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Pharm Fall '24 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Somatic nervous system controls what?

A

Voluntary muscle movements

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2
Q

Autonomic nervous system controls what?

A

Involuntary functions

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3
Q

What is included in the autonomic nervous system?

A

Sympathetic, parasympathetic and enteris

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4
Q

Sympathetic nervous system mediates what response?

A

Fight or flight

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5
Q

what does the fight or flight response do?

A

Increase HR, BP and Breathing

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6
Q

What does the parasympathetic nervous system mediate?

A

Rest and digest

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7
Q

what does rest and digest do?

A

conserve energy. slow HR and promote digestion

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8
Q

Parasympathetic nervous system involves primarily cranial nerve _____

A
  1. Vagus nerve
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9
Q

what is the enteric nervous system?

A

complex network of neurons controlling gastrointestinal functions

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10
Q

Parasympathetic nervous system has ____(longer/shorter) preganglionic and _____(longer/shorter) postganglionic fibers

A

longer
shorter

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11
Q

Sympathetic has ____(longer/shorter) preganglionic and _____(longer/shorter) postganglionic fibers

A

shorter
longer

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12
Q

Parasympathetic nervous system primarily uses ____ as a neurotransmitter, while sympathetic nervous system primarily uses _____

A

Acetylcholine
Norepi

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13
Q

____ receptors are mainly muscarinic and nicotinic, while ____ receptors are mainly alpha and beta adrenergic.

A

Parasympathetic
Sympathetic

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14
Q

_____ are clusters of neuron cell bodies in the sympathetic nervous system, located close to the spinal cord.

A

Chain ganglia

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15
Q

_____ are networks of neurons in the enteric nervous system, similar in function to the chain ganglia.

A

PNS plexi

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16
Q

What are sympathomimetics?

A

Drugs that mimic the effects of the sympathetic nervous system

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17
Q

What are parasympathomimetic (cholinomimetic)

A

Drugs that mimic the effects of the parasympathetic nervous system.

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18
Q

What are sympathoplegic (α and β blockers)?

A

Drugs that block the sympathetic nervous system.

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19
Q

What are parasympathoplegics (anticholinergics)

A

Drugs that block the parasympathetic nervous system.

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20
Q

List the sympathetic receptors, subtypes, and second messengers

A

Receptor: Adrenergic receptors
Subtype: Alpha and Beta
Second messengers: cAMP, IP3, DAG

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21
Q

List the parasympathetic receptors, subtypes and second messengers

A

Receptor: Cholinergic receptors
Subtype: Muscarinic and Nicotinic
Second messengers: cAMP, IP3, DAG

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22
Q

What are the adrenergic alpha receptor subtypes?

A

Alpha 1 and 2

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23
Q

What are the adrenergic Beta receptor subtypes?

A

Beta 1 and 2

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24
Q

What G protein is coupled with Alpha 1, Alpha 2, Beta 1 and Beta 2?

A

QISS
A1: Gq (activates phospholipase C)
A2: Gi (inhibitory..inhibit adenylate cyclase)
B1/B2: Gs (stimulates..increase cAMP)

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25
Q

Where are alpha 1 receptors found and what do they cause?

A

Vascular smooth muscle, causing vasoconstriction.

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26
Q

Where are the Alpha-2 adrenergic receptors found and what does this cause?

A

Presynaptic, inhibiting neurotransmitter release.

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27
Q

Where are the Beta-1 adrenergic receptors found and what does this cause?

A

Cardiac muscle, increasing heart rate and contractility.

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28
Q

Where are the Beta-2 adrenergic receptors found and what does this cause?

A

Vascular smooth muscle, causing vasodilation. Bronchi causing bronchodilation

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29
Q

Where are the Muscarinic cholinergic receptors found and what does this cause?

A

Smooth muscle (relax)
Heart (decrease HR and contractility)

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30
Q

Where are the Nicotinic cholinergic receptors found and what does this cause?

A

Skeletal muscle (muscle contraction.)

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31
Q

How does the autonomic (sympathetic and parasympathetic) feedback loop work in terms of MAP

A

Sympathetic: vasoconstriction, increase HR, increase contractile force, increase venous tone = increased BP

Parasympathetic: vasodilation, decrease HR = decrease BP

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32
Q

How does the hormonal feedback loop work in terms of MAP

A

Decreased blood pressure is sensed by the kidneys, leading to renin release, angiotensin II production, and aldosterone secretion to increase blood volume and pressure.

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33
Q

What are the organ system effects of stimulation of the parasympathetic system?

A

Slowed heart rate, bronchoconstriction, increased digestive activity.

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34
Q

What are the organ system effects of stimulation of the sympathetic system?

A

Increased heart rate, bronchodilation, decreased digestive activity.

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35
Q

describe how vasodilation occurs in skeletal muscle blood vessels.

A

vasodilation of skeletal muscle blood vessles via acetylcholine released from postganglionic parasympathetic fibers.

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36
Q

List the six main classes of neurotransmitters

A

1.esters of choline
2.monoamines
3.amino acids
4. purines
5. peptides
6. inorganic acids

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37
Q

Example of esters of choline neurotransmitter (1)

A

Acetylcholine

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38
Q

Example of monoamines neurotransmitter (3)

A

norepi
dopa
serotonin

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39
Q

example of amino acids neurotransmitter (2)

A

glutamate
gaba

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40
Q

example of purines neurotransmitter (2)

A

adenosine and ATP

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41
Q

example of peptides neurotransmitter (2)

A

substance P
endorphins

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42
Q

example of inorganic acids neurotransmitter (1)

A

nitric oxide

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43
Q

Recall the function of three CNS neurotransmitters in emotion.

A

Dopamine
Serotonin
Norepo

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44
Q

List three types of synapses described in lecture.

A

chemical synapses
electrical synapses
on-pause synapses.

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45
Q

Describe the possible fate of neurotransmitters in the synapse. (4)

A
  1. diffusion away from synapse
  2. degraded by enzymes
  3. uptake into pre-synaptic cell
  4. uptake into surrounding cells
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46
Q

What is the difference between excitatory and inhibitory neurotransmitters

A

Excitatory: Cause depolarization (e.g., glutamate).

Inhibitory: Cause hyperpolarization (e.g., GABA).

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47
Q

What role does CHT play in the presynaptic neuron?

A

Choline transporter into neuron

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48
Q

Describe the formation of acetylcholine

A

acetyl-CoA + choline via ChAT

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49
Q

Describe the transport of acetylcholine (specifically VAT)

A

VAT transports ACh into vesicle

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50
Q

Describe the enzymatic cleavage of acetylcholine

A

enzymatic cleavage occurs by acetylcholinesterase (AChE)

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51
Q

What is the SNARE complex?

A

Anchoring (docking). includes SNAP-25 and VAMP

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52
Q

List targets for drug action in the synapse. (5)

A

Synthesis
Storage
Release
Receptors
Degradation/Reuptake

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53
Q

What is an example of drug action for the synthesis synapse

A

Inhibition of tyrosine hydroxylase to block norepinephrine synthesis

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54
Q

What is an example of drug action for the storage synapse

A

Reserpine to inhibit vesicular storage of neurotransmitters

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55
Q

What is an example of drug action for the release synapse

A

Botulinum toxin to block neurotransmitter release

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56
Q

What is an example of drug action for the receptors synapse

A

Agonists and antagonists acting on muscarinic, nicotinic, alpha, beta, dopamine, and serotonin receptors

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57
Q

What is an example of drug action for the reuptake synapse

A

SSRI - reuptake inhibitor

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58
Q

List the major clinical uses of cholinomimetic agonists (cholinergic agonists). (4)

A

Acetylcholine - pupillary constriction

Methacholine - astha (Dx)

Carbachol - Decrease IOP

Bethanechol – Bladder dysfunction, GERD

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59
Q

Describe direct-acting cholinomimetic agent

A

Mimic activity of acetylcholine. (bind to and activate M or N receptors)

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60
Q

Describe indirect-acting cholinomimetic agent

A

Block acetylcholinesterase

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61
Q

The indirect cholinomimetic ______ is useful in the diagnosis of Myasthenia gravis

A

Edrophonium

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62
Q

Describe the differences between a nicotinic and muscarinic receptor.

A

Nicotinic receptors are ion channels
muscarinic receptors are G-protein coupled receptors.

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63
Q

List the effects of cholinomimetics in the major organ systems (eye, CV system, respiratory system and GI)

A

eye (pupillary constriction)

cardiovascular system (decreased peripheral resistance, increased heart rate)

respiratory system (bronchoconstriction)

gastrointestinal tract (increased secretions and motility).

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64
Q

What are the two different types of glaucoma?

A

Open-angle and closed-angle

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65
Q

Cholinomimetics are used for which type of glaucoma and contraindicated in what other type of glaucoma?

A

used for - open-angle
contraindicated for: closed-angle

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66
Q

List the major signs and symptoms of organophosphate insecticide poisoning

A

“SLUDGE-M”

salivation
lacrimation
urination
defecation
gastrointestinal motility
emesis
miosis

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67
Q

List the major signs and symptoms of acute nicotine toxicity.

A

tremors
vomiting
respiratory stimulation
convulsions
coma

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68
Q

What is the function of acetylcholinesterase?

A

Breaks down acetylcholine

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69
Q

what is the function of organophosphate aging?

A

organophosphates can irreversibly inhibit this enzyme through covalent binding and “aging”.

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70
Q

Antimuscarinics: main uses for the following according to lecture:
Atropine is for _____
Scopolamine is for ____
Tropicamide is for _____
Ipratopium is for _____

A
  1. bradycardia
  2. motion sickness
  3. eye
  4. COPD
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71
Q

Describe the effects of atropine on the major organ systems. (Eyes, CV system, Respiratory system, GI)

A

atropine can reverse the effects of cholinomimetics

eye (pupillary dilation)

cardiovascular system (increased heart rate)

respiratory system (bronchodilation)

gastrointestinal tract (decreased secretions and motility).

72
Q

Symptoms of atropine overdose

A

BRAND

Blind
Red
Absent bowel sounds
Nuts (cray cray)
Dry

73
Q

Treatment of atropine overdose

A

neostigmine or pyridostigmine

74
Q

the use of cholinomimetics myasthenia gravis

A

Neostigmine:
treat the muscle weakness by increasing acetylcholine levels at the neuromuscular junction.

75
Q

the use of cholinomimetics glaucoma

A

pilocarpine:
open-angle glaucoma

increasing drainage of aqueous humor.

Atropine can be used in open angle with caution

76
Q

the use of cholinomimetics in post-operative ileus.

A

neostigmine:

used to treat the paralysis of the gastrointestinal tract that can occur after surgery.

77
Q

List the major clinical indications for the use of muscarinic antagonists such as atropine.

A

poisonous mushrooms (muscarinic excess)

Organophosphare exposure

Premedication before anesthesia to reduce secretions

78
Q

List the major clinical contraindications for the use of muscarinic antagonists such as atropine.

A

Closed-angle glaucoma - Atropine can worsen the condition by further constricting the angle and impeding drainage

79
Q

Name the two categories of muscle relaxants.

A

Depolarizing muscle relaxants

Non-depolarizing muscle relaxants

80
Q

Differentiate depolarizing muscle relaxants and give examples

A

(e.g., succinylcholine) cause initial depolarization of the muscle followed by paralysis.

81
Q

Describe non-depolarizing muscle relaxants and give examples

A

(e.g., rocuronium, vecuronium) competitively block acetylcholine at the NMJ without causing depolarization.

derivatives of curare

82
Q

Recall the basic structure of catecholamines.

A

catechol group (a benzene ring with two hydroxyl groups) and an amine group.

83
Q

Mechanism of Action (MOA) of Direct Acting Catecholamines

A

These directly bind to and activate adrenergic receptors

84
Q

Mechanism of Action (MOA) of Indirect Acting Catecholamines

A

Release catecholamines from presynaptic terminal

85
Q

Why cant catecholamines be taken orally?

A

because it is broken down in the gut by COMT

86
Q

Describe what happens in the cardiovascular system after the administration of an alpha-agonist

A

vasoconstriction

87
Q

Describe what happens in the cardiovascular system after the administration of an a beta-agonist

A

Beta 1- increase HR, increase contractility

Beta 2- bronchodilation, vasodilation = decrease BP

88
Q

Describe what happens in the cardiovascular system after the administration of a mixed agonist.

A

mixed agonists like epinephrine (increase both blood pressure and cardiac output).

89
Q

Norepi has effects on ____ and ____receptors and has little effect on _____ receptors.

A

Alpha
Beta 1
Beta 2 (little effect)

90
Q

Name a typical nonselective α agonist

A

Phenylephrine

91
Q

Name a typical selective α2 agonist (2)

A

Dexmedatomidine and Clonidine

92
Q

Name a typical nonselective β agonist

A

Isoproterenol

93
Q

Dobutamine is a _____ selective agonists and is used for treating ______ and ______

A

beta 1
cardiac shock
acute heart failure

94
Q

Name a typical selective β2 agonists.

A

Albuterol

95
Q

List tissues that contain significant numbers of α1 receptors.

A

peripheral vasculature

96
Q

List tissues that contain significant numbers of α2 receptors.

A

central nervous system.

97
Q

Tissues Containing Significant β1 Receptors

A

Heart (increases heart rate and contractility).

Kidney (renin release).

98
Q

Tissues Containing Significant β2 Receptors

A

Bronchial smooth muscle (bronchodilation).

Vascular smooth muscle in skeletal muscle (vasodilation).

99
Q

Define the triphasic effects of dopamine.

A

low doses cause vasodilation

medium doses increase cardiac effects

high doses increase blood pressure.

100
Q

List the most common toxicities associated with sympathomimetics.

A

Cardiac arrhythmias
Addiction
CNS effects

101
Q

Effects of an α Blocker on blood pressure

A

Vasodilation, lower BP

102
Q

phentolamine, prazosin, terazosin, and doxazosin are examples of what?

A

alpha blockers

103
Q

Phentolamine and phenoxybenzamine can be used in the treatment of _____ linked to pheochromocytoma (tumor of the adrenal glands that secrete epi and norepi)

A

Hypertension

104
Q

propranolol, metoprolol, atenolol, lebetalol and esmolol are examples of what?

A

beta blockers

105
Q

What are the clinical uses for alpha and beta blockers?

A

hypertension, angina, certain arrhythmias, and pheochromocytoma (for alpha blockers)

106
Q

Explain the following sentence: Phentolamine converts a pressor (epinephrine) into a depressor.

A

phentolamine, an alpha blocker, can block the pressor effects of the alpha agonist epinephrine, leading to a decrease in blood pressure.

107
Q

Selective beta-blockers metoprolol and atenolol are typically safer for treating ____ and _____ and are mainly beta _____ selective.

A

COPD and diabetics
beta 1

108
Q

non-selective beta-blocker propranolol works on which beta receptor

A

beta 1 and 2

109
Q

Describe the clinical indications of typical α and β blockers.

A

hypertension, angina, certain arrhythmias, and pheochromocytoma (for alpha blockers).

110
Q

Describe the toxicities of typical α and β blockers.

A

bradycardia, bronchospasm, hypoglycemia, and weight gain (for long-term use of beta blockers).

111
Q

How do you calculate MAP

A

diastolic pressure plus 1/3 of the difference between systolic and diastolic pressures.

112
Q

Cardiac output as a regulator of BP

A

Increased CO raises BP

113
Q

PVR as a regulator of BP

A

Resistance in the arteries; increased PVR leads to higher BP

114
Q

Four main anatomic control sites for blood pressure.

A

the resistance arterioles

the capacitance venules

the pump output of the heart

the renin-angiotensin-aldosterone system.

115
Q

non-pharmacologic intervention for elevated blood pressure.

A

Controlling salt intake, weight and stress

116
Q

List 4 major groups of antihypertensive drugs

A
  1. Diuretics
  2. Sympathoplegics
  3. direct vasodilators
  4. anti-angiotensins
117
Q

Hydralazine, minoxidil, nitroprusside and fenoldopam are examples of what class of antihypertensives?

A

Vasodilators

118
Q

______ and _____ are centrally acting sympathoplegic drugs that primarily act on _____ receptors

A

Methyldopa
Clonidine
Alpha 2

119
Q

Methyldopa is typically used to treat ______.

A

pregnancy induced hypertension

120
Q

Clonidine is (1)_____ soluble. It is used as a backup (2)_____. More commonly it is used for (3)_____, (4)_____, and (5)_____

A
  1. lipid
  2. antihypertensive
  3. ADHD
  4. tourettes
  5. Withdrawl symptoms
121
Q

A major side effect of both clonidine and methyldopa is _____

A

sedation

122
Q

List the major sites of action of peripheral sympathoplegic drugs in clinical use and give examples of drugs that act at each site.

A

sympathetic ganglia, the adrenergic nerve terminals, the alpha receptors, and the beta receptors.

Examples of drugs acting at these sites include phenoxybenzamine (alpha blocker), propranolol (beta blocker), and labetalol (alpha and beta blocker).

123
Q

MOA of vasodilators

A

Relax smooth muscle in blood vessels

124
Q

4 classifications of vasodilators

A

Calcium channel blockers

NO donors

K channel openers

Alpha blockers

125
Q

Describe the compensatory responses to vasodilators.

A

increased sympathetic outflow, increased renin release, and sodium and water retention.

126
Q

List the major antihypertensive vasodilator drugs and describe their effects. (2)

A

Hydralazine and Minoxidil

K channel activation, hyperpolarization of smooth muscle

127
Q

What is sodium nitroprusside typically used for and what are concerns for using this drug?

A

HTN emergencies. However, it has high toxicity due to the cyanide molecules in its structure.

128
Q

List the three classes of CCBs and major target of each.

A

Verapamil- More targeted towards the heart

Dihydropyridines (e.g., nifedipine, amlodipine) - More targeted towards the peripheral vasculature

Diltiazem - Somewhere in between the other two classes in terms of its effects on the heart and peripheral vasculature.

129
Q

Describe the differences between ACE inhibitors and Angiotensis receptor blockers

A

ACE inhibitors (e.g., captopril) - Block the conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin.

Angiotensin receptor blockers (ARBs) - Directly block the binding of angiotensin II to its receptors, without affecting the production of angiotensin II.

130
Q

What is the side effect of ACE inhibitors that everyone hates and what causes this?

A

Dry cough. ACE inhibitors lead to an increase in bradykinin levels

131
Q

List and describe mechanisms of action for pulmonary hypertension therapeutics. (2)

A

Prostaglandins (e.g., prostacyclin) - Cause vasodilation in the pulmonary vasculature.

Endothelin receptor antagonists - Block the endothelin receptors, which are involved in vasoconstriction and smooth muscle proliferation in the lungs. (Bosentan)

132
Q

Define hypertensive urgency

A

hypertensive urgency is defined as blood pressure greater than 180/110 mmHg without end-organ damage

133
Q

Define hypertensive crisis.

A

hypertensive emergency is the same high blood pressure with acute end-organ damage.

134
Q

TX for mild/mod HTN

A

diet, exercise

single-drug therapy (diuretic, Beta-blocker, Ca channel blocker)

135
Q

Treatment for severe/emergent HTN

A

Continuous IV infusion of parenteral antihypertensives like sodium nitroprusside or fenoldopam.

136
Q

What is arterial tone responsible for?

A

regulating vascular resistance and blood pressure.

137
Q

What is capillary tone used for?

A

important for distributing blood flow to different tissues based on their metabolic needs

138
Q

What is venous tone responsible for?

A

The primary function is to conduct blood back to the heart, rather than regulate pressure.

139
Q

Describe the pathophysiology of effort angina

A

Effort angina is caused by decreased blood flow to the heart due to coronary artery disease, leading to an imbalance between oxygen demand and supply.

140
Q

Describe the pathophysiology of vasospastic angina

A

caused by temporary spasm of the coronary arteries, rather than fixed blockages.

141
Q

Describe the major determinants of cardiac oxygen consumption.

A

heart rate, contractility, and wall tension.

142
Q

Explain the following: coronary blood flow is directly related to duration of diastole.

A

Coronary blood flow occurs mainly during diastole when the heart muscle relaxes and perfusion to the coronary arteries increases.

143
Q

Strategies and Drug Targets for Anginal Pain Relief

A

Reduce Oxygen Demand: Use beta blockers or calcium channel blockers.

Increase Oxygen Supply: Use nitrates to dilate coronary vessels.

144
Q

Molecular Pathways of Vascular Tone and Drug Targets

A

Nitric Oxide Pathway: NO activates guanylyl cyclase, increasing cGMP and leading to vasodilation. Drugs like nitroglycerin target this pathway.

145
Q

name the Primary Nitrates and Nitrites. What do they treat

A

Nitroglycerin and isosorbide dinitrate.

Angina and heart failure

146
Q

MOA of Primary Nitrates and Nitrites

A

Donate NO, increasing cGMP for vasodilation.

147
Q

Concerns with Overexposure to Nitrates/Nitrites

A

Tolerance: Continuous use can lead to decreased efficacy.

Methemoglobinemia: Overexposure can cause abnormal hemoglobin formation.

148
Q

Receptor Differences in Epicardial Arteries

A

Alpha and Beta Receptors: Epicardial arteries contain both alpha (vasoconstrictive) and beta (vasodilatory) receptors.

149
Q

Is Ranolazine a pFOX inhibitor?

A

yes

150
Q

Describe MOA of pFOX inhibitors

A

Inhibit fatty acid oxidation, shifting metabolism to glucose, reducing oxygen consumption.

151
Q

Therapeutic and Adverse Effects of Nitrates for Angina

A

Vasodilation, but can cause headaches and hypotension.

152
Q

Therapeutic and Adverse Effects of Beta Blockers for Angina

A

Reduce heart rate, but can cause fatigue and bradycardia.

153
Q

Therapeutic and Adverse Effects of CCBs for Angina

A

Vasodilation, but may cause edema and reflex tachycardia.

154
Q

Why would we combine Nitrate with Beta Blocker or CCB

A

Combining nitrates with beta blockers or CCBs can reduce compensatory mechanisms like reflex tachycardia, providing better angina control.

155
Q

Medical Therapy for Angina

A

Focuses on reducing oxygen demand and increasing supply (e.g., drugs like nitrates, beta blockers).

156
Q

Surgical therapy for angina

A

Coronary interventions like angioplasty or bypass surgery improve coronary blood flow mechanically

157
Q

Define heart failure

A

Heart cant pump enough blood to meet body’s needs

158
Q

The four factors of cardiac performance

A

Preload

Afterload

Contractility

Heart rate

159
Q

Define the Starling law.

A

force of cardiac muscle contraction is directly proportional to the initial length of the muscle fiber (preload).

This means that increased ventricular filling (preload) leads to a more forceful contraction, up to an optimal point.

160
Q

How does ESV contribute to EDV

A

End-systolic volume (ESV) - Higher ESV leads to higher end-diastolic volume (EDV) through the Frank-Starling mechanism.

161
Q

How does passive filling contribute to EDV

A

Increased venous return and ventricular compliance during diastole contribute to higher EDV.

162
Q

How does atrial contraction contribute to EDV

A

The “atrial kick” at the end of diastole further increases EDV by actively filling the ventricles

163
Q

treatment for acute heart failure

A

Diuretics: Furosemide.

Vasodilators: Nitroglycerin, sodium nitroprusside.

Positive Inotropes: Dobutamine, milrinone.

164
Q

Treatment for chronic HF

A

ACE inhibitors: Lisinopril.

Beta blockers: Carvedilol, metoprolol.

Aldosterone antagonists: Spironolactone.

ARNI (angiotensin receptor-neprilysin inhibitor): Sacubitril/valsartan.

165
Q

Molecular Mechanisms Controlling Normal Cardiac Contractility

A

Calcium influx during the plateau phase of the action potential triggers calcium release from the sarcoplasmic reticulum, which binds to troponin C, leading to actin-myosin interaction and muscle contraction.

166
Q

Describe the mechanism of action of digitalis and its major effects.

A

Digitalis (e.g., digoxin) inhibits the Na+/K+ ATPase pump in cardiac myocytes, leading to increased intracellular sodium.

This, in turn, increases intracellular calcium through the Na+/Ca2+ exchanger, enhancing calcium-mediated contraction of the myofibrils.

The major effects of digitalis include increased contractility, decreased heart rate, and increased cardiac output.

167
Q

Describe the nature and mechanism of digitalis’s toxic effects on the heart.

A

Digitalis toxicity can lead to cardiac arrhythmias, such as atrial and ventricular tachyarrhythmias.

This is due to the drug’s effects on the Na+/K+ ATPase pump, which can disrupt the normal electrical activity of the heart when present in excess.

168
Q

Positive Inotropic Drugs for Heart Failure (Other than Digitalis)

A

Dobutamine: Beta-1 agonist, increases contractility.

Milrinone: Phosphodiesterase-3 inhibitor, increases cAMP, enhancing contractility and vasodilation.

169
Q

Reasoning for Beta Blockers in Heart Failure

A

Chronic sympathetic stimulation is harmful in HF. Beta blockers reduce heart rate, improve ejection fraction over time, and prevent adverse remodeling.

170
Q

Effects of Non-Inotropic Drugs in Heart Failure

A

Diuretics: Reduce preload and alleviate fluid overload.

Vasodilators: Decrease afterload (e.g., ACE inhibitors, hydralazine).

ACE Inhibitors: Reduce RAAS activity, decreasing afterload and preload, and preventing remodeling.

Beta Blockers: Reduce sympathetic overactivity, slow heart rate, and prevent remodeling.

171
Q

Non-Pharmaceutical Interventions for Heart Failure

A

Lifestyle modifications: Low-sodium diet, fluid restriction.

Exercise: Cardiac rehabilitation.

Surgery: Bypass, VAD

172
Q

List the different types of arrhythmias.

A

Bradycardia
Tachycardia
Heart block
Bundle branch block
Atrial fibrillation
Ventricular fibrillation

173
Q

Intrinsic Conduction System and EKG Reading

A

Conduction System: SA node → AV node → Bundle of His → Right and left bundle branches → Purkinje fibers.

174
Q

EKG interpretation

A

P wave (atrial depolarization), QRS complex (ventricular depolarization), and T wave (ventricular repolarization).

175
Q

Compare the different types of ion channels, their operation, and contribution to the cardiac action potential.

A

Sodium Channels: Rapid depolarization (Phase 0).

Calcium Channels: Plateau phase (Phase 2).

Potassium Channels: Repolarization (Phase 3).

176
Q

Describe the process of sodium channel recycling and the positions of the m and h gates.

A

m gate: Activation gate, opens during depolarization.

h gate: Inactivation gate, closes during depolarization, reopens during repolarization.

177
Q

Cardiac Action Potential Phases

A

Phase 0: Rapid depolarization (Na+ influx).

Phase 1: Initial repolarization (K+ efflux).

Phase 2: Plateau (Ca2+ influx).

Phase 3: Repolarization (K+ efflux).

Phase 4: Resting potential.

Pharm Fall '24 (7 decks)

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