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Pathophysiology > Chapters 26 & 27 (NO shock) > Flashcards

Chapters 26 & 27 (NO shock) Flashcards

1
Q

the large

A

aorta

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2
Q

medium

A

coronary

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3
Q

small

A

ulcers

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4
Q

pathology occurs by

A

impairment of blood flow

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5
Q

ischemia

A

reduction in flow insufficient to meet oxygen demands of tissues

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6
Q

injury

A

reversible

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7
Q

infarction

A

irreversible with necrosis

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8
Q

what has an active role in controlling vascular function

A

endothelium

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9
Q

dysfunctional cells produce

A

inflammatory cytokines

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10
Q

endothelial dysfunction

A

endothelial dysfunction describes potentially reversible changes in endothelial function that occur in response to environmental stimuli

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11
Q

endothelial dysfunction: products that cause inflammation

A

cytokines, bacteria, viruses, hemodynamic stresses, lipid products, hypoxia

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12
Q

dyslipidemia is a major cause of

A

atherosclerosis

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13
Q

dyslipidemia is a imblance of

A

lipid components (triglycerides, phospholipids and cholesterol)

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14
Q

5 types of lipoproteins but we only will be focusing on 2, what are they

A

LDL and HDL

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15
Q

where is the synthesis of lipoproteins

A

small intestine and liver

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16
Q

primary dyslipidemia

A

may have genetic basis, defective synthesis of apoproteins may occur, defective or lack of lipid receptors

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17
Q

familial hypercholesterolemia is what kind of dyslipidemia

A

primary

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18
Q

familial hypercholesterolemia ___ receptor is deficient of defective, autosomal _________ disorder. cholesterol levels can be as high as 1000

A

LDL, dominant

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19
Q

secondary dyslipidemia

A

dietary, obesity, metabolic changes associated with DMT2

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20
Q

hypercholesterolemia

A

increase in serum cholesterol levels

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21
Q

screening for hypercholesterolemia is appropriate for children as young as two who have

A

a family history of heart disease or high cholesterol

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22
Q

LDL is good or bad

A

bad, LOSER CHOLESTEROL

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23
Q

LDL is the main carrier for

A

cholesterol

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24
Q

LDL receptors predominantly located in

A

hepatocytes

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25
Q

_______ plays critical role in metabolism of LDL

A

liver

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26
Q

LDL removal by scavenger cells such as

A

monocytes and macrophages

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27
Q

uptake of LDL by macrophages in the arterial wall can result in accumulation of

A

insoluble cholesterol esters, foam cells, and atherosclerosis

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28
Q

HDL

A

good, HAPPY CHOLESTEROL

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29
Q

inverse relation between HDL and development of

A

atherosclerosis

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30
Q

HDL facilitates in the clearance of cholesterol from atheromatous plaques and transports it back to the

A

liver

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31
Q

HDL is responsible for

A

reverse cholesterol transport (returns excess cholesterol from tissues to liver)

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32
Q

HDL inhibits uptake of _____ into arterial wall

A

LDL

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33
Q

what increases HDL

A

regular exercise and moderate alcohol consumption

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34
Q

what are associated with decreased levels of HDL

A

smoking and diabetes

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35
Q

major risk factor for atherosclerosis is

A

hypercholesterolemia and elevations of LDL

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36
Q

non modifiable risk factors for atherosclerosis is

A

age, gender, genetic history, family of premature CAD in a first degree relative

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37
Q

nontraditional risk for atherosclerosis is

A

elevated serum C reactive protein

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38
Q

inflammation marked by

A

elevated C reactive protein

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39
Q

C reactive protein is

A

non specific

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40
Q

nontraditional risk factors for coronary artery disease

A

c reactive protein, microbiome, medications, infection, airpolution

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41
Q

modifiable risk factors for coronary artery disease

A

dislipidemia, hypertension, cigarette smoking, diabetes, obesity

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42
Q

one pack of cigarette smoking a day _____ endothelial damage

A

doubles

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43
Q

DM+hypertension+dyslipidemia= increases risk

A

20 times

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44
Q

mechanisms for development of coronary artery disease

A

endothelial injury, fatty streak present in first year of life, fibrous atheromatous plaque, complicated lesion

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45
Q

endothelial injury causes a migration of inflammatory cells which leads to ______ accumulation and smooth muscle ________ and ______ development

A

lipid, proliferation, plaque

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46
Q

fatty streak

A

macrophages and smooth muscle cells distended with lipid to form foam cells

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47
Q

fibrous atheromatous plaque

A

basic lesion accumulation of lipids, proliferation, scar tissue and calcification

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48
Q

complicated lesion

A

hemorrhage, ulceration and scar tissue deposits with thrombosis

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49
Q

vaculitides is a group of vascular disorders that cause ___________ injury and ________ of the blood vessel wall

A

inflammatory, necrossi

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50
Q

vasculitides when in the large vessel is called

A

giant cell (temporal) arteritis

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51
Q

giant cell (temporal) arteritis (AKA vasculitides) mainly affects arteries of the ______, this is a disease of the _______, symptoms may include:
inflammation of ophthalmic artery involvement can cause ______

A

head, elderly, stiffness of shoulder and headache and tenderness of temporal artery, blindness

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52
Q

peripheral arterial disease is systemic atherosclerosis distal to the

A

arch of the aorta

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53
Q

peripheral arterial strongest risk factors

A

smoking and DM

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54
Q

peripheral arterial when you finally get symptoms you are already at __% narrowing

A

50

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55
Q

peripheral arterial symptom will include

A

intermitten claduication or pain with walking in the calf
atrophic changes and thinning of the skin and sub q
ischemic pain at rest
ulceration and gangrene will develop

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56
Q

why will you get pain in calf with peripheral arterial

A

because the gastrocnemius has the highest oxygen consumption of any muscle group in leg during walking

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57
Q

it is important in peripheral arterial to look at what body part

A

feet

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58
Q

acute arterial thrombus formation

A

activation of the coagulation cascade, intimal irritation and roughening, inflammation, trauma, infection, low BP, obstructions

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59
Q

the 7 P’s of acute arterial embolism

A

pistol shot (acute onset)
pallor
polar
pulselessness
pain
paresthesia
paralysis

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60
Q

arterial disease of extremities peripheral vascular disorders

A

thromobangitis obliterans (Buerger’s Disease), Raynaud’s disease

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61
Q

Buerger’s Disease is ______ of medium arteries, usually affects ____, this is very ________

A

vaculitis, men, inflammed

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62
Q

Raynaud’s disease is caused by intense _______ of arteries and arterioles in ______, this is seen in _______, appear pale looking

A

vasospasm, fingers, women

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63
Q

aneurysm is a localized _______ of blood vessle

A

dilatation

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64
Q

aneurysm tension wall diameter increases with increasing size and may lead to

A

rupture

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65
Q

aortic aneurysm is more frequent in men who are __________, most are _______

A

hypertensive, asymptomatic

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66
Q

aortic dissection is acute and

A

life threatening

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67
Q

aortic dissection is the hemorrhage into the vessel wall with

A

longitudinal tearing or separation of the vessel wall to form a blood filled channel

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68
Q

aortic dissection is common with

A

Marfans syndrome

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69
Q

BP is calculated how

A

cardiac output X peripheral vascular resistance

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70
Q

pulse pressure

A

difference between systolic and diastolic

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71
Q

systolic is normally the smaller or larger number

A

larger

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72
Q

diastolic is normally the smaller or larger number

A

smaller

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73
Q

mean arterial pressure

A

average blood pressure in systemic circulation

74
Q

how to calculate mean arterial pressure

A

1/3PP+DP

75
Q

mean arterial pressure is a good indicator of

A

tissue perfusion

76
Q

cardiovascular center is located in ____ and _______ where intergration with ANS occurs

A

pons, medulla

77
Q

pressure sensitive _________ are located in the blood vessels and heart

A

baroreceptors

78
Q

baroreceptors induces

A

heart rate increase and vasconstriction

79
Q

arterial chemoreceptors are located in _____ and _______ and respond to changes in oxygen, CO2 and H+, these control _________ and induce widespread ___________

A

carotids, aorta, ventilation, vasoconstriction

80
Q

Humoral BP regulation is regulated by

A

RAA, Vasopressin (ADH)

81
Q

RAA system steps

A

renin secreted by kidney in response to low BP, ECF volume/EC sodium,
renin converts to angiotensin to angiotensin 1
angiotensin 1 is converted to angiotensin II by enzyme in endothelial in lung

82
Q

Angiotensin 2 does what

A

its a strong vasoconstrictor and stimulates aldosterone

83
Q

aldosterone

A

secreted from adrenal glands which contributes to long term regulation by increasing salt and water retention by kidney

84
Q

undercuffing BP cuff

A

overestimates BP

85
Q

overcuffing BP cuff

A

underestimates BP

86
Q

primary/essential hypertension

A

no evidence of other disease, caused by consittutional or lifestyle,

87
Q

primary hypertension risk factors are things that cannot be changed like

A

genes, race, DM, age, gender

88
Q

primary hypertension lifestyle contributes

A

High NA intake, excessive calorie intake, obesity, inactivity, alcohol

89
Q

secondary hypertension may be

A

corrected or cured

90
Q

secondary hypertension causes

A

renal hypertension, pheochromocytoma, oral contraceptives, cocaine, amphetamines

91
Q

renal hypertension

A

largest single cause is renal disease, excess production of aldosterone and excess levels of glucocorotcoid

92
Q

pheochromocytoma

A

tumor of chromatin tissue which contains sympathetic nerve cells most often in adrenal medulla

93
Q

target organs of hypertension

A

heart, brain, kidney

94
Q

ACE inhibitors

A

inhibit conversion of angiotensin I to II reducing effect on vasoconstriction and aldosterone

95
Q

unique hypertensive situations include

A

pregnancy, elderly, children, orthostatic

96
Q

orthostatic

A

abnormal drop in standing position

97
Q

orthostatic is a sustained reduction in systolic pressure of at least __mmHg

A

20`

98
Q

causative factors of orthostatic hypotension

A

fluid deficit, medications, aging, defective function of ANS, effects of immobility

99
Q

disorders of venous circulation (one we need to know)

A

venous thrombosis

100
Q

venous thrombosis can be caused by

A

venous stasis

101
Q

venous stasis causes

A

bed rest, immobility, spinal cord injury. acute MI, congestive heart failure, shock, venous obstruction

102
Q

virchows triad associated with venous thrombosis

A

statuses of blood, increased blood coagulability, vessel wall injury

103
Q

hyperrreactivty genetic disease name

A

leiden 5 diease

104
Q

disorders of the cardiac pericardium

A

pericardial effusion, cardiac tamponade

105
Q

cardiac tamponade starts off as

A

pericardial effusion

106
Q

cardiac tamponade is an increase in

A

intrapericardial pressure

107
Q

cardiac tamponade is caused by

A

accumulation of fluid or blood in the pericardiac sac, trauma, cardiac surgery, cancer, uremia, cardiac rupture

108
Q

symptoms of cardiac tamponade depends on

A

how rapidly the fluid accumulates

109
Q

pulsus paradoxus

A

when you inspire your SBP drops a small amount

110
Q

in cardiac tamponade you have an exaggerated

A

pulsus paradoxus

111
Q

consequences of pericardial effusion

A

restricts heart expansion which causes the left ventricle to not accept enough blood which leads to decreased cardiac output and decreased BP and shock. This also causes the right ventricle to not accept enough blood which causes increased venous pressure; jugular distension

112
Q

right coronary artery supplies the ________ wall of the ventricle

A

inferior

113
Q

RCA supplies what else besides the inferior wall

A

SA and AV node

114
Q

left coronary artery has __ main branches

A

2

115
Q

what artery is known as your widowmaker

A

left coronary

116
Q

coronary heart disease is impaired coronary blood flow that may cause

A

angina, MI, cardiac arrhythmias, conduction defects, heart failure and sudden death

117
Q

coronary heart disease can be caused by

A

atherosclerotic plaques

118
Q

atherosclerotic plaques are made up of

A

soft lipid rich core with fibrous cap

119
Q

coronary heart disease plaque can occur with and without

A

thrombus

120
Q

_______ play a major role in linking plaque disruption to acute coronary syndrome

A

platelets

121
Q

in coronary heart diease with disruption platelets aggregate and release substances that

A

further propagate aggregation, vasoconstriction, and thrombus formation

122
Q

plaque disruption may occur

A

spontaneously

123
Q

plaque disruption could be triggered by

A

hemodynamic factors

124
Q

Diurnal variation

A

first hour after arising may favor platelet aggregation and fibrinolytic activity

125
Q

unstable plaque with ulceration or rupture and thrombosis could lead to

A

acute coronary syndromes

126
Q

you need 3 things to diagnosis a MI

A

patient history, ECG changes, serum cardiac markers (troponin)

127
Q

STEMI has what elevation

A

ST elevation

128
Q

NSTEMI has no ___ _________

A

ST elevation

129
Q

angina could be 2 types

A

stable and unstable

130
Q

stable angina

A

pain when hearts oxygen demand increases

131
Q

unstable angina

A

the pain has a more persistent and severe course and is characterized by at least one of three features

132
Q

unstable angina characterized by 1 of 3 factors

A

occurs at rest, lasting more than 20 mins
severe and described as pain and of new onset
occurs with a pattern that is more severe, prolonged, or frequent than previously experienced

133
Q

unstable angina causes

A

NSTEMI

134
Q

unstable angina NSTEMI occurs at rest with minimal exertion usually lasting more than

A

20 mins

135
Q

NSTEMI reflects

A

ischemia server enough to cause myocardial damage which releases serum cardiac markers

136
Q

STEMI is a

A

MI

137
Q

STEMI is not treated by

A

nitroglycerin

138
Q

be careful with what 2 groups when they have a STEMI because they presentation is not conventional

A

women an diabetics

139
Q

STEMI diabetic may

A

not experience pain

140
Q

STEMI women may

A

present with fatigue or shortness of breath

141
Q

referred pain

A

pain not related to origin

142
Q

if you have a 12 lead EKG change, markers and a clinical presentation you have

A

STEMI

143
Q

what part of the EKG will be changed when you have a STEMI

A

ST wave elevation

144
Q

cardiomyopathies

A

heterogenous group of diseases of the myocardium associated with mechanical and/or electrical dysfunction that usually exhibit inappropriate ventricular hypertrophy or dilatation and that are due to a variety of causes that frequently are genetic

145
Q

a example of a primary genetic cardiomyopathy is

A

hypertrophic

146
Q

an example of secondary cardiomyopathy found in women who just gave birth are

A

peripartum

147
Q

hypertrophic cardiomyopathy

A

unexplained ventricular hypertrophy with disproportionate thickening of the septum, abnormal diastolic filling and cardiac arrhythmias

148
Q

what is the most common cause of death in young athletes

A

hypertrophic cardiomyopathy

149
Q

syncope

A

fainting

150
Q

hypertrophic cardiomyopathy is the enlargement of

A

myocardium

151
Q

mitral valve prolapse

A

floppy valve

152
Q

mitral valve prolapse is symptomatic or asymptomatic

A

asymptomatic

153
Q

mitral valve is most commonly found in

A

females

154
Q

stenosis

A

narrowing of the valve opening, so it does not open properly

155
Q

if a valve is stenotic you will hear

A

murmur of blood shooting through the narrow opening when the valve is open

156
Q

incompetent or regurgitant valve

A

permits backward flow to occur when the valve should be closed

157
Q

if a valve is regurgitant you will hear

A

murmur of blood leaking back through when the valve should be closed

158
Q

decrease in cardiac output with a consequent decrease in blood flow to

A

kidneys and other organs and tissues

159
Q

inotropic influence

A

is one that increases the ability of contractile elements of the heart muscle to interact and shorten against a load

160
Q

positive inotropic influence is caused by

A

sympathetic

161
Q

negative inotropic influences is caused by

A

acidosis

162
Q

SNS and RAA increase

A

heart rate

163
Q

what is preload

A

volume you have

164
Q

what is the resistance heart has to pump against

A

afterload

165
Q

how does tachycardia impact cardiac output and coronary artery filling

A

decreases time for coronary filling and ventricular filling leading to decreased cardiac output

166
Q

myocardial hypertrophy and remodeling is part of

A

RAA

167
Q

angiotensin II causes

A

vasoconstriction (which leads to increased AL) and myocardium remodeling

168
Q

deleterious effects of norepinephrine and SNS

A

increased LV volumes and pressures, LV hypertrophy< arrhythmias, apoptosis

169
Q

left sided vs right sided heart failure: left

A

decreased cardiac output and pulmonary congestion which leads to impaired gas exchange (leads to cyanosis and hypoxia) and pulmonary edema (leads to cough with frothy sputum, orthopena, paroxysmal nocturnal dyspnea)

170
Q

left sided vs right sided heart failure: right

A

congestion of peripheral tissues which leads to dependent edema and ascites, GI tract congestion (anorexia, GI distress and weight loss) and liver congestion

171
Q

symptoms of heart failure

A

orthopena, paroxysmal nocturnal dyspnea, fatigue, RUQ fullness and pain, anorexia, nausea and vomitting

172
Q

signs of heart failure

A

jugular venous distension, pulmonary crackles, cheyne stokes, S3 gallop, narrow pulse pressure, pale cool skin, decreased urine output

173
Q

cheyne stokes

A

gasping breathing

174
Q

pulmonary edema happens in

A

extreme heart failure

175
Q

pulmonary edema happens when capillary fluid moves into

A

alveoli

176
Q

in pulmonary edema the hemoglobin is not completely

A

oxygenated

177
Q

as you get older in reaction to you cardiac function

A

increased vascular stiffness, left ventricular hypertrophy, heart compliance, reduced response to beta adrenergic

178
Q

atrial fibrillation the blood is stagnant

A

in the atrias

179
Q

atrial fibrillation is

A

irregularly irregular

180
Q

when in atrial fibrillation you at risk for ______ ____, assess anticoagulant status

A

mural thrombi

181
Q

a person with a MI is releasing angiotensin II. how should the clinician interpret this findinf

A

counter productive, it causes the heart to work harder

Pathophysiology (44 decks)

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