CVS 2 Flashcards
Diagnostic criteria for SHHD
LVH, concentric
HTN
Absence of other CVS lesions that could cause hypertrophy (valves)
Microscopic examination reveals myocytes aligned circumferentially. What disease?
Cor pulmonale
RV dilation without hypertrophy (after pulmonary embolization)
acute cor pulmonale
Chronic RV pressure –> RV hypertrophy. Main feature of what disease?
chronic cor pulmonale
Microscopic examination revealed:
1) increase in transverse diameter of myocytes
2) box-like appearance of myocytes
3) diffused interstitial fibrosis
systemic hypertensive heart disease
SSHD
Most common type of CMP
dilated CMP
congestive CMP
CMP associated with B-MHC gene
hypertrophic CMP (obstructive)
CMP with decreased ejection fraction, CO and hypocontracting heart
dilated CMP
CMP with decreased cardiac compliance –> impaired ventricular filling, decrease LV ejection fraction
restrictive CMP
In acute cor pulmonale, RV dilation by lead to _____ regurgitation
tricuspid
Characteristic of this CMP:
Hypertrophied IV septum too close to mitral valve –> leads to obstruction
hypertrophic CMP
Causes of this type of CMP include: AABBCCD Alcohol Adrimycin Beriberi B12 def. Coxsackie B Cobalt Doxorubicin
dilated CMP
What type of CMP is associated with pregnancy?
dilated CMP
also classified as peripartum CMP
Banana-like ventricular cavity –> obstruction of blood flow. What CMP?
hypertrophic CMP
Major causes of this CMP:
sarcoidosis, amyloidosis, post-radiation fibrosis
restrictive CMP
Mural thrombi common in this CMP
dilated CMP
CMP with massive hypertrophy but without ventricular dilatation
hypertrophic CMP
Thick fibroelastic tissue in endocardium of young children
endocardial fibroelastosis (type of R CMP)
endomyocardial fibrosis with a prominent eosinophilic infiltrate
Loffler’s syndrome (type of R CMP)
Most common etiologic agent of myocarditis
viruses: Coxsackie A and B enterovirus CMV HIV
Parasitic etiologies of myocarditis:
Chagas disease
txoplasmosis
trichinosis
Bacterial etiologies of myocarditis
Lyme disease
diphtheria
Myocarditis with these features:
edema
mononuclear infiltrates
myocyte degeneration and necrosis
acute viral myocarditis
aka Fiedler’s myocarditis
giant cell myocarditis
Myocarditis with these features:
macrophage and eosinophil infiltrate
little to no necrosis
no granulomas
hypersensitivity myocarditis
Methyldopa can cause this myocarditis
hypersensitivity myocarditis
Most common chromosomal defect resulting in CHD
trisomy 21
Trisomies that are highly associated with CHD
13, 15, 18, 21
Infections causing CHDs
rubella
Teratogen causing CHD
thalidomide
Early cyanotic (blue baby) CHDs are usually
R to L shunt
unoxygenated blood bypass pulmonary circulation and sent to systemics
Most common CHD
VSD
Most common asymptomatic CHD
ASD
Direction of low shunted from LA to RA
ASD
Most common type of ASD
secundum ASD
CHD that can manifest pulmonary congestion due to volume overload in RV
VSD
Indomethacin used to treat this CHD
PDA
CHD has this characteristic machinery-like murmur
PDA
Late clinical manifestation of ASD
ASD pulmonary HTN occurs in the 2nd or 3rd decade of life
Most common type of ASD
secundum ASD
Type of ASD where defect is located near entrance of SVC.
May be associated with total anomalous pulmonary venous return (TAPVR)
sinus venosus
CHD due to fenestrated fossa ovale
secundum ASD
CHD due to incomplete closure of AV septum and associated with cleft of anterior mitral valve
primum ASD
primum ASD + cleft of anterior mitral valve = partial AVSD)
Most VSD occur in this part of the septum
membranous (superior) VSD
Type of VSD located below pulmonary valve
infundibular VSD
Type of VSD located near atrioventricular valve
membranous VSD
Type of VSD showing Swiss-cheese septum
muscular VSD
Type VSD with high incidence of spontaneous closure
muscular VSD (50%)
CHD where there is a single large common AV valve and free communication of all four chambers
Complete AVSD
Shunting of blood from aorta to pulmonary artery
Patent ductus arteriosus PDA
PDA may be beneficial in:
TGV
TOF
Maintains patency of ductus arteriosus
PGE
Right to Left shunts?
5 T's Tetralogy Transposition Trucus Tricuspid TAPVR
Main problem in TOF. Causes the cyanosis and most common reason for R to L shunting.
Pulmonary stenosis
TOF components
- Pulmonary stenosis
- RVH
- Aorta overriding VSD
- VSD
Blue baby CHD characterized by RV hypoplasia
Tricuspid Atresia (absent tricuspid valve is obviously the most important characteristic)
Results from unequal division of AV canal
Tricuspid atresia
Pulmonary artery and aorta are a single great artery in this CHD.
PTA (patent Truncus Arteriosus)
Due to failure of the aorticopulmonary septum to spiral during embryogenesis
TGV
Lesion most associated with PTA
VSD
Patient learns to compensate for symptoms by squatting.
TOF
compression of femoral arteries –> increased TPR –> decreased right to left shunt
Compression causes pressure.
Pulmonary veins drain into right heart circulation (SVC, coronary sinus, etc.). What CHD?
TAPVR
CHD featuring RVH and LV hypoplasia
TGV
RV becomes systemic ventricle
LV wastes because no blood flows here
Boot-shaped heart
RVH seen in TOF
Cyanotic CHD featuring hypoplastic LA with right-sided dilation and hypertrophy,
TAPVR
The pulmonary veins drain into right side (cause of dilation and hypertrophy) instead of LA (hypoplasia)
TGV is incompatible with life unless paired with these defects
PDA, ASD, VSD
There has to be a shunt to allow mixing of blood since the systemic and pulmonary circulations are separated.
What CHD? Inability of the great vessel to rotate during embryogenesis resulting in an incomplete migration of the great vessels to their normal positions.
TOF
Congenital narrowing or constriction of the aorta
Coarctation of aorta
COA type associated with Turner syndrome
Infantile type
In TGV aorta arises from where? pulmonary artery from where?
Aorta arises from RV
Pulmonary artery from LV
COA type where stenosis is distal to ligamentum arteriosum (closed ductus arteriosus).
Adult type has a postductal constriction
Infantile type has a preductal constriction
COA + PDA manifests symptoms when?
Early childhood.
Without COA, adulthood.
Hypertension in upper extremities and weak pulse in lower extremities.
Adult COA or postductal COA
The pressure is higher proximal to the coarctation point (thus higher BP for upper circulation and lower BP for abdominal aorta)
Most common valvular defect
calcific aortic valve stenosis
Usually acquired and the result of wear and tear.
Libman-Sacks endocarditis found in patients with:
SLE
Serotonin-induced fibrosis of tricuspid and pulmonary valves causing Right-sided insufficiency
carcinoid heart disease
Immune-mediated inflammatory disease folowing group A (beta hemolytic) strep
RF
Pathognomonic for RF
Anitschkow cells - enlarged macrophages found within granular tissue in RF
Heaped-up calcified masses within aortic cusps
calcific aortic valve stenosis
Common in eldery women with myxomatous mitral valve and elevated LV pressure
mitral annular calcification
Colonization or invasion of valves or mural endocardium by microbe forming bulky vegetations
infective endocarditis
Marantic endocarditis aka
non bacterial thrombotic endocarditis
associated with malnutrition
Antibodies aginst M protein (strep) react with glycoproteins of heart
RF
Bulky, friable vegetations on valves
IE
Necrotic vegetations on lines of valve closure
verrucae (RF)
Major bacterial causes of IE
Strep viridans
Staph aureus (esp. IV drug users)
pneumococci
ricketssia/chlamydia
Type of IE arising in previously diseased valve
subacute IE (usually by less virulent organisms like viridans)
Defect that causes a mid-systolic click
MVP
Irregular thickenings caused by regurgitation and induced by verrucae usually seen in LA
Seen in RF
MacCallum plaques
Mechanical prosthetic valves are prone to:
thrombosis
Fish mouth or buttonhole stenosis seen in:
RF
extreme narrowing of valve, usually MITRAL
Roth spots can be seen in which heart disease?
subacute bacterial endocarditis
x
x
Associated with cancer and Trousseau syndrome
NBTE
Non-tender erythematous/heemorrhagic lesions in palms or soles? What disease?
Janeway lesions
PATHOGNOMONIC of IE
“caterpillar cells” aka
Anitschkow cells
Irregular, stony, hard nodules behind MV leaflets
mitral annular calcification
Splinter hemorrhage seen in what heart disease
IE
nails
Sterile, nondestructive vegetations on valves
NBTE
Central zone of degenerating, hypereosinophilic ECM infiltrated by lymphocytess, plasma cells, and plump activated macro phages are:
Found in what disease?
Aschoff bodies
acute RF
Unequal-sized bicuspid valve with midline “raphe’ resulting from incomplete commissural separation during development.
congenital bicuspid aortic valve calcification
CVS disease most associated with Marfan’s
MVP
Most common valvular disease in INDUSTRIALIZED countries
MVP
Bioprosthetic valves are prone to
deterioration and calcification
Pericarditis caused by SLE, RHD, scleroderma, tumors
serous (noninfectious, inflammatory diseases)
Pericarditis caused by Dressler syndrome
fibrinous
Caseous pericardits caused by
tuberculous foci
Soldier’s plaque seen in this pericarditis
chronic/healed
Pericarditis caused by TB, tumor metastasis, bacteria
hemorrhagic
Loud pericardial friction rub is heard in this pericarditis
fibrinous
Viruses cause this form of pericarditis
serous
When pericardial effusion affects heart function by restricting cardiac filling:
cardiac tamponade
Bread and butter pericarditis
fibrinous
Most common primary heart tumor in adults
myxoma
Most common primary heart tumor in children
rhabdomyoma
Causes wrecking ball effect to valve leaflets:
myxoma tumors
Cardiac tumor associated with tuberous sclerosis
rhabdomyoma
Spider cells
rhabdomyoma
Left atrium tumor
myxoma
Left ventricle tumor
rhabdomyoma
