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Advanced Pharmacology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Epinephrine MOA (3)

A

alpha - vasoconstriction

beta 1 - positive inotrope & chronotrope

beta 2 - dilates skeletal muscles and bronchioles

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2
Q

Tyramine

A

Precusor

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3
Q

Norepinephrine MOA (2)

A

alpha - vasoconstriction, increase BP

beta 1-vagal reflex overcomes chronotropic effects

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4
Q

Isoproterenol MOA

A

Beta 1 agonist, beta 2 agonist

Increase CO, Increase HR, Decrease MAP

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5
Q

Dopamine MOA (2)

A

D1 receptors-dilates kidney vessels

(mimics epinephrine at higher doses)

Beta 1-increase HR, increase CO

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6
Q

Dobutamine MOA & Use

A

Beta 1-increase HR, increase BP

CARDIAC SHOCK
ACH

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7
Q

Neo-synephrine (phenylephrine) MOA

A

alpha ONLY

Increase BP, vasoconstriction, NO HR EFFECTS

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8
Q

Neo-synephrine (phenylephrine) Use (2)

A

Nasal Decongestant
Tetralogy of Fallot

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9
Q

Midodrine

A

alpha 1-Increases BP

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10
Q

Ephedrine

A

releases stored catecholamines

nasal decongestant

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11
Q

Amphetamines

A

mimic SNS effects

crosses BBB

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12
Q

Cocaine MOA

A

indirect, mimics amphetamines

crosses BBB

Inhibits dopamine reuptake –> addiction

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13
Q

Clonidine MOA

A

alpha 2 adrenergic agonist

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14
Q

Clonidine Side Effects

A

Sedation

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15
Q

What is clonidine used for?

A

Treats HTN

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16
Q

Dexmedetomidine MOA

A

alpha 2 adrenergic agonist - sedation

-blocks NE release

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17
Q

Monoamine Oxidase Inhibitors (MAOI) MOA

A

Inhibits reuptake of NE

Increases BP

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18
Q

Monoamine Oxidase Inhibitors (MAOI) Interactions

A

FOODS WITH TYRAMINE INCREASE BP WITH MAOI’S

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19
Q

What medication should you choose for HTN

A

alpha agonists (NE, neo)

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20
Q

What medication should you choose for cardiac shock and why?

A

Beta 1, dobutamine

No vasoconstriction peripherally

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21
Q

What medication should you choose for heart block and why?

A

Epinephrine or Isoproterenol

Vasodilates cardiac arteries

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22
Q

What medication should you choose for asthma

A

Beta 2
Albuterol

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23
Q

Afferent

A

Going towards CNS, brings info in

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24
Q

Somatic Nervous System

A

CONSCIOUS control, no ganglion

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25
Q

Autonomic Nervous System

A

UNCONSCIOUS control –> smooth muscle, cardiac muscle, glands

(SNS & PNS)

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26
Q

Axons (preganglionic)

A

(first) neuron, lightly myelinated axon

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27
Q

Axons (ganglionic)

A

(second) neuron, extends to an effector organ

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28
Q

SNS

A

Ergotropic - thoracolumbar

Fight or flight

Short preganglion, Long Post ganglioin

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29
Q

PNS

A

Trophotropic - craniosacral

Rest and digest

Long preganglion, short post ganglion

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30
Q

Inotropic

A

Change of force of contraction

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31
Q

Chronotropic

A

Change in rate

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32
Q

What are reversible Alpha Antagonists (4)

A

Phentolamine, tolazoline, prazosin, labetalol

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33
Q

Name an Irreversible Alpha Antagonist and WHY is it irreversible?

A

COVALENT BONDED
Phenoxybenzamine

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34
Q

Phentolamine MOA

A

Competitive alpha 1 and alpha 2 antagonist

decrease BP through blockage of alpha 1

Blocks alpha 2 –> increase NE release in synapse –> reflex tachy

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35
Q

What is Phentolamine used for?

A

Treats HTN, Erectile Dysfunction

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36
Q

Phentolamine Side Effects

A

Nausea, Vomiting, Diarrhea, Priapism

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37
Q

Phenoxybenzamine MOA

A

MOA: inhibits NE reuptake –> reflex tachycardia

Somewhat selective for alpha 1

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38
Q

What is Phenoxybenzamine used to treat?

A

Pheochromocytoma

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39
Q

Prazosin MOA

A

MOA: relaxes arterial & venous smooth muscle

Alpha 1 antagonist selective

Low Alpha 2 affinity (NO stimulation of NE)

Less cardiac effect

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40
Q

What is Prazosin used for?

A

HTN & BPH

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41
Q

What are 4 Alpha-1 antagonist selective drugs and what are they used to treat?

A

Terazosin
Doxazosin
Alfozosin
Tamsulosin

BPH

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42
Q

What are 2 Alpha-2 antagonist selective drugs?

A

Yohimbine & Ergotamine

NO CLINICAL USE

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43
Q

Propranolol MOA

A

B1 and B2 antagonist selective (beta blockers)

Decrease force & rate

Increase airway tone

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44
Q

Propranolol has a _____ first pass metabolism

A

HIGH

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45
Q

Propranolol Adverse Effects

A

Bradycardia, rash, fever, sedation, depression, worsening asthma

D/C use gradually

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46
Q

What is Propranolol’s effect on kidneys

A

Inhibits renin production

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47
Q

Atenolol & Metoprolol MOA, good for patients with what disease?

A

Beta 1 Antagonist

No airway effects

Safer in COPD patients

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48
Q

What is the MOST selective beta 1 antagonist?

A

Nebivolol

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49
Q

Nadalol MOA

A

Beta 1 & Beta 2 antagonist

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50
Q

Pindolol, Acebutalol, Carteolol, Penbutolol Use

A

Treats HTN & angina

Less likely to cause bradycardia

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51
Q

Labetalol MOA

A

MOA: Decrease HR & Contractility

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52
Q

Labetalol is a ______ mixture and has ___ different isomers

A

Racemic, 4

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53
Q

What are the different isomers of Labetalol? Which forms are inactive?

A

Racemic Mixture (3 isomers due to 2 areas of asymmetry)

  1. S,S (INACTIVE)
  2. R,S (INACTIVE)

3.S,R –> POTENT ALPHA BLOCKER

  1. R,R –> POTENT BETA BLOCKER
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54
Q

Which isomer of labetalol is a potent ALPHA blocker?

A

(S,R)-Labetalol

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55
Q

Which form of labetalol is a potent BETA blocker?

A

(R,R)-Labetalol

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56
Q

Esmolol MOA

A

MOA: Beta 1 antagonist selective

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57
Q

What is Esmolol used to treat?

A

Intraoperative tachycardia and supraventricular arrhythmias

Steady state infusion

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58
Q

What is Esmolol’s half-life?

A

about 10 minutes

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59
Q

When should you use Beta Blockers (5)

A

HTN (alone or with diuretic)

Ischemic Heart Disease

Cardiac Arrhythmias

Obstructive cardiomyopathy

Dissecting aortic aneurysm

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60
Q

Beta 1 drugs primarily work on the _____

A

Heart

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61
Q

Beta 2 drugs primarily work on the _____

A

Lungs

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62
Q

What is Cardiac Output Formula

A

CO = HR X SV

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63
Q

How do you calculate MAP

A

Diastolic + (1/3) X (Systolic - Diastolic)

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64
Q

What is ESV

A

End Systolic Volume

The lowest volume of blood in a ventricle at end of systole

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65
Q

What is EDV

A

End Diastolic Volume

The amount of blood in a ventricle at end of filling at diastole

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66
Q

What 3 things affect peripheral vascular resistance

A

Diameter
Viscosity
Length

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67
Q

What area of the brain is responsible for alpha-2 agonist

A

Vasomotor Cortex
(causes vasodilation)

can stimulate BOTH PNS & CNS

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68
Q

Name the 4 drug classes that treat HTN

A
  1. Diuretics
  2. Sympathoplegics
  3. Direct vasodilators
  4. Anti-angiotensins
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69
Q

How do diuretics affect BP

A

Lowers BP 10-15mm Hg

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70
Q

What is the toxicity associated with diuretics

A

Potassium depletion

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71
Q

Sympathoplegics MOA

A

Stimulates vagus nerve –> increase release of ACh –> increase binding to mACh receptors –> decreasing CO

Decrease PVR and CO

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72
Q

Direct Vasodilators MOA

A

Relax vascular smooth muscle to reduce PVR and MAP in both arterioles and veins

Direct effect on arterial system

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73
Q

Anti-angiotensin MOA

A

blocks activity/production of angiotensin

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74
Q

What anti-hypertensive drug class is methyldopa in?

A

CNS sympathoplegics

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75
Q

What is the MOA of Methyldopa

A

Alpha adrenoceptor agonist. Blocks sympathetic response in periphery by activating alpha 2 receptors

Prodrug that becomes activated

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76
Q

What is the primary use of methyldopa and why?

A

Pregnancy induced HTN

doesn’t cross placental barrier

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77
Q

What anti hypertensive drug class is Clonidine in

A

Sympathoplegics

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78
Q

What is the MOA of clonidine

A

Inhibits sympathetic outflow –> inhibiting release of NE –> decreasing overall effect

79
Q

What are side effects of clonidine

A

Sedation, dry mouth

80
Q

What are the common uses of clonidine (3)

A

ADHD
Tourettes
Withdrawal Symptoms

81
Q

What are the off-label uses of clonidine (3)

A

Anxiety
PTSD
Sedative –> prolong anesthesia

82
Q

What drug class is dexmedetomidine in and what receptor does it target

A

Sympathoplegics

Alpha 2

83
Q

What is the typical side effect of dexmedetomidine?

A

Sedation (intended to decrease HR & BP, but does it so well that we see sedation)

84
Q

What drug class is Hydralazine in

A

Vasodilator

85
Q

Hydralazine MOA

A

ARTERIOLE system

releases NO to dilate blood vessels

86
Q

How does hydralazine release NO

A

Increasing cGMP –> increased activation of guanalyl cyclas –> NO release

87
Q

What are the side effects of hydralazine?

A

INITIAL ONLY

HA, nausea, sweating, flushing, symptoms resembling SLE

88
Q

What drug class is minoxidil in

A

Vasodilators

89
Q

What is the MOA of minoxidil

A

ARTERIAL SYSTEM

Hyperpolarization of smooth muscle membrane through opening of potassium channels

90
Q

What are the side effects of Minoxidil

A

HA, sweating, palpitations, tachycardia, angina, HYPERTRICHOSIS (hair growth)

91
Q

What is the MOA of nitroprusside?

A

Releases NO into smooth muscle to dilate blood vessels

92
Q

Step by step process of NO dilating vessels

A

crosses smooth muscle, activates cGMP, relaxes smooth muscle surrounding vasculature

93
Q

What is nitroprusside used for?

A

HTN emergencies

94
Q

What is the MOA of calcium channel blockers (CCB)

A

Reduction of calcium influx in arterial smooth muscle through blockage of L-type calcium channels

Decreases contractility and HR

95
Q

What are calcium channel blockers used for? (3)

A

HTN
Angina
Arrhythmias

96
Q

what drug class does fenoldopam belong to?

A

vasodilators

97
Q

What are the 3 main groups of calcium channel blockers?

A

Verapamil
Diltiazem
Dihydropyridine Family

98
Q

What is the MOA of fenoldopam?

A

activates dopamine receptors in renal bed

99
Q

What part of the body does Verapamil work more on?

A

Heart

but can also affect calcium channels in peripheral vasculature

100
Q

What happens when dopamine receptors in the renal bed are activated?

A

Increase blood flow to kidneys, more urine produced, low BP

101
Q

What are 4 drugs in the dihydropyridine family?

A

Nicardipine
Amlodipine
Clevidipine
Nifedipine

102
Q

Explain the angiotensin pathway

A

Angiotensinogen is activated by Renin to create angiotensin 1, angiotensin converting enzyme converts angiotensin 1 to angiotensin 2. Angiotensin 2 works on vasoconstriction and aldosterone secretion. Vasoconstriction leads to increased peripheral vascular resistance. Aldosterone leads to increased water and sodium retention. Overall effect: increased blood pressure.

103
Q

Where do dihydropyridine drugs primarily work

A

Targeted toward periphery and NOT the heart

104
Q

What is pulmonary hypertension?

A

Increased pressure in pulmonary arteries –> leakage in pulmonary arteries –> fluid build up in the lungs –> pneumonia/death

105
Q

How is pulmonary hypertension diagnose?

A

Echocardiogram
Cardiac Cath Lab

106
Q

What causes pulmonary HTN? (5)

A

High BP
Congenital
Emphysema
Blood Clots
Heart Failure

107
Q

What types of drugs can treat pHTN?

A

Prostaglandins
Endothelin Receptor Antagonists

108
Q

What drug acts on renin?

A

Aliskiren

109
Q

What do prostaglandins do?

A

Vasodilate

110
Q

What are examples of prostaglandins and where are they primarily used?

A

Prostacyclin (Epoprostenol)

In the hospital setting as a continuous infusion

111
Q

What are 2 examples of Endothelin Receptor Antagonists

A

Bosentan (Tracleer)
Tezosentan

112
Q

What drug class blocks angiotensin converting enzymes?

A

ACE Inhibitors

113
Q

What is the MOA of endothelin receptor antagonists?

A

Blocks endothelin type receptors (ETA & ETP)

Causes HIGH shear stree –> NO release –> decrease in BP

Prevents additional proliferation of endothelial cells

114
Q

What if the suffix associated with ACE inhibitors

A

“-pril”

115
Q

Overall MOA of ACE Inhibitors

A

decreased pvr, CO, HR

116
Q

What do ETA and ETP normally do?

A

Causes vasoconstriction –> proliferation of smooth muscle (after prolonged activation of receptors)

117
Q

what pathway do ACE inhibitors also work on?

A

Inflammation pathway

118
Q

what do ACE inhibitors do to bradykinins?

A

Increases bradykinins present in blood

119
Q

Where do Endothelin cells come from?

A

Comes from vascular endothelium (the cells that line the blood vessels)

Produced by low shear stress release of angiotensin II, release of cytokines, and thrombin

120
Q

What is the pathway of bradykinins when acted on by ACE inhibitors

A

Prostaglandins are stimulated, vasodilation occurs

121
Q

What are the adverse effects of Endothelin Receptor Antagonists?

A

HA, edema, rash, hepatoxicity, and teratogenesis

122
Q

What is the side effect associated with bradykinins and what causes that side effect?

A

Cough

Prostaglandins increase secretions in lungs which increases secretions in respiratory tract

123
Q

What is the BP range for Initial (pre) HTN

A

SBP 120-140

124
Q

How do you treat pre-hypertension?

A

Non-pharmacological approach

Decrease sodium intake
Exercise
Weight Reduction
Evaluate drugs increasing BP in patient

125
Q

Toxicity associated with ACE inhibitors (3)

A

severe hypotension, teratogenic in first trimester, rashes

126
Q

What are some drugs/things that can increase BP in patient? (5)

A

Decongestants, NSAIDs, contraceptives, some herbal medications, and alcohol use

127
Q

What drug class blocks Angiotensin 2

A

Angiotensin receptor blockers

128
Q

What drug class toxicity do ARBs resemble?

A

ACE inhibitors

129
Q

What is the SBP range for MILD HTN

A

SBP 140-160

130
Q

How do you treat mild HTN

A

Single Drug

131
Q

Why would someone choose an ARB over an ACE inhibitor?

A

No cough associated with ARBs

132
Q

What are the first-line drugs for mild HTN

A

Low dose diuretic
Beta Blocker
Calcium channel blocker

133
Q

What is the safest and easiest to prescribe first-line drug for HTN

A

low dose diuretics

134
Q

______ leads to angina?

A

HTN

135
Q

characteristics of veins

A

large blood capacitance
returns blood to heart
less vascular tone than arteries

136
Q

How do you treat moderate HTN and why?

A

DUAL therapy

Single drug might not be enough because of side effects like reflex tachycardia

Combine drugs with different sites of action

137
Q

What happens with venous constriction?

A

increased EDV, increased stretch of cardiac myocytes, increased force of contraction, increased SV, CO, BP

138
Q

What are 3 examples of fixed dose combinations available

A

Tenoretic :beta blocker & diuretic
Lopressor: beta blocker & diuretic
Lotrel: CCB & ACE inhibitor

139
Q

What is hypertensive crisis?

A

BP is too high –> risk rupturing arterioles, capillaries, and possible arterial rupture–>stroke, aneurysm, death

140
Q

venous dilation

A

decreased VR, CO, BP, stretch, EDV

141
Q

What is angina?

A

not enough BF to heart

142
Q

What is Hypertensive URGENCY

A

(SBP >180/110) WITHOUT acute end organ damage

143
Q

Difference in smooth muscle contraction and cardiac muscle contraction?

A

cardiac shortens in one direction
smooth muscle bunches up/contracts in all directions

144
Q

What percentage of hypertensive crises are Hypertensive URGENCY

A

99%1

145
Q

What is Hypertensive EMERGENCY

A

(SBP >180/110) WITH acute end organ damage, kidney failure, infarct, and stroke

146
Q

How do you treat HTN Emergency

A

ICU monitoring of continuous BP
Monitor fluid intake, output, and body weight
Parenteral anti-hypertensives to lower BP

147
Q

What causes angina? (metabolism)

A

build up of metabolites from anaerobic metabolism causes the ischemia (lack of O2 supply)

148
Q

whats the first course treatment of angina?

A

Nitroglycerin

149
Q

What percentage of Hypertensive crises are Hypertensive Emergencies

A

<1%

150
Q

how does nitroglycerin treat angina?

A

increases oxygen supply to heart, vasodilation

151
Q

What are the most common drugs to treat hypertensive emergencies?

A

Sodium nitroprusside & Fenoldepam

152
Q

What are the three types of angina?

A

Classic angina
Variant angina
Unstable angina

153
Q

What does Fenoldepam do for hypertensive emergencies?

A

Increase kidney perfusion

154
Q

What are other drugs that can treat hypertensive emergencies?

A

Labetalol, CCB, hydralazine/methyldopa

154
Q

What’s the worst angina someone could have?

A

unstable angina

155
Q

Causes of classic angina

A

decreased BF to cardiac myocytes (CAD, atherosclerosis) + working out, decrease in O2 supply
anaerobic metabolism
ischemia

156
Q

How does smooth muscle normally contract in vasculature that feeds a cardiac myocyte

A

Calcium influxes in and binds to calmodulin creating calmodulin complex.

It then activates MLCK (myosin-light chain kinase) to phosphorylate MLC (myosin light chains), interacting with actin to cause a contraction

157
Q

Causes of variant angina

A

temp O2 decreased supply due to vasospasm
SUPER RARE 2%

158
Q

How to treat variant angina

A

potent vasodilators

159
Q

does unstable angina go away with rest?

A

no, it’s an emergency

160
Q

Is a beta blocker a vasodilator?

A

no, decreases O2 demand by B1 dilating microarterioles but they also cause vasoconstriction on epicardial arteries

161
Q

How can you relax vascular tone with CCB

A

CCB inhibits the influx of calcium into myocyte preventing the binding of calmodulin

162
Q

How can you relax vascular tone with Nitrates?

A

Nitrates release NO that increases cGMP resulting in vasodilation/relaxation

Increase blood flow and oxygen to heart

163
Q

How can you relax vascular tone with B2 agonists

A

B2 agonists dephosphorylate myosin light chains PO4 resulting in vasodilation/relaxation

164
Q

__________ cells release NO in response to high shear stress

A

Endothelial

165
Q

_________ inhibits breakdown of cGMP which increases relaxation

A

Sildenafil

166
Q

What is the MOA of Nitroglycerin

A

Releases NO from nitroglycerin compound –> vascular smooth muscle relaxation

167
Q

What are hemoglobin interactions with nitrates

A

Causes methemoglobin (increases nitrate attachment)

Lowers affinity for O2

168
Q

What are pFOXs?

A

lipid, fatty acid chains that utilizie anaerobic metabolism. they break down fatty acids for energy

169
Q

What blocks pFOXs?

A

pFOX inhibitors

170
Q

What is the MOA of pFOX

A

decrease pFOX by increase glucose utilization, resulting in more aerobic metabolism, less ischemia

171
Q
A
172
Q

what is GABAs intent in the brain

A

Inhibitory

173
Q

what is glutamates intent in the brain

A

Excitatory

174
Q

What type of drug is edrophonium and what does it treat?

A

Cholinesterase inhibitor, MG and ileus

175
Q

What type of drug is neostigmine and what does it treat?

A

cholinesterase inhibitor, MG and ileus

176
Q

what type of drug is pyridostigmine and what does it treat?

A

Cholinesterase inhibitor, treats MG

177
Q

Echothiophate drug class

A

Cholinesterase inhibitor, treats glaucoma, organophosphate

178
Q

How long does the organophosphate echothiophate last for when treating glaucoma?

A

100 hours

179
Q

What medication do we give when we SLUDGE-M side effects (cholinergic OD)

A

Atropine

180
Q

MAOI mechanism of action

A

Inhibits the reuptake of NE

181
Q

What foods to avoid with MAOIs

A

Foods high in tyramine, beer, cheese, wine

182
Q

Where does alpha-1 work and is it excitatory and inhibitory and what second messengers does it utilize

A

Smooth muscle, excitatory, IP3, DAG

183
Q

Where does alpha-2 work, excitatory or inhibitor =y and what 2nd messenger

A

Smooth muscle and CNS, inhibitory, cAMP decreases

184
Q

Where does beta 1 work, excitatory or inhibitory, 2nd messenger used

A

Heart, ciliary body, epithelium, excites, cAMP

185
Q

Where does beta 2 work, excitatory or inhibitory, 2nd messenger

A

Lungs, smooth muscle and skeletal muscle, DILATION, cAMP

186
Q

What happens when dopamine receptors on the renal vessels are stimulated?

A

Vasodilation

187
Q

What receptors use GPCRs?

A

Beta, alpha, mACh, dopamine

188
Q

What drugs should you give with hypotension

A

Alpha agonists, norepinephrine and neosynephrine

189
Q

What should you give with cardiac shock?

A

beta-1, dobutamine, NO VASOCONSTRICTION peripherally

190
Q

What drugs to give with heart block?

A

Vasodilate the arteries, epi and isoproterenol

191
Q

What drug to give during asthma attack?

A

Albuterol, B-2

192
Q

Where are n-ACh-R found and what effects when stimulated?

A

Skeletal muscles, BBB, increased awake and alertness, tremors w OD

193
Q

Where are mACh-R found and what are their effects when stimulated (M1,3,5) (M2,4)

A

Heart, periphery,

M2- decreases HR (inhibitory)
M3 - bladder contracted, vasodilation, bronchioles contracted, (excitatory)

Advanced Pharmacology (2 decks)

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