module 10 HTN and disorders Flashcards

1
Q

preeclampsia

A

HTN during pregnancy

  • 5-12% of pregnancies
  • inc. risk of maternal, fetal, and neonatal morbidity and mortality
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2
Q

complications associated with preeclampsia

A
preterm labor
abruptio placentae
disseminated intravascular coagulation
hemorrhagic stroke
liver failure
acute renal failure
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3
Q

aortic aneurysm

A

saclike enlargement in wall of aorta often assoc. with atherosclerosis
bulging -> inc. wall stress through inc. radius
-> dec. wall thickness -> red. ability to withstand stress.
Rupture: internal hemorrhage, fatal

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4
Q

Aortic aneurysm risk factors

A
HTN
smoking
obesity 
atherosclerosis
hypercholesterolemia
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5
Q

dissection

A

aortic aneurysm

bleeding into the vascular wall through a tear in the inner layer (intima)

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6
Q

true aneurysm saccular

A

involves all 3 tunicae

ballooning on one side

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7
Q

true aneurysm fusiform

A

involves all 3 tunicae

ballooning on both sides

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8
Q

false aneurysm

A

at least one tunicae unaffected
- muscle tissue and fascia confine blood
- r/t trauma more often
hematoma

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9
Q

dissecting aortic aneurysm

A

tear creats channel for blood flow

  • between intima and media or media and adventitia
  • > inc. blood flow -> inc separation -> inc. weakness -> aortic rupture -> death
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10
Q

Atherosclerosis

A

endothelial dysfunction -> inflammation
oxidized LDL -> inflammation
foam cell formation (macrophage engulfs ox-LDL)
smooth muscle cell migration, proliferation, secretion

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11
Q

intimal thickening and atherosclerosis

A

smooth muscle cells migrate to intima

  • cell mitosis
  • elaboratoin of extracellular matrix (concrete that cell sits on)
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12
Q

clinical manifestations of systemic atherosclerosis (peripheral vascular disease)

A
skin
- cool ot touch
- dec. or absent hair
- dry, thin, glossy appearance
- thickened nails
- pallor when elevated, rubor/blush when dependent
- diminished pulses
pain
- sharp and stabbing
- intensified with activity
- relieved by rest or dependency 
Ulcer
- severely painful
- pale, gray base
- well- defined edges 
- located on heels, lateral malleolus, distal phalanges, pretibial area
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13
Q

Atheroma/plaque

A

intimal lesion from fatty streak: lipid core covered by fibrous cap.

  • Cells (smooth muscle cells, monocytes, and leukocytes), collagen, elastic fibers, and proteoglycans as well as lipids make up the fibrous cap.
  • necrotic center: cell debris, cholesterol crystals, foam cells, calcium
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14
Q

atherosclerosis steps

A

damage to endothelium -> inflammatory response and inc. in vessel wall permeability

  • > low density lipo-proteins breach intimal layer
  • > lipids become oxidized -> further vessel damage
  • > platelet aggregation -> release of growth factor
  • > growth of smooth muscle cells in media layer
  • > smooth muscle cells migrate to intima and proliferate
  • > atherosclerotic plaque
    • SMC, lipoproteins, and inflammatory debris
  • > inc. plaque size -> dec. lumen size -> dec. perfusion
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15
Q

Atherosclerotic plaque rupture

A
  • can lead to platelet aggregation and clot formation -> complete vessel occlusion (MI)
  • Can also rupture without superimposed thrombus
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16
Q

atherosclerosis on supply and demand

A
coronary plaque
- dec. perfusion
- dec. arterial oxygen content
increased demand
- inc. HR
- inc. preload
- inc. afterload
- inc contractility
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17
Q

risk factors for atherosclerosis

A
modifiable
- smoking
- HTN
- glucose intolerance
- elevated cholesterol and LDL
- dec. physical activity
- obesity
- wt. fluctuations
- ineffective stress management 
Non-modifiable 
- age
- gender
- ethnicity 
- heredity
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18
Q

3 layers of heart

A

epicardium: external
myocardium
endocardium: internal

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19
Q

ischemic heart disease

A
imbalance in myocardial O2 demand and supply 
supply < demand -> ischemia 
syndromes associated: 
- angina pectoris
- acute MI
- sudden cardiac death
- chronic ischemic heart disease
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20
Q

angina pectoris

A

75% reduction in lumen.
intermittent chest pain d/t transient reversible myocardial ischemia
Stable: upon exertion
Variant: rest or in sleep
Unstable: increased frequency of pain
Platelet aggregation, vasoconstriction, and formation of mural (heart wall) thrombus -> dec. O2

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21
Q

Acute MI

A

Heart attack

complete occlusion

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22
Q

Sudden cardiac death

A

PE, ruptured aortic aneurysm, and infections

ventricular arrhythmias, in particular ventricular fibrillation

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23
Q

chronic ischemic heart disease

A

congestive heart failure
progressive form
degeneration of the myocardium with angina or myocardial infarction

24
Q

s/s of acute MI

A
severe chest pain that may radiate
may last several hours to days
diaphoretic 
pulmonary edema 
cardiogenic shock
25
progression of necrosis during MI
caused by local ischemia zone of perfusion, area that occlusion is depriving of O2 cells furthest away die off first.
26
lab evaluation during MI
creatine kinase: dimers M, B are found in derived from brain, myocardium, skeletal muscle tissue - CK-MB primarily form the myocardium - - activity increases 2-4hr, peaks at 18, normal by 48 - Cardiac troponins T and I: more specific to heart cells - - increase after infarct but remain elevated 4-7 days
27
infarction
area of ischemic necrosis d/t occlusion of arterial supply or venous drainage Classified based on color - hemorrhage: red/white - Microbial infection: septic/bland
28
preexisting collaterals
blood flow can get to a specific area multiple ways - vessels connected - blockage in one vessel, blood can "go around"
29
Management of blocked coronary arteries
- thrombolysis: drugs to remove thrombus - percutaneous transluminal coronary angioplasty: scratches plaque off -> inflammation -> re-occulsion - Placement of stent to prevent reocclusion - coronary artery bypass, grafting a surgical placement of new conduit around occluded area
30
rate of coronary perfusion impaired by
large stable atherosclerotic plaque acute platelet aggregation and thrombosis vasospasm failure of autoregulation by microcirculation poor perfusion pressure
31
causes of Cardiomyopathy
``` "heart muscle disease" cardiac structural changes in disease - valvular disease -systemic or pulmonary HTN -heart failure - aortic stenosis - mitral incompetence ```
32
pulmonary hypertension and cardiomyopathy
right ventricular hypertrophy may occur in response to increased work of the right ventricle
33
aortic stenosis and cardiomyopathy
narrowing of aortic valve | - left ventricular hypertrophy occurs in response to greater work load
34
mitral incompetence and cardiomyopathy
left atrial dilation may develop as a result of the elevation of left atrial pressure and volume cause by mitral regurgitation
35
dilated cardiomyopathy
progressive form of cardiac hypertrophy associated with dilation and cardiac systolic dysfunction - one or both ventricles - Tends to affect all chambers of heart. 1 chamber -> all
36
dilated cardiomyopathy risk factors
alcohol toxicity genetic component: dystrophin -> dec. contractility -> systolic dysfunction pregnancy postviral myocarditis
37
hypertrophic cardiomyopathy
asymmetric septal hypertrophy or idopathic hypertrophic subaortic stenosis -abnml diastolic filling - intermittent ventricular outflow obstruction stiff thick wall -> impaired diastolic filling
38
hypertrophic cardiomyopathy risk factors
genetic: autosomal dominant | - abnormal sarcomere proteins
39
s/s of hypertrophic cardiomyopathy
septal hypertrophy - strenous activity - > inc. outflow obstruction - > negligible SV - > sudden death - dyspnea - angina
40
restrictive cardiomyopathy
rarest form decrease in ventricular compliance -> impaired ventricular filling during diastole -> dec. force of systole dec. SV
41
common causes of restrictive cardiomyopathy
``` endomyocardial fibrosis cardiac amyloidosis (deposition of protein in wall) sarcoidosis glycogen storage disease iron overload scleroderma radiation inj ```
42
s/s of restrictive cardiomyopathy
exercise intolerance dyspnea weakness
43
congestive heart failure
build up of fluid forward failure: systemic hypertension, mitral/aortic valve disease, ischemic heart backward failure: venous backup
44
CHF pressure load
concentric hypertrophy - heart working to overcome pressure - > dec. chamber volume r/t inc. wall size
45
CHF volume load
eccentric hypertrophy - increased volume in chamber - dilation of chamber
46
compensated HF
maintain O2 in blood
47
decompensated HF
pulmonary congestion, edema, venous congestion, systemic edema
48
CHF s/s
dec. lung compliance during exertion -> dyspnea increased venous return -> orthopnea cyanotic and/or acidotic
49
Left sided HF
``` most associated with LV infarction and systemic HTN backward effect - dec. ejection fraction -> inc. preload -> inc. atrial pressure -> pulmonary dysfunction -> inc. pressure in pulmonary veins and capillaries -> fluid forced into interstitial and alveoli -> edema forward effect: - dec. CO -> RAAS activation -> fluid retention -> dec. tissue perfusion ```
50
S/S of LSHF
``` cough crackles (rales) hypoxemia increased left atrial pressure blood tinged sputum and frothy cyanosis ```
51
acute cardiogenic pulmonary edema
life threatening associated with LHF | severely impaired gas exchange
52
s/s of LHF
``` severe dyspnea anxiety bolt-upright posture crackles throughout pink frothy sputum inc. HR tissue hypoxia ```
53
RSHF
``` LV failure -> inc. workload of RV -> RV failure isolated RV rare: r/t infarction or pulmonary disease - cor pulmonale: RV hypertrophy -> failure backward effect: - dec. ejection fraction -> inc. RV preload -> systemic congestion Forward effects: dec. output to left ventricle -> dec. CO -> dec. tissue perfusion -> RAAS activation -> fluid retention -> inc. RV preload ```
54
S/S of RSHF
``` Backward effects - hepatomegaly - ascites - splenomegaly - anorexia - subQ edema - jugular vein distention Forward Effects: - fatigue - oliguria - inc. HR - fait pulses - restlessness - confusion - anxiety ```
55
Cor Pulmonae
Heart disease caused by lung disease result of pulmonary HTN leads to cardiac hypertrophy and dilation
56
biventricluar HF
result of primary LV failure -> RSHF dec. CO inc. Pulmonary congestion systemic venous congestion