Test 2 - RU Heart Flashcards

(66 cards)

1
Q

chronic inflammatory response in the walls of arteries

A

atherosclerosis

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2
Q

inflammatory disease of blood vessels

A

vasculitides

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3
Q

S/S of vasculitides

A

fever, malgias, athralgais

ischemia, thrombus formation

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4
Q

M/C arteritis after 50 yrs

involves medium and small arteries

granulomatous formation is T cell mediated

A

giant cell arteritis

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5
Q

ocular disturbances and weakened upper extremity pulse

A

takayasu arteritis

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6
Q

typically involves small and medium arteries, especially renal vessels

autoimmune

affects young adults

transmural inflammation of the arterial wall

nodular formation causes segmental weakening resulting in rupture

A

polyarteritis nodosa (PAN)

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7
Q

autoimmune

acute necrotizing granulomas in respiratory tract

renal disease - “crescentic glomerulonephritis”

A

wegener’s granulomatosis

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8
Q

onset before age 35

affects heavy smokers

involves segmental thrombosing and inflammation of medium and small arteries

A

thromboangiitis obliterans “buerger disease”

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9
Q

localized, abnormal dilation of a blood vessel wall or wall of the heart

A

aneurism

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10
Q

true vs false aneurism

A

true: involves all layers: atherosclerotic, symphilitis, congenital vascular aneurism, left vascular aneurism (MI)
false: leak in the vessel wall leading to a hematoma (PAN)

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11
Q

blood enters the vessel wall and forms a hematoma resulting in a dissection of the layers of the wall

usually caused by atherosclerosis and cyctic median necrosis

A

dissection

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12
Q

affects mainly men 50+

mostly results from atherosclerosis

abdominal aorta - below renal artery but above the bifercation

obstruction, shock, aneuris, embolism

A

abdominal aortic aneurism

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13
Q

typically men between 40-60 with history of hypertension

thoracic aorta

S/S: aortic valve insufficiency, difficulting breathing, encroachment of mediastinal structures

A

syphilitic (leutic) and aortic dissection

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14
Q

benign, malformation of the endothelial cells lining blood vessels

majority are superficial, occuring in the head, neck and liver

A

hemangioma

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15
Q

located in skin, sub-cutaneous tissue and mucus membranes of oral cavities and lips

A

capillary hemangioma

juvenile : strawberry patch seen in new borns

cavernous : large, often located in the brain or brainstem

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16
Q

most often seen in AIDS patients

A

karposi sarcoma

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17
Q

malignant endothelial neoplasm

most common primary malignancy of the heart

A

angiosarcoma

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18
Q

most frequently occurring cardiac tumor and is found most often in adults; benign

A

myxoma of the left atrium

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19
Q

most common in infants and young children

notable for its association with tuberous sclerosis; benign

A

rhabdomyoma

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20
Q

5 principles of cardiac dysfunction

A
  1. failure of the pump - muscle contracts weakly, incomplete emptying of chambers, insufficient ventricular filling
  2. obstruction of flow: incomplete valve opening, increased ventricular pressure
  3. flow regurgitation: insufficient closure of the valve casuing blood to flow backwards
  4. disorders of conduction: due to heart-block or arhythmeas
  5. disruption of the continuity of the circulatory system
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21
Q

group of syndromes caused by myocardial ischemia

A

ischemic heart disease

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22
Q

acute heart attack

A

myocardial infarction

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23
Q

severe chest pain (stable, prinzmetal, and unstable)

A

angina pectoris

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24
Q

unstable angina, MI, sudden death

A

acute coronary syndromes

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25
blood supply to the heart is interrupted
myocardial infarction
26
transmural MI involves ischemic necrosis of the full thickness of the \_\_\_\_\_\_\_
ventricular wall
27
morphologic changes of MI 4hrs 4-24 hrs 1-3 days 3-7 \>7
4hrs - no gross damage 4-24hrs - collagen necrosis 1-3 days - necrosis with inflammation (neutrophilic infiltrate) 3-7 days - dying neutrophils and necrosis \>7 days - necrosed myocardium is replaced with connective tissue (fibrosis)
28
consequences of MI
contractile dysfunction arrhythmias pericarditis ventricular anurism myocardial rupture
29
usually caused by significant coronary occlusion congenital, structural coronary arterial abnormalities aortic valve stenosis mitral valve prolapse dialted or hypertrophic cardiomyopathy pulmonary hypertension
sudden cardiac death
30
hear tis large and heavy due to left ventricular hypertrophy and dilation myocardial hypertrophy found with ischemic cardiomyopathy
chronic ischemic heart disease
31
sustained diastolic blood pressure \> 90mmHg or sustained systolic blood pressure \> 140mmHg
hypertension
32
priamary vs secondary hypertension
primary: abnormality in the rennin-angiotensin system resulting in an increase in blood volume, increase in peripheral resistance secondary: often caused by renal disease, caused by adrenohyperfunction (cushing syn), caused by pregnancy, stress, and cardiovascular pathology
33
found in elderly patients without hypertension leakage of plasma components across vascular wall increase in extra-cellular matrix production by smooth muscle cells hyaline deposition
hyaline atherosclerosis
34
acute or rapid elevation in blood pressure narrowing of the arteriole lumen due to a concentric laminated thickening (onion skin) smooth muscle cells thicken and replicate the basement membrane results in fibrinoid deposition and acutre necrosis of the vessel
hyperplastic atherosclerosis
35
hypertension retinopathy 1 2 3 4
1 - generalized narrowing of the arterioles 2 - grade 1 + focal arteriole spasms 3 - grade 2 + flame shpaed hemorrhages, cotton wool spots and hard waxy exudates 4 - grade 3 + optic disc edema
36
inflammation of the endothelial and subendothelial tissues
endocarditis
37
autoimmune occurs after strep infections produces Macculm plaques - subendocardial thickening from regurgitation, left atrium changes usually occur in mitral valve leaflet thickening commissural fusion shortening and thickening of cordea tendenea
rheumatic valvulitis
38
autoimmune involves the mitral and tricuspid valves small vegetations on both sides of valves found in fibrinoid necrosis
liebman - sacks (SLE)
39
caused by highly virulent bacteria: strep aureus / viridans commonly involves aortic or pulmonary valves devastating destruction of the valves
acute INFECTIVE endocarditis
40
caused by low virulence bacteria: alpha hemolytic Streptococci - S. milleri, S. Mutans and S. salivarus, S. bovis. Staphylococcus aureus or E.coli. results in large irregular vegetations involving valves and cords
subacute bacterial endocarditis
41
seen in debilitated patients (cancer, sepsis, etc) causes vegetations containing fibrin and platelts (thrombus) no bacteria seen with: venous thrombosis, pulmonary embolism, hypercoagulability
non-bacterial thrombotic endocarditis (NBTE)
42
inflammation of myocardium infections - viral coxsackie A bacterial - diphtheria, lyme disease immune - SLE, rheumatic idopathic - sarcoidosis
myocarditis
43
deterioration of the heart
cardiomyopathy
44
acquired via alcoholism or pregnancy hypertrophy followed by dilation, impairment of contractility, systolic dysfunction enlarged heart
dialated cardiomyopathy (congestive carediomyopathy)
45
hypertrophy and fibrosis, impairment of compliance, diastolic dysfunction
hypertrophic (obstructive) cardiomyopathy
46
least common of cardiomyopathy amyloidosis, sarcoidosis, radiatio, fibrosis pericardial constriction, diastolic and systolic dysfunction
restrictive cardiomyopathy
47
inflammation of pericardium
pericarditis
48
fibrinous: bread and butter appearance
pericarditis
49
risk factors of CHD
preterm infants genetic factors (trismony 13,15,18,21, turner syndrome) enviromental factors (rubella, toxoplasma infections)
50
abnormal communication between chambers or vessels direction of blood flow is dependent on pressure relationship between chambers
shunt
51
atrial septal defect (ASD) ventricular septal defect (VSD) patent ductus arteriosis (PDA) atrioventricular septal defect (AVSD) all part of ______ shunt: ___ cyanosis
left to right shunt late cyanosis
52
tetralogy of fallout transposition of greater vessels tricuspid atresia anomalies (connections) all part of ______ shunt: ____ cyanosis
right to left shunt early cyanosis
53
obstructive CHD
coarctiation of aorta aortic valve stenosis and atresia pulmonary valve stenosis and atresia
54
asymptomatic until adulthood seen with volume hypertrophy of the ventricles types: secundum: most common, defect on fossa ovale primum: occurs adjacent to atrioventricular valves (cleft mitral valve leaflet) sinus venosus: near the entrance of the superior vena cava
atrial septal defect L -\> R shunt
55
most common congenital anomaly usually closes by itself types: membranous: upper part of septum muscular: lower part of septum early - R to L shunt (no cyanosis) right ventricle responds with hypertrophy shunt shifts to L to R shunt with cyanosis
ventricular septal defect
56
connection between aorta and pulmonary artery mostly asymptomatic pulmonary hypertension which causes a reversal of the shunt to the R to L machine like 'harsh murmur' can be heard
patent ductus arteriosus
57
R to L shunt 1. ventricular septal defect 2. pulmonary valve or subpulmonary valve stenosis 3. overriding of the aorta over the ventricular septal defect 4. right ventricular hypertrophy (heart becomes 'boot shaped') child is born with cyanosis
tetralogy of fallot R to L shunt
58
congenital anomaly where the aorta narrows where the ductus arteriosis inserts infantile: aortic hypoplasia proximal to the patent ductus arteriosis adult: rigid like folding the aorta opposite to the closed ductus arteriosis. higher blood pressure in the upper extrem than in lower extrem
coarctation of aorta
59
inability of the heart to pump blood at a rate commensurate with the demand of the tissues at normal pressure
heart failure
60
enhanced contractility with icnreased preload heart failure
frank sterling mechanism
61
heart rate and contractility increased heart failure
norepinephrine release
62
to increase blood volume heart failure
activation of the renin-angiotensin-aldosterone system
63
pathophys of systolic failure vs diastolic failure
systolic - deterioration of myocardial contractility diatole - inability of muscle to relax (decreased filling)
64
etiology: ischemic heart disease, angina, cardio myopathy, MI results in decreased perfusion to the kidneys (prerenal azotemia) and brain hypoxic encephalopathy
left sided heart failure
65
blood backs up into the venous system results in: congestive hepatomegaly centrilobar hemorrhagic necrosis cardiac clerosis portal hypertension venous congestion in the brain
right sided heart failure
66