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Pharmacology: Exam 2 > Lecture 1: Autonomic Nervous System Pharmacology > Flashcards

Lecture 1: Autonomic Nervous System Pharmacology Flashcards

1
Q

List the (3) important drug classes (Catecholamine)

HIGH yield

A
  • Natural Catecholamine
  • Indirect-acting Sympathomimetics
  • Mixed-action Sympathomimetics
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2
Q

What are the drugs under the natural cathecholamine drug class?

HIGH yield

A
  • Dopamine
  • Epinephrine
  • Noreinephrine
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3
Q

What are the drugs under the indirect-acting sympathomimetics drug class?

HIGH yield

A
  • Cocaine
  • Amphetamine
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4
Q

What are the drugs under the mixed-action sympathomimetics drug class?

HIGH yield

A
  • Ephedrine
  • Pseudoephedrine
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5
Q

Describe the general mechanism of action for natural catecholamines

A

They directly stimulate the adrenergic receptors

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6
Q

Describe the general mechanism of action for indirect-acting symphathomimetics

A
  • They DO NOT directly stimulate the adrenergic receptors
  • They elevate the levels of natural catecholamines
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7
Q

Describe the general mechanism of action for mixed-action sympathomimetics

A
  • Have some effects like natural catecholamines and some effects like indirect-acting symphathomimetics (mainly amphetamine effects)
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8
Q

What are the target tissues of the autonomic nervous system?

A

visceral organs, glands, smooth muscle

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9
Q

What is the target tissue of the somatic nervous system?

A

skeletal muscle

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10
Q

What is the distal location of the autonomic nervous system?

A

peripheral ganglia

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11
Q

What is the distal location of the somatic nervous system?

A

cerebrospinal axis

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12
Q

Are the postsynaptic nerves myelinated or non-myelinated in the autonomic nervous system?

A

non-myelinated

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13
Q

Are the postsynaptic nerves myelinated or non-myelinated in the somatic nervous system?

A

myelinated

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14
Q

Does the autonomic nervous system form networks?

A

Yes

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15
Q

Does the somatic nervous system form networks?

A

No

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16
Q

What is the result of denervation in the autonomic nervous system?

A

spontaneous activity

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17
Q

What is the result of denervation in the somatic nervous system?

A

paralysis, atrophy

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18
Q

Describe the preganglionic neurons in the sympathetic nervous system

A
  • Short
  • Cholinergic (ACh) receptors
  • leave CNS to innervate ganglia
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19
Q

Describe the postganglionic neurons in the sympathetic nervous system

A
  • Long
  • adrenergic (NE) receptors
  • leave ganglia to innervate effector
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20
Q

What are the primary neurotransmitters of the sympathetic autonomic nervous system?

  • Cholinergic:
  • Adrenergic:
  • Dopaminergic:
A
  • Cholinergic=Acetylcholine
  • Adrenergic=Norephinephrine
  • Dopaminergic=Dopamine
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21
Q

Describe preganglionic and post ganglionic neurons in parasympathetic system?

A

preganglionic = long cholinergic
postganglionic = short cholinergic

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22
Q

What are the primary neurotransmitters of the the parasympathetic autonomic nervous system?

A
  • Cholinergic: Acetylcholine
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23
Q

List the 8 receptors of the Sympathetic Nervous Sytem

A
  1. ⍺1
  2. ⍺2
  3. β1
  4. β2 (often d/t circulating epinephrine)
  5. β3
  6. Dopaminergic
  7. Muscarinic
  8. Nicotinic
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24
Q

What occurs to heart rate and contractility during sympathetic stimulation?

A
  • Heart rate: Accelerates
  • Contractility: Increases

which increases cardiac output

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25
Q

What occurs to blood vessels in the skeletal muscles and to the liver/GI tract during sympathetic stimulation?

A
  • Increases dilation to increase blood flow to the muscles
  • Increases contraction to decrease blood flow to the GI tract and liver
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26
Q

What happens to fat (metabolism) during sympathetic stimulation?

A
  • Increase fat breakdown to produce energy
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27
Q

What happens to the lungs during sympathetic stimulation?

A

Increases dilation to relax lungs to breathe more

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28
Q

What body organs (3) DO NOT receive parasympathetic stimulation?

A
  • Adrenal medulla
  • Sweat glands
  • Blood vessels
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29
Q

What occurs in the GI tract during parasympathetic stimulation?

A
  • Increase motility and tone (contracts)
  • Sphincters relaxes
  • Increase secretion of enzymes and acids to help digest food
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30
Q

What occurs in the heart during parasympathetic stimulation?

A
  • Decreases heart rate
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31
Q

What occurs in the urinary system during parasympathetic stimulation?

A
  • Bladder constricts
  • Sphincter relaxes allowing voiding (peeing)
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32
Q

What occurs in the lungs during parasympathetic stimulation?

A
  • Bronchi constriction
  • Increased fluid in lungs
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33
Q

Which organ has dual innervation of the ANS?

A

The eye

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34
Q

Explain the Sympathetic control of the eye

  • Receptor
  • Muscles affected
  • Action
A
  • Adrenergic
  • Radial muscle
  • Dilation of eyes for better vision
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35
Q

Explain the Parasympathetic Control of the Eye

  • Receptor
  • Muscles affected
  • Action
A
  • Cholinergic
  • Circular muscle & Ciliary muscle
  • Constricts the eye. (Ciliary muscle interacts with the trabecular network to release aqueous humor that repairs the eye)
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36
Q

How is homeostasis maintained in the ANS?

A

Combinations of neurons that send out a signal (efferent) and neurons that are sensing a variety of things from distension to chemicals (afferent)

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37
Q

What are afferent and efferent neurons?

A

Afferent: Signal going TO CNS
Efferent: Signal going AWAY from CNS

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38
Q

What is the short-term response that helps maintain homeostasis in the cardiovascular system? Where can they be found and what triggers a response?

A
  • Baroreceptors (chemo-and mechanoreceptor)
  • Carotid sinus and body & Arch of aorta
  • Respond to changes in blood pressure
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39
Q

What is the name of a common feedback loop in the ANS?

A

The Baroreceptor Reflex

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40
Q

What happens to the baroreceptor reflex when mean arterial pressure (BP) is high?

HIGH yield

A

Increased BP signals the stretch baroreceptors (carotid sinus, arch of aorta) → signal increases firing to the Vasomotor center→PARASYMPATHETIC output ACTIVATED→ which decreases heart rate (& little contractile force)→ decreases cardiac output→ decreases BP

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41
Q

What parts of the heart are not affected by the parasympethetic output of the baroreceptors?

HIGH yield

A
  • NO effect on peripheral resistance and venous tone
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42
Q

Why is there NO effect on peripheral resistance and venous tone durring the parasympethic output of the baroreceptors?

HIGH yield

A

Blood vessels do NOT recieve any parasympthetic stimulation

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43
Q

What occurs to the barorecptor reflex when mean arterial pressure (BP) is low?

HIGH yield

A

Decreased BP signals the strectch baroreceptors (cartoid sinus, arch of aorta) → signal decreases firing to the Vasomotor center→SYMPATHETIC output ACTIVATED→ which increases heart rate, restistance (constriction), contractile force, and venous tone→ increases cardiac output & stroke volume→ Increases BP

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44
Q

What are the common responses of the sympathetic output involved in baroreceptor reflex?

HIGH yield

A
  • Normal physiological responses
  • Pathophysiological (disease or injury) responses (e.g Cardiac Heart Failure)
  • Unwanted side effects (E.g vasodilator)
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45
Q

What disease occurs when the sympathetic output of the baroreceptor reflex is inhibited?

HIGH yield

A
  • Orthostatic hypotension
  • BP drops when standing up (Can cause appearance of floaties. Older pts tend to fall and substain hip damage)
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46
Q

What does both parasympathetic and sympathetic GANGLIA have?

A

Both have Presynaptic Cholinergic Neurons

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47
Q

What are the synapses for all parasympathetic target organs?

A

Cholingeric synapses

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48
Q

A few Sympathetic target organs have cholinergic synapses. What are they?

A
  • Sweat Glands
  • Vascular system (blood vessels)
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49
Q

Acetylcholine is the primary neurotransmitters in which organs/systems?

A
  • Adrenal gland
  • Skeletal muscle
  • All ganglia
50
Q

What is the primary neurotransmitter in the somatic nervous system and where is it located?

A
  • Acetylcholine
  • Located in the Neuromusclar Junction (NMJ)
51
Q

List the steps of the synthesis, storage, and release of Acetylcoline

A
  1. Choline transported into the cell, Acetyl CoA originates from pyruvates
  2. Acetyl CoA +Choline→becomes Acetylcholine (ACh) via Choline Acetly Transferase (outside of the vesicle)
  3. ACh transported and stored inside the vesicle
  4. Ca2+ increases and ACh is released
  5. Binds to receptor (nicotonic or muscarinic) and depending on receptor/location causes effect
52
Q

How is Acetylcholine terminated in the post synapse of the cell?

A
  1. The excess ACh is mainly broken down by Acetylcholine esterase
  • Very little ACh diffuses out of the cell b/c ACh rarely leaves the synapse
  1. Choline is pumped back into the cell to make more ACh
53
Q

What are the type of receptors located in the post-synaptic cell of the cholinergic juncture?

A
  • Cholinergic
  • Autoreceptors
  • Heteroreceptors
  • Other receptors
54
Q

What are the main receptors for Acetylcholine?

A
  • Muscarinic Receptors
  • Nicotinic Receptors
55
Q

Muscarinic are what type of receptors and what is the normal speed?

A
  • G-Coupled Protein Receptor (GPCR)
  • SLOW transmission
56
Q

Nicotinic are what type of receptor and what is the normal speed?

A
  • Ligand-gated ion channel
  • FASTER transmission
57
Q

Where are nictonic receptors mainly distributed in the body? And what type of autonomic response do they cause?

A
  • Found in the ganglia, skeletal muscle (NMJ) and adrenal medulla
  • Has both sympathetic and parasympethic effects
58
Q

What are the nicotinic receptor subtype? And are they excitatory or inhibitory?

A
  • Nm (muscle contraction)
  • Nn (nueronal)
  • Excitatory
59
Q

For the nicotinic receptor subtype, Nm list the:

  • Location
  • Effector
  • Physicological response
A
  • Location: Neuromuscular juncture (NMJ)
  • Effector: Na+, Ca2+ channels (opens them)
  • Skeletal muscle contraction
60
Q

For the nicotinic receptor subtype, Nn lists the following:

  • Location
  • Effector
  • Physiological response
A
  • Location: Autonomic ganglia, brain
  • Effector: Na+, Ca2+ channels (opens them)
  • Physiological response: Ganglionic transmission (action potentials)
61
Q

What is the primary agonist for muscarinic receptors?

A

Muscarine (dervied from the Amanita muscaria plant)

NOTE: the main NT is still Acetylcholine

62
Q

Where are muscarnic receptors mainly distributed in the body? And what type of autonomic response do they cause?

A
  • Found in Cardiac and smooth muscle, gland cells, nerve terminals
  • Response is mainly parasympathetic
  • Very few sympathetic response found in sweat glands and a few vascular smooth muscle
63
Q

What are the muscarnic receptor subtype? And are they excitatory or inhibitory?

A
  • M1, M2, M3, M4, M5
  • Excitatory (Odd: M1, M3, M5) and Inhibitory (M2, M4)
64
Q

List the G-proteins involved with muscarinic receptors and their effects

Cholinergic

A
  • Gi=Inhibitory→decreases cAMP
  • Gq=”different stimulatory”→Increase IP3, DAG→ increases Ca2+
65
Q

What effect do all Excitatory muscarinic receptors (M1, M3, M5) have?

A
  • All increase calcium
  • Increase secretion
66
Q

For the muscarinic receptor subtype, M1 list the:

  • G protein
  • Location
  • Biochemical Effectors
  • Physicological response
A
  • G-protein: Gq /G11
  • Location: Nerves
  • Biochemical Effectors: PLC, IP3, DAG, ↑intracellular Ca2+
  • Physiological Response: Depolarization of neuron, activation of myenteric plexus
67
Q

For the muscarinic receptor subtype, M3 list the:

  • G protein
  • Location
  • Biochemical Effectors
  • Physicological response

MAIN EXCITATORY RECEPTOR ACTIVATED

A
  • G-protein: Gq /G11
  • Location: Glands, smooth muscle, endothelium, nerves
  • Biochemical Effectors: PLC, IP3, DAG, ↑intracellular Ca2+
  • Physiological Response: Contraction of GI and bronchial smooth muscle, ↑GI secretion
68
Q

For the muscarinic receptor subtype, M5 list the:

  • G protein
  • Location
  • Biochemical Effectors
  • Physicological response
A
  • G-protein: Gq /G11
  • Location: CNS
  • Biochemical Effectors: PLC, IP3, DAG, ↑intracellular Ca2+
  • Physiological Response: Modulate neuroexcitability and vascular tone
69
Q

What effect do all Inhibitory muscarinic receptors (M2& M4) have?

A
  • All decrease cAMP, decrease SA node firing and slow HR
  • Increase K+, Hyperpolarize (No action potential)
70
Q

For the muscarinic receptor subtype, M2 list the:

  • G protein
  • Location
  • Biochemical Effectors
  • Physicological response

MAIN INHIBITORY RECEPTOR ACTIVATED

A
  • G-protein: Gi /Go
  • Location: Heart, nerves, smooth muscle
  • Biochemical Effectors: Inhibit adenylyl cyclase (decreases cAMP), activates K+ channels, inhibits Ca2+ channels
  • Physiological Response: ↓SA Node firing rate (negative chronotropic), ↓Ventricular contractile force (negative inotropic)
71
Q

For the muscarinic receptor subtype, M4 list the:

  • G protein
  • Location
  • Biochemical Effectors
  • Physicological response
A
  • G-protein: Gi /Go
  • Location: Nerves, CNS
  • Biochemical Effectors: Inhibit adenylyl cyclase (decreases cAMP), activates K+ channels, inhibits Ca2+ channels
  • Physiological Response: Modulate neuro-excitability?
72
Q

Where are adrenergic synapses located? and what neurotransmitters have an effect?

A
  • Located at target organ
  • Norepinephrine(NE)-main NT and Dopamine(D)
73
Q

Adrenergic receptors target which autonomic nervous system? And which organs are targeted?

A
  • Sympathetic (Fight or Flight)
  • Adrenergic (NE) : Cardiac and smooth muscle, gland cells, nerve terminals
  • Dopamenergic (D): Renal vascular smooth muscle
74
Q

Explain the steps of synthesis, storage and release of Norepinephrine (NE) at the Noradrenergic juncture?

A
  1. Tyrosine is transported into the cell (by A)
  2. Combined with DOPA to create Dopamine
  3. Dopamine gets taken up into the vesicle (by B):Dopamenergic
  4. Dopamine converts to Norepinephrine INSIDE VESICLE
  5. Ca2+ releases causes release of NE from vesicle: Adrenergic

A: Na-dependent tyrosine carrier
B: Vesicular Monoamine transporter

75
Q

Explain the steps of termination of action of NE at the Noradrenergic juncture?

A

(Uptake 1) NE is actively pumped back into the presynaptic neuron (most important step)

  • Some is recycled into vesicles
  • Some metabolized by monoamine oxidase (MAO)

(Uptake 2) A smaller portion is transported into post-junctional cell and metabolized by cathechol-O-methyl transferase (COMT)

Both MAO and COMT degrade the NT (and other catecholamines) BUT Action is terminated by REUPTAKE
1-Norepinephrine transporter (NET)
2-Non-neuronal NET

76
Q

What are the adrenergic receptor subtypes? Are they excitatory or inhibitory?

A
  • ⍺1(⍺1A, ⍺1B, ⍺1D)= Excitatory
  • ⍺2 (⍺2A, ⍺2B, ⍺2C)=Inhibitory
  • β (β1, β2, β3)= Excitatory
77
Q

List the G-proteins involved with adrenergic receptors and their effects

A
  • Gs=Stimulatory→increases cAMP
  • Gi=Inhibitory→decreases cAMP
  • Gq=”different stimulatory”→Increase IP3, DAG→ increases Ca2+
78
Q

For the alpha adrenergic receptor subtype, ⍺1 list the:

  • G protein
  • Location
  • Biochemical Effectors
  • Physicological response
A
  • G-protein: Gq
  • Location: Vascular smooth muscle, heart, liver
  • Biochemical Effectors: PLD, PLA2, PLC, IP3, DAG, ↑ intracellular Ca2+
  • Physiological response: Vasoconstriction, ↑ contractile force, glycogenolysis, gluconeogenesis (Symph MAINLY)

Excitatory (⍺1A, ⍺1B, ⍺1D)

79
Q

For the alpha adrenergic receptor subtype, ⍺2 list the:

  • G protein
  • Location
  • Biochemical Effectors
  • Physicological response
A
  • G protein: Gi
  • Location: Pancreas islets (β cells), Nerve terminals, vascular smooth muscle
  • Biochemical Effectors: Inhibit adenylyl cyclase (↓ cAMP), activate K+ channels, inhibit Ca2+ channels
  • Physicological response: ↓ insulin secretion (Parasymp, dec. NT release)

Inhibitory (⍺1A, ⍺1B, ⍺1C)

80
Q

For the alpha adrenergic receptor subtype, β1 list the:

  • G protein
  • Location
  • Biochemical Effectors
  • Physicological response
A
  • G protein: Gs
  • Location: Heart, juxtaglomerular cells
  • Biochemical Effectors: Stimuate adenylyl cyclase (↑ cAMP) and L-type Ca2+ channels
  • Physicological response: ↑ force and rate of contraction, ↑renin secretion (Symph for heart)

Excitatory

81
Q

For the alpha-adrenergic receptor subtype, β2 list the:

  • G protein
  • Location
  • Biochemical Effectors
  • Physicological response
A
  • G protein: Gs
  • Location: Smooth muscle (vascular, bronchial, GI), bronchial glands, liver
  • Biochemical Effectors: Stimulate adenylyl cyclase (↑ cAMP)
  • Physicological response: Relaxation (vasodilation, bronchodilation), ↑bronchial secretions, glycogenolysis, gluconeogenesis, ↑insulin secretion (Symph for BV and lungs)

Excitatory

82
Q

For the alpha adrenergic receptor subtype, β3 list the:

  • G protein
  • Location
  • Biochemical Effectors
  • Physicological response
A
  • G protein: Gs
  • Location: Adipose tissue
  • Biochemical Effectors: Stimulates adenylyl cyclase (↑cAMP)
  • Physicological response: Lipolysis, Nitric Oxide release (Fat breakdown)
83
Q

What are the 4 components affecting Blood Pressure?

A
  1. Resistance
  2. Cardiac Output
  3. Volume
  4. Capacitance
84
Q

What tissues do ⍺1 adrenergic receptor target and what is the effect of each?

A
  • Most vascular smooth muscle: Contraction
  • Heart: Increased force
  • Prostate: Contraction
  • Pupillary dilator muscle: Contraction (pupil dilation)

Excitatory-Gq

85
Q

What tissues do ⍺2 adrenergic receptors target and what are the effect of each?

A
  • Postsynaptic CNS-Multiple (↓SNS tone)
  • Presynaptic ANS-Decrease NT release
  • Some vascular smooth muscle-Contraction

Inhibitory-Gi

Bolded-most important to remember

86
Q

What tissues do β1 adrenergic receptors target and what are the effect of each?

A
  • Heart-Increased force and rate
  • Juxtaglomerular cells-Increased renin release (fluid retention to maintain BP)

Excitatory-Gs

Bolded-most important to remember

87
Q

What tissues do β2 adrenergic receptors target and what are the effect of each?

A
  • Skeletal muscle blood vessels-Relaxation (increase blood flow to skeletal muscle)
  • Bronchial smooth muscle-Relaxtion
  • Liver-Glycogenolysis and gluconeogenesis
  • Uterus-Relaxation

Excitatory-Gs

Bolded-most important to remember

88
Q

What tissues do β3 adrenergic receptors target and what are the effect of each?

A
  • Fat cells- Increased lipolysis
  • Endothelial cells-Nitric oxide production

Excitatory-Gs

Bolded-most important to remember

89
Q

Explain the reuptake and repacking of NE

A
  • Occurs in the postganglionic nerve ending
  • Important transporters include:
  • Vesicular Monoamine Transporter (VMAT)-transporter for NE to be repackage into vesicle
  • Norepinephrine Transporter (NET)-Brings NE into the cell
90
Q

List drugs that are indirect-acting sympathomimetics

Also known as Drugs that Enhance Noradrenergic Transmission

A
  • Cocaine
  • Amiphetamine
  • Tyramine
91
Q

Explain the mechanism of action and effect of Cocaine

Indirect-acting sympathomimetics

A
  • Blocks NET (norepinephrine transporter)→NE build up in the synapse (causes sympathetic responses)
  • Increase HR
  • Increases Contractility
  • Increases activity of Pacemakers
  • Vasoconstriction

Can have negative effects on the heart

Indirect-DOES NOT bind to receptor

92
Q

Explain the mechanism of action and effects of Amphetamine and Tyramine

Indirect-acting sympathomimetics

A

Non-Vesicular release:

  1. These drugs get taken up into cells by NET and VMAT imports them into the vesicle, and the vesicle gets filled up
  2. Vesicle then dumps everything into the pre-synaptic terminal causing NE buildup and NON-vesicular release

Indirect-DOES NOT bind to receptor

93
Q

List drugs that are mixed-action sympathomimetics

Also known as Drugs that Enhance Noradrenergic Transmission

A
  • Ephedrine
  • Pseudoephedrine
94
Q

Explain the mechanism of action and effects of Ephedrine Pseudoephedrine

Mixed- action symphathomimetics

A

MIxed-action

  • Causes Non-Vesicular Release (like amphetamines) but
  • Also affects adrenergic receptors

Think Epi and amphetamines
Binds to ⍺ and β receptors

95
Q

List drugs that are natural catecholamine

A
  • Dopamine
  • Epinephrine
  • Norepinephrine
96
Q

For Epinephrine explain:

  • Hormone (type)
  • Mechanism of Action (MOA)
  • Effects (Cardiac, Vascular, Smooth muscle, Metabolic)
A
  • Flight or Fight Hormone (Adrendal gland)
  • MOA: Activates ALL adrenergic receptors (⍺1, ⍺2, β1, β2 and β3)
  • Effects:
  • Cardic- positive inotropic and chronotropic effect:β1
  • Vascular-Vasoconstriction (splanchnic) and vasodilation (skeletal muscle): β2
  • Smooth Muscle: Relaxation of Smooth of GI, uterine and bronchial: β2
  • Metabolic-Elevates serum glucose and free fatty acids:β3
97
Q

Explain why Epinephrine at low dosage has an increased pulse rate, increased blood pressure but decreased resistance

A
  • β1 receptor are responsible for the increased HR
  • Increased HR causes the heart to pump faster which increases the blood pressure
  • Due to low dosage β2 receptor is the main effector on the heart. β2 decreases resistance

When Epi is at low dosage β receptors control the effects

98
Q

What occurs when the dosage of Epinephrine is high?

A
  • Changes from a β response into an ⍺ response
  • ⍺1 increases the resistance, heart rate and blood pressure
99
Q

List the overall cardiovascular effects of Epinephrine

A
  • Increase Vasoconstriction (⍺1)
  • Decreases peripheral resistance to skeletal (β2)
  • Net effect of activation ⍺1 and β2=Decrease in Resistance
100
Q

What are 3 clinical uses for epinephrine and be specific as to which receptors are activates?

A
  • Anaphylaxis: (Can’t breathe)→Administer Epi→activate β2→Bronchodilation to breathe again
  • Septic shock: Decrease in BP→Administer Epi→activate ⍺1 for vasoconstriction to increase BP
  • Cardiac Arrrest: Heart stop beating→Adminster Epi→activate β1 to increase pumping of the heart
101
Q

Pharmacokinetics of Epinephrine:

  • Administration
  • Metabolism
  • Exertion

LOW yield

A
  • Administered injectable, topical, or inhalation. NOT administered orally (d/t first pass effect)
  • Metabolized in the gut and liver (abundance of COMT)
  • Excerted in the urine
102
Q

List the adverse effects that can occur due to Epinepherine

A

Exaggeration of physiological effects, including CNS reaction

  • Angina
  • Anxiety/fear
  • Cardiac arrhythmias (β1)
  • Dyspnea
  • Headache
  • Hypertension (⍺1)
  • Peripheral vasoconstriction
  • Tissue necrosis (END ARTERIES)
  • Tremor
103
Q

For Norepinephrine explain:

  • Mechanism of Action (MOA)
  • Effects (Cardiac, Vascular, Smooth muscle, Metabolic)
A
  • MOA: Activates all receptors EXCEPT β2
  • Effects:
  • Similar to Epi
  • EXCEPT, NO relaxation of bronchial smooth muscle and NO relaxation of smooth muscle vasculature(Increases in BP are more exaggerated)
104
Q

Explain why Norepinephrine causes an decreased pulse rate (HR), increased blood pressure and increased resistance

A
  • Increase BP b/c ⍺1 causes Vasoconstriction
  • Increase Resistance b/c no β2 activation only ⍺1
  • Decrease HR due to an increase in BP and resistance
105
Q

Why is there a decrease in HR when given norepinephrine?

A

A dramatic increase in resistance→increases BP→Body responses by activating parasympathetic NS to decrease HR

106
Q

What are 3 clinical uses of Norepinephrine?

A
  1. Septic shock= septic =vasodilation-> need to vasoconstrict to incr BP (1st choice)
  2. Hypotension
  3. Vasopressor support in other types of shock
107
Q

Why would you not use Norepinephrine to treat anaphylaxis?

A

Lack of β2 receptor, cannot vasodilate

108
Q

Pharmacokinetics of Norepinephrine:

  • Administration
  • Metabolism
  • Excretion

Low yield
Similar to Epi

A
  • Administered injectable, topical, or inhalation. NOT administered orally (d/t first pass effect)
  • Metabolized in the gut and liver (abundance of COMT)
  • Excreted in the urine
109
Q

What are the adverse effects of Norepinephrine?

A
  • Similar to Epi
  • EXCEPT, hypertension is more pronounced d/t ⍺1 stimulation without β2 balance
110
Q

List the receptors that Dopamine activate

A
  • D1
  • D2
  • β1
  • ⍺1
111
Q

When dopamine binds to D1 receptors what occurs?

A

Vasodilation. including renal vaculature, diuresis/natriuresis. Hypotensive effect

112
Q

When dopamine binds to D2 receptors what occurs

A

(Presynaptic receptors) Negative feedback to inhibit further norepinephrine, and possibly dopamine releases

113
Q

When dopamine binds to β1 receptors what occurs?

A
  • Positive inotropic and chronotropic effect (increases contraction & HR)
  • At high levels of dopamine only
114
Q

When dopamine binds to ⍺1 receptor what occurs?

A
  • Seen only at high doses
  • Causes vasoconstriction
115
Q

What are some clinical uses for dopamine?

A
  1. Cardiogenic shock
  2. Septic shock
  3. Hypotension

For cardiogenic shock, heart is not beating strong enough, want to increase force of contraction, and increase CO w/o increase afterload

116
Q

Which receptors does a high dose of Dopamine stimulate?

A

⍺1 and β1 receptors just like norepinephrine

117
Q

Which of the following is innervated by the Parasympathetic Nervous system?
a. Adrenal Medulla
b. Salivary Glands
c. Sweat Glands
d. Blood vessels
e. All of the above

A

b. Salivary glands

118
Q
  1. Which of the following receptor types would have faster effects?
    a. M3
    b. M2
    c. B1
    d. A2
    e. Nm
A

e.Nm

119
Q
  1. Which drug type could possibly be a contraindication for hyperglycemic patients?
    a. ⍺1 Agonist
    b. ⍺2 Antagonist
    c. β1 Agonist
    d. β2 Agonist
    e. β2 Antagonist
A

d. β2 Agonist

120
Q
  1. A patient walks into the ER with an increased blood pressure and HR. Upon a drug screening the patient tested positive for cocaine. What is the mechanism of action that caused these symptoms?
    a. Non-Vesicular release of Norepinephrine
    b. Agonist to all Epinephrine receptors
    c. Blocks NET leading to increased NE half-life
    d. Blocks VMAT leading to increased presynaptic epinephrine
A

c. Blocks NET leading to increased NE half-life

121
Q
  1. A patient in the ICU presents with hypotension, increased heart rate, and a high fever. You diagnose the patient with septic shock. Which of the following is first line use?
    a. Dopamine
    b. Epinephrine
    c. Norepinephrine
    d. Isoproterenol
A

c. Norepinephrine

Pharmacology: Exam 2 (10 decks)

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