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Z-Advanced Pharmacology > Exam 2 - Cholinergic, muscarinic, alpha, and beta > Flashcards

Exam 2 - Cholinergic, muscarinic, alpha, and beta Flashcards

1
Q

Briefly describe the autonomic nervous system and what are its subdivisions?

A

Contains systems not under our concious control including: symapathetic, parasympathetic, and enteric.

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2
Q

What is the “fight or flight” mode and its responses?

A

Activation of the sympathetic nervous system that increases HR and BP, dilates bronchioles and pupils, and shunts blood to needed muscles.

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3
Q

What is the ergotropic response?

A

Movement related response that requires energy during sympathetic activation.

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4
Q

What is the “rest and digest” mode and its responses?

A

Activation of the parasympathetic nervous system leads to energy conservation and shunting blood to endocrine, GI, and urogenital organs.

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5
Q

What is trophotropic response?

A

Means leading to growth. Describes parasympathetic response.

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6
Q

Where are the pre and postganglionic fibers located in the sympathetic nervous system?

A

In the thoracolumbar region. The preganglionic fibers terminate in the paravertebral chain ganglia. The postganglionic fibers innervate the affected organs.

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7
Q

Where are the pre and postganglionic fibers of the parasympathetic nervous system located?

A

In the craniosacral region.The preganglionc fibers leave the CNS through the cranial nerves and sacral spinal roots (there is no chain ganglion)

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8
Q

What is the differences between the cell bodies of the somatic nervous system and autonomic nervous system?

A

In the SNS the cell bodies are located within the brain/spinal cord and called nuclei. In the ANS they are located outside the brain/spinal cord and clusterd together to form ganglia.

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9
Q

Describe the nerve fibers in the sympathetic nervous system?

A

The preganglionc fibers are short while the postganglionic fibers are long. The fibers form a chain so that activation will activate the entire pathway. The ganglia are close to the spinal cord.

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10
Q

Describe the nerve fibers in the parasympathetic nervous system?

A

The preganglionc fibers are long and the postganglionic fibers are short. The ganglia are in the effector organs.

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11
Q

What is the length of effects of the parasympathetic nervous system? why?

A
  • They are short lived
  • Once the intended effect is reach, there is no more need to keep effect going

Ex: HR is 120 PNS brings down to 70 and then shuts off.

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12
Q

What are the effector organs of the autonomic nervous system?

A

Cardiac muscle, smooth muscle, and glands (not skeletal)

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13
Q

What do all preganglionic fibers of the ANS release?

A

Aceytlcholine

Both sympathetic and parasympathetic

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14
Q

What do the postganglionic fibers of the ANS release?

A

Both ACh and norepiniphrine to either stimulate or inhibit.

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15
Q

What are sympathomimetics and the two different types?

A
  • Drugs that mimic the action of norepinehrine
    -Ionotropy, chronotropy, vasoconstriction, bronchodilation
  • Direct or indirect.

Direct: epinephrine, isoproterenol, albuterol
Indirect: Ephedrine and amphetamines.

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16
Q

What are sympatholytics and the different types?

A
  • Block the effects of the sympathetic nervous system
  • Beta and alpha blockers
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17
Q

What are the different receptors in the autonomic nervous system? What ligand do they respond to?

A
  • Cholinergic - respond to aceytlcholine
    -Muscarinic
    -Nicotinic
  • Adrenergic - respond to norepinephrine/epinephrine
    -Alpha
    -Beta
    -Dopamine
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18
Q

What are the muscarinic receptor subtypes? Define if excitatory or inhibatory.

A
  • Muscarinic M1 - Excitatory
  • Muscarinic M2- Inhibitory
  • Muscarinc M3- Excitatory
  • Muscarinic M4- Inhibitory
  • Muscarinc M5- Excitatory
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19
Q

What are the nicotinic receptor subtypes?

A
  • Nicotinic Nn (neuronal)
  • Nicotinic Nm (muscular)
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20
Q

What are the alpha adrenoreceptor subunits? What is their signal transduction pathway?

A
  • Alpha 1 - activates Gq GPCR which acivates phospholipase C and IP3/DAG as 2nd messengers.
  • Alpha 2 - activates Gi GPCR that inhibits adenylate cyclase which decreases cAMP production
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21
Q

What are the beta adrenoreceptor subunits? What is their signal transduction pathway?

A
  • Beta 1, 2, 3 - all activate Gs GPCR that stimulates adenylate cyclase and increases cAMP production.
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22
Q

Describe the pathway of norepinephrine activated alpha 1 receptors?

A
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23
Q

Describe the pathway of B1/B2 stimulation in a cardiac myocyte?

A

Alpha 2 is inhibitory and prevents the release of norepinephrine

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24
Q

Describe the pathway of Beta 2 stimulation in peripheral smooth muscle?

A

cAMP inhibts MLCK (myosin light chain kinase) and leads to relaxation

alpha 1 consticts in vascular smooth muscle and beta 2 dilates peripheral smooth muscle = more blood flow to muscles during fight or flight

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25
Describe the pathway of the different muscarinic and nicotinic cholinergic receptors when bound by ACh?
* **M1,M2, M3** - activate Gq and activate phospholipase * **M2, M4** - activate Gi and inhibit adenylate cyclase * **Nicotinc**- Bind to ion channels
26
Describe the autonomic and hormonal feedback loops that regulate changes in MAP?
27
What is the function of chain ganglia?
They allow multiple organs to be effected by the stimulation of one neuron. Happens during fight or flight
28
Define heteroreceptors and autoreceptors? What are the types of autoreceptors?
**Heteroreceptors** - receptors on the neuron that can bind to molecules other than the released neurotransmitter. **Autoreceptors** - bind to the neurotransmitter released by the neuron. * can be inhibitory (negative feedback) or excitatory (positive feedback) * *Inhibitory* = a2 receptor on noradrenergic nerve terminal * *Excitatory* = B receptor on noradrenergic nerve terminal
29
What is the effects of stimulation of sympathetic and parasympathetic activity in the heart?
30
What is the effects of stimulation of sympathetic and parasympathetic activity in the blood vessels?
31
What is the effects of stimulation of sympathetic and parasympathetic activity in the bronchioles?
32
What is a cholinomimetic (parasympathomimetic)?
A drug that mimics the actions of acetylcholine
33
What is a parasympatholytic (antimuscanaric)?
A drug that inhibts the effects of Ach and the parasympathetic nervous system.
34
What types of receptors are involved in skeletal muscle blood vessels? What is there effect when stimulated? What is the normal skeletal circulating blood volume when at rest and stimulated?
At rest 20%, up to 80% during fight or flight
35
What is the structure of a neuron?
* Information is recieved in the dendrites * The cell body decides whether or not to send a signal * The axon hillock generates the action potential * The signal reaches the telondendrion * The neurotransmitter is relased from the synaptic bouton
36
What is the structure of the synapse?
* Comprised of the presynpatic and postsynaptic terminals * Neurotransmitters are stored in secretory vesicles that will bind with the presynaptic membrane and enter the synaptic space where it can ineract with receptors on the postsynaptic membrane
37
What are the 3 types of synapses?
* Chemical - release neurotransmitters * Electrical - gap junctions * En passant - synapses connect to the middle of the axon
38
What are the 4 fates of neurotransmitters in the synapse?
* Diffuses away from synapse * Degraded by enzymes (acetylcholinesterase) * Uptake into pre-synaptic cell * Uptake into surrounding cell
39
What are the 6 main neurotransmitter classes and examples of each?
1.Esters - Acetylcholine (R-COOR) 2.Monamines - Norepinephrine, serotonin, dopamine 3.Amino Acids - GABA, glutamate 4.Purines - Adenosine, ATP 5.Peptides - Substance P, endorphins 6.Inorganic gases - Nitric oxide (not stored, made as needed) PIMPEA
40
What are the 3 neurotransmitters involved in emotion?
* Norepinephrine * Dopamine * Serotonin
41
What are examples of excitatory and inhibitory NT?
* Excitatory - Glutamate * Inhibitory - GABA and glycine ## Footnote Remember: excitatory leads to depolarization; inhibitory leads to hyperpolarization
42
What is the pathway for ACh release and degradation?
*Dependent on extracellular calcium* - Action potential reaches terminal – Triggers Ca2+ influx – Ca2+ destabilizes storage vesicles – Fusion of vesicle with terminal membrane – Exocytosis – release of contents into synaptic cleft – ACh plus cotransmitters (ATP, peptides) – ACh broken down by AChE
42
Where and how is ACh synthesized? Where is stored?
* Made in the cytoplasm * Acetyl-CoA and Choline turned into ACh by Choline acetyltransferases (ChAT) * Stored in vesicles in quanta by VAT (1000-50,000 per vesicle)
43
How is acetylcholine transported into the cell? Into the vesicle?
* CHT (choline transporter) - into neuron * VAT (vesicular acetylcholine transporter) - into vesicle ## Footnote Ach pnemonic: CHT ChAT VAT
44
How is the vesicle anchored (docked)?
* SNARE complex: - Syntaxin - SNAP - 25 - VAMP = vesicular associated membrane protein | "loading" gun
45
What is priming of a vesicle?
-It is ATP dependent and allows for rapid exocytosis -"Cocking" gun
46
Draw out the entire pathway from acetylcholine production to release in the synapse.
47
What are some targets for cholinergic inhibition in the synapse/neuron and examples?
* Voltage gated ion channels - Calcium channel blockers * Acetylchoinesterase inhibitor - Sarin nerve gas (atropine is treatment), neostigmine, pyridostigmine * Botox - inhibits vesicle release from storage proteins by cleaving SNAP
48
What is the precursor to adrenergic neurotransmitters?
* Tyrosine - can be converted to dopa, dopamine, epinephrine, or norepinephrine
49
How is norepinephrine taken back up into the neuron?
NET - norepinephrine transporter
50
How is NE degraded in the synapse?
MAO (mono-amine oxidase)
51
Draw the entire pathway of NE release from a neuron.
52
What are some targets for adrenergic inhibition in the synapse and examples?
* **Cocaine & tricyclic antidepressants** - inhibit NET (as well as serotonin reuptake) * **MAOIs** - Inhibit NE degradation
53
What is the difference in signaling between muscarinic and nicotinic cholinocepters?
* Muscarinic - GPCR * Nicotinic - Ion channels
54
What are the direct acting cholinomimetic groups? Examples of each?
* Esters of choline (*permanently charged, do not cross barriers well*) - **succinylcholine**, carbachol (decrease IOP), methacholine (diagnosis of asthma), bethancol (bladder dysfunction). * Alkaloids -Pilocarpine, **nicotine** *(lipid soluble)*, arecoline (betel nut)
55
What are some effects of cholinomimetic agonists in the eye?
Causes pupil constriction which increases intraocular drainage
56
What are some effects of cholinomimetic agonists in the CV system?
* Reduction in peripheral vascular resistance * Vasodilation = lowering of BP, reflexive HR increase - bradycardia in overdose
57
What are some effects of cholinomimetic agonists in the lungs?
* Bronchial smooth muscle contraction * Tracheobronchial mucosa secretion increased ## Footnote We want a normal tone in our bronchioles; decreases flow and increases surface area to remove foreign particulate This can be bad for asthmatics
58
What are some effects of cholinomimetic agonists in the GI system?
* Increase motor and secretory activity * Salivary and gastric gland stimulation * Sphincters relax
59
What are some effects of cholinomimetic agonists in the brain?
Nicotine has alerting response and causes release of dopamine (addiction), serotonin, GABA, NE In large doses can causes toxicity and death
60
What are the different types of glaucoma?
* Open angle - drainage into canal of schlemm partially blocked leading to increased IOP * Narrow angle - **iris** is bulged forward and narrowed, partially blocking the canal of schlemm
61
What drug is contraindicated in closed angle glaucoma? Why?
Atropine - it causes relaxation of ciliary smooth muscle causing complete obstruction of drainage of aqueous humor (**medical emergency**)
62
How do indirect acting cholinomimetics work?
They block or inhibit acetylcholinesterase
63
What are examples of indirect cholinomimetics?
* Alcohols - Edrophonium * Carbamates - Neostigmine, pyridostigmine * Organophosphates - Echothiophate (covalent bond formed, somewhat irreversible) ## Footnote **Note the difference in durations of action!!!**
64
What drugs can be used to diagnose and treat myasthenia gravis?
* Cholinesterase inhibitors - edrophonium used as diagnostic (short half life); can be treated with neostigmine or pyridostigmine to increase the amount of ACh in the synapse
65
How are acetylcholinesterase inhibitors used in surgical anesthesia?
We can use a drug like neostigmine to reverse the effects of NMB (pancuronium)
66
What are the symptoms of organophospate posioning (pesticides)? What is the treatment?
* SLUDGE - M: Salivation, Lacrimation, Urination, Defecation, GI upset, Emesis, Miosis * Atropine and pralidoxime
67
Be able to describe this pathway
68
What are the symptoms of nicotine toxicity?
Headaches, nausea, dizziness, collapse, breathlessness, loss of conciousness
69
How does pralidoxime treat organophosphate toxicity?
It prevents aging of the organophosphate and regenerates acetylcholinesterase
70
What is atropines MOA?
Atropine is an antimuscarinic and competitively inhibits muscaniric receptors to aceytlcholine.
71
How can atropine be used preoperatively?
* Help prevent vagal stimulation and potential bradycardia * Reduce respiratory secretions * Block unwanted GI activity * Postoperative nausea (scopalamine patch)
72
What are indications for atropine in the respiratory system?
To treat bronchospasm in COPD to bronchodilate | Atrovent
73
What are atropine's effects on the eye?
* Dilation - used in cycloplegia (tropicamide) * Decreased watering
74
What are atropine's effect on the heart?
Increase in HR, treatment for bradycardia
75
What are the clinical indications for atropine?
Parkinson's - adjunctive Motion sickness - scopalamine Opthalmic - dilation of the eye (tropicamide) Asthma- ipratropium bromide Bradycardia - Atropine IV
76
What are the clinical contraindications for atropine?
* Glaucoma patients * Elderly men with known BPH (atropine causes swelling of the prostate gland)
77
What are the symptoms of atropine overdose?
**Hot** as a hare **Blind** as a bat **Dry** as a bone **Red** as a beet **Mad** as a hatter
78
What is te treatment for atropine overdose?
Pyridostigmine or other parasympathomimetic
79
What are the two categories of muscle relaxants?
Depolarizing and non-depolarizing
80
What is a depolarizing muscle relaxant? How does it work? What are its effects?
* Succinylcholine * Strucurally resembles ACh and acts as ACh receptor agonist. - This causes continuous end plate depolarization (cell cannot repolarize) resulting in relaxation/paralysis
81
What are the non-depolarizing muscle relaxants? How do they work?
* Pancuronium, Atrocurium, Mivacurium * They are competitive antagonists of ACh. They do not depolarize the motor end plate.
82
How can you reverse the effects of NMB?
Neostigmine or suggamadex (roc and vec)
83
What are the two types of nicotinic antagonists?
Ganglion blockers (Nn) and neuromuscular blockers (Nm)
84
What is the MOA of direct and indirect adregenergic agonists?
* **Direct** - bind dierectly to and activate adrenergic receptors * **Indirect** - cause an increase in the amount of norepinephrine in the synapse
85
What is the basic structure of a catecholamine?
* Benzene ring with OH group at 3 and 4 carbons. * Amine group opposite the ring
86
How do substitutions on the benzene ring of catecholamines effect their degredation?
* Greatly reduces their potency
87
How do substitutions at the alpha carbon effect catecholamine degredation?
They have a prolonged action because oxidation by MAO is blocked ## Footnote Phenylephrine, ephedrine, amphetamine
88
What are the major adrenergic receptor types and subtypes?
* **Alpha**- alpha 1 and alpha 2 * **Beta** - Beta 1, 2, and 3 * **Dopamine** - dopamine 1-5
89
What are the effects in the CV system after administering an alpha agonist?
* Strong increase in vascular tone * Strong increase in BP * No real effect on contraction
90
What are the effects on the CV system by a beta agonist?
* Decreased vasular tone * Strongly increases contractility and HR * Decreases blood pressure
91
What are the effects on the CV system by a mixed alpha and beta agonist?
* Mixed increase/decrease vascular tone and HR * Strong increase in contractility * Increase in BP ## Footnote Ex: Epinephrine and norepinephrine
92
Name a nonselective alpha agonist?
Epinephrine and phenylephrine
93
Name a selective alpha 2 agonist?
Clonidine, methyldopa, and dexmedetomidine
94
Name a non-selective beta agonist?
Isoproterenol
95
What is a selective beta 1 agonist?
Dobutamine
96
What is a selective beta 2 agonist?
Albuterol
97
What tissues contain significant numbers of alpha 1? Which tissues contain alpha 2 receptors?
**Alpha 1**- Most vascular smooth muscle, prostate, heart **Alpha 2** - Adrenergic and cholinergic nerve terminals
98
What tissues contain significant numbers of beta 1 receptors? What tissues contain beta 2 receptors?
**Beta 1** - Heart **Beta 2** - Respiratory, uterine, and skeletal muscle vasculature
99
What are the major clinical effects of adrenoreceptor agonist in different organs?
* **Eye** - Alpha agonist = dilation * **Lungs** - Beta 2 = bronchodilation * **GI** - alpha and beta = relaxation * **CNS** - catecholamines don't cross BBB unless very large doses - leads to feelings of “impending doom”
100
What are the triphasic effects of dopamine?
* **Low dose** - DA1 in kidney = diuresis * **Moderate dose** - B1 = increase in contraction * **High dose** - alpha = increase in PVR/BP
101
What adrenergic agonist would be best for hypotensive emergency?
* Direct acting alpha agonist -Norepinephrine, phenylephrine
102
What adrenergic agonist would be best for CV syndrome or cardiogenic shock?
* Beta 1 agonist -Dobutamine, isoproterenol Milrinone: PDE3 inhibitor | Avoid peripheral vasoconstriction
103
What adrenergic agonists are best for non-cardiogenic shock?
* Volume replacemet (treat underlying cause) * Vasoconstrictors or dilators -Norepinephrine
104
What adrenergic agonist would you chose to reduce blood flow?
* Alpha receptor agonist -Ex: lido + epi, phenylephrine
105
What adrenergic agonist would be best for complete HB and caridac arrest?
* Target dilation of coronary arteries -Isoproterenol, epinephrine, atropine
106
What adrenergic agonist would be best for airway constricton?
* B2 selective agonists -Albuterol, terbutaline, metaproterenol
107
What adrenergic agonist is best for anaphylaxis?
* Epinephrine -Both alpha and beta effects
108
What drugs are alpha 2 agonists? What are the indications?
* Clonidine - hypertension, diarrhea, hot flashes, **hemodynamic instability during anesthesia** (blunts sympathetic outflow) * Dexmedetomidine - Sedation, very highly selective alpha 2 agonists * Methyldopa - pregnancy induced HTN
109
What are some of the toxicities associated with sympathomimetics?
Pressors * Hypertension * Cerebral hemorrhage * Angina * MI CNS * catecholamines in high doses lead to feeling of imending doom * cocaine can lead to convulsions and MI
110
What alpha antagonist is irreversibly bound?
* Phenoxybenzamine -recovery requires new receptors due to covalent bonding
111
What are the effects of an alpha blocker?
* Decreased BP, sedation, relaxation of vascular smooth muscles
112
What side effect may you see with non-selective alpha blockers? Why?
* Reflex tachycardia -Decrease in PVR leads the body to compensate by increasing CO (HR) - Alpha 2 is being blocked so NE is still being released
113
What are the indications for phentolamine?
Competitive antagonist for alpha 1 and alpha 2 * Reduces PVR * Reduces BP * Treatment of ED - *Some cardiac stimulation from alpha 2 inhibition*
114
How does phentolamine convert a pressor (epi) into a depressor?
Phentolamine is a competitive antagonist at alpha 1 and alpha 2. Epi is a competitive agonist of the same receptors. When phentolamine is given after epi, the pressor effects (vasoconstriction) are reversed.
115
What is the clinical use for phenoxybenzamine? What is important to know about this drug?
* Hypertension associated with pheochromocytoma (tumors producing NE) * It is covalently bound and irreversible
116
What are the clinical indications for prazosin?
* Hypertension and BPH -highly selective alpha 1 antagonist (has little effect on HR) -relaxes venous, arterial, and prostatic smooth muscle
117
What is the difference between selective and non-selective beta blockers?
* Non-selective: block both beta1 and beta 2 leading to decrease in HR and contractility and increase in bronchial tone. * Selective: Selective for beta 1 and safer for COPD and diabetics
118
What are the pharmacologic effects (good and bad) of beta blockers?
* Increased airway resistance (beta 2) * Decrease in HR and contractility * Decreased IOP by decreasing aqueous humor production * Inhibits lipolysis and glycogenolysis * Long term use can cause decrease in HDL and increase in LDL
119
Why can beta blockers be used with local anesthetics?
Cause local blockade of sodium channels
120
What is the non-selective beta blocker described in class? What's important about it?
* Propanolol * Undergoes extensive first pass metabolism
121
What are the selective oral beta blockers discussed?
Metoprolol and Atenolol
122
What beta blocker is used for intraoperative tachycardia? Why?
* Esmolol - Has an ultra short lifespan (safer in critically ill patients) - Highly beta 1 selective
123
When should beta blockers be used?
* Hypertension * Ischemic heart disease * Arrhythmias
124
What are the toxic effects of beta blockers?
* Bradycardia * Sedation * Worsening of asthma * Hypoglycemia in diabetics
125
What would be the effect of phentolamine and propanolol in the abscence of a competitive agonist?
There would be no effect
126
What would be the effects of propanolol in the prescence of epinephrine?
Epi would still cause constriction of peripheral vasculature (alpha 1) but propanolol would prevent dilation of skeletal smooth muscle (blocking beta 2)
127
Describe the 2 phases of succinylcholine block?
Phase 1: Depolarization Phase 2: Desensitization and prevention of ACh binding; acts as antagonist
128
Describe the 2 vesicle fusion hypothesis?
* Kiss and run - vesicle fuses and then removes it self from the membrane to return to the cytoplasm as a vesicle * Clatherin coated pit - the vesicle is endocytosed by clatherin pits where it can be reused in the cytoplasm
129
What enzyme degrades catecholamines in the gut? Why do some drugs not undergo this?
* COMT - catechol-O-methyltransferase * Phenylephrine does not have OH groups on the benzene ring, preventing breakdown by COMT
130
Why may you see a transient increase in BP when clonidine is first given?
It will agonize alpha 1 first leading to vasoconstriction before it crosses the BBB and agonizes alpha 2 leading to decrease in BP

Z-Advanced Pharmacology (17 decks)

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