Ischaemic Heart Disease/HTN Flashcards

1
Q

normal bp

A

<80

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2
Q

prehypertensive

A

120-139/80-89

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3
Q

hypertensive I

A

140-160/90-99

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4
Q

hypertension II

A

> 160/>100

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5
Q

list risk factors of developing essential hypertension

A
related to increased CO and increased TPR
age
obesity
diabetes
physical inactivity
excess salt intake
excess alcohol intake
family history
black>white> asian
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6
Q

describe acute end organ damage

A
encephalopathy
stroke
retinal hemorrhages, exudats, hemorrhages
MI
HF
aortic dissection
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7
Q

hypertensive predisposes to:

A
coronary artery disease
LVH
HF
atrial fibrillation
aortic dissection
aortic aneurysm
stroke
chronic kidney disase
retinopathy
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8
Q

signs of hyperlipidemia

A

xanthomas, tendinous sxanthoma, corneal arcus

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9
Q

hyaline arteriosclerosis

A

diabetes and essential hypertension due to thicekenign of vessel walsl - leaking

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10
Q

hyperplastic hypertension

A

onion skinning in severe hypertension due to proliferation of smooth muscle cells.

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11
Q

what is monckeberg?

A
medial calcific sclerosis
affects medium sized arteries
calcification of elastic lamina of arteris - stiffening without cobstriuction
PIPESTEM on CXR
no obstruction fo blood flow
intima is not involved
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12
Q

describe what vessels atherosclerosis affects

A

elastic arteries
large and medium sized muscular arteries
a form of arteriosclerosis caused by buildup of cholesterol plaques

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13
Q

risk factors

A

modifiable: smoking, hypertension, hyperlipidemia, diabetes
nonmodifiable: age, sex - men and post menopausal women, family history

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14
Q

describe progressin of atherosclerosis

A

inflammation tis important
endothelia cell dysfunction – MO and LDL accumulation – foam cell formation – fatty streaks – smooth muscle cell migration (PDGF, and FGF) – proliferation and extracellular matrix deposition – fibrous plaque – complex atheromas when calcified

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15
Q

complciations of atherscloersis

A

aneurysms, ischemia, infarcts, peripheral vascular disease, thrombus, emboi

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16
Q

most common locatiosn of atherosclerosi

A

abdominal aorta > carotid arteries > popliteal artery > coronary artery

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17
Q

symptoms of atherosclerosis

A

angina, claudication, ASXTIC MOSTLY

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18
Q

abdominal aorti aneurysm associated with?

A

atherosclerosis

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19
Q

RF for abdominal aortic aneurysm

A

tobacco use
increased age
male
family history

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20
Q

RF for thoracic aortic aneurysms

A

hypertension
bicuspid aortic valve
Marfan
tertiary syphillis

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21
Q

assicated with aortic diseection are?

A

hypertension
bicuspid aortic valve
marfan
same as thoracic aneurysm minus syphillis

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22
Q

what is an aortic dissection?

A

longitudinal intimal tear forming a false lumen -

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23
Q

cxpx of aortic dissection?

A

tearing chest pain of acute onset radiating to the back with or without markedly unequal bp in arms

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24
Q

standor type A aortic dissecation

A

ascending aorta and may extend to aortic arch fo descending aorta
treatment is surgery

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25
Q

Stanford type B aortic dissection

A

descending and or aortic arch, no ascending

treat with beta blockers then vasodilators

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26
Q

complicatiosn of aortic dissection

A

rupture
pericardial tamponade
fatal

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27
Q

describe stable angina

A

secondary to atherosclerosis
extertional chest pain in classic disctribugion
ST depression
resolves with rest or NO

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28
Q

describe variant angina

A

occurs at rest secondary to vascular spasm
transient ST elevation
triggers: tobacco, cocaine, triptans
treat with CCB, nitrates, smoking cessation

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29
Q

describe unstable angina

A

thrombobsis with incomplete coronary artery occution
with or without ST elevation and or T wave inversion
no cardiac biomarker elevation
increased frequency or intesnsitiy of chest pain or any chest pain at rest

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30
Q

coronary steal syndrome

A

distal to coronary stenosis vessels are maximally dialted at baseline. so if give casodilators - dilates normal vessels and shunts blood away from post stenotic region resulting in decreased flow and iscahemia
STRESS TEST

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31
Q

myocardial infarction

A

most often due to acute thrombosis due to rupture of coronary artery atherosclerotic plaque

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32
Q

ECG in transmural MI

A

STEMI elevated + cardiac biomarkers

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33
Q

ECK in subendocardiacl MI

A

NSTEMI depressed + Cardiac biomarkers

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34
Q

sudden cardiac death

A

death from cardiac causes within one hour of onset of symptoms.
most commonly due to lethal arrhythmia
associated with CAD, cardiomyopathy, hereditary ion channelopathies

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35
Q

chronic ischemic heart disease

A

progressive onset of HF over many years odue to chronic myocardial damage

36
Q

what are most commonly occluded coronary arteries

A

LDA >RCA> LCX

37
Q

MI presentation

A

diaphoresis, n/v, severe retrosternal pain, pain in let arm and or jaw, SOB, fatigue

38
Q

0-4 hours of MI

A

no gross
no LM
increased risk of arrhtymia, cardiogenic shock, HF

39
Q

4-24 horus of MI

A

gross: dark mottling, pale with tetrazolium stain
LM: early coagulative necrosis - edema, hemorrhage, wavy fibres
reperfusion injury causes CONTRACTION BANDS
increased risk of arrhythmia, cardiogenic shock, HF

40
Q

1-3 days of MI

A

gross - red due to hyperemia
LM: extensive coagulative necrosis, PMN infiltration
risk of post infarction fibrinous pericarditis

41
Q

3-14 days of MI

A

gross: yellow-brown softening - maximammly yellow and soft by 1- days
LM:

42
Q

3-14 days of MI

A

gross: yellow-brown softening - maximammly yellow and soft by 1- days
LM: MO and then granulation tissue at margins
risk of free wall rupture s- tamponade
risk of papillary muscel rupture - mitral regurgitation
interventricular rupture - LV pseudoaneurysm or vsd
due to MO cleaning up

43
Q

2 weeks to several months

A

gray white noncontractile tiss;ue
contracted scar complete
risk of Dressler syndrome, HG, arrhythmias, true ventricular aneurysm (mural thrombus)

44
Q

time courase of CKMB

A

increases 6-12 hours, stays for 48 hours

godo for reinfarction

45
Q

time course fo troponins

A

increased after 4 hours and stay up for 7 to 10 days

46
Q

ECG changes with MI

A
St elevation  = STEMI, transmural
ST depression - NSTEMI, subendocardial
hyperacute/peaked T waves
T wave inversion
new LBBB
pathologic Q wave or poor R wave - evolving or old transmural infarct
47
Q

leads V1-V2 Mi

A

anteroseptal LAD

48
Q

leads V3-V4 Mi

A

anteroapical distal LAD

49
Q

leads V5-V6 Mi

A

anterolateral LAD or LCX

50
Q

leads I, aVL Mi

A

lateral LCX

51
Q

leads II, III, aVF

A

inferior RCA

52
Q

when is ggreatest risk of rupture following MI?

A

3-14 days post

MO going to town before scar tissue formed

53
Q

what is a ventricular pseudoaneurysm ?

A

contained free wall rupture
decreased CO
increasd risk fo arrhtmia
embolus from mural rthrombus

54
Q

when is greatest risk for ventricular pseudoanuerysm?

A

3-14 days tis a rupture

55
Q

what is atrue ventricular aneurysm?

A

outward buldge during systole a dyskinesia.

fibrosis

56
Q

when does a true ventricular aneurysm occur?

A

greatest risk 2 weeks to several motnsh

57
Q

greatest risk of postinfarction fibrinous pericarditis?

A

1-3 days post MI

58
Q

risk for dresslers?

A

2-12 weeks

59
Q

how to treat unstable angina/NSTEMI

A
anticoagulation - heparin
antiplatelet - aspirin, clopidogrel
bbs
ACEis
statins
control symptoms with nitroglycerin and morphine
60
Q

how to treat a STEMI

A

heparin, aspirin and clopidogrel, bbs, ACEis, statins and reperfusion therapy is most important - percutaneous coronary intervention > fibrinolysis

61
Q

what causes dilated cardiomyopathy

A
idiopathic/familial. ABCCCDHSP
alcohol abuse
wet beri beri
chronic cocain
chagas disease
coxsackie B virus
doxorubicin
hemochromatosis
sarcoidosis
peripartum cardiomyopathy
increased preload
62
Q

result of dilated cardiomyopathy?

A

increased preload - eccentric hypertrophy - in series - systolic dysfunction - S3

63
Q

cxfx of dilated cardiomyopathy?

A

HF, S3, systolic regurgitant murmur, dilated heart on echocardiogram, ballone appearance of heart on CXR

64
Q

treatment of dilated cardiomyopathy?

A

na restriction, ACEi, bb, diuretics, digoxin, ICD, heart transplant

65
Q

findings with hypertrophic cardiomyopathy?

A

S4
systolic murmur
mitral valve regurgitation bc it cant close

66
Q

treatment of hypertrophic cardiomyopathy?

A

cessation fo high intensity athletics
BB, CCB
ICD if at high risk

67
Q

result of hypertrophic cardiomyopathy?

A

increased afterload - concentric hypertrophy in parallel - diastolic dysfunction

68
Q

what is obstructive hypertrophic cardiomyopathy

A

assymetric septal hypertrophy and systolic anterior motion fo the mitral valve - outflow obstruction - dyspnea nad syncope

69
Q

what causes restrictive/infiltrative cardiomyoatphy

A
sarcoidosis
amyloidosis
endocardial fibroelastosis
Loffler syndrome
hemochromatosis
70
Q

what is endocardial fibroelastosis

A

in children - thick fibroelastic tissue in endocardium

71
Q

what is lofflers syndrome?

A

endomyocardial fibrosis with prominent eosinophilic infiltrate

72
Q

what casues dilated and restrictive/infiltrative cardiomyopathy?

A

hemochromatosis can!

73
Q

restrivitev/infiltrative cardiomyoatphy causes?

A

increased afterload - concentric hypertrophy - in parallele - diastolic dysfunction

74
Q

describe the ECG in restrictive/infiltrative cardiomyopathy

A

can hav elow voltage ECG despite thick myocardium - especially amyloidosis

75
Q

describe systolic dysfunction leading to congestive heart failure

A

increased preload - ischemia/MI or dilated cardiomyopathy - eccentric - inseries
reduced EF, increased EDV
decreased contractility

76
Q

describe diastolic dysfunction leading to congestive heart failure

A

decreased compliance secondary to myocardial hypertrophy
increased afterload - concentric - parallel
normal EF, normal EDV

77
Q

symptomso of LVF

A

orthopnea, paroxysmal nocturnal dyspnea, pulmonary oedema

78
Q

symptoms of RVF

A

hepatomegaly/nutmeg liver/cardia cirrhosis
jufular venous distension
peripheral oedema

79
Q

describe hypovolemic shock

A

caused by hemorrhage, dehydration burns
decreased CVP**, decreased CO, increased TPR
treat with IV fluids

80
Q

describe cardiogenic shock

A

caused by acute MI, HF< valvular dysfunction, ;arrhythmia
increased CVP, decreased CO**, increased TP
treat with inotropes and diuresis

81
Q

describe obstructive shock

A

caused by cardiac tamponase and PE
increased CVP , decreased CO **, increased TPR
treat by reliveing obstruction

82
Q

describe distributive shock

A

caused by sepsis, CNS injury, anaphylaxis
decreased TPR** decreased CVP, increased CO
treat with pressors and IV fluid

83
Q

what is systemic inflammatory response?

A

more than two of

a) fever
b) tachycardia
c) tachypnea
d) leukocytosis/leukopenia

84
Q

what is the fist sign of shock?

A

tachycardia

85
Q

which type of shock moves CVP in opposite direction of others

A

cardiogenic/obstructive - has increased CVP

86
Q

which type of shock moves CO in opposite direction of others?

A

distributive - has increased CO

87
Q

which type of shock moves TPR in opposite direction of others?

A

distributive - has decreased TPR