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PAS 753 (Molecular Pathophysiology) > Cardiovascular Disease > Flashcards

Cardiovascular Disease Flashcards

1
Q

two divisions of cardiovascular disease

A

peripheral vascular disease

heart disease

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2
Q

two branches of peripheral vascular disease

A

atherosclerotic

vasculitis

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3
Q

four divisons of heart disease

A

coronary artery disease

valvular disease

HTN heart disease

cardiomyopathy

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4
Q

T/F cardiovascular illness is the most common serious disorder in the US

A

true

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5
Q

what percent of the following have cardiovascular disease

people at age 20

people over 75

total population

A

5%

75%

20%

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6
Q

what is the most common cause of death in the US

A

cardiovascular disease

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7
Q

systolic pressure

A

pressure at which blood flow resumes in an occluded arterty

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8
Q

diastolic reading

A

pressure at which flow returns to normal in an occluded artery

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9
Q

most current guidelines for blood pressure

Normal

elevated

Stage 1

Stage 2

A

normal: 120/80

elevated: systolic >120, diastolic >80

stage 1 HTN: >/= 130/80

stage 2 HTN: >/= 140/90

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10
Q

based on new HTN guidelines how many people are afflicted

A

103million

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11
Q

of the 75% of the patients who have HTN and are aware of it, how many are getting treated?

how many are controlled?

A

50% are being treated

25% are under control

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12
Q

Dr Dodges suggested take home messages regarding HTN

A
  1. 140/90 is still a reasonable threshold for the intiation of medical treatment of HTN
  2. lifestyle modification are useful for patients with elevate BP
  3. patients with diabetes or other comorbidities, medical treatment should be considered
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13
Q

four classifications of HTN

A

primary/essential/idiopathic

renal

endocrine

pregnancy induced

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14
Q

what is the most common form of HTN

A

primary/essential/idiopathic

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15
Q

two conditioned associated with renal hypertension

A

narrowed renal artery

chronic renal disease

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16
Q

three endocrine conditions associated with HTN

A

cushings

pheochromcytoma

congenital adrenal hyperplasia

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17
Q

three conditions associated with pregnancy induced HTN

A

toxemia

pre-eclampsia

eclampsia

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18
Q

pheochromocytoma

5 primary symptoms

A

a rare tumor of the adrenal medulla or sympathetic ganglion that secretes norepinephrine

  1. severe headaches
  2. diaphoresis
  3. palpitation
  4. tremor
  5. anxiety
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19
Q

T/F HTN is generally asymptomatic

A

true

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20
Q

what are three general symptoms associated with HTN

A

Headaches

malaise/fatigue

symptoms of complications

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21
Q

where are BP recordings most accurate

A

at home and work, not in the office

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22
Q

the hydraulic equation

define the variables

A

BP = CO x PVR

BP = cardiac output x peripheral resistance

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23
Q

three ways to decrease BP by decreasing CO

A

reduce HR

reduce contractility

reduce venous return/decrease blood volume

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24
Q

how to reduce BP by decreasing PVR

two methods to achieve this

A

vasodilation

  1. direct action on the vessels
  2. CNS control
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25
Q

two key elements manipulated to regulate blood pressure

A

sympathetic nervous system input

renal blood flow

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26
Q

two primary sympathetic receptors manipulated to control BP

A

Alpha 1 vascular receptors

Beta 1 cardiac receptors

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27
Q

two factors related to renal blood flow that can be manipulated to regulate BP

A

renin-angiotensin-aldosterone pathway

total vascular volume

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28
Q

descrive the RAA pathway (5)

A
  • renin is released by the kidneys in response to decreasing BP
  • renin converts angiotensinogen to angiotensin I
  • angiotensin converting enzyme converts angiotensin I to II
  • angiotensin II stimulated an increase in BP and the release of aldosterone from the kidney
  • Aldosterone causes salt retension
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29
Q

two key RAA hormones

A

Angiotensin II

aldosterone

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30
Q

what is the function of aldosterone II

A

triggers vasoconstriction

aldosterone production and release from the adrenal cortex

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31
Q

three facts about aldosterone

A

most potent natural mineralocorticoid

helps with sodium and fluid retention

also induces cardiac growth

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32
Q

what is the sympathetic response to decreased BP

A
  • activation of Beta adrenergic receptors in the heart
  • activation of Alpha adrenergic receptors in smooth muscle
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33
Q

what is the effect of sympathetic activation of Beta receptors in response to Decreased BP

A

increased cardiac output through contractility

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34
Q

what is the effect of sympathetic stimulation of alpha receptors in response to decreased BP

A

increased peripheral resistance through vasoconstriction

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35
Q

what is the renal response to decreased blood pressure

A

decreased renal blood flow

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36
Q

what happens in response to decreased renal blood flow

A

renin is released

glomerular filtration is decreased

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37
Q

what has been the primary reason for decreasing number of cardiac death since the 1970

A

decreased in smoking

improved treatment

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38
Q

what two factors increase water retention in response to decreased blood pressure

A

decreased glomerular filtration

aldosterone production

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39
Q

what is the result of increased sodium and water retention in response to low BP

A

increasd blood volume, which increases cardiac output

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40
Q

what is the effect of angiotensin to released in response to renin production

A

aldosterone production leading to increased salt and water retention

increased peripheral resistance

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41
Q

two HTN treatment strategies

A

reduce cardiac output

reduce peripheral vascular resistance

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42
Q

two methods to reduce cardiac out in HTN treatment

A

block beta 1 sympathetic action

reduce blood volume

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43
Q

what is the result from blocking beta 1 sympathetic action

A

reduced cardiac rate and contractility

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44
Q

three methods to reduce peripheral resistance in HTN treatment

A

block alpha 1 sympathetic action

block central sympathetic action

directly dilate the blood vessels

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45
Q

four groups of drugs used to treat HTN

A

diuretics

sympathetic receptor blocker

direct vasodilators

RAA blockers

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46
Q

how do diuretic function to decrease blood pressure

A

lower blood volume

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47
Q

how do sympathetic receptors blockers function to lower HTN

A

block alpha and beta receptors

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48
Q

what is the function of direct vasodilators in the treatment of HTN

A

reduce peripheral vascular resistance

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49
Q

what is the function of blocking RAA in treating HTN

A

reduce blood volume and peripheral resistance

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50
Q

three common diuretics (examples)

A

thiazides (hydrochorthiazide)

loop diuretics (furosimide)

potassium sparring diuretics (spironolactone)

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51
Q

four common sympathetic receptor blockers (examples)

A

beta blocker (atenolol, propanolol)

alpha blockers (prazosin, terazosin)

alpha and beta (labetalol)

centrally acting (methyldopa, clonidine)

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52
Q

thee common vasodilators (examples)

A

calcium channel blockers (diltiazem, amlodipine)

arterial (hydralazine, minoxidil, diazoxide)

arterial and venous (nitroprusside)

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53
Q

four common RAA blockers (examples)

A

angiotensin converting enzyme (ACE) inhibitors (catopril, benazopril)

angiotensin II receptor antagonist (losartan)

aldosterone antagonist (spironolactone)

renin inhibitor (aliskiren)

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54
Q

thee factors that influence cardiac output

A

HR

contractility

filling pressure

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55
Q

thee factors that influence PVR

A

arterial diameter

arterial length

elasticity

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56
Q

distinguish between treatments for mild and severe HTN

A

mild to moderate HTN usually uses one drug

severe HTN uses multiple drugs

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57
Q

mitigating factors to consider in treatment of HTN

A

other medical conditions

RAA work less well on african americans

cost

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58
Q

why are ACE inhibitors effective

A

because angiotensin I is really just a precuros without much effect on blood pressure

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59
Q

what angiotensin II a potent actor on BP

A

it triggers the aldosterone production to increase blood volume

it acts on the blood vessels to increase peripheral resistance

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60
Q

three popular single drugs used in intial HTN treatment

A

ACE inhibitor

calcium channel blocker

diuretic

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61
Q

the useful conbinations of drugs used in intitial treatment of HTN

A

ACE inhibitor + diuretic

Beta blocker + diuretic

beta blocker + alpha blocker

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62
Q

what is the goal of HTN treatment

A

maintenance of 120/80 BP for high risk patients

<135/85 for mild to moderate risk patients

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63
Q

limbo goal for high risk hypertensives

A

trying to go as low as is safely possible for people with severe comorbities (diabetes, CAD, CVA)

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64
Q

what is the risk of decreasing blood pressure too low

A

toxicity

orthostatic hypertension

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65
Q

three common side effects of HTN treatment

A

electrolyte imbalances

annoying dry cough

malaise, fatigue

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66
Q

why drugs used to treat HTN will cause low potassium?

high?

A

diuretics

ACE and aldosterone inhibitors

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67
Q

what common HTN treatment will cause annoying dry cough

A

ACE inhibitors

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68
Q

what common HTN treatment can cause malaise and fatigue

A

beta blockers

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69
Q

what constitutes a “hypertensive emergency”

A

200/140

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70
Q

how would treatment differ for a patient with BP <200/140 vs >200/140

A

over 200/140 needs hospitalization due to stroke or MI concerns

below 200/140 can be managed outpatient

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71
Q

does HTN mangement need to be life long

A

preferably not, as long as necessary but short as possible

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72
Q

step down strategy for HTN treatment

A

decreasing dose based on stable normal pressures attained through lifestyle changes

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73
Q

what is the main cause of cardiovascular disease

A

atherosclerosis

74
Q

atherosclerosis

A

vessel narrowing due to fatty deposits in the arteries related to lipid metabolism and cholesterol

75
Q

two sources of cholesterol

A

exogenous (diet and absorption)

endogeneous (production of cholesterol from the liver)

76
Q

lipoproteins

A

macromolecule consisting of lipid and protein

77
Q

LDL

A

transporter of endogeneous cholesterol

78
Q

HDL

A

removes LDL cholesterol and triglycerides

79
Q

best goal of LDL/HDL

why is this a good goal

A

make your lows low and highs high

decreasing LDL reduces risk of atherosclerosis

increased HDL decreases risk

80
Q

how is HDL increased

A

weight loss and exercise

81
Q

HDL paradox

A

drugs that decrease LDL reduce risk

drugs that increase HDL do not reduce risk

82
Q
A
83
Q

atherosclerotic process

A
  • fatty streaks
  • monocyte aggregation
  • LDL oxidation
  • formation of foam cells
  • inflammation leading to LDL accumulation
84
Q

fatty streaks

A

LDL accumulation under endothelium

85
Q

what causes the oxidation of LDL in fatty streaks

A

monocytes

86
Q

foam cells

A

monocytes that become macrophages and ingest oxidized LDL

87
Q

what is considered the unifying element in the pathogenesis of atherosclerosis

how was this decided

A

inflammtion

inflammatory markers correlate to CV disease risk

88
Q

C reactive protin

A

an inflammtion marker related to heart disease

89
Q

risk factors for atherosclerosis

A
  • smoking
  • hypertension
  • diabetes
  • family HX
  • age
  • dyslipidemia
  • lifestyle
90
Q

age range for increased atherosclerosis risk for men and women

A

>/=45 men

>/= 55 for women

91
Q

dyslipidemia related to atherosclerosis

A

high LDL

low HDL

92
Q

three lifestyle issues that increase risk of atherosclerosis

A

obesity

physical inactivity

atherogenic (inflammatory) diet

93
Q

why is the age related risk for athersclerosis different for men and women

A

women haver higher HDL

estrogen raises HDL

94
Q

two chronic effects of atherosclerosis

A

coronary effects

peripheral vascular disease

95
Q

two coronary effects of chronic atherosclerosis

A

angine pectoris

congestive or chronic heart failure

96
Q

three peripheral vascular disease associated with the effects of chronic atherosclerosis

A

renal artery stenosis

femoral/popliteal stenosis

aortic aneurysm formation

97
Q

T/F most myocardial infarctions are caused by HTN

A

false, caused by atherosclerotic plaque rupture

98
Q

what happens when an atherosclerotic plaque ruptures

A

a blood clot forms around the rupture and blocks the artery

99
Q

four treatments for atherosclerosis

A

lifestyle changes

treatment of hyperlipidemia with statins

treat HTN

treat diabetes

100
Q

when are symtpoms of mild atherosclerosis noticed?

severe?

A

50% occulsion, usually on exertion

80%, effects can be felt at rest

101
Q

5 lipid lowering agents

A

niacin

bile acid binding agents

HMG-CoA reductase inhibitors

fibric acid derivatives

inhibitors of sterol absorption

102
Q

common name of HMG-CoA reducatse inhibitors

A

statins

103
Q

what is the effect of statin drug treatment

A

reduction of endogenous cholesterol synthesis

lowers LDL

104
Q

three common statins

A

atorvastatin (lipitor)

simvastatin (zocor)

lovastatin (mevacor)

105
Q

two adverse effects of statins

A

liver damage

muscle damage

106
Q

what must be monitored during statin treatment due to the liver damaging side effects

A

liver enzymes

107
Q

two conditions related to muscle damage from statin drugs

A

myopathy

rhabdomyolysis

108
Q

when are statins contraindicated

A

pregnacy

children

109
Q

what is a lesser known issue with statin?

what is the result

A

muscle weakness

reduction in activities

110
Q

PCSK9 inhibitors

A

new drug that stimulated production of an enzyme show to decrease LDL and decrease risk of heart disease

111
Q

two PCSK9 drugs

A

alirocumab (praluent)

evolcumab (repatha)

112
Q

what is the benefit of PCSK9 treatment

drawback?

A

produce better lipid reduction that statins

very expensive

113
Q

three causes of ischemia

A

vessel stenosis or occulsion

vasospasm

pump failure

114
Q

what is the key component of ischemia

A

O2 supply is not sufficient for demand

115
Q

other oxygen transport issues related to heart damage that arent ischemia

A

hypotension

chronic anemia

increased metabolism

116
Q

three causes of hypotension that can result ischemia

A

acute blood loss

anesthesia

cardiac arrhythmia

117
Q

causes of increased metabolism related to cardiac ischemia

A

hyperthyroid

fever

118
Q

symptoms of

acute

subacute

chronic

ischemia

A

acute: acute coronary syndrome
subacute: angina

chronic : CHF

119
Q

acute coronary syndromes

A

acute MI with ST segment elevation

acute MI without St elevation

unstable angina

120
Q

three main forms of coronary heart disease (CHD)

A

acute coronary syndrome

stable angina

CHF

121
Q

acute myocardial infarction

A

mycardial death due to abrupt reduction in coronary blood flow almost always caused by atherosclerosis

122
Q

what is the intitial event of an acute MI

A

a plaque rupture

123
Q

how many AMIs occur yearly

what percent are fatal

A

1.1 million

20-40%

124
Q

T/F more than 50% of AMI death occur suddenly

A

true

125
Q

symptoms of acute MI

A

squeezing pressure chest pain

can be felt in the stomach or left arm, face, shoulder

anxiety

diaphoresis

GI distress

126
Q

T/F 30% of AMIs are asymptomatic

A

treu

127
Q

what percent of AMIs are precipitated by strenous events

A

50%

128
Q

why are AMIs more common in the AM

A

BP is higher

increased blood viscosity

cortisol secretion is at its highest

129
Q

T/F most women have atypical AMI presentation

A

true, more likely to be Dx as gi

130
Q

STEMI is usually indicative of what

A

transmural ischemia (involves the full thickness of the cardiac wall)

131
Q

what is more common, STEMI or NSTEMI

A

NSTEMI (55-60%)(

132
Q

NSTEMI is indicative of what

A

ischemia that is subendocardial rather than transmural

133
Q

NSTEMI treatment

A

supportive measures

anticoagulation

134
Q

NSTEMI supportive treatments

A

rest

oxygen

sedation/analgesia

control of arrhytmia

135
Q

differentiate between the vascular causes of STEMI vs NSTEMI

A

STEMI is more likely to be in one of the great vessels

NSTEMI usually comes from a small vessel

136
Q

anticoagulation therapy for NSTEMI

A

heparin

antiplatelets

137
Q

STEMI treatment

A

reperfusion

supportive measures similar to NSTEMI

138
Q

two methods for reperfusion in response to STEMI

A

percutaneous coronary intervention

thrombolytic therapy

139
Q

supportive measures for STEMI

A

aspirin

oxygen

decrease myocardial oxygen demand

control arrhytmia

140
Q

PCI vs thrombolysis

preference

when would thrombolysis be used

A

PCI is preferred

thrombolytics are indicated with PCI isn’t available and early treatment

early is key

141
Q

PCI

A

stent placement

142
Q

AMI prognosis factors

A

age

size of vessel

prior infarctions

nature of treatment

143
Q

T/F the risk of death within 90 days of AMI is 75%

A

false, 1-22%

144
Q

two main causes of MI mortality

A

cardiac arrhythmia (v fib)

pump failure (cardiogenic shock)

145
Q

when is cardiogenic shock the more common cause of MI mortality

A

in the case of large infarctions

146
Q

treatment of v fib

A

cardioversion (defibrilation)

147
Q

three treatments of cardiogenic shock

A

vasopressors (maintain pressure)

inotropic agents to improve contractility

mechanical assist deveices

148
Q

two types of mechanical assist devices used in cardiogenic shock

A

balloon pumps

LVADs

149
Q

preventing the recurrance of MI

A

lifestyle changes

beta blockers

statins

ACE inhibitors

antiplatelet drugs

150
Q

three faces of angina pectoris

A

stable

unstable

variant

151
Q

stable angina

A

recurring episodes of chest pain brought on by exertion and relieved by rest

152
Q

unstable angina

A

angina that occurs with minimal activty or at rest

153
Q

variant (prinzmetal) angina

A

extreme fatigue associated with minimal exertion related to coronary vasospasm

154
Q

pathophysiology of stable angina

A

unmet oxygen demand cuased by coronary atherosclerosis, anemia, fever, hyperthyroid

155
Q

typical anginal episode

A

lasts 2-15 minutes

substernal pain with radiation

intiated by lifting, eating, emotions, cold weather

156
Q

treatment of stable angina

A

acute treatment with vasodilation

decrease frequency of attacks

157
Q

how to decrease stable angina attacks

A

HTN control

lipid management

lifestyle modification

cononary revascularization

158
Q

three drugs used in the treatment of stable angina

A

nitrates

beta blockers

calcium channel blockers

159
Q

prognonsis for stable angina

A

some will improve, but most will develop CHF or have progress to acute cononary syndrome within 3-5 years

160
Q

chronic heart failure 9CHF) definition

A

ventricular function insufficent to meet the metabolic and blood flow demands

161
Q

why is the indicidence of CHF increasing

A

people who used to die from AMIs are now living with decreased heart function

162
Q

two types of CHF

A

CHF with reduced EF (systolic heart failure)

CHF with preserved heart failure (diastolic heart failure)

163
Q

ejection fraction

A

fraction of ventricular volume eject by each beat of the heart, normally 50-65%

164
Q

how is EF determined

A

echocardiogram

165
Q

visious cycle of CHF

A

chronic ischemia damages myocardium

remodeling occurs due to stretching leads to cardiomegaly

overstretched remodeled myocardium reduces ventricular function leads to fluid overload and high BP

leads to increased ischemia

166
Q

four factors to prevent CHF

A

lipid control

HTN treatment

lifestyle changes

prevent or reduce damage from AMI

167
Q

CHF symptoms

A

dyspnea, orthopnea, edema

168
Q

CHF signs

A

peripheral edema, JVD

169
Q

CHF signs on CXR

A

cardiomegaly, pulmonary edema

170
Q

CHF signs on echocardiogram

A

ventricular ejection fraction

171
Q

CHF lab signs

A

elevated BNP

172
Q

BNP

A

brain natriuretic peptide

173
Q

CHF EKG signs

A

left ventricular hypertrophy

174
Q

orthopnea

A

the inability to sleep supine without breathing issues

175
Q

CHF treatment strategy I

A

reduce cardiac work load (limit activity, reduce weight, control HTN)

reduce blood volume (decrease Na, diuretics)

176
Q

CHF treatment strategy II

A

reduct cardiac remodeling (aldosterone antagonists)

treat hyperlipidemia (statins, even if lipids are normal)

177
Q

two agents that improve survival with CHF

A

beta blockers

ACE inhibitors

178
Q

dyspnea as it relates to CHF

A

air hunger with minimal exertion

179
Q

what is the 5 year survival rate once diagnosed with CHF

A

50%

180
Q

who is usually victim of idiopathic cardiomyopathy

A

young and healthy people, generally with a precipitating even (viral infection, pregnancy)

181
Q

what is the treatment for idiopathic cardiomyopathy

A

spontaneous remission, but LVADs or transplant can be required

PAS 753 (Molecular Pathophysiology) (17 decks)

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