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Pathophysiology > module 10 HTN and disorders > Flashcards

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
Q

progression of necrosis during MI

A

caused by local ischemia
zone of perfusion, area that occlusion is depriving of O2
cells furthest away die off first.

26
Q

lab evaluation during MI

A

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
Q

infarction

A

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
Q

preexisting collaterals

A

blood flow can get to a specific area multiple ways

  • vessels connected
  • blockage in one vessel, blood can “go around”
29
Q

Management of blocked coronary arteries

A
  • 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
Q

rate of coronary perfusion impaired by

A

large stable atherosclerotic plaque
acute platelet aggregation and thrombosis
vasospasm
failure of autoregulation by microcirculation
poor perfusion pressure

31
Q

causes of Cardiomyopathy

A 
"heart muscle disease" 
cardiac structural changes in disease 
- valvular disease
-systemic or pulmonary HTN
-heart failure
- aortic stenosis
- mitral incompetence
32
Q

pulmonary hypertension and cardiomyopathy

A

right ventricular hypertrophy may occur in response to increased work of the right ventricle

33
Q

aortic stenosis and cardiomyopathy

A

narrowing of aortic valve

- left ventricular hypertrophy occurs in response to greater work load

34
Q

mitral incompetence and cardiomyopathy

A

left atrial dilation may develop as a result of the elevation of left atrial pressure and volume cause by mitral regurgitation

35
Q

dilated cardiomyopathy

A

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
Q

dilated cardiomyopathy risk factors

A

alcohol toxicity
genetic component: dystrophin -> dec. contractility -> systolic dysfunction
pregnancy
postviral myocarditis

37
Q

hypertrophic cardiomyopathy

A

asymmetric septal hypertrophy or idopathic hypertrophic subaortic stenosis
-abnml diastolic filling
- intermittent ventricular outflow obstruction
stiff thick wall -> impaired diastolic filling

38
Q

hypertrophic cardiomyopathy risk factors

A

genetic: autosomal dominant

- abnormal sarcomere proteins

39
Q

s/s of hypertrophic cardiomyopathy

A

septal hypertrophy

  • strenous activity
  • > inc. outflow obstruction
  • > negligible SV
  • > sudden death
  • dyspnea
  • angina
40
Q

restrictive cardiomyopathy

A

rarest form
decrease in ventricular compliance -> impaired ventricular filling during diastole
-> dec. force of systole
dec. SV

41
Q

common causes of restrictive cardiomyopathy

A 
endomyocardial fibrosis
cardiac amyloidosis (deposition of protein in wall)
sarcoidosis
glycogen storage disease
iron overload
scleroderma 
radiation inj
42
Q

s/s of restrictive cardiomyopathy

A

exercise intolerance
dyspnea
weakness

43
Q

congestive heart failure

A

build up of fluid
forward failure: systemic hypertension, mitral/aortic valve disease, ischemic heart
backward failure: venous backup

44
Q

CHF pressure load

A

concentric hypertrophy

  • heart working to overcome pressure
  • > dec. chamber volume r/t inc. wall size
45
Q

CHF volume load

A

eccentric hypertrophy

  • increased volume in chamber
  • dilation of chamber
46
Q

compensated HF

A

maintain O2 in blood

47
Q

decompensated HF

A

pulmonary congestion, edema, venous congestion, systemic edema

48
Q

CHF s/s

A

dec. lung compliance during exertion
-> dyspnea
increased venous return -> orthopnea
cyanotic and/or acidotic

49
Q

Left sided HF

A 
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
Q

S/S of LSHF

A 
cough
crackles (rales)
hypoxemia
increased left atrial pressure
blood tinged sputum and frothy
cyanosis
51
Q

acute cardiogenic pulmonary edema

A

life threatening associated with LHF

severely impaired gas exchange

52
Q

s/s of LHF

A 
severe dyspnea 
anxiety
bolt-upright posture
crackles throughout
pink frothy sputum 
inc. HR
tissue hypoxia
53
Q

RSHF

A 
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
Q

S/S of RSHF

A 
Backward effects
- hepatomegaly
- ascites
- splenomegaly
- anorexia
- subQ edema
- jugular vein distention 
Forward Effects: 
- fatigue
- oliguria
- inc. HR
- fait pulses
- restlessness
- confusion
- anxiety
55
Q

Cor Pulmonae

A

Heart disease caused by lung disease
result of pulmonary HTN
leads to cardiac hypertrophy and dilation

56
Q

biventricluar HF

A

result of primary LV failure -> RSHF
dec. CO
inc. Pulmonary congestion
systemic venous congestion

Pathophysiology (80 decks)

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