Iron overload
69
Q

What is takotsubo cardiomyopahy?

(associated with, what is released, what happens to L. ventricle, what does it mimic, result in?)

A
  • “Broken heart syndrome”
  • associated with emotional distress
  • Sudden surge of catecholamines
  • Apical ballooning of left ventricle
  • signs and sx of acute MI
  • can result in Ischemic cardiomyopathy or cardiac death
  • Epidemiology is 90% women
70
Q

What are characteristics of hypertrophic cardiomyopathy? Mutation?

A
  • Characterized by myocyte hypertrophy and myocyte disarray
  • Myocyte hypertrophy is marked with septal prominence
  • Genetic disorder with male predominance
  • Numerous mutations involving sarcomeric proteins most commonly, B-myosin heavy chain (B-MHC)
71
Q

Classic presentation of hypertrophic cardiomyopathy?

A
  • Most are asx but can present with:
    • Sudden unexplained death in an athlete during exercise
    • Systolic ejection murmur (mitral valve gets pushed to the septum)
72
Q

What causes restrictive cardiomyopathy?

A
  • Decreased ventricular compliance (increased stiffness) leading to diastolic function (impaired filling)
    • amyloid
    • increased fibrosis (radiation)
73
Q

How is amyloidosis related to restrictive cardiomyopathy?

A
  • Can involve different parts of the heart but when it invovles the myocardium restrictive cardiomyopathy is the result
74
Q

What can amyloidosis be due to?

A
  • myeloma
  • chronic inflammatory states
  • Mutated versions of transthyretin
  • Senile amyloidosis
75
Q

What is amyloid?

A
  • deposition of proteins forming an insoluble beta pleated sheet
  • can see apple green birefringence with congo red stain
76
Q

What is endomyocardial fibrosis?

A
  • Seen in young children young adults in tropical and subtropical regions (africa)
  • Fibrosis of the endocardium and subendocardium
77
Q

Loeffler endocarditis?

A
  • Eosinophilic infiltration
  • Part of spectrum of endomyocardial fibrosis
  • Associated myeloproliferative (leukemia/lymphoma)
78
Q

Endocardial fibroelastosos?

A
  • Fibroelastic thickening of left ventricle endocardium in the first two years of life
  • associated with congenital heart defects
79
Q

What is arrhythmogenic right ventricular cardiomyopathy?

A
  • Defective cell adhesion proteins in desmosomes that link adjacent cardiac myocytes
  • Many cases are familial and AD
  • myocardium of right ventricular wall replaced by adipose and fibrosis with dilation
  • Causes ventricular tachycardia, premature contractions or fibrillation leading to sudden death
80
Q

What is Naxos syndrome?

A
  • ARVC with plantar and palmar hyperkeratosis of plantar palmar skin surfaces and wooly hair
  • Mutations in the gene encoding desmosome associated protein Plakoglobin
81
Q

Myocarditis clinical presentation? Most common cause?

A
  • Viral infection by Coxsackie B and covid 19 are most common cause
  • asymptomatic to heart failure to arrhythmia and death
  • Troponin can be elevated and heart can show motion anomalies on echocardiogram
82
Q

How does chagas disease relate to infectious myocarditis?

A
  • amastigotes encyst in tissue cells in the heart
83
Q

How does trichinosis cause infectious myocarditis?

A
  • The worm larvae encysts in muscle and that can include heart muscle
84
Q

How does Lyme disease relate to the heart?

A
  • Carditis with heart block in early disseminated phase of lyme disease
    • along with migratory polyarthritis and facial palsy and meningitis
85
Q

Lymphocytic myocarditis?

A
  • most common form of myocarditis
  • Viral/post viral infection, autoimmune or idiopathic
86
Q

Eosinophilic myocarditis?

A
  • Characterized by marked increase of eosinophils
    • Hypersensitivity myocarditis:
      • due to underlying allergy/hsn rxn typically to drugs
    • need to eliminate potential parasite infectio
87
Q

Idiopathic Giant cell Myocarditis?

A
  • Aggressive with poor prognosis, survival is <3months from diagnosis
  • Giant cells admixed with variable mixed inflammation
88
Q

Myocardial Sarcoidosis?

A
  • Idiopathic process rare cause of myocarditis with variable presentation
  • Giant cells with non necrotizing granulomas
89
Q

What congenital heart disease will not present with cyanosis immediately after birth?

  • Tetralogy of Fallot
  • Transposition of great arteries
  • Tricuspid atresia with septal defect
  • Coarctation of aorta with PDA
  • VSD
90
Q

You have a patient with metastatic cancer and bx of solid cystic ovarian mass shows mucinous cystadenocarcinoma, what type of cardiac abnormality is associated with this?

A

Non bacterial thrombotic endocarditis

91
Q

Causes of prinzmetal angina?

A
  • Cocaine abuse
  • Elevated T4
  • Caffeine use
  • Autoantibodies
  • Pheochromocytoma

CPR 2 Exam 1 (21 decks)

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