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Cardio > HTN > Flashcards

HTN Flashcards

1
Q

Changes in heart rate by an increase in the firing of the SA node

A

chronotropy

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2
Q

Pacemaker cells are influenced by the ___________

A

autonomic nervous system

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3
Q

Affects permeability of K+, Na+, and Ca2+

A

pacemaker cells

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4
Q

______________ increases heart rate (positive chronotropy)

A

sympathetic nervous system

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5
Q

______________ decreases heart rate (negative chronotropy)

A

parasympathetic nervous system

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6
Q

Changes in the conduction velocity in the pacemaker cells at the AV node resulting in an altered interval

A

dromotropy

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7
Q

Force of contraction

A

inotropy

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8
Q

Inotropy is influenced by __________

A
  • preload
  • afterload
  • free cytosolic Ca2+
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9
Q

Inotropy is commonly influenced by the ________

A

sympathetic nervous system (norepinephrine)

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10
Q

This is the end diastolic volume related to right atrial pressure

A

preload

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11
Q

An (increase/decrease) in end diastolic volume (increases/decreases) contractility

A

increase, increase

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12
Q

An increase in venous return will _________

A
  • increase prelaod
  • stretches the sarcomere
  • increases contractility
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13
Q

This is the arterial pressure that must be overcome by the ventricle

A

afterload

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14
Q

(Increase/decrease) in work load can worsen ______

A

increase, ischemia

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15
Q

Responsible for transitioning blood from a pulsatile flow into a smooth, continuous flow

A

arteries

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16
Q

________ of arteries allows greater pressure control

A

elasticity

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17
Q

During systole, arteries _______ and store some of the stroke volume (1/3 of the time in healthy arteries)

A

expand

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18
Q

What is the greatest pressure exerted on the arteries?

A

systolic blood pressure

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19
Q

During diastole, arteries ________ and create a smooth blood flow (2/3 of the time in healthy arteries)

A

recoil

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20
Q

What is the lowest arterial blood pressure?

A

diastolic blood pressure

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21
Q

DBP is largely affected by the _____________

A

elasticity of the arteries

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22
Q

Wide pulse pressure indicates (increased/decreased) elasticity or (increased/decreased) stiffness

A

decreased, increased

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23
Q

Average blood pressure over time; typically set at 100 mmHg

A

mean arterial pressure (MAP)

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24
Q

What is the formula for MAP?

A

MAP=2/3(DPB) + 1/3(SBP)

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25
Q

Name the catecholamines

A
  • norepinephrine (NE)
  • dopamine (DA)
  • epinephrine (EPI)
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26
Q

Which catecholamine is of main importance in HTN?

A

norepinephrine

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27
Q

Name the adrenergic receptors

A
  • alpha 1 adrenoreceptor
  • alpha 2 adrenoreceptor
  • beta 1 adrenoreceptor
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28
Q

Which adrenergic receptor is located on the post synaptic cell of smooth muscle tissue and the heart?

A

alpha 1

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29
Q

Which adrenergic receptor regulates smooth muscle contraction (vascular tone) and myocardial inotropy (force)?

A

alpha 1

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30
Q

In alpha 1 adrenreceptors, NE causes __________

A

vasoconstriction in smooth muscle and increased contractility in the heart

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31
Q

Which adrenergic receptor is located on presynaptic cells and regulates NE?

A

alpha 2

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32
Q

Activation of alpha 2 (increases/decreases) NE release?

A

decreases

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33
Q

Which adrenergic receptor is located in the heart, kidney, and adipose tissue?

A

beta 1

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34
Q

Activation of beta 1 causes _____________

A

increases in HR and force of contraction, stimulates lipolysis in fat cells, and stimulates renin activity from the kidney

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35
Q

What is the rate limiting step in the RAAS?

A

production of renin

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36
Q

What is the function of renin?

A

angiotensinogen to angiotensin I

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37
Q

What is the function of angiotensin converting enzyme (ACE)?

A

converts angiotensin I to angiotensin II

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38
Q

What cleaves peptides such as bradykinin, LH releasing hormone, and substance P?

A

ACE

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39
Q

What receptors does Ang II have?

A

AT1 receptor and AT2 receptor

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40
Q

Which receptor increases vasoconstriction, aldosterone secretion, sodium reabsorption, and release of ADH?

A

AT1 receptor

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41
Q

Which receptor stimulates formation of superoxide?

A

AT1

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42
Q

What is the function of superoxide?

A

deactivates NO

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43
Q

What is the function of NO?

A

causes vasodilation

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44
Q

What is the function of the AT2 receptor?

A

antagonizes the effects of AT1 (causes vasodilation and natiuresis)

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45
Q

Why is HTN more prevalent in AAs?

A

they have tissues that can produce Ang II independent of the RAAS

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46
Q

What does Ang II do?

A

increases BP

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47
Q

Tissue Ang II contributes to __________

A

blood pressure, inflammation, fibrosis, and remodeling

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48
Q

What is the function of the ANS?

A

monitors and regulates HR, blood flow, and BP

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49
Q

What is the function of the medulla?

A

maintains SNS activity using information from baroreceptors and chemoreceptors

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50
Q

What is the function of the hypothalamus?

A

regulates BP using neurohormonal feedback

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51
Q

What is the function of cortical/subcortical areas?

A

effect CV function based on emotion and stress

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52
Q

Name the arterial baroreceptors

A
  • stretch receptors

- mechanoreceptors or “high pressure” receptors

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53
Q

Where are the arterial baroreceptors located?

A
  • aortic arch
  • carotid bifurcation
  • kidney
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54
Q

What does the baroreceptor reflex do?

A

decreases in MAP result in result in decreased stretch in arteries and decreased baroreceptor stimulation

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55
Q

What is the result from decreased baroreceptor stimulation?

A

decreased nerve signals to the medulla oblongata

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56
Q

What is the result of decreased nerve signals to the medulla due to decreased baroreceptor stimulation?

A

decrease in parasympathetic outflow and an increase in sympathetic outflow

57
Q

What is the function of postganglionic nerve fibers from the baroreceptor reflex?

A

innervate the heart and blood vessels to release NE

58
Q

What are the “low pressure” receptors?

A

cardiopulmonary receptors

59
Q

Where are cardiopulmonary receptors located?

A
  • cardiac atria
  • ventricles
  • lungs
60
Q

What is essential HTN known as and what percentage of people does it effect?

A

primary HTN; 95%

61
Q

What is the cause of essential HTN?

A

it is idiopathic or unknown

62
Q

What is the cause of secondary HTN and what percentage of people does it effect?

A

related to a specific, known cause; 5%

63
Q

What are some disease states that are related to HTN?

A

CKD, obstructive sleep apnea (OSA), aldosteronism, renal artery stenosis, thyroid disease, and pheochromocytoma

64
Q

What are some common medications related to HTN?

A

amphetamines, corticosteroids, decongestants, estrogen, NSAIDs

65
Q

What are some other factors that lead to HTN?

A

nicotine, cocaine, sodium, low potassium diet, and increase BP

66
Q

What is the predominant form of HTN in adolescents and young adults?

A

isolated systolic HTN (ISH)

67
Q

What is the cause of ISH?

A

increased stroke volume

68
Q

ISH increases again in PTs >50 years of age due to ___________

A

vascular stiffness

69
Q

What is the reasoning behind increased ISH in PTs over 50 yo?

A

rise in SBP, decrease in DBP, thus a rise PP

70
Q

What is the predominant form of HTN in those aged 30-50?

A

diastolic HTN

71
Q

What causes diastolic HTN?

A

increased vascular resistance (decreased elastin, increased collagen and calcium deposits in arteries)

72
Q

What is a major predictor of IHD before age 50?

A

diastolic HTN

73
Q

(Central/Peripheral) obesity is more closely associated with HTN than (central/peripheral) obesity

A

Central; peripheral

74
Q

What is the function of insulin?

A

increases sodium and water retention, increases adrenergic activity, and causes smooth muscle hypertrophy

75
Q

What happens with insulin resistance?

A

diminishes insulin-mediated vasorelaxation

76
Q

What do obese patients have that largely distributes centrally?

A

higher total body volume

77
Q

What does increases fluid volume cause?

A

increased ventricular filling and cardiac output

78
Q

Sympathetic activity in the kidneys is likely related to ___________

A

elevated leptin levels

79
Q

Where is leptin produces and what is its function?

A

located in adipose tissue and regulates food intake

80
Q

What does leptin do that causes an elevated BP?

A

increases sympathetic outflow

81
Q

What is the effect of chronic infusion of leptin?

A

decreases natiuresis and NO production

82
Q

BMI is correlated with ___________

A

increased plasma angiotensinogen, renin activity, ACE concentration and aldosterone

83
Q

What initiates/maintains the low-grade inflammation present in HTN?

A

inflammatory cytokines released from adipose tissue

84
Q

What is a common cause of resistant HTN?

A

sleep apnea

85
Q

What triggers an increase in sympathetic activity?

A

decreased oxygenation due to apnea

86
Q

What is present during sleep and wakeful periods?

A

increased sympathetic activity

87
Q

What aspects of the RAAS are associated with OSA?

A

elevated ang II and aldosterone

88
Q

What impairs endothelin function?

A

hypoxia (endothelin increases, NO decreases)

89
Q

What kind of vascular remodeling is associated with OSA?

A

OSA leads to increased carotid intima-media thickness and arterial stiffness

90
Q

True of false: most patients are asymptomatic when it comes to HTN?

A

true

91
Q

What type of organ damage can occur with the heart with HTN?

A
  • left ventricular hypertrophy and diastolic dysfunction
  • chronic HF
  • vascular remodeling and microvascular changes
  • oxidative stress
  • endothelial dysfunction
92
Q

What type of organ damage can occur with the brain in HTN?

A
  • stroke/TIA
  • hypertensive encephalopathy
  • cognitive impairment and dementia
93
Q

What type of organ damage can occur with the kidney in HTN?

A
  • nephrosclerosis

- CKD

94
Q

True or false? Diagnosis of HTN requires 3 or more separate readings

A

False; 2 readings

95
Q

What is resistant HTN?

A

inability to achieve BP goals with 3 or more antihypertensive agents including a diuretic

96
Q

What should a patient do with their diet if they are hypertensive?

A
  • salt reduction
  • increase potassium
  • increase fresh fruits and veggies
97
Q

Where do thiazides bind?

A

bind to receptors on the luminal side of the DCT

98
Q

What is the function of thiazides?

A

compete for the Cl binding site and thus inhibit the Na, Cl symporter causing increased secretion of Na, Cl, H2O, and K

99
Q

What is the starting/max dose for thiazides and when should they be taken?

A

12.5-25 mg/day in pm/HS

100
Q

What can decrease the efficacy of thiazides?

A

CrCl

101
Q

Where do the loop diuretics bind?

A

bind receptors on the luminal side of the thick ascending limb of the loop of Henle

102
Q

What is the function of the loops?

A

compete for the Cl binding site of the Na, K, 2Cl symporter causing increased excretion of Na, Cl, H20, K, Ca, and Mg

103
Q

What is the function of Na channel blockers (amiloride, triamterene)?

A

block Na channels in the late distal tubule and collecting duct; rarely used for HTN alone

104
Q

Where do the aldosterone inhibitors (spironolactone, eplerenone) bind?

A

bind the mineralocorticoid receptor in the late distal tubule and collecting duct

105
Q

What is the effect of the aldosterone inhibitors?

A

blockade of Na movement from luminal to interstitial space through Na channels and pumps

106
Q

When should aldosterone antagonists be used?

A

they are rarely used unless other comorbidities exist such as HF, alcohol liver disease, post-MI, refractory HTN
-can be useful in resistant HTN

107
Q

Which medication can cause gynecomastia?

A

spironolactone

108
Q

What is the MOA of ACE inhibitors?

A
  • inhibits conversion of ang I to ang II

- inhibits conversion of active bradykinin to inactive bradykinin

109
Q

What is the function of active bradykinin and what is its result?

A

stimulates NO and prostaglandin release; result is vasodilation and Na excretion

110
Q

Which class of drugs is most useful for renal protection in patients with DM by decreasing glomerular filtration pressures?

A

ACE-Is

111
Q

ACE-Is are less effective in _______ due to lower renin release

A

african americans

112
Q

What are some side effects associated with the ACE-Is?

A
  • cough due to bradykinin build up in lungs
  • hyperkalemia
  • acute renal failure
  • hypotension
  • angioedema (more common in AAs)
113
Q

What is the MOA for ARBs?

A

inhibits the effects of ang II at its various sites of action

  • decrease SVR
  • increase Na and H20 excretion
114
Q

What is the MOA for direct renin inhibitors?

A

inhibits the conversion of angiotensinogen to ang I via direct renin inhibition

  • decrease SVR
  • increase Na and H20 excretion
115
Q

What class of drug is contraindicated with ACE-I or ARB?

A

direct renin inhibitor

116
Q

What is the MOA for CCBs?

A

blocks transmembrane influx of calcium into smooth muscle (heart and vascular muscles)

117
Q

Which type of CCB is more selective for vascular smooth muscle?

A

dihydropyridine (amlodipine/felodipine)

118
Q

Which type of CCB is more likely to have a depressant effect on the heart and can lead to leaky vasculature which will lead to edema?

A

non-dihydropyridine (verapamil/diltiazem)

119
Q

Which CCB should not be used in heart failure or in conjunction with BBs?

A

non-dihydropyridine

120
Q

What is the MOA of beta blockers?

A
  • decrease NE binding at beta 1 receptors resulting in decreased HR and CO
  • decrease renin release due to beta 1 blockade in kidneys
121
Q

In which type of patient should a beta 1 selective BB such as metoprolol be used in?

A

patient with asthma/COPD due to potential for beta 2 blockade

122
Q

What is the MOA for the alpha 2 agonist (clonidine)?

A
  • centrally acting

- decreases CO by decreasing HR and SVR through decreased sympathetic activity

123
Q

What is the MOA for alpha 1 antagonists (doxazosin/terazosin)?

A

block postsynaptic alpha 1 receptors resulting in vasodilation and decreases SVR
-located postsynaptically in the vasculature

124
Q

Which class of drug can be used to treat BPH in men?

A

alpha 1 antagonists

125
Q

Which class of drug can be used to help with PTSD?

A

alpha 1 antagonists

126
Q

What is the MOA for methyldopa?

A

centrally acting agent that decreases SVR as well as HR and CO to some extent

127
Q

Which drug is preferred for HTN during pregnancy?

A

methyldopa

128
Q

Which drug(s) is a direct arteriolar vasodilator?

A
  • hydralazine

- minoxidil

129
Q

Which drug is used more commonly in HR and hypertensive crisis?

A

hydralazine

130
Q

Is minoxidil or hydralazine more potent of the arteriolar vasodilators?

A

minoxidil

131
Q

Which arteriolar vasodilator stimulates hair growth?

A

minoxidil

132
Q

What is the MOA of reserpine?

A

depletes central and peripheral stores of NE, DA, and 5-HT. BP lowering is accomplished through decreased sympathetic activity

133
Q

Which drug frequently causes sedation, mental depression, and parkinsonian symptoms?

A

reserpine

134
Q

HOPE

A

ramipril reduced incidence of CV events and death in high risk patients including patients with diabetes and prior stroke

135
Q

ALLHAT

A

Patients either give chlorthalidone, amlodipine, or lisinopril. Primary outcome is combined fatal CHD or non-fatal MI

136
Q

ONTARGET

A

telmisartan and ramipril have similar outcomes with regard to renal protection; combination therapy is not warranted although it may decrease albuminuria

137
Q

RENAAL

A

ARBs are effective for treating patients with type 2 DM and nephropathy though they have not been shown to reduce mortality

138
Q

PROGRESS

A

ACE-I with a diuretic for secondary stroke prevention

139
Q

When should aspirin be administered to a patient with DM?

A

should only be initiated when BP is controlled due to increased risk of hemorrhagic stroke

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