Test 2 - RU Heart Flashcards

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
Q

blood supply to the heart is interrupted

A

myocardial infarction

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26
Q

transmural MI involves ischemic necrosis of the full thickness of the _______

A

ventricular wall

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27
Q

morphologic changes of MI

4hrs

4-24 hrs

1-3 days

3-7

>7

A

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
Q

consequences of MI

A

contractile dysfunction

arrhythmias

pericarditis

ventricular anurism

myocardial rupture

29
Q

usually caused by significant coronary occlusion

congenital, structural coronary arterial abnormalities

aortic valve stenosis

mitral valve prolapse

dialted or hypertrophic cardiomyopathy

pulmonary hypertension

A

sudden cardiac death

30
Q

hear tis large and heavy due to left ventricular hypertrophy and dilation

myocardial hypertrophy found with ischemic cardiomyopathy

A

chronic ischemic heart disease

31
Q

sustained diastolic blood pressure > 90mmHg

or

sustained systolic blood pressure > 140mmHg

A

hypertension

32
Q

priamary vs secondary hypertension

A

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
Q

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

A

hyaline atherosclerosis

34
Q

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

A

hyperplastic atherosclerosis

35
Q

hypertension retinopathy

1

2

3

4

A

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
Q

inflammation of the endothelial and subendothelial tissues

A

endocarditis

37
Q

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

A

rheumatic valvulitis

38
Q

autoimmune

involves the mitral and tricuspid valves

small vegetations on both sides of valves

found in fibrinoid necrosis

A

liebman - sacks (SLE)

39
Q

caused by highly virulent bacteria: strep aureus / viridans

commonly involves aortic or pulmonary valves

devastating destruction of the valves

A

acute INFECTIVE endocarditis

40
Q

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

A

subacute bacterial endocarditis

41
Q

seen in debilitated patients (cancer, sepsis, etc)

causes vegetations containing fibrin and platelts (thrombus) no bacteria

seen with: venous thrombosis, pulmonary embolism, hypercoagulability

A

non-bacterial thrombotic endocarditis (NBTE)

42
Q

inflammation of myocardium

infections - viral coxsackie A

bacterial - diphtheria, lyme disease

immune - SLE, rheumatic

idopathic - sarcoidosis

A

myocarditis

43
Q

deterioration of the heart

A

cardiomyopathy

44
Q

acquired via alcoholism or pregnancy

hypertrophy followed by dilation, impairment of contractility, systolic dysfunction

enlarged heart

A

dialated cardiomyopathy (congestive carediomyopathy)

45
Q

hypertrophy and fibrosis, impairment of compliance, diastolic dysfunction

A

hypertrophic (obstructive) cardiomyopathy

46
Q

least common of cardiomyopathy

amyloidosis, sarcoidosis, radiatio, fibrosis

pericardial constriction, diastolic and systolic dysfunction

A

restrictive cardiomyopathy

47
Q

inflammation of pericardium

A

pericarditis

48
Q

fibrinous: bread and butter appearance

A

pericarditis

49
Q

risk factors of CHD

A

preterm infants

genetic factors (trismony 13,15,18,21, turner syndrome)

enviromental factors (rubella, toxoplasma infections)

50
Q

abnormal communication between chambers or vessels

direction of blood flow is dependent on pressure relationship between chambers

A

shunt

51
Q

atrial septal defect (ASD)

ventricular septal defect (VSD)

patent ductus arteriosis (PDA)

atrioventricular septal defect (AVSD)

all part of ______ shunt: ___ cyanosis

A

left to right shunt

late cyanosis

52
Q

tetralogy of fallout

transposition of greater vessels

tricuspid atresia

anomalies (connections)

all part of ______ shunt: ____ cyanosis

A

right to left shunt

early cyanosis

53
Q

obstructive CHD

A

coarctiation of aorta

aortic valve stenosis and atresia

pulmonary valve stenosis and atresia

54
Q

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

A

atrial septal defect

L -> R shunt

55
Q

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

A

ventricular septal defect

56
Q

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

A

patent ductus arteriosus

57
Q

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

A

tetralogy of fallot

R to L shunt

58
Q

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

A

coarctation of aorta

59
Q

inability of the heart to pump blood at a rate commensurate with the demand of the tissues at normal pressure

A

heart failure

60
Q

enhanced contractility with icnreased preload

heart failure

A

frank sterling mechanism

61
Q

heart rate and contractility increased

heart failure

A

norepinephrine release

62
Q

to increase blood volume

heart failure

A

activation of the renin-angiotensin-aldosterone system

63
Q

pathophys of systolic failure vs diastolic failure

A

systolic - deterioration of myocardial contractility

diatole - inability of muscle to relax (decreased filling)

64
Q

etiology: ischemic heart disease, angina, cardio myopathy, MI

results in decreased perfusion to the kidneys (prerenal azotemia) and brain hypoxic encephalopathy

A

left sided heart failure

65
Q

blood backs up into the venous system

results in:

congestive hepatomegaly

centrilobar hemorrhagic necrosis

cardiac clerosis

portal hypertension

venous congestion in the brain

A

right sided heart failure

66
Q
A