Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
134 Cards in this Set
- Front
- Back
|
what types of clinical manifestations can you get for ischemic heart disease?
|
1. silent
2. angina pectoris 3. MI |
|
|
who is predisposed to IHD?
|
- metabolic sydrome:
- central obesity, artherogenic lipid patterns, hypertension, insulin resistance, proinflammatory state with C-reactive protein |
|
|
what is angina pectoris
|
- chest pain caused by inadequate oxygenation of the myocardium
1. stable angina 2. unstable angina 3. prinzmetal angina |
|
|
stable angina
|
- most common form
- pain that is precipitated by exertion - caused by severe narrowing of artherosclerotic coronary vessels - relieved by nitroglycerin or cessation of activity |
|
|
unstable angina
|
- prolonged or recurrent pain at rest
- indicative of imminent MI - cuased by disruption of an atherosclerotic plaque with superimposed thrombus - can also be caused by embolization or vasospasm |
|
|
prinzmetal angina
|
- intermittent chest pain at rest
- caused by vasospasm |
|
|
what type of necrosis is characteristic of MI?
|
- myocardial coagulative necrosis caused by coroanry artery occlusion is characteristic
|
|
|
what is released during an MI?
|
- MI is marked by changes in gross and microscopic appearance
- release of myocardial enzymes into the bloodstream b/c of altered permeability of necrotic blood cells |
|
|
what type of cellular involvement is found in MI?
|
- cellular involvement: neutrophils, macrophages, fibroblasts
|
|
|
what type of cellular involvement is not found in MI?
|
- lymphocytes and plasma cells
|
|
|
which proteins/enzymes do you see in serum following MI?
|
1. Creatine Kinase MB fraction (CK-MB)
2. Troponin-I 3. Lactate dehydrogenase (LDH) |
|
|
when do you see CK-MB after an MI?
|
- peaks at 24 h
- gone by 3 days |
|
|
when do you see Troponin-I after an MI?
|
- peaks at 24 h
- persists to a week |
|
|
when do you see LDH after an MI?
|
- peaks at 3 days
- persists to a week |
|
|
what are the 2 patterns of myocardial ischemic necrosis?
|
1. transmural infarction: traverses the entire ventricular wall, from teh endocardium to the epicardium
2. subendocardial infarction: limited to the interior 1/3 of the wall of the LV |
|
|
list some complications following MI
|
1. arrhythmia
2. myocardial (pump) failure 3. myocardial rupture 4. ruptured papillary muscle 5. mural thrombosis 6. ventricular aneurysm |
|
|
what is the most common complication in the first several hours after MI?
|
- arrhythmia
|
|
|
what can pump failure lead to?
|
- CHF and/or shock
- likelihood det by size and location of the lesion |
|
|
myocardial rupture
|
- occurs within the first 4-7 days and may result in death from cardiac tamponade
|
|
|
what is a mural thrombus?
|
- a thrombus formed at the endocardium overlying the infarct -> can lead to left sided embolism
|
|
|
define rheumatic fever
|
- multisystem inflammatory disorder with major cardiac manifestations and sequelae, most often affecting children between 5-15 years of age
|
|
|
what else do you have when you get rheumatic fever?
|
- a transient mild migratory polyarthritis
|
|
|
when does rheumatic fever occur?
|
- about 1-4 weeks after tonsillitis or another infection caused by GROUP A B-HEMOLYTIC STREPTOCOCCI
|
|
|
what blood test can you do to determine recent streptococcal infection?
|
- elevated antistreptolysin O (ASO)
|
|
|
what is a classic lesion of RF?
|
- Achoff body
- area of focal interstitial myocardial inflammation - characterized by fragmented collagen and fibrinoid material, by large cells (Anitschkow myocytes), and by multinucleated giant cells (Aschoff cells) |
|
|
what other anatomical changes do you get with rheumatic fever (pancarditis)?
|
1. pericarditis
2. myocarditis 3. endocarditis |
|
|
what happens with pericarditis?
|
can get pericardial, pleural or other serous effusions
|
|
|
what happens with myocarditis?
|
- can lead to cardiac failure
- cause of moth deaths during the early stages of acute RF |
|
|
what happens with endocarditis?
|
- leads to valvular damage
- usually occurs in areas of greatest hemodynamic stress (e.g. points of valve closure and the posterior wall of the L. atrium) -> MacCallum plaque |
|
|
which valves are most likely to be affected in RF?
|
- mitral and aortic, which are subject to more pressure and turbulence
|
|
|
what happens in the early stage of endocarditis?
|
- valve leaflets are red and swollen, and tiny, warty, bead-like, rubbery vegetations (verrucae) form along the lines of closure on the leaflet
- these are nonfriable and are NOT a source of emboli |
|
|
what are verrucae?
|
swollen, and tiny, warty, bead-like, rubbery vegetations form along the lines of closure on the leaflet
|
|
|
what happens with leaflet healing during RF endocarditis?
|
- fibrosis causes valves to be thickened and deformed
- fusion of cusps and thickening of the chordae tendineae - calcification is prominent --> rheumatic heart disease |
|
|
which valve is most often involved in Rheumatic heart disease?
|
- mitral valve
- is the only valve affected in 50% of cases - can be affected by stenosis with fish-mouth buttonhole deformity, insufficiency, or both - Mitral stenosis -> diastolic pressure is higher in the LA than in the LV |
|
|
which other valves are affected during rheumatic heart disease?
|
- the aortic valve -> either stenosis or insufficiency
|
|
|
how often is the tricuspid valve involved in rheumatic heart disease?
|
- 5%
|
|
|
which valve is rarely involved in rheumatic heart disease?
|
- pulmonic valve
|
|
|
list the noncardiac manifestations of acute rheumatic fever
|
1. fever, malaise, and increased e. sedimentation rate
2. joints: arthralgia, arthritis, migratory polyarthritis 3. skin lesions: subcutaneous nodules, erythma marginatum 4. CNS: sydenham chorea |
|
|
define arthralgia
|
- joint poaint without clinically evident inflammation
|
|
|
define migratory polyarthritis
|
sequential involvement of multiple joints
|
|
|
what are subcutaneous nodules?
|
- small painless swellings over bony prominences
|
|
|
what is erythema marginatum?
|
- skin rash characteristic of rheumatic fever, often involving the trunk and extremities
|
|
|
what is sydenham chorea?
|
- involuntary, purposeless muscular movements, bizarre grimaces, and emotional liability
|
|
|
list the other types of endocarditis
|
1. infective endocarditis
2. nonbacterial endocarditis 3. Libman-Sacks endocarditis 4. Endocarditis of the carcinoid syndrome |
|
|
infective endocarditis
|
- bacterial or fungal infection of endocardium. often involves valvular surfaces
|
|
|
what characterizes infective endocarditis?
|
- large, soft, friable, easily detached vegetations formed from fibrin and intermeshed inflammatory cells and bacteria
|
|
|
what are some complications of infective endocarditis?
|
- ulceration, with performation of valve cusps or rupture of chordae tendineae
|
|
|
what are the two subtypes of infective endocarditis?
|
- acute endocarditis
- subacute (bacterial) endocarditis |
|
|
acute endocarditis
|
- caused by staph aureas in 50% of the cases
- seen secondary to infection occuring elsewhere in the body |
|
|
subacute (bacterial) endocarditis
|
- caused by less virulent organisms: strep viridans in more than 50% of the cases
- tends to occur in patients with congenital HD or preexisting valvular HD, often rheumatic in origin (then go to dentist) |
|
|
which valves are most often involved in infective endocarditis?
|
- mitral
- both mitral and aortic involved in 40% of cases - tricuspid valve is involved in >50% of cases involving IV drug users -> caused by staphlococcus infection |
|
|
what are some complications of infective endocarditis?
|
1. distant embolization
2. emboli can result in septic infarcts in the brain 3. renal glomeruli may be the site of focal glomerulonephritis (focal necrotizing glomerulitis) caused by immune complex disease or by septic emboli |
|
|
nonbacterial thrombotic endocarditis
|
- aka marantic endocarditis
- associated with debilitating disorders (e.g. metastatic cancer) - small, sterile firbin deposits randomly arrange along the line of closure on valve leaflets - can result in peripheral embolization, but these emboli are sterile |
|
|
Libman-Sacks endocarditis
|
- occurs in SLE
- small vegetations are found on both surfaces of the valve leaflets |
|
|
Endocarditis of the carcinoid syndrome
|
- caused by secretory products of carcinoid tumors (vasoactive peptides and amines, esp 5-HT
- results in thickened endocardial plauqes involving the mural endocardium or the valvular cusps of the RH |
|
|
what are carcinoid tumors?
|
Carcinoid tumors are discrete, yellow, well-circumscribed tumors that can occur anywhere along the gastrointestinal tract (GI). These tumors are unique in that they are endocrine in nature. They secrete hormones into the blood stream, which then travel to end organs and act upon them via appropriate receptors. Although quite rare, carcinoid tumors account for 75% of GI endocrine tumors.
|
|
|
why don't you see LH valvular involvement in endocarditis of the carcinoid syndrome?
|
- 5-HT and other carcinoid secretory products are detoxed in the lung
|
|
|
what types of disease can you get with the mitral valve?
|
1. prolapse
2. stenosis 3. insufficiency |
|
|
what types of disease can you get with the aortic valve?
|
1. stenosis
2. insufficiency |
|
|
what types of diseases can you get with the tricuspid valve?
|
rarely involved ALONE in rheumatic heart disease, but may be involved together with the mitral and aortic valves.
- accounts for 5% of cases - may also be involved in carcinoid sydrome |
|
|
what diseases are associated with the pulmonary valve?
|
- most commonly affected by congenital malformations (e.g. tetrology of Fallot)
- rarely invovled in rheumatic heart disease - may be involved in carcinoid syndrome |
|
|
mitral valve prolapse
|
- most frequent valvular lesion
- occurs in 7% of the population, most often young women |
|
|
what are characteristics of mitral valve prolapse?
|
- myxoid degeneration of the ground substance of the valve -> stretching of the posterior valve leaflet -> parachute deformity with prolapse in systole
|
|
|
define myxoid
|
resembling mucous
|
|
|
what do you hear with mitral valve prolapse?
|
- systolic murmur with a midsystolic click
|
|
|
what can mitral valve prolapse result in?
|
- mitral insufficiency/regurg
- assocaited with arrhythmias and predisposes to infective endocarditis |
|
|
what is another word for insufficiency?
|
regurge
|
|
|
Mitral valve stenosis
|
- almost always due to RH disease
|
|
|
Mitral valve insufficiency
|
- usually results from rheumatic heart disease
- can also result from mitral valve prolapse, infective endocarditis, damamge to a papillary muscle from MI - can be secondary to LV dilation with stretching of the mitral ring |
|
|
Aortic valve disease
|
- frequently involved in rheumatic heart disease and infective endocarditis, along with the mitral valve
|
|
|
Aortic valve stenosis
|
- often presents as calcific aortic stenosis caused by calcification:
1. degenerative calcific aortic stenosis 2. congenital bicuspid aortic valve 3. valve affected by RH dsease- scarring may be seen as fusion of valve commisures |
|
|
degenerative calcific aortic stenosis
|
age-related degenerative chagne.
- most common cause of calcific aortic stenosis in persons older than 60 - used only when teh stenotic valve has three cusps |
|
|
aortic valve insufficinecy
|
can be caused by:
1. nondissecting aortic aneurysm from cystic medial necrosis 2. RH disease, in association with mitral valve disease 3. Syphilitic (luetic) aortitis- dilation of the aortic ring |
|
|
anatomic changes seen in atrial septal defects
|
1. patent foramen ovale
2. septum primum 3. septum secondum 4. sinus venosus 5. lutembarcher syndrome |
|
|
septum primum
|
affects lower part of septum
- if large, may be associated with deformalities of the AV valves |
|
|
define atrial septum defect
|
hole between the two atria
|
|
|
septum secondum
|
- defect in the fossa ovalis
|
|
|
sinus venosus
|
- affects the upper part of the septum, near the entrance of the SVC
|
|
|
lutembacher syndrome
|
atrial septal defect with mitral stenosis
|
|
|
what are the clinical manifestations of ASDs?
|
- often delayed until adult life
- pulmonary hypertension and reversal of flow with resultant cyanosis are late complications -> can lead to paradoxic embolism |
|
|
paradoxical embolism
|
if there is an ASD, a clot can cross from the right to the left side of the heart, then pass into the arteries. Once in the arterial circulation, a clot can travel to the brain. Because of the risk of stroke, it is usually recommended that even small ASDs be repaired.
|
|
|
anatomic changes in ventricular septal defects
|
- can vary greatly in size
- small defects can close spontaneously - large defects -> pulmonary hypertension -> right sided HF -> reversal of flow and late cyanosis |
|
|
tetralogy of fallot
|
1. pulmonary infundibular or valvular stenosis
2. VSD 3. overriding aorta 4. RV hypertrophy |
|
|
what are the clincial manifestations of tetrology of Fallot
|
- cyanosis from birth
- patients squat to lessent right to left shunting |
|
|
patent ductus arteriosus
|
- failure to close the ductus arteriosus -> pulmonary hypertension, RV hypertrophy, reversal of blood flow -> cyanosis
|
|
|
why does the ductus arteriosus stay open during fetal stages?
|
- low oxygen tension and prostaglandin synthesis
|
|
|
how do you treat a patent ductus arteriosus pharmacologically?
|
- indomethacin: a NSAID that blocks the production of prostaglandins
|
|
|
coarctation of the aorta
|
narrowing of the aorta, usually distal to the origin of the subclavian arteries -> extensive developmet of collateral circulation with dialtion of intercostal arteries
|
|
|
what are the clinical features of coarctation of the aorta?
|
- hypertension limited to the upper extremities and cerebral vessels
- notching of the ribs seen on x-ray |
|
|
transposition of the great vessels
|
- aorta arises from the RV, pulmonary arteries from the LV
- a patent ductus arteriosus is necessary for survival |
|
|
what genetic defects cause congenital heart disease?
|
- trisomies (Down's) and turner syndrome
|
|
|
what is turner's syndrome associated with?
|
- coarctation of the aorta
|
|
|
how does Down's syndrome lead to congenital heart defects?
|
- endocardial cushion defects -> atrail and ventricular septal defects and atrioventricular valve deformities
|
|
|
which children have a higher incidence of patent ductus arteriosis?
|
- patients that live at high altitude -> possibly an association with fetal O2 deprivation
|
|
|
what is an infectious etiology of congenital heart disease?
|
- rubella (german measles)
- congenital rubella syndrome: mothers with rubella during the first trimester -> infants with CV defects, microcephaly with mental retardation, deafness, cataracts, and growth retardation |
|
|
what cardiac malformations do you get in congenital rubella syndrome?
|
- patent ductus arteriosus, aortic stenosis, VSD, pumonary infundibular or valvular stenosis, sometimes tetrology of fallot
|
|
|
how do you determine a mother's immune status to rubella?
|
- IgM antirubella antibodies: recent primary infection
- IgG antirubella antibodies: either recent primary infection, past infection, or reinfection |
|
|
is tetralogy of fallot seen in families?
|
- yes. possibly due to multifactorial inheritance
|
|
|
noncyanotic diseases
|
- those with no shunt (aortic stenosis, coarctation of the aorta)
- L to R shunt: patent ductus arteriosus, atrial or VSD |
|
|
cyanotic diseases
|
- transposition of the great vessels (you need a shunt between the L and R ventricles to survive)
- malformations with a R to L shunt (e.g. tetrology of fallot) - reversal of shunt direction: late cyanosis, tardive cyanosis |
|
|
cardiomyopathy- define!
|
diseases of the heart nmuscle that are noninflammatory and are not associated with hypertension, congenital heart disease, valvular disease, or coronary artery disease
|
|
|
how is cardiomyopathy characterized?
|
- usually by unexplained ventricular dysfunction (HF that is unresponsive to digitalis, ventricualr enlargement, ventricular arrhythmias)
|
|
|
list the different types of cardiomyopathy
|
1. congestive or dilated
2. Restrictive 3. Hypertrophic |
|
|
congestive or dilated cardiomyopathy
|
- most common form of cardiomyopathy
- 4 chamber dilation and hypertrophy - R and L sided intractable HF - etiology is unknown - sometimes related to alcoholism, thiamine deficiency, or prior myocarditis |
|
|
what causes thiamine deficiency?
|
- beriberi
|
|
|
restrictive cardiomyopathy
|
- infiltrative processes within the myocardium that stiffens the muscle -> can't pump
- exemplified by cardiac amyloidosis -> L and R sided HF |
|
|
hypertrophic cardiomyopathy
|
- autosomal dominant
- hypertrophy of all chamber walls, esp the ventricular septum (asymmetric septal hypertrophy) - tangled and hypertrophied myocardial fibers - LV outflow obstruction -> syncope and sudden death (young athletes) |
|
|
myocarditis
|
- presents as biventricular HF in young people without valvular, rheumatic, or congenital Heart disease
|
|
|
what morphologic characteristics do you see in myocarditis?
|
- diffuse myocardial degeneration and necrosis, with inflammatory infiltrate
|
|
|
what causes myocarditis?
|
- viruses: coxsackievirus
|
|
|
what causes myocarditis in south america?
|
- trypanosoma cruzi -> chagas disease
|
|
|
non-inflammatory pericardial disease
|
1. hydropericardium
2. hemopericardium |
|
|
hydropericardium
|
- accumulation of serous transudate in teh pericardial space
- results from systemic edema - caused by CHF or edematous conditions (hypoproteinemia seen in nephroic syndrome and chronic liver disease) |
|
|
hemopericardium
|
- accumulation of blood in pericardial sac.
- caused by traumatic perforation of the heart or aorta - can also be caused by myocardial rupture associated with acute MI |
|
|
acute pericarditis
|
1. serous pericarditis
2. fibrinous or serofibrinous pericarditis 3. purulent or suppurative pericarditis 4. hemorrhagic pericarditis |
|
|
serous pericarditis
|
- assocaited wtih SLE, RF, and viral infections
- production of clear, staw-colored, protein rich exudate containing some inflammatory cells |
|
|
fibrinous or serofibrinous pericarditis
|
- fibrin rich exudate
- caused by uremia, MI, or acute RF |
|
|
purulent or suppurative exudate
|
- almost always caused by bacterial infection
- grossly cloudy or frankly purulent inflammatory exudate |
|
|
hermorrhagic pericarditis
|
- bloody inflammatory exudate
- results from tumor invasion of the pericardium - can also result from TB or bacterial infection |
|
|
chronic (constrictive) pericarditis
|
- usually caused by TB or pyogenic staph
- thickening and scarring of the pericardium -> loss of elasticity (mimics the symptoms of RH failure) - proliferation of fibrous tissue with small foci of calcification |
|
|
primary tumors of the heart
|
1. myxoma of the Left atrium
2. Rhabdomyoma |
|
|
myxoma of the l. atrium
|
- most frequently occurring cardiac tumor
- found in adults |
|
|
Rhabdomyoma
|
- most comon in infants and young childrne
- assocaited with tuberous sclerosis |
|
|
metastatic tumors of the heart
|
- found more frequently than primary tumors
|
|
|
what type of assay can you run to differentiate heart failure from asthma, acute coronary syndrome, COPD, or PE?
|
- look for B-type natriuretic peptide: elevated in HF
|
|
|
causes of Left sided Heart Failure
|
1. Ischemic heart disease
2. hypertension 3. aortic and mitral valvular disease 4. myocardial diseases |
|
|
what are the clinical manifestations of Left sided heart failure?
|
- dyspnea and orthopnea (from pulm congestion and edema)
- pleural effusion with hydrothorax - reduction in renal perfusion (less frequent) - cerebral anoxia (less frequent) |
|
|
define hydrothorax
|
- A type of pleural effusion
- hydrothorax: pus - In hemothorax this fluid is blood (as in major chest injuries), in pyothorax the fluid is pus (resulting from chest infections), in chylothorax it is chylus (resulting from rupture of the thoracic duct). |
|
|
what causes right sided heart failure?
|
1. left sided heart failure
2. left sided lesions (e.g. mitral stenosis) 3. pulmonary hypertension (from cor pulmonale) 4. vardiomyopathy and diffuse myocarditis 5. tricuspid or pulmonary valvular disease |
|
|
define cor pulmonale
|
change in structure and function of the right ventricle of the heart as a result of a respiratory disorder. RVH (right ventricular hypertrophy) is the predominant change in chronic cor pulmonale, however in acute cases dilation dominates.
|
|
|
what are the clinical manifestations of right sided heart failure?
|
- renal hypoxia -> fluid retention and peripheral edema (more so than in LH failure!)
- enlarged and congested liver and spleen -> chornic passive congestion of the ventriloobular veins of liver -> nutmeg liver - distension of neck veins |
|
|
what is LV hypertrophy caused by?
|
- mainly hyerptension and aortic or mitral valvular disease
|
|
|
what is RV hypertrophy caused by?
|
- LV failure
- chronic lung disease - mitral valve disease - congenital heart disease (L to R shunt) |
|
|
define cor pulmonale again
|
- RV hypertrophy and or dilation secondary to lung disease or primary disease of the pulmonary vasculature (e.g. primary pulmoanry hypertension)
- emphysema is a frequent cause |
