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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
What occurs to blood vessels in the skeletal muscles and to the liver/GI tract during sympathetic stimulation?
* Increases dilation to increase blood flow to the muscles * Increases contraction to decrease blood flow to the GI tract and liver
26
What happens to fat (metabolism) during sympathetic stimulation?
* Increase fat breakdown to produce energy
27
What happens to the lungs during sympathetic stimulation?
Increases dilation to relax lungs to breathe more
28
What body organs (3) DO NOT receive parasympathetic stimulation?
* Adrenal medulla * Sweat glands * Blood vessels
29
What occurs in the GI tract during parasympathetic stimulation?
* Increase motility and tone (contracts) * Sphincters relaxes * Increase secretion of enzymes and acids to help digest food
30
What occurs in the heart during parasympathetic stimulation?
* Decreases heart rate
31
What occurs in the urinary system during parasympathetic stimulation?
* Bladder constricts * Sphincter relaxes allowing voiding (peeing)
32
What occurs in the lungs during parasympathetic stimulation?
* Bronchi constriction * Increased fluid in lungs
33
Which organ has dual innervation of the ANS?
The eye
34
Explain the Sympathetic control of the eye * Receptor * Muscles affected * Action
* Adrenergic * Radial muscle * Dilation of eyes for better vision ## Footnote
35
Explain the Parasympathetic Control of the Eye * Receptor * Muscles affected * Action
* Cholinergic * Circular muscle & Ciliary muscle * Constricts the eye. (Ciliary muscle interacts with the trabecular network to release aqueous humor that repairs the eye)
36
How is homeostasis maintained in the ANS?
Combinations of neurons that send out a signal (efferent) and neurons that are sensing a variety of things from distension to chemicals (afferent)
37
What are afferent and efferent neurons?
**Afferent**: Signal going **TO** CNS **Efferent**: Signal going **AWAY** from CNS
38
What is the short-term response that helps maintain homeostasis in the cardiovascular system? Where can they be found and what triggers a response?
* Baroreceptors (chemo-and mechanoreceptor) * Carotid sinus and body & Arch of aorta * Respond to changes in blood pressure
39
What is the name of a common feedback loop in the ANS?
The Baroreceptor Reflex
40
What happens to the baroreceptor reflex when mean arterial pressure (BP) is high? ## Footnote HIGH yield
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**
41
What parts of the heart are not affected by the parasympethetic output of the baroreceptors? ## Footnote HIGH yield
* NO effect on peripheral resistance and venous tone
42
Why is there NO effect on peripheral resistance and venous tone durring the parasympethic output of the baroreceptors? ## Footnote HIGH yield
Blood vessels do NOT recieve any parasympthetic stimulation
43
What occurs to the barorecptor reflex when mean arterial pressure (BP) is low? ## Footnote HIGH yield
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
44
What are the common responses of the sympathetic output involved in baroreceptor reflex? ## Footnote HIGH yield
* Normal physiological responses * Pathophysiological (disease or injury) responses (e.g Cardiac Heart Failure) * Unwanted side effects (E.g vasodilator)
45
What disease occurs when the sympathetic output of the baroreceptor reflex is inhibited? ## Footnote HIGH yield
* Orthostatic hypotension * BP drops when standing up (Can cause appearance of floaties. Older pts tend to fall and substain hip damage)
46
What does both parasympathetic and sympathetic GANGLIA have?
Both have Presynaptic Cholinergic Neurons
47
What are the synapses for all parasympathetic target organs?
Cholingeric synapses
48
A few Sympathetic target organs have cholinergic synapses. What are they?
* Sweat Glands * Vascular system (blood vessels)
49
Acetylcholine is the primary neurotransmitters in which organs/systems?
* Adrenal gland * Skeletal muscle * All ganglia
50
What is the primary neurotransmitter in the somatic nervous system and where is it located?
* Acetylcholine * Located in the Neuromusclar Junction (NMJ)
51
List the steps of the synthesis, storage, and release of Acetylcoline
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
How is Acetylcholine terminated in the post synapse of the cell?
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 2. Choline is pumped back into the cell to make more ACh
53
What are the type of receptors located in the post-synaptic cell of the cholinergic juncture?
* **Cholinergic** * Autoreceptors * Heteroreceptors * Other receptors
54
What are the main receptors for Acetylcholine?
* Muscarinic Receptors * Nicotinic Receptors
55
Muscarinic are what type of receptors and what is the normal speed?
* G-Coupled Protein Receptor (GPCR) * SLOW transmission
56
Nicotinic are what type of receptor and what is the normal speed?
* Ligand-gated ion channel * FASTER transmission
57
Where are nictonic receptors mainly distributed in the body? And what type of autonomic response do they cause?
* Found in the **ganglia, skeletal muscle (NMJ) and adrenal medulla** * Has both sympathetic and parasympethic effects
58
What are the nicotinic receptor subtype? And are they excitatory or inhibitory?
* Nm (muscle contraction) * Nn (nueronal) * Excitatory
59
For the nicotinic receptor subtype, Nm list the: * Location * Effector * Physicological response
* Location: Neuromuscular juncture (NMJ) * Effector: Na+, Ca2+ channels (opens them) * Skeletal muscle contraction
60
For the nicotinic receptor subtype, Nn lists the following: * Location * Effector * Physiological response
* Location: Autonomic ganglia, brain * Effector: Na+, Ca2+ channels (opens them) * Physiological response: Ganglionic transmission (action potentials)
61
What is the primary agonist for muscarinic receptors?
Muscarine (dervied from the Amanita muscaria plant) ## Footnote NOTE: the main NT is still Acetylcholine
62
Where are muscarnic receptors mainly distributed in the body? And what type of autonomic response do they cause?
* 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
What are the muscarnic receptor subtype? And are they excitatory or inhibitory?
* M1, M2, M3, M4, M5 * Excitatory (Odd: M1, **M3**, M5) and Inhibitory (**M2**, M4)
64
List the G-proteins involved with muscarinic receptors and their effects ## Footnote Cholinergic
* **Gi**=Inhibitory→decreases cAMP * **Gq**="different stimulatory"→Increase IP3, DAG→ increases Ca2+
65
What effect do all Excitatory muscarinic receptors (M1, M3, M5) have?
* All increase calcium * Increase secretion
66
For the muscarinic receptor subtype, **M1** list the: * G protein * Location * Biochemical Effectors * Physicological response
* G-protein: **Gq** /G11 * Location: Nerves * Biochemical Effectors: PLC, IP3, DAG, **↑intracellular Ca2+** * Physiological Response: Depolarization of neuron, activation of myenteric plexus
67
For the muscarinic receptor subtype, **M3** list the: * G protein * Location * Biochemical Effectors * Physicological response | MAIN EXCITATORY RECEPTOR ACTIVATED
* 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
For the muscarinic receptor subtype, **M5** list the: * G protein * Location * Biochemical Effectors * Physicological response
* G-protein: **Gq** /G11 * Location: CNS * Biochemical Effectors: PLC, IP3, DAG, **↑intracellular Ca2+** * Physiological Response: Modulate neuroexcitability and vascular tone
69
What effect do all Inhibitory muscarinic receptors (M2& M4) have?
* All decrease cAMP, decrease SA node firing and slow HR * Increase K+, Hyperpolarize (No action potential)
70
For the muscarinic receptor subtype, **M2** list the: * G protein * Location * Biochemical Effectors * Physicological response | MAIN INHIBITORY RECEPTOR ACTIVATED
* 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
For the muscarinic receptor subtype, **M4** list the: * G protein * Location * Biochemical Effectors * Physicological response
* 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
Where are adrenergic synapses located? and what neurotransmitters have an effect?
* Located at target organ * **Norepinephrine(NE)-main NT** and Dopamine(D)
73
Adrenergic receptors target which autonomic nervous system? And which organs are targeted?
* **Sympathetic** (Fight or Flight) * Adrenergic (NE) : Cardiac and smooth muscle, gland cells, nerve terminals * Dopamenergic (D): Renal vascular smooth muscle
74
Explain the steps of synthesis, storage and release of Norepinephrine (NE) at the Noradrenergic juncture?
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** ## Footnote A: Na-dependent tyrosine carrier B: Vesicular Monoamine transporter
75
Explain the steps of termination of action of NE at the Noradrenergic juncture?
**(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) ## Footnote 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
What are the adrenergic receptor subtypes? Are they excitatory or inhibitory?
* ⍺1(⍺1A, ⍺1B, ⍺1D)= Excitatory * ⍺2 (⍺2A, ⍺2B, ⍺2C)=Inhibitory * β (β1, β2, β3)= Excitatory
77
List the G-proteins involved with adrenergic receptors and their effects
* **Gs**=Stimulatory→increases cAMP * **Gi**=Inhibitory→decreases cAMP * **Gq**="different stimulatory"→Increase IP3, DAG→ increases Ca2+
78
For the alpha adrenergic receptor subtype, **⍺1** list the: * G protein * Location * Biochemical Effectors * Physicological response
* 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)** ## Footnote Excitatory (⍺1A, ⍺1B, ⍺1D)
79
For the alpha adrenergic receptor subtype, **⍺2** list the: * G protein * Location * Biochemical Effectors * Physicological response
* 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)** ## Footnote Inhibitory (⍺1A, ⍺1B, ⍺1C)
80
For the alpha adrenergic receptor subtype, **β1** list the: * G protein * Location * Biochemical Effectors * Physicological response
* 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)** ## Footnote Excitatory
81
For the alpha-adrenergic receptor subtype, **β2** list the: * G protein * Location * Biochemical Effectors * Physicological response
* 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)** ## Footnote Excitatory
82
For the alpha adrenergic receptor subtype, **β3** list the: * G protein * Location * Biochemical Effectors * Physicological response
* G protein: **Gs** * Location: Adipose tissue * Biochemical Effectors: Stimulates adenylyl cyclase **(↑cAMP)** * Physicological response: Lipolysis, Nitric Oxide release **(Fat breakdown)**
83
What are the 4 components affecting Blood Pressure?
1. Resistance 2. Cardiac Output 3. Volume 4. Capacitance
84
What tissues do ⍺1 adrenergic receptor target and what is the effect of each?
* **Most vascular smooth muscle: Contraction** * Heart: Increased force * Prostate: Contraction * Pupillary dilator muscle: Contraction (pupil dilation) | Excitatory-Gq
85
What tissues do ⍺2 adrenergic receptors target and what are the effect of each?
* **Postsynaptic CNS-Multiple (↓SNS tone)** * **Presynaptic ANS-Decrease NT release** * Some vascular smooth muscle-Contraction | Inhibitory-Gi ## Footnote Bolded-most important to remember
86
What tissues do β1 adrenergic receptors target and what are the effect of each?
* **Heart-Increased force and rate** * **Juxtaglomerular cells-Increased renin release** (fluid retention to maintain BP) | Excitatory-Gs ## Footnote Bolded-most important to remember
87
What tissues do β2 adrenergic receptors target and what are the effect of each?
* **Skeletal muscle blood vessels-Relaxation** (increase blood flow to skeletal muscle) * **Bronchial smooth muscle-Relaxtion** * **Liver-Glycogenolysis and gluconeogenesis** * Uterus-Relaxation | Excitatory-Gs ## Footnote Bolded-most important to remember
88
What tissues do β3 adrenergic receptors target and what are the effect of each?
* **Fat cells- Increased lipolysis** * **Endothelial cells-Nitric oxide production** | Excitatory-Gs ## Footnote Bolded-most important to remember
89
Explain the reuptake and repacking of NE
* 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
List drugs that are indirect-acting sympathomimetics | Also known as Drugs that Enhance Noradrenergic Transmission
* **Cocaine** * **Amiphetamine** * Tyramine
91
Explain the mechanism of action and effect of Cocaine ## Footnote Indirect-acting sympathomimetics
* 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 ## Footnote Indirect-DOES NOT bind to receptor
92
Explain the mechanism of action and effects of **Amphetamine** and Tyramine ## Footnote Indirect-acting sympathomimetics
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** ## Footnote Indirect-DOES NOT bind to receptor
93
List drugs that are mixed-action sympathomimetics | Also known as Drugs that Enhance Noradrenergic Transmission
* **Ephedrine** * **Pseudoephedrine**
94
Explain the mechanism of action and effects of Ephedrine Pseudoephedrine ## Footnote Mixed- action symphathomimetics
MIxed-action * Causes Non-Vesicular Release (like amphetamines) but * Also affects adrenergic receptors ## Footnote Think Epi and amphetamines Binds to ⍺ and β receptors
95
List drugs that are natural catecholamine
* Dopamine * Epinephrine * Norepinephrine
96
For Epinephrine explain: * Hormone (type) * Mechanism of Action (MOA) * Effects (Cardiac, Vascular, Smooth muscle, Metabolic)
* 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
Explain why Epinephrine at low dosage has an increased pulse rate, increased blood pressure but decreased resistance
* 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 ## Footnote When Epi is at low dosage β receptors control the effects
98
What occurs when the dosage of Epinephrine is high?
* Changes from a β response into an ⍺ response * ⍺1 increases the resistance, heart rate and blood pressure
99
List the overall cardiovascular effects of Epinephrine
* Increase Vasoconstriction (⍺1) * Decreases peripheral resistance to skeletal (β2) * Net effect of activation ⍺1 and β2=Decrease in Resistance
100
What are 3 clinical uses for epinephrine and be specific as to which receptors are activates?
* **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
Pharmacokinetics of Epinephrine: * Administration * Metabolism * Exertion ##Footnote## LOW yield
* 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
List the adverse effects that can occur due to Epinepherine
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
For Norepinephrine explain: * Mechanism of Action (MOA) * Effects (Cardiac, Vascular, Smooth muscle, Metabolic)
* 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
Explain why Norepinephrine causes an decreased pulse rate (HR), increased blood pressure and increased resistance
* 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
Why is there a decrease in HR when given norepinephrine?
A dramatic increase in resistance→increases BP→Body responses by activating parasympathetic NS to decrease HR
106
What are 3 clinical uses of Norepinephrine?
1. Septic shock= septic =vasodilation-> need to vasoconstrict to incr BP (1st choice) 2. Hypotension 3. Vasopressor support in other types of shock
107
Why would you not use Norepinephrine to treat anaphylaxis?
Lack of β2 receptor, cannot vasodilate
108
Pharmacokinetics of Norepinephrine: * Administration * Metabolism * Excretion ## Footnote Low yield Similar to Epi
* 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
What are the adverse effects of Norepinephrine?
* Similar to Epi * EXCEPT, hypertension is more pronounced d/t ⍺1 stimulation without β2 balance
110
List the receptors that Dopamine activate
* D1 * D2 * β1 * ⍺1
111
When dopamine binds to D1 receptors what occurs?
**Vasodilation**. including renal vaculature, diuresis/natriuresis. Hypotensive effect
112
When dopamine binds to D2 receptors what occurs
(Presynaptic receptors) Negative feedback to **inhibit further norepinephrine**, and possibly dopamine releases
113
When dopamine binds to β1 receptors what occurs?
* Positive inotropic and chronotropic effect (increases contraction & HR) * At high levels of dopamine only
114
When dopamine binds to ⍺1 receptor what occurs?
* Seen only at high doses * Causes vasoconstriction
115
What are some clinical uses for dopamine?
1. Cardiogenic shock 2. Septic shock 3. Hypotension ## Footnote For cardiogenic shock, heart is not beating strong enough, want to increase force of contraction, and increase CO w/o increase afterload
116
Which receptors does a high dose of Dopamine stimulate?
⍺1 and β1 receptors just like norepinephrine
117
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
b. Salivary glands
118
2. Which of the following receptor types would have faster effects? a. M3 b. M2 c. B1 d. A2 e. Nm
e.Nm
119
3. 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
d. β2 Agonist
120
4. 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
c. Blocks NET leading to increased NE half-life
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5. 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
c. Norepinephrine

Pharmacology: Exam 2 (10 decks)

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