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Cardio > Cardio Path Review > Flashcards

Cardio Path Review Flashcards

1
Q

cardiogenesis timing

A
  • weeks 3-6
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2
Q

heart tissue originates from ____ and starts as ____.

A
  • mesoderm

- a single tube

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3
Q

direction of heart tube looping

A
  • right or D-looping
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4
Q

____ are necessary for normal AV valve formation and arch development

A
  • neural crest cells
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5
Q

____ assist w/ septation and form ____

A
  • endocardial cushions

- AV valves

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6
Q

CHD incidence

A
  • 0.6% of all full term births

- 1-8 per 1,000

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7
Q

CHD etiology

A
  • multifactorial/unknown: 90%
  • genetic (chromosomal, single gene): 8%
  • environmental (rubella): 2%
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8
Q

right to left shunt outcomes

A
  • cyanosis

- emboli arising in peripheral veins can enter systemic circulation

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9
Q

left to right shunt outcomes

A
  • RV hypertrophy and overload
  • progressive pulmonary HTN
  • pulmonary obstructive vascular disease
  • reversal of shunt with cyanosis
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10
Q

In utero, pulmonary circulation is a ____ flow, ____ resistance circuit.

A
  • low

- high

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11
Q

After birth, pulmonary circulation is a ____ flow, ____ resistance circuit, due to ____.

A
  • high
  • low
  • reduction of pulmonary vascular resistance and higher partial pressure of O2
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12
Q

Spontaneous heart closures after birth

A
  • umbilical arteries -> umbilical ligaments
  • ductus venosus (umbilical vein blood to IVC) -> ligamentum venosum
  • foramen ovale -> fossa ovalis
  • ductus arteriosus (PA/Aorta shunt) -> ligamentum arteriosum
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13
Q

The atrial septum develops from

A
  • septum secundum
  • septum primum
  • endocardial cushion tissue
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14
Q

septum secundum

A
  • infolding of muscular roof of common atrium (door frame of foramen ovale)
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15
Q

septum primum

A
  • thin sheet of tissue that grows to fill in archway formed by septum secundum
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16
Q

endocardial cushion tissue

A
  • develops into portion of atrial septum adjacent to AV valves
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17
Q

AV junction tissue contributes to development of

A
  • AV valves

- portions of atrial septum and ventricular septum

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18
Q

trisomy 21 cardiac associations

A
  • 40% have heart abnormalities
  • endocardial cushion defects (AV canal common)
  • VSD, ASD, PDA
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19
Q

turner syndrom cardiac associations

A
  • coarctation of aorta
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20
Q

trisomy 18 cardiac associations

A
  • VSD
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21
Q

septum secundum defect

A
  • foramen ovale
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22
Q

LV hypoplasia

A
  • aortic stenosis
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23
Q

situs inversus abnormality associations

A
  • polysplenia
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24
Q

persistent truncus arteriosus

A
  • one aortic and pulmonic outflow tract
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25
Q

ASD types

A
  • left to right shunt
  • secundum (most common) or primum
  • sinus venous defect, coronary sinus septal defect
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26
Q

VSD types

A
  • left to right shunt
  • paramembranous (most common): involves membranous septum
  • muscular (second common): little functional disturbance, loud
  • AV canal
  • conal septum/muscular septum malalignment
  • subarterial (conal septal defect)
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27
Q

Tetralogy of Fallot (pathology)

A
  • right to left shunt
  • VSD, subpulmonary obstruction, overriding (r deviation) aorta, RV hypertrophy
  • boot shaped heart
  • squatting improves symptoms
  • all caused by displaced infundibulum
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28
Q

Tetralogy of Fallot (etiology)

A
  • most common cyanotic congenital heart malformation
  • 6-10% of CHD
  • embryology not completely understood: abnormal endocardial cushion development of conotruncus
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29
Q

Transposition of great Arteries

A
  • right to left shunt
  • circulation in parallel (D-TGA)
  • aorta anterior to PA
  • must have ASD/VSD (mixing) to survive
  • PDA improves mixing
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30
Q

hypoplastic left heart syndrome

A
  • spectrum of disease resulting in LV not sufficient to support systemic circulation
  • assoc: mitral/aortic stenosis/atresia, rv hypertrophy, coarctation of aorta
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31
Q

true aneurysm

A
  • involves all three layers of artery or of heart wall

- atherosclerotic and syphilitic, congenital vascular, ventricular resulting from transmural myocardial infarctions

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32
Q

pseudoaneurysm

A
  • wall defect leading to formation of extravascular hematoma that communicates with intravascular space
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33
Q

aneurysms are classified by ____.

A
  • macroscopic shape and size
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34
Q

aneurysms classifications

A
  • saccular: spherical outpouchings involving only portion of vessel wall; often contain thrombus
  • fusiform: diffuse, circumferential dilations; aortic arch, abdominal aorta, iliac arteries
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35
Q

aortic aneurysms predisposing conditions

A
  • atherosclerosis (most common): abdominal aorta, iliac arteries, aortic arch, descending thoracic aorta
  • cystic medial degeneration
  • other: trauma, congenital defects (berry), vasculitis, infections
36
Q

AAA pathogenesis

A
  • men, smokers, > 50 years
  • atherosclerosis major cause: destruction and thinning of underlying aortic media
  • hereditary defects in aorta
37
Q

AAA morphology

A
  • below renal arteries, above bifurcation of aorta

- saccular or fusiform

38
Q

syphilitic aneurysm

A
  • tertiary syphilis
  • obliterative endarteritis of small vessels in any part of body
  • ischemic medial injury leading to aneurysmal dilatation or aorta
39
Q

intracranial aneurysm

A
  • cerebral vascular disorder: weakness in wall causes dilatation or ballooning
  • majority occur in circle of willis
  • hemorrhage is catastrophic
  • risk factors: age, HTN, smoking, alcohol abuse
40
Q

aneurysm signs and symptoms

A
  • small, unchanging = few if any symptoms
  • before rupture: no symptoms, severe headache, nausea, vision impairment, vomiting, loc
  • rupture: sudden/severe headache, nausea/vomiting, drowsiness/confusion/loc, visual abnormalities
41
Q

DVT: clinical features

A
  • local: distal edema, cyanosis, superficial vein dilation, heat, tenderness, redness, swelling, pain
  • PE
42
Q

DVT primary risk factors

A
  • common: factor V mutation, prothrombin mutation, increased factor VIII/IX/XI/fibrinogen
  • rare: antithrombin/proteinC/proteinS deficiencies
43
Q

DVT secondary risk factors

A
  • high: immobilization, MI, tissue injury, cancer, heparin thrombocytopenia, anti-phospholipid Ab syndrome
  • lower: cardiomyopathy, nephrotic syndrome, hyperestrogenic, oral contraceptive, sickle cell, smoking
44
Q

secondary heart tumors

A
  • 20-40 times more common than primary
  • 5% of patients die
  • lung, breast, melanoma
45
Q

myxomas

A
  • most common primary in adult
  • benign
  • 90% atrial, 80% LA
  • clinical manifestation: valvular obstruction, embolization, constitutional
46
Q

rhabdomyoma

A
  • most common primary in children
  • valvular obstruction
  • 50% assoc with tuberous sclerosis
  • spider cells: large round/polygonal with glycogen rich vacuoles
47
Q

tuberous sclerosis complex

A
  • AD multisystem disease that causes tumor growth
  • TSC1 (hamartin) or TSC2 (tuberin) mutation
  • TSC2 more common/severe
48
Q

kaposi sarcoma

A
  • vascular neoplasm caused by herpesvirus
  • most common in AIDS
  • 4 types: classic, endemic african, transplantation-assoc, AIDS-assoc
49
Q

AIDS-assiciated (epidemic) KS

A
  • most common HIV-related malignancy
  • often involves lymph nodes and disseminates widely to viscera early
  • endoscopy shows red spotted tissue
  • histology: dilated, irregular, not well-formed vascular channels with extravasated erythrocytes, hemosiderin-laden macrophages
50
Q

cardiomyopathy types

A
  • dilated or congestive (90%)
  • hypertrophic (6%)
  • restrictive or obliterative (4%)
51
Q

dilated CMP definition

A
  • progressive cardiac dilation and contractile dysfunction usually w/ hypertrophy
  • global LV systolic dysfunction, increased LV cavity diameter, absence of htn/valve disease/sig CAD
52
Q

dilated CMP etiology

A
  • 30-50% inherited disease; mutations: cytoskeletal myocyte proteins of sarcolemma and nuclear membrane
  • viruses: autoimmune attack on myocardium after viral myocarditis
  • immunologic abnormalities
53
Q

dilated CMP gross pathology

A
  • tripled heart weight
  • 4 chamber dilatation (ventricles more severe), formation of mural thrombi of apex
  • flabby/pale myocardium with subendocardial scars
54
Q

dilated CMP assoc conditions

A
  • alcoholism
  • pregnancy/peripartum
  • drug induced (antrhacycline toxicity)
55
Q

hypertrophic CMP etiology

A
  • uncommon
  • cardiac hypertrophy disproportionate to heart load
  • 40-50% cases are familial (AD)
  • mutation in genes encoding proteins of cardiac contractile elements
  • most: B-myosin heavy chain (chr14)
56
Q

hypertrophic CMP clinical features

A
  • variable: young male, sudden cardiac death after exertion

- decreased LV compliance, reduced chamber size due to impaired diastolic filling

57
Q

hypertrophic CMP pathology

A
  • gross: LV hypertrophy w/ asymmetric bulging of iv septum into LV
  • histo: myofiber disarray in iv septum
58
Q

restrictive CMP definitions

A
  • myocardial or endocardial abnormalities limit diastolic filling resulting in decreased CO with normal systolic function
  • may mimic constrictive pericarditis
59
Q

restrictive CMP causes

A
  • interstitial infiltration of amyloid
  • metastatic carcinoma
  • sarcoidosis
  • storage diseases (hemochromatosis)
60
Q

amyloidosis

A
  • heart usually affected in general forms
  • restrictive CMP most common cause of death in AL amyloidosis
  • right sided symptomatology (CHF, peripheral edema, poor response to digitalis)
  • cardiomegaly promenent
  • apple green on congo red
61
Q

myocarditis causes (infectious)

A
  • viral (coxackie, flu, hiv)
  • rickettial
  • bacterial
  • fungi
  • parasites
62
Q

myocarditis causes (non-infectious)

A
  • hypersensitivity and immunology related (rheumatic fever, lupus, RA)
  • radiation
  • misc (sarcoidosis, uremia)
63
Q

viral myocarditis

A
  • hx of viral upper resp infection
  • recover or die of CHF/arrhythmia
  • severe in pregnant or children
  • patchy/diffuse interstitial infiltrate of T lymphocytes, macrophages, rare giant cells, with focal myocyte necrosis
64
Q

chagas disease

A
  • trypanosoma cruzi transmitted by kissing bug

- organisms fill pseudocyst in myocardial fiber

65
Q

giant cell myocarditis

A
  • rare, rapidly fatal
  • unknonw etiology
  • young to middle age patients
  • no effective treatment
  • flabby/dilated heart
  • histo: myocardial necrosis and giant cells (no granulomas)
66
Q

pericarditis

A
  • inflammation of visceral or parietal pericardium with formation of pericardial effusions
  • most acute rxns, chronic less common
67
Q

pericarditis etiology

A
  • infectious: virus, bacteria, tb, fungi, parasites
  • immune: rheumatic fever, collagen disease, postcardiotomy, post MI, drug rxn
  • misc: uremia, neoplasia, trauma, radiation
68
Q

acute pericarditis

A
  • most due to viral infections (coxsackie)

- classified according to gross appearance: serous, fibrinous, purulent, hemorrhagic, caseous

69
Q

fibrinous pericarditis

A
  • inflam rxn of epicardial and pericardial surfaces in form of exudate, with or without resolution
  • most common type
  • loud pericardial friction rub
  • causes: MI, uremia, chest radiation, rheumatic fever, lupus, trauma
70
Q

ischemic heart disease definition

A
  • consequence of atherosclerosis

- in acute coronary syndromes, coronary atherosclerotic plaque rupture or disruption w/ assoc platelet-fibrin thrombus

71
Q

MI macroscopic features

A
  • 30 min: none
  • 0.5-12hrs: none or unstained zone
  • 12-24hrs: pallor or red-blue hue
  • 2-4 days: mottling w/ yellow-tan center
  • 5-10 days: hyperemic border, central yellow-tan softening
  • 10 days - 2 wks: depressed, soft, infarct borders, gelatinous
  • 2-8wks: gray-white scar
  • > 2 months: scar complete
72
Q

MI microscopic features: 0 to 24hrs

A
  • 30 min: none
  • 0.5-24hrs: wavy fibers, coagulative necrosis, myocyte eosinophilia, edema, hemorrhage, contraction band necrosis, myocytosis
73
Q

MI microscopic features: 2-4 days

A
  • coagulation necrosis w/ loss of nuclei and striations, interstitial infiltration of PMNs, interstitial edema, hemorrhage
74
Q

MI microscopic features: 5-7 days

A
  • disintegration of dead myofibers, dying PMNs, macrophages w/ phagocytosis of dead cells
75
Q

MI microscopic features: 7-10 days

A
  • well-developed phagocytosis of dead cells, early formation of fibrovascular granulation tissue at margins, few PMN
76
Q

MI microscopic features: 2-8 weeks

A
  • well-established granulation tissue w/ new blood vessels and increased collagen deposition w/ decreased cellularity
77
Q

MI microscopic features: >2 months

A
  • dense collagenous scar
78
Q

major causes of valve disease

A
  • aging
  • congenital
  • rheumatic heart disease
  • infective endocarditis
79
Q

calcific aortic stenosis

A
  • one of most common
  • congenital bicuspid valve predisposes to calcification
  • acquired: aging degeneration of valve
80
Q

myxomatous degeneration of mitral valve (definition)

A
  • aka prolapse, floppy valve disease
  • very common
  • anomaly of connective tissue
  • floppy enlargement of mitral leaflets w/ redundant tissue and myxoid change
81
Q

floppy valve disease features

A
  • young female
  • midsystolic click
  • dyspnea, angina, fatigue, depression
  • complications: mitral incompetence, emboli, infective endocarditis, arrhythmia, sudden death
82
Q

RF jones crireria

A 
MAJOR:
- J: migratory polyarthritis of large joints
- O: carditis
- N: subcutaneous nodules
- E: erythema marginatum
- S: Sydenham's chorea
MINOR:
- fever, arthralgia, acute phase reactants
DIAGNOSIS: 2 major or 1 major + 2 minor
83
Q

RF pathogenesis

A
  • streptococcal pharyngitis
  • Ab produced
  • cross rxn with glycoproteins
  • cumulative effects on heart
  • chronic valve disease, arrhythmias, infective endocarditis
84
Q

acute rheumatic carditis pathology

A
  • Aschoff bodies: fibrinoid necrosis and inflammatory cells (lymph, histiocytes [Aschoff, Anitschkow])
  • pancarditis: peri, myo, endocardium
85
Q

rheumatic endocarditis

A
  • acute: vegetations on closure line of cusps
  • chronic: organization/fibrosis, valve distortion, cusp thickening, commissure fusion, chordae thickening/shortening/fusion, calcification
86
Q

infective endocarditis types

A
  • acute: normal valve, virulent organism, marked destruction, high mortality
  • subacute: abnormal valve, low virulence of organisms, less destruction, low mortality
87
Q

infective endocarditis predisposing factors

A
  • RHD
  • abnormal valve
  • prosthetic valve
  • immunosuppression, IV lines/drugs
  • sites of infection

Cardio (4 decks)

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