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331 test 2 Flashcards

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1
Q

nervous system can be separated into

A

central and peripheral

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2
Q

central nervous system

A

brain and spinal cord

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3
Q

peripheral nervous system broken down into

A

somatic and autonomic

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4
Q

somatic

A

skeletal muscle

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5
Q

autonomic nervous system can be broken down into

A

parasympathetic and sympathetic

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6
Q

parasympathetic

A

rest and digest. cholinergic receptors

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7
Q

sympathetic

A

fight or flight. adrenergic receptors with alpha and beta receptors

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8
Q

what does parasympathetic do to your eyes, SA node, bronchial muscle, arteriole, and gastric motility

A

constriction in eyes and brachial muscles, SA node decrease, arteriole dilation, increase in gastric motility

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9
Q

what neurotransmitter is connected with parasympathetic

A

acetylcholine

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10
Q

inotropic

A

contractibility of the heart

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11
Q

chronotropic

A

effect heart rate

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12
Q

dromotropic

A

electrical conduction of the heart

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13
Q

glycogenolysis

A

breaking down of glycogen into glucose

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14
Q

sympathetic neurotransmitter

A

norepinephrine and epinephrine

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15
Q

what is epinephrine? and what does it do?

A

nonselective adrenergic agonist for both beta 1&2 and alpha 1. vasoconstrictor, bronchodilator, and increases inotropic, chronotropic, and dromotropic

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16
Q

PEA

A

pulseless electrical activity

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17
Q

indications for epinephrine

A

PEA, asystole, bradycardia

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18
Q

asystole

A

cardiac arrest rhythm with no discernible electrical activity on the EKG monitor. It is a flatline EKG, P Waves and QRS complexes are not present The heart is not functioning.

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19
Q

miosis

A

pupillary constriction

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20
Q

what can increase chances of hypertenstion

A

age, diabetes, being African American, and diet (obesity)

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21
Q

what diseases are associated with hypertension

A

MI, renal disease, stroke

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22
Q

what 2 systems are involved in hypertension

A

RAAS (renal) and central nervous system

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23
Q

what is the most common primary diagnosis in the US

A

hypertension

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24
Q

what can lead to an increase in circulating volume

A

an increase in intake of Na and/or decrease excretion of Na and K, Ca, Mg deficiency

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25
Q

ANP

A

Atrial Natriuretic Peptide

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26
Q

BNP

A

Brain natriuretic peptide

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27
Q

CNP

A

C-type natriuretic peptide still need to figure out what this does

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28
Q

urodilatin

A

hormone that causes natriuresis through increasing renal blood flow

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29
Q

natriuretic hormones

A

ANP, BNP, CNP, urodilatin

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30
Q

what causes hypertension?

A

sustained increase in peripheral resistance and cardiac output

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31
Q

SVR

A

systemic vascular resistance. reflects changes in the arterioles, which can affect emptying of the left ventricle

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32
Q

increase in RAAS leads to

A

decreased renal salt excretion so increase salt retention

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33
Q

what does sympathetic nervous system do to you HR and vessels

A

increase heart rate and vasoconstrict

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34
Q

what can prolonged hypertension do to your body?

A

vascular remodeling, increase renin/angiotensin, renal sodium retention, and procoagulant

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35
Q

primary hypertension

A

due to genetics and environment

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36
Q

secondary hypertension

A

usually from disease process. Is reversible

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37
Q

complicated hypertension

A

leads to target organ damage such as LVH, HF, CAD

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38
Q

LVH

A

left ventricular hypertrophy

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39
Q

CAD

A

coronary artery disease

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40
Q

CVA

A

cerebral vascular accident (stroke)

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41
Q

TIA

A

Transient ischemic attack (mini stroke)

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42
Q

what can complicated hypertension do to your body?

A

LVH, HF, CAD, kidney damage with microalbuminuria, stroke, vascular sclerosis

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43
Q

microalbuminuria

A

albumin in urine – sign of kidney damage (something bad is going to happen)

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44
Q

hypertensive crisis

A

BP 180/110+, rapid onset. can cause organ damage, CVA, or stroke

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45
Q

what can cause a hypertensive crisis

A

alcohol withdrawal, stimulant drugs, or pregnancy

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46
Q

High blood pressure guidelines

A

Normal: Less than 120/80 mm Hg;
Elevated: Systolic between 120-129 and diastolic less than 80;
Stage 1: Systolic between 130-139 or diastolic between 80-89;
Stage 2: Systolic at least 140 or diastolic at least 90 mm Hg;
Hypertensive crisis: Systolic over 180 and/or diastolic over 120, with patients needing prompt changes in medication if there are no other indications of problems, or immediate hospitalization if there are signs of organ damage

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47
Q

Microvascular

A

arteries, veins, capillaries

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48
Q

microvascular dysfunctions stems from?

A

stems from constant state of increased volume and increased vasoconstriction

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49
Q

adipokines

A

inflammatory mediators released by adipocytes

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50
Q

adipokines release

A

leptin and adiponectin

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51
Q

leptin control what in the body?

A

appetite suppression and increase metabolic rate

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52
Q

what happens to leptin and adiponectin when you are obese?

A

increase in leptin and decrease in adiponectin

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53
Q

what do adiponectins deal with

A

insulin

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54
Q

what do increased levels of leptin do?

A

cause resistance by increases SNS, decreasing renal sodium excretion, and causing inflammation

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55
Q

what does a decreased amount of adiponectin do to your body?

A

increases SNS, increases RAAS, and decreases nitric oxide

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56
Q

Bariatric surgery

A

weight loss surgery. usually beings hypertension back to secondary

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57
Q

what does microvascular dysfunction lead to?

A

vascular remodeling, endothelial dysfunction, decrease in vasodilator release, and sustained HTN

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58
Q

salt retention and increased volume =

A

vascular resistance

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59
Q

what causes salt retention

A

increased Na intake, renin secretions which would stimulate RAAS, and decrease of K, Ca, and Mg

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60
Q

what does angiotensin do?

A

stimulates the release of aldosterone from the adrenal cortex to promote sodium retention by the kidneys

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61
Q

Atherogenesis

A

plaque formation. a disorder of the artery wall that involves adhesion of monocytes and lymphocytes to the endothelial cell surface

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62
Q

Atherosclerosis

A

plaque with the addition of inflammation around vessel

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63
Q

what does increased angiotensin 2 do?

A

systemic vasoconstriction, arteriolar remodeling, endothelial dysfunction, insulin resistance, platelet aggregation, Hypertension end-organ damage

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64
Q

Increases platelet aggregation =

A

increase risk of blood clot

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65
Q

what can cause increased volume?

A

renal injury that causes renal vasoconstriction, tissue ischemia that causes inflammation and sodium retention

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66
Q

tissue ischemia

A

a restriction in blood supply to tissues, causing a shortage of oxygen

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67
Q

proper function of natriuretic hormones

A

vasodilation, sodium excretion, decrease BP

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68
Q

improper function of natriuretic hormones

A

increase vascular tone, sodium retention that increases blood volume, and increase in BP

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69
Q

BNP test

A

blood test that measures levels of a protein called BPN that is made by your heart and blood vessels.

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70
Q

what does higher levels of BNP mean? what is considered normal?

A

less than 100 = normal. higher than 100 = heart failure, increase in volume, or ventricle stretch

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71
Q

decrease in venous return =

A

decrease preload

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72
Q

increased ANP/BNP levels linked to

A

heart failure, ventricular hypertrophy, atherosclerosis

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73
Q

ANP linked to

A

right atrium

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74
Q

two things that affect cardiac output

A

stroke volume and heart rate

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75
Q

what affects stroke volume and heart rate

A

preload, after load, and contractility

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76
Q

how does the body compensate when BP drops

A

increase HR, increase contractility, increase preload, vasoconstriction by SNS and RAAS

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77
Q

dysfunction of the natriuretic hormones can be due to

A

low levels of Ca, K, or Mg

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78
Q

vomiting and diarrhea may cause toxicity for which drug?

A

digoxin cause vomit and diarrhea can make you lose potassium and hypokalemia increases potential digoxin toxicity

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79
Q

most common reason for people over 65 years old to be admitted into hospital

A

heart failure

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80
Q

what does left heart failure (systolic) do to CO and EF?

A

decrease CO and EF is less than 40%

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81
Q

what is EF?

A

EF is the ejection fraction. a measurement, expressed as a percentage, of how much blood the left ventricle pumps out with each contraction

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82
Q

what affects Stroke volume

A

contractility, preload, and after load

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83
Q

what happens with contractility and preload during left systolic heart failure?

A

decrease in contractility and increase in pre load

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84
Q

why would preload increase during left heart failure?

A

decrease contractility and increased vascular volume

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85
Q

what leads to decreased contractility during left sided heart failure

A

myocyte disfunction

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86
Q

constant ischemia in the heart leads to

A

increase workload which causes hypertrophy, increase RAAS and SNS and myocardial remodeling

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87
Q

what does decrease CO lead to?

A

decrease in renal percussion, increase in RAAS which increases after load and preload. Also activates bars-receptors which increase ADH which increase SNS which increase after load and preload.

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88
Q

LVH

A

Left ventricular hypertrophy is enlargement and thickening (hypertrophy) of the walls of your heart’s main pumping chamber (left ventricle)

89
Q

LVEDV

A

Left Ventricular End-Diastolic Volume.

90
Q

effects of decrease contractility

A

increase preload - stretching of myocardium and decrease of lumen coronary arteries - myocardial ischemia - leads right back to more decreased contractility

91
Q

effects of increased afterload

A

increases left ventricle workload - increase RAAS and SNS which causes hypertrophy causes increases demand for oxygen causes ventricular remolding which leads to decrease in contractility which increases RAAS and SNS and leads to more vascular resistance

92
Q

how does a patient present with left systolic heart failure

A

fatigue, pulmonary edema, dyspnea, orthopnea, cough with frothy sputum, S3 heart sound

93
Q

orthopnea

A

shortness of breath while laying down

94
Q

what tests should you run with heart failure

A

echocardiogram and BNP

95
Q

ASA

A

aspirin which is an anti platelet

96
Q

Ace inhibitors and ARBs

A

reduce preload and after load, decrease volume and PVR, are cardio and renal protective

97
Q

diuretics do what to preload

A

reduce preload by reducing volume

98
Q

treatment for heart failure

A

beta blocker, anti platelet, salt restriction, diuretic, ACE inhibitor or ARB

99
Q

what is a first line treatment for HTN if no other comorbidities exist?

A

diuretic - decrease BP, CO, and preload

100
Q

what should you do when administering diuretic

A

monitor electrolytes, BUN, and creatine

101
Q

lasix

A

Furosemide - antihypertensive and diuretic

102
Q

adverse affects of lasix

A

vertigo, hypotension, hypokalemia, fatal skin rash

103
Q

Cardiac glycosides Mechanism of actions and what do they do to inotrope, chronotrpe, and dromotrope

A

increase sodium and calcium (positive inotrope), augments parasympathetic stimulation (negative chronotrope), prolongs conduction (negative dromotrope)

104
Q

what cardiac glycoside did we learn

A

Digoxin

105
Q

what do you have to be careful with when using digoxin?

A

toxicity = bradycardia, confusion, and visual disturbances

106
Q

what do you use to reverse digoxin toxicity?

A

digoxin immune FAB (digifab)

107
Q

if someone presents with hyperkalemia and life threatening cardiac dysrhythmias what do you give them?

A

digoxin immune FAB (digifab)

108
Q

if calcium is not leaving the cells within the heart what happens

A

there’s an inability to relax the heart

109
Q

DOE

A

dyspnea on exertion

110
Q

Left heart diastolic failure

A

filling problem with normal EF and CO

111
Q

patient presentation with Left heart diastolic failure

A

DOE, fatigue, S4 heart sound, pulmonary edema and hypertension

112
Q

right heart failure

A

seen with CHF and pulmonary hypertension because there is inadequate blood flow to the lungs

113
Q

what will you see with right heart failure

A

peripheral edema, hepatosplenomegaly, venous congestion, COPD, pulmonary endothelial remodeling, hypoxic vasoconstriction

114
Q

hepatosplenomegaly

A

enlarged liver and spleen

115
Q

High output failure

A

ineffective tachycardia but CO in normal

116
Q

what can cause high output failure?

A

anemia by decreasing oxygen carrying capability or sepsis by vasodilation and anaerobic metabolism

117
Q

LLMs

A

lipid - laden macrophages

118
Q

what do LLMs release?

A

inflammatory cytokines which causes oxidation of LDL

119
Q

stages of atherosclerosis

A

damaged endothelium, cholesterol sticks to vessel to “repair”, leads to a fatty streak, foam cells, and platelets attach to endothelium, fibrous tissue encapsulates lipid areas and causes plaque buildup. then thinning of college cap leads to rupture and capsule breaking off and forming a blood clot

120
Q

inflammatory cytokines

A

interleukins, interferons

121
Q

risk factors to atherosclerosis

A 
Poor diet
High cholesterol 
Smoking
Sedentary lifestyle
Hypertension (biggest risk factor)
122
Q

intermittent claudication

A

pain with walking

123
Q

how does peripheral artery disease present?

A

can be asymptomatic but if not will show as intermittent claudication, severe color change, loss of pulse, severe pain

124
Q

how do you test and treat peripheral artery disease?

A

test with ankle/brachial index and treat with anti platelets and reducing risk factors

125
Q

coronary artery disease

A

hardening or narrowing of arteries which impairs heart pumping ability

126
Q

risk factors for coronary artery disease

A

Hypertension
Endothelial injury from a constant state of high pressure
Hypertrophy – vascular remodeling from constant pressure and stretch

127
Q

path from HTN to ischemia

A

HTN-endothelial injury-hypertrophy-increased oxygen demand-increased SNS-increased RAAS - ischemia

128
Q

first line drug therapy for hypercholesterolemia

A

antilipemics HMG-CoA reductase inhibitor, also known as statins. reduces LDL and plasma triglycerides and increases HDL

129
Q

Statin Adverse effects

A

elevated liver enzymes, myopathy, rhabdomyolysis

130
Q

what is dark urine a sign of while taking statin

A

sign of rhabdomyolysis

131
Q

what is rhabdomyolysis

A

muscle breakdown and myoglobin protein end up in urine

132
Q

process of going from atherosclerosis to myocardial ischemia

A

plague-thrombus formation-ischemia

133
Q

what happens after ischemia to the heart

A

there is glucose deprivation which lead to aerobic metabolism which causes lactic acid to build up and cause pain

134
Q

after myocardial ischemia how lung do you have until MI?

A

20 minutes

135
Q

fatal arrhythmias

A

V fib and V tac

136
Q

types of angina

A

stable, prinzmetal, and unstable

137
Q

stable angina

A

predictable shows a lot like MI

138
Q

prinzmetal angina

A

unpredictable and occurs at rest, usually at night.

139
Q

unstable angina

A

results from reversible myocardial ischemia but on your way to MI

140
Q

silent ischemia

A

mental stress induced ischemia

141
Q

STEMI

A

ST elevation = infarction = tissue death

142
Q

non-STEMI

A

ST segment depression = ischemia = lack of blood flow

143
Q

CPK-MB

A

creatine phosphokinase MB

144
Q

what happens when you go through myocardial infarction

A

decrease contractibility, altered LV compliance, decrease stroke volume and ejection fraction, SA node malfunction, increased left ventricular end diastolic volume, inflammation, and angiotensin 2 release, myocyte remodeling

145
Q

CRP

A

A plasma protein that rises in the blood with the inflammation

146
Q

what can be signs of inflammation

A

CRP and leukocytosis

147
Q

you get a surge of what during MI?

A

catecholamines

148
Q

what tests should you use for MI

A

CPK-MB, troponin, CRP

149
Q

MI does what to contractibility?

A

decreases it

150
Q

what does decreased contractibility do?

A

decrease EF and renal perfusion (increase preload), increase LVEDV and renin/angiotensin (increase after load)

151
Q

how will a patient present with MI?

A

depends on stage of progression, but will have pain, SOB, impending doom, could look pale and be cool

152
Q

MONA

A

Morphine, oxygen, nitroglycerin, and aspirin

153
Q

you do not want to use what with nitroglycerin?

A

erectile dysfunction meds

154
Q

Nitroglycerin

A

anti anginas therapy - decreases preload and after load. coronary artery dilation

155
Q

nitroglycerin contraindicated for

A

anemia and ED drugs

156
Q

adverse effects of nitroglycerin

A

headache, hypotension, tachycardia

157
Q

when is preload increased?

A

hypervolemia, regurgitation of cardiac valves, and heart failure

158
Q

when is after load increased

A

hypertension and vasoconstriction

159
Q

calcium channel blockers

A

inhibit calcium entry into cardiac/smooth muscle cells and promotes muscle relaxation

160
Q

what calcium channel blockers did we learn

A

amlodipine and diltiazem

161
Q

what does amlodipine do?

A

decreases after load, reduced cardiac workload, reduces oxygen demand

162
Q

what does diltiazem do?

A

negative inotrope, dromotrope, and chronotrope

163
Q

when and how should you take amlodipine

A

orally for angina or HTN

164
Q

when and how should you take diltizem

A

IV for a-fib, A-flutters, or SVT

165
Q

SVT

A

Supraventricular tachycardia

166
Q

when is troponin considered elevated

A

when its over 0.04 and we usually want to test every 3 hours

167
Q

beta blockers

A

end in “olol” decrease contractibility, decrease HR

168
Q

what can beta blockers mask

A

hypoglycemia so be careful when giving to diabetics

169
Q

ACE inhibitors

A

end in “pril” decrease preload and after load and stops the conversion of angiotensin 1 to angiotensin 2

170
Q

ARBS

A

“artan” decrease preload and after load

171
Q

all ACE inhibitors have a black box warning of

A

fetal toxicity

172
Q

phentalomine

A

causes vasodilation

173
Q

first dose phenomenon

A

causes orthostatic hypertension

174
Q

first dose phenomenon

A

fall in blood pressure

175
Q

decreased mg, ca, and K can lead to

A

high BP

176
Q

when is troponin released

A

with cardiac cell death

177
Q

an echocardiogram shows us what

A

EF

178
Q

what does your blood concentration look like during Heart failure?

A

diluted so your sodium looks low due to all the fluid retention

179
Q

what happens with renin during HF

A

renin is recreated due to low blood flow to kidneys due to vasoconstriction

180
Q

what happens with renin during HF

A

renin is recreated due to low blood flow to kidneys due to vasoconstriction

181
Q

epinephrin

A

alpha and beta agonist

182
Q

tamsulosin (flomax)

A

alpha 1 blocker

183
Q

clonidine (catapres)

A

alpha 2 agonist

184
Q

metaprolol (lopressor)

A

beta 1 blocker

185
Q

carvedilol (coreg)

A

nonselective beta and alpha blocker

186
Q

lisinopril

A

ace inhibitor

187
Q

losartan (cozaar)

A

ARB

188
Q

enalopril

A

ACE INHIBITOR

189
Q

hydralazine

A

vasodilator

190
Q

amlodipine (norvasc)

A

calcium channel blocker

191
Q

diltiazem

A

calcium channel blocker

192
Q

Lipitor

A

Statin

193
Q

furosemide (lasix)

A

loop diuretic

194
Q

nitroglycerin (nitrostat)

A

nitrate

195
Q

Digoxin

A

cardiac glycoside

196
Q

what do alpha receptors do

A

vasoconstrict cardiovascular, bladder constriction, promote glycogenolysis, mydriasis

197
Q

what do beta 1 receptors do

A

increase contractility in heart, increase HR, promote renin secretion

198
Q

what do beta 2 receptors do

A

bronchodilate, glycogenolysis, vasodilation

199
Q

adrenergic agonist (alpha and beta)

A

promote SNS. low dose beta, high dose alpha

200
Q

alpha 1 blocker

A

smooth muscle relaxation, vasodilation. used for men with enlarged prostates and rhaynaud’s disease

201
Q

rhaynaud’s disease

A

fingertips and toes start to turn blue due to low perfusion.

202
Q

alpha 2 agonist

A

centrally acting, blocks SNS activity, decreases PVR, BP, and HR. used for opioid withdraws and hypertension

203
Q

alpha 2 agonist adverse effects

A

bradycardia, hypotension, or rebound hypertension if stopped abruptly,

204
Q

Beta 1 blocker

A

negative ionotrope (SNS blocked), negative chronotrope (SNS blocked), and negative domotrope (fills ventricle), brings workload of heart down, O2 demand down, and renin secretion down

205
Q

beta 1 blocker indication

A

MI and angina

206
Q

Nonselective beta and alpha blocker

A

blocks glycogenolysis, inhibits insulin secretion, brings workload of heart down so can mask hypoglycemia symptoms so be careful when giving to diabetic patients

207
Q

indication for Nonselective beta and alpha blocker

A

heart failure, beneficial for hypertension and angina

208
Q

Ace inhibitor

A

blocks AG1 to AG2, brings SVR down which decreases after load, blocks aldosterone which prevents sodium and water retention which brings volume down and decreases preload

209
Q

ace inhibitor indicator and what do they protect

A

hypertension or heart failure, protect both heart and renal

210
Q

adverse effects of ACE inhibitors

A

dry cough, hyperkalemia, acute renal injury, angio edema

211
Q

what is a serious concern for ACE inhibitors

A

black box warning of fetal toxicity

212
Q

ARBs

A

blocks vasoconstriction of vascular smooth muscle, and blocks production of aldosterone. with being a vasodilator is decreases SVR which brings afterload down

213
Q

ARBs indication

A

hypertension and heart failure, lowers mortality after MI

214
Q

Vasodilator drugs

A

directly causes arteriolar and venous smooth muscle relaxation, decreases SVR which decreases afterload

215
Q

Vasodilator drug indication and contraindication

A

used for hypertension. do not use with CAD or diastolic dysfunction

216
Q

what do nitrates do

A

coronary vasodilator and antianginal can cause headache

217
Q

what do calcium channel blockers do

A

relax vascular smooth muscle, effective in treating angina

218
Q

what are cardiac glycosides used for

A

heart failure

219
Q

what are statins used for

A

to bring cholesterol down

NURSING School (17 decks)

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