Cardio Path Review Flashcards
cardiogenesis timing
- weeks 3-6
heart tissue originates from ____ and starts as ____.
- mesoderm
- a single tube
direction of heart tube looping
- right or D-looping
____ are necessary for normal AV valve formation and arch development
- neural crest cells
____ assist w/ septation and form ____
- endocardial cushions
- AV valves
CHD incidence
- 0.6% of all full term births
- 1-8 per 1,000
CHD etiology
- multifactorial/unknown: 90%
- genetic (chromosomal, single gene): 8%
- environmental (rubella): 2%
right to left shunt outcomes
- cyanosis
- emboli arising in peripheral veins can enter systemic circulation
left to right shunt outcomes
- RV hypertrophy and overload
- progressive pulmonary HTN
- pulmonary obstructive vascular disease
- reversal of shunt with cyanosis
In utero, pulmonary circulation is a ____ flow, ____ resistance circuit.
- low
- high
After birth, pulmonary circulation is a ____ flow, ____ resistance circuit, due to ____.
- high
- low
- reduction of pulmonary vascular resistance and higher partial pressure of O2
Spontaneous heart closures after birth
- umbilical arteries -> umbilical ligaments
- ductus venosus (umbilical vein blood to IVC) -> ligamentum venosum
- foramen ovale -> fossa ovalis
- ductus arteriosus (PA/Aorta shunt) -> ligamentum arteriosum
The atrial septum develops from
- septum secundum
- septum primum
- endocardial cushion tissue
septum secundum
- infolding of muscular roof of common atrium (door frame of foramen ovale)
septum primum
- thin sheet of tissue that grows to fill in archway formed by septum secundum
endocardial cushion tissue
- develops into portion of atrial septum adjacent to AV valves
AV junction tissue contributes to development of
- AV valves
- portions of atrial septum and ventricular septum
trisomy 21 cardiac associations
- 40% have heart abnormalities
- endocardial cushion defects (AV canal common)
- VSD, ASD, PDA
turner syndrom cardiac associations
- coarctation of aorta
trisomy 18 cardiac associations
- VSD
septum secundum defect
- foramen ovale
LV hypoplasia
- aortic stenosis
situs inversus abnormality associations
- polysplenia
persistent truncus arteriosus
- one aortic and pulmonic outflow tract
ASD types
- left to right shunt
- secundum (most common) or primum
- sinus venous defect, coronary sinus septal defect
VSD types
- 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)
Tetralogy of Fallot (pathology)
- right to left shunt
- VSD, subpulmonary obstruction, overriding (r deviation) aorta, RV hypertrophy
- boot shaped heart
- squatting improves symptoms
- all caused by displaced infundibulum
Tetralogy of Fallot (etiology)
- most common cyanotic congenital heart malformation
- 6-10% of CHD
- embryology not completely understood: abnormal endocardial cushion development of conotruncus
Transposition of great Arteries
- right to left shunt
- circulation in parallel (D-TGA)
- aorta anterior to PA
- must have ASD/VSD (mixing) to survive
- PDA improves mixing
hypoplastic left heart syndrome
- spectrum of disease resulting in LV not sufficient to support systemic circulation
- assoc: mitral/aortic stenosis/atresia, rv hypertrophy, coarctation of aorta
true aneurysm
- involves all three layers of artery or of heart wall
- atherosclerotic and syphilitic, congenital vascular, ventricular resulting from transmural myocardial infarctions
pseudoaneurysm
- wall defect leading to formation of extravascular hematoma that communicates with intravascular space
aneurysms are classified by ____.
- macroscopic shape and size
aneurysms classifications
- saccular: spherical outpouchings involving only portion of vessel wall; often contain thrombus
- fusiform: diffuse, circumferential dilations; aortic arch, abdominal aorta, iliac arteries
aortic aneurysms predisposing conditions
- atherosclerosis (most common): abdominal aorta, iliac arteries, aortic arch, descending thoracic aorta
- cystic medial degeneration
- other: trauma, congenital defects (berry), vasculitis, infections
AAA pathogenesis
- men, smokers, > 50 years
- atherosclerosis major cause: destruction and thinning of underlying aortic media
- hereditary defects in aorta
AAA morphology
- below renal arteries, above bifurcation of aorta
- saccular or fusiform
syphilitic aneurysm
- tertiary syphilis
- obliterative endarteritis of small vessels in any part of body
- ischemic medial injury leading to aneurysmal dilatation or aorta
intracranial aneurysm
- 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
aneurysm signs and symptoms
- 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
DVT: clinical features
- local: distal edema, cyanosis, superficial vein dilation, heat, tenderness, redness, swelling, pain
- PE
DVT primary risk factors
- common: factor V mutation, prothrombin mutation, increased factor VIII/IX/XI/fibrinogen
- rare: antithrombin/proteinC/proteinS deficiencies
DVT secondary risk factors
- high: immobilization, MI, tissue injury, cancer, heparin thrombocytopenia, anti-phospholipid Ab syndrome
- lower: cardiomyopathy, nephrotic syndrome, hyperestrogenic, oral contraceptive, sickle cell, smoking
secondary heart tumors
- 20-40 times more common than primary
- 5% of patients die
- lung, breast, melanoma
myxomas
- most common primary in adult
- benign
- 90% atrial, 80% LA
- clinical manifestation: valvular obstruction, embolization, constitutional
rhabdomyoma
- most common primary in children
- valvular obstruction
- 50% assoc with tuberous sclerosis
- spider cells: large round/polygonal with glycogen rich vacuoles
tuberous sclerosis complex
- AD multisystem disease that causes tumor growth
- TSC1 (hamartin) or TSC2 (tuberin) mutation
- TSC2 more common/severe
kaposi sarcoma
- vascular neoplasm caused by herpesvirus
- most common in AIDS
- 4 types: classic, endemic african, transplantation-assoc, AIDS-assoc
AIDS-assiciated (epidemic) KS
- 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
cardiomyopathy types
- dilated or congestive (90%)
- hypertrophic (6%)
- restrictive or obliterative (4%)
dilated CMP definition
- progressive cardiac dilation and contractile dysfunction usually w/ hypertrophy
- global LV systolic dysfunction, increased LV cavity diameter, absence of htn/valve disease/sig CAD
dilated CMP etiology
- 30-50% inherited disease; mutations: cytoskeletal myocyte proteins of sarcolemma and nuclear membrane
- viruses: autoimmune attack on myocardium after viral myocarditis
- immunologic abnormalities
dilated CMP gross pathology
- tripled heart weight
- 4 chamber dilatation (ventricles more severe), formation of mural thrombi of apex
- flabby/pale myocardium with subendocardial scars
dilated CMP assoc conditions
- alcoholism
- pregnancy/peripartum
- drug induced (antrhacycline toxicity)
hypertrophic CMP etiology
- 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)
hypertrophic CMP clinical features
- variable: young male, sudden cardiac death after exertion
- decreased LV compliance, reduced chamber size due to impaired diastolic filling
hypertrophic CMP pathology
- gross: LV hypertrophy w/ asymmetric bulging of iv septum into LV
- histo: myofiber disarray in iv septum
restrictive CMP definitions
- myocardial or endocardial abnormalities limit diastolic filling resulting in decreased CO with normal systolic function
- may mimic constrictive pericarditis
restrictive CMP causes
- interstitial infiltration of amyloid
- metastatic carcinoma
- sarcoidosis
- storage diseases (hemochromatosis)
amyloidosis
- 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
myocarditis causes (infectious)
- viral (coxackie, flu, hiv)
- rickettial
- bacterial
- fungi
- parasites
myocarditis causes (non-infectious)
- hypersensitivity and immunology related (rheumatic fever, lupus, RA)
- radiation
- misc (sarcoidosis, uremia)
viral myocarditis
- 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
chagas disease
- trypanosoma cruzi transmitted by kissing bug
- organisms fill pseudocyst in myocardial fiber
giant cell myocarditis
- rare, rapidly fatal
- unknonw etiology
- young to middle age patients
- no effective treatment
- flabby/dilated heart
- histo: myocardial necrosis and giant cells (no granulomas)
pericarditis
- inflammation of visceral or parietal pericardium with formation of pericardial effusions
- most acute rxns, chronic less common
pericarditis etiology
- infectious: virus, bacteria, tb, fungi, parasites
- immune: rheumatic fever, collagen disease, postcardiotomy, post MI, drug rxn
- misc: uremia, neoplasia, trauma, radiation
acute pericarditis
- most due to viral infections (coxsackie)
- classified according to gross appearance: serous, fibrinous, purulent, hemorrhagic, caseous
fibrinous pericarditis
- 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
ischemic heart disease definition
- consequence of atherosclerosis
- in acute coronary syndromes, coronary atherosclerotic plaque rupture or disruption w/ assoc platelet-fibrin thrombus
MI macroscopic features
- 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
MI microscopic features: 0 to 24hrs
- 30 min: none
- 0.5-24hrs: wavy fibers, coagulative necrosis, myocyte eosinophilia, edema, hemorrhage, contraction band necrosis, myocytosis
MI microscopic features: 2-4 days
- coagulation necrosis w/ loss of nuclei and striations, interstitial infiltration of PMNs, interstitial edema, hemorrhage
MI microscopic features: 5-7 days
- disintegration of dead myofibers, dying PMNs, macrophages w/ phagocytosis of dead cells
MI microscopic features: 7-10 days
- well-developed phagocytosis of dead cells, early formation of fibrovascular granulation tissue at margins, few PMN
MI microscopic features: 2-8 weeks
- well-established granulation tissue w/ new blood vessels and increased collagen deposition w/ decreased cellularity
MI microscopic features: >2 months
- dense collagenous scar
major causes of valve disease
- aging
- congenital
- rheumatic heart disease
- infective endocarditis
calcific aortic stenosis
- one of most common
- congenital bicuspid valve predisposes to calcification
- acquired: aging degeneration of valve
myxomatous degeneration of mitral valve (definition)
- aka prolapse, floppy valve disease
- very common
- anomaly of connective tissue
- floppy enlargement of mitral leaflets w/ redundant tissue and myxoid change
floppy valve disease features
- young female
- midsystolic click
- dyspnea, angina, fatigue, depression
- complications: mitral incompetence, emboli, infective endocarditis, arrhythmia, sudden death
RF jones crireria
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
RF pathogenesis
- streptococcal pharyngitis
- Ab produced
- cross rxn with glycoproteins
- cumulative effects on heart
- chronic valve disease, arrhythmias, infective endocarditis
acute rheumatic carditis pathology
- Aschoff bodies: fibrinoid necrosis and inflammatory cells (lymph, histiocytes [Aschoff, Anitschkow])
- pancarditis: peri, myo, endocardium
rheumatic endocarditis
- acute: vegetations on closure line of cusps
- chronic: organization/fibrosis, valve distortion, cusp thickening, commissure fusion, chordae thickening/shortening/fusion, calcification
infective endocarditis types
- acute: normal valve, virulent organism, marked destruction, high mortality
- subacute: abnormal valve, low virulence of organisms, less destruction, low mortality
infective endocarditis predisposing factors
- RHD
- abnormal valve
- prosthetic valve
- immunosuppression, IV lines/drugs
- sites of infection
