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Pharm Block 11 > Cardiovascular Pharmacology I > Flashcards

Cardiovascular Pharmacology I Flashcards

1
Q

What is considered high BP?

A

140/90
Either one of these can be high, doesn’t have to be both
-repeated high measurements

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2
Q

What causes hypertension

A
  • 10% of patients are the only ones that have a specific cause, and they are secondary to another disease, causing secondary HTN
  • 90% of patients we dont know the cause of it
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3
Q

How do we cure HTN in the people with secondary HTN (due to another disease/10%)

A

Treat the other disease

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4
Q

How do we treat primary HTN? (90% of patients, dont know what it causes)

A

HTN drugs

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5
Q

Patients that exhibit no specific causes of HTN are said to have

A

Primary or essential HTN

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6
Q

What is blood pressured maintained by

A

Arterioles
Postcapillary venules
Heart
Kidneys

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7
Q

How do the kidneys regulate BP

A

Regulating the intravascualr fluid

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8
Q

How do the arterioles, venules, heart, and kidney work to regular blood pressure?

A

Baroreflexes

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9
Q

What is cardiac performance influenced by

A
  • Parasympathetic innervation (vagus)

- sympathetic innervation

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10
Q

Heart rate is decreased by

A

Parasympathetic activity at the SA node

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11
Q

Heart rate is increased by

A

Sympathetic activity at the SA node

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12
Q

Is parasympathetic or sympathetic dominant on HR

A

Parasympathetic

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13
Q

Contractile force of heart is reduce by

A

Parasympathetic activity to atrial and ventricular muscles

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14
Q

Contractile force of the heart is increased by

A

Sympathetic activity to atrial and ventricular muscles

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15
Q

Vascular smooth muscle constricts when

A

In response to sympathetic stimulation

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16
Q

Parasympathetic and vascular smooth muscle

A

Doesn’t affected it much

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17
Q

Constriction of veins in vascular smooth muscle

A

Increases CO

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18
Q

Constriction of arteries in vascular smooth muscle

A

Reduces CO by increases after load

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19
Q

Sympathetic actions on the kidney

A

Renin release

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20
Q

Causes sodium and water retention (increased fluid volume, increased CO, increased BP)

A

Renin

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21
Q

Helps achieve minute to minute control of blood pressure

A

Baroreceptor reflex

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22
Q

How do the baroreceptors work

A

The nerve endings detect stretch due to arterial pressure, the reflex is to increase parasympathetic and decrease sympathetic (efferent via vagus)

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23
Q

If arterial pressure declines, what does the baroreceptor do

A

Causes an increase in sympathetic and a decrease in parasympathetic activation

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24
Q

What happens when changes in blood pressure persist beyond a few minutes?

A

Reflex autonomic responses diminish

  • this is called barorefelx adaptation
  • increased BP, increased HR in exercise instead of anticipated reflex bradycardia
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25
Q

What does the renin-angiotensin-aldosterone system (RAAS) do

A

Maintains BP

  • decreased BP: decreased renal blood flow:renin release which activates the RAAS to increase BP
  • sympathetic also causes renin release as well
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26
Q

What kind of receptors causes the release of renin

A

B1

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27
Q

What are the important target areas for controlling BP with drugs in the RAAS

A

Targeting B1 receptors and targeting the RAAS system

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28
Q

Decreased arterial pressure and the baroreceptor reflex

A

Increases sympathetic nervous system activity

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29
Q

Increased sympathetic nervous system on the heart

A
  • Increased force and rate of contraction=increased CO

- renin release: renal retention of Na and water (increased blood volume)

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30
Q

What does ADH do

A

Decreases arterial pressure causes a baroreflex-mediated release of this.
-acts on the renal collecting duct to enhance water retention

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31
Q

What areas do we target to decreased blood pressure with drugs?

A

Blood vessels
Heart
Kidney
Some brain

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32
Q

First line treatment for HTN

A

Thiazides
ACEI
CCB

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33
Q

Of the first line medications (thiazides, ACEI, and CCBs), which one is more effective

A

They are all equally effective

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34
Q

Patients requiring combination therapy, the most popular choice is

A

ACEI with a long lasting CCB

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35
Q

Of the first line HTN drugs, which one is most often given because it is cheap

A

Thiazides

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36
Q

Which do you use first, ACEI or ARB?

A

ACEI

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37
Q

What drugs do you want to use or combination therapy?

A

Pick a combination of 2 of the first line drugs

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38
Q

Long term benefit of diuretics

A

Hyperpolarization, decrease vascular effect, decreased BP

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39
Q

MOA of diuretics

A

Reduce fluid volume, reusults in water and electrolyte excretion, which decreases CO

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40
Q

What happens after several days of treatment with diuretics

A

Urinary excretion returns to normal, and later CO and blood volume return to pretreatment values, but blood pressure remains reduced

  • decreased vascular reactivity to NE and decreased structural vascular resistance
  • decreases vascular activity
  • hyperpolarization of smooth muscle, basically in vessels, maybe due to decreased Na
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41
Q

Why is that after taking a diuretic for a few days, urine excretion and blood volume return to pretreatment levels, but BP stays low?

A

Hyperpolarization: decreased vascular effect, decreased BP

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42
Q

Therapeutic use of thiazides (diuretics)

A

HTN, particularly in black or elderly patients

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43
Q

Adverse effects of thiazides (diuretic)

A

Potassium depletion which could affect:

  • chronic arrhythmia
  • acute MI
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44
Q

Are thiazides potassium wasting or sparing

A

Wasting

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45
Q

What are the 2 most common thiazides (diuretics)

A 
Chlorthalidone
Hydrochlorothiazide (HCTZ)
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46
Q

What do calcium channel blockers work on

A

Heart and blood vessels

  • Slow conduction=decreased CO=decreased BP
  • thiazides on BV=vasodilation=decreased TPR=decreased BP
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47
Q

What kind of calcium channel do calcium channel blockers work on

A

L-type in heart and BV

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48
Q

Therapeutic use for calcium channel blockers (CCB)

A

HTN

-works well in co-morbid conditions. Popular in patients with multiple conditions

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49
Q

Adverse effects to CCBs

A
  • Consitpation (block Gi tract Ca2+ channels)

- gingival hyperplasia (red, bleeding gums)

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50
Q

What HTN medication can cause red, bleeding gums?

A

CCBs (dipines)

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51
Q

What is a common name for CCBs

A

“-dipine”

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52
Q

What are the two CCBs for cardiac calcium channels

A

Verapamil and diltiazem

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53
Q

What drug works on vascular calcium channels

A

Amlodipine

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54
Q

Which CCB is most cardiodepressant

A

Verapamil

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55
Q

Which CCBs is good vasodilator

A

Dipines (amlodipine)

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56
Q

Which CCBs most likely to cause reflex tachycardia?

A

Dipines

  • decreased BP=reflex tachy
  • verapamil works directly on the heart, so it doesn’t have that reflex
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57
Q

Which CCB works on the heart and on the vacualtrue

A

Diltiazem

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58
Q

Which CCB consistently slows heart rate and vasodilates?

A

Diltiazem

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59
Q

MOA of ACEI

A

Block the enzyme ACE

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60
Q

What does the enzyme ACE do

A
  • Converts angiotensin I to angiotensin II

- acts on bradykinin to make it inactive

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61
Q

What does angiotensin II do

A
  • Causes vasoconstriction, increases peripheral vascular resistance, which increases BP
  • also causes release of aldosterone, which increases Na and water retention, which increases BP
62
Q

What receptor does angiotensin II bind to

A

AT-1

63
Q

ACEI effect on bradykinin

A

Causes increased levels of bradykinin, this promotes vasodilation, which decreases blood pressure.

64
Q

Bradykinin in the presence of ACE enzyme

A

ACE inactivates bradykinin, but bradykinin’s actions are to vasodilation, decrease peripheral vascular resistance,and decrease BP

65
Q

What does Renin do

A

It’s an enzyme that converts angiotensinogen into angiotensin I

66
Q

What does aliskiren work on

A

It is a renin inhibtor

67
Q

What substance accumulates when you take aliskiren?

A

Angiotensinogen

68
Q

The production of what is immediately inhibited when taking aliskiren

A

Angiotensin I

69
Q

What does ACEI prevent

A

The conversion of angiotensin I to angiotensin II

70
Q

What receptor does angiotensin II bind

A

AT-1

-vasocontricts

71
Q

Where are AT-1 receptors found

A

Blood vessels and adrenal cortex

72
Q

What kind of G protein coupled receptor is AT-1 receptor

A

Go

73
Q

What does aldosterone do

A

Increases water and Na retention, which increases BP

74
Q

What does ARB2 do

A

Blocks AT-1 receptors

75
Q

Which drug that targets the RAAS system does not affect Bradykinin?

A

ARB2

-works on lower part of the pathway

76
Q

Which drug that works on the RAAS will not cause a cough as a side effect

A

ARB2 because it does not work on Bradykinin

77
Q

If a patient is on an ACEI and complains of a cough, what is something that can be done

A

Switch to ARB2

-we don’t initially start people on these because they are more expensive

78
Q

No matter what drug you use to target the RAAS pathway and no matter what part of the pathway is being targeted, the same things happen:

A

Same net effect

  • deceased aldosterone
  • decrease vasoconstriction
  • decrease Na and water retention
  • decreased BP
79
Q

What does the RAAS pathway normally do?

A

Increases BP

80
Q

Is bradykinin a vasodilator or vasoconstrictor

A

Vasodilator

81
Q

What does ACE do it bradykinin and why do we want to stop it

A

ACE inactivates Bradykinin
-ACE inhibitor will allow more bradykinin to be active, and since bradykinin is a vasodilator, it will decrease BP on its own

82
Q

Therapeutic use for ACEI

A
  • HTN in young, white patients
  • CHF given 24 hours after MI
  • diabetic nephropathy (delay renal disease)
83
Q

What drug can you give to a diabetic to help with diabetic nephroapthy?

A

ACEI

84
Q

Adverse effects of ACEI

A

Dry cough in 30% of patients
-most people can live with it, they dont discontinue
-mediated by bradykinin
Angioedema
Teratogenic
Acute renal failure in bilateral renal artery stenosis

85
Q

What is the most common side effect of ACEI

A

Dry cough

86
Q

What is the most severe side effect of ACEI

A

Angioedema

87
Q

What is the one exception to giving ACEI to someone for renal problems

A

Normal its good for renal problems such as diabetic nephropathy, but in the case of bilateral renal artery stenosis, it could cause renal failure

88
Q

What are the names of ACEI

A

End in “pril”
Captopril
Lisinopril

89
Q

What does angiotensin II do at the level of the glomerulus

A

Constricts the efferent arterioles

90
Q

What do prostaglandins do at the level of the glomerulus

A

Dilated the afferent arterioles

91
Q

How does ACEI help diabetics

A
  • saves kidneys
  • stops production of Ang II, efferent side dilates, decreases filtration, decreases GFR, reducing work of kidneys, will decreased amount of protein in urine
92
Q

Why is ACEI bad in someone with bilateral renal stenosis

A
  • pt already has low GFR
  • kidneys are already struggling
  • very low GFR can cause renal failure
93
Q

MOA of ARBs

A

Inhibit angiotensin type I receptor (AT-1)

-blocks actions of angiotensin II, but does not affect bradykinin metabolism

94
Q

Use of ARBs

A

HTN, CHF, diabetic nephropathy

95
Q

Adverse effects of ARBs

A

Better than ACEI, teratogenic, acute renal failure in those with bilateral renal stenosis

96
Q

ARB drugs

A

“Artan”

Losartan

97
Q

Patients age 18 and older regardless of race with chronic kidney disease and HTN should receive _______ to improve kidney outcomes

A

ACEI or ARB

-check GFR first to make sure its not too low though

98
Q

What is the name of the renin inhibitor

A

Aliskiren

99
Q

MOA of aliskiren

A

Direct renin inhibitor preventing the conversion of angiotensinogen to angiotensin I

100
Q

Therapeutic use of aliskiren

A

HTN as a single agent or in combination

101
Q

Adverse affects of aliskiren

A

Teratogenic

-very slight chance of angioedema and slight cough, but you would suspect ACEI before this as the culprit)

102
Q

How do B blockers work for HTN

A
  • B1 activation of adrenoreceptors on heart=decreased CO
  • decreases renin, which decreases angiotensin II, which decreases aldosterone, which decreases dosing and water retention, which decreases blood volume

These all decrease BP

103
Q

Therapeutic use of B1 blockers

A

HTN but not first line unless patient has comorbid condition.

104
Q

Who benefits greater from B blockers

A

Younger white patients.

105
Q

Why are B1 blockers not the best choice for elderly or black patients

A

They have low-renin HTN

-use CCB or thiazides

106
Q

General rule for B blockers and cardiac conditions

A

Use B1 selective drugs for cardiac conditions

107
Q

Adverse effects of B blockers

A

Nonspecific B clockers can block B2 receptors in the lungs (bronchoconstriction) and disrupt glucose control
-contraindicated in asthmatics and diabetics

108
Q

When are B blockers contraindicated

A

In asthmatics and diabetics

109
Q

What drugs are B blockers

A

Atenolol and metoprolol

B1 selective

110
Q

MOA of alpha 1 blockers

A

Block a1 receptors in a arterioles and venules

111
Q

Therapeutic use of alpha 1 blockers

A

HTN, benign prostatic hyperplasia

112
Q

Adverse effects of alpha 1 blockers

A

Postural hypotension, dizziness

113
Q

What drug is an alpha 1 blocker

A

Prazosin

114
Q

What drug do we use for HTN and BPH?

A

Prazosin

115
Q

What drugs for HTN work in the CNS

A

Central A2 agonists

116
Q

MOA of central A2 agonists

A

Act on a2 receptors to reduce sympathetic outflow

117
Q

What is the reason that central a2 agonists are not first line, even though they are very powerful

A

Because they work in the CNS and can cause fatigue

118
Q

Therapeutic use of central a2 agonist

A

Drug of choice for HTN during pregnancy

119
Q

What is the drug of choice for HTN during pregnancy

A

Methyldopa, a central a2 agonists

120
Q

What is the only HTN drug that is safe during pregnancy

A

Methyldopa, a central a2 agonist prodrug

121
Q

Adverse effects of methyldopa (central a2 agonist)

A
  • Sedation
  • Sudden discontinued use causes rebound HTN which may be severe
  • hemolytic anemia if positive Coombs test
122
Q

What test tells you if you are likely to be at risk for hemolytic anemia

A

Positive Coombs test

123
Q

Multiple action drugs

A

Labetolol
Carvedilol
Nebivolol

124
Q

How are labetolol and carvedilol multiple action drugs

A

Block a1, b1, and b2 receptors

-decrease BP

125
Q

How is nebivolol a multiple action drug

A

Blocks B1 and vasodilates via nitric oxide release, lower BP

Even though it starts with N and ends in olol, it is not a nonspecific B blocker. Works on B1 and uses NO

126
Q

Therapeutic use for multiple action drugs

A

HTN

127
Q

This occurs when HTN is severe enough to cause end-organ damage

A

HTN emergencies

128
Q

What drug is used as IV therapy for HTN emergencies

A

Labetolol

129
Q

Stage 1 HTN gets what kind of drugs

A

Single drug

130
Q

Stage 2 HTN gets what kind of drugs

A

Combo drugs

131
Q

Highly lethal condition with pulmonary congestion and and peripheral edema

A

Congestive heart failure

132
Q

Left heart failure

A

Pulmonary congestion

133
Q

Right heart failure

A

Peripheral edema

134
Q

What are the first targets you want to hit to treat CHF

A

BV and kidney

135
Q

What all happens in CHF

A
  • decreased contractility;
  • cardiac failure;
  • increased symp activity (compensation), which leads to increased arterial constriction (afterload), increased blood volume, increased preload, and increased HR
136
Q

What is the main thing causing the heart to fail in CHF

A

Decreased contractility

137
Q

What does the compensatory increased sympathetic firing in CHF affect?

A

Too much of a good thing

  • increased HR
  • constricts arterioles (increased afterload)
  • increased blood volume
138
Q

How can we fix the increased HR in CHF?

A

Low dose B blocker

139
Q

How do we fix the constricted arterioles and the increased afterload

A

We want to dilate the arterioles and decrease afterload

140
Q

How do we fix the increased blood volume in CHF

A

Decrease preload with diuretics or ACEI

-or can decrease preload with venodilators

141
Q

What is the compensation for the cardiac failure in CHF

A

Increases sympathetic activity

142
Q

What dose of B blocker is essential when treating CHF and getting the HR to lower

A

Low dose. If you give high dose, you could make the CHF worse

143
Q

What is cardiac remodeling

A

Excess fibrosis after cardiac failure (CHF) causing a decrease in function from over stimulating the heart

144
Q

What are the causes of cardiac remodeling?

A
  1. Aldosterone
    - 20x the normal level
    - heart has receptors for aldosterone so we need to target them
  2. NE and epi
    - too much sympathetic compensation
145
Q

What drugs do we used to treat cardiac remodeling

A

ACEI and ARBs for the aldosterone levels and B blockers to stop the epi and NE

146
Q

What is the number one benefit of ACEI and ARBs in CHF

A

Decreased cardiac remodeling

147
Q

If you inhibit remodeling, what do you do to survivial

A

Increase it

148
Q

If you increase survival, what do you do to remodeling

A

Inhibitit

149
Q

What is the main thing you want to do to stop remodeling

A

Stop aldosterone!

150
Q

Myocardial hypertrophy in CHF

A

Left ventricle gets large, leads to cardiac remodeling

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