Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > Autonomic Pharmacology > Flashcards

Autonomic Pharmacology Flashcards

1
Q

Autonomic Nervous System

A

Controls subconscious or unconscious functions such as peristalsis, temperature, and heart rate. Functions that are necessary for life to be sustained. Two branches: parasympathetic and sympathetic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Parasympathetic system

A

Long presynaptic fibers, often synapse with postsynaptic neuron right in the target tissue. Do not synapse in the ganglia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Parasympathetic primary neurotransmitter

A

ACH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Sympathetic system

A

Synapse in the ganglion, shorter fibers. Long postsynaptic going to end organs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Sympathetic primary neurotransmitter

A

NE. Can have ACH or Dopamine as well. ACH in the ganglion, NE in target tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Modified pathway

A

Neuron from the spinal cord to the adrenal gland, will release Epi or NE “fight or flight” response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Somatic system

A

Volunatry muscle control. Long fibers run from spinal cord to muscle tissue, synapses in the neuromuscular junction. ACH is primary.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Enteric nervous system

A

GI tract. Motor and secretory function. Esophagus through the colon.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Neurotransmitter chemistry

A

Neurotransmitters synthesized in the neuron that releases them. Quantities vary. Some neurotransmitter functions will increase or decrease the function or the target tissue/organ.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cholinergic junction

A

Cholinergic synapse, small vesicles containing ACH. Choline brought into neuron by transporter, combined with acetyl-CoA through certain enzymes, synthesizes ACH to be stored in a vesicle. Neuron has ACH receptor that serves as negative feedback to stop releasing ACH, we do not recycle ACH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

“-ase’s”

A

Enzymes. Acetylcholinesterase metabolizes ACH, very quick metabolism in synapse.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Drug actions affecting ACH synthesis

A

We can block choline entering the neuron, decreasing ACH production. We can block transporters that take drugs into the vesicle, decreasing ACH. Calcium is needed to bind vesicle to the receptor to release ACH, botox interferes with calcium aspect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Release of ACH

A

Dependent on extracellular calcium. Action potential reaches the terminal and triggers opening of calcium channels, allowing influx of calcium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cholinoceptors

A

7 types of ACH receptors. 5 Muscarinic, 2 Nicotinic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

M1 receptor

A

CNS neurons, sympathetic postganglionic neurons, some presynaptic sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

M2 receptor

A

Myocardium, smooth muscle, some presynaptic sites, CNS neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

M3 receptor

A

Exocrine glands, vessels (smooth muscle and endothelium), CNS neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

M4 receptor

A

CNS neurons, possibly vagal nerve endings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

M5 receptor

A

Vascular endothelium, especially cerebral vessels, CNS neurons

20
Q

Catecholamines

A

Neurotransmitters in sympathetic or adrenergic system. All come from tyrosine. Tyrosine transported into cell, tyrosine hydroxylase enzyme converts it to dopamine or NE (adrenal gland further metabolizes to Epi), transported into storage vesicle. Receptors on postsynaptic membrane and neuron, negative feedback.

21
Q

Catecholamine metablism

A

REUPTAKE. NE is taken back into neuron and stored away, or MAO (lives in synapse) will metabolize NE, Epi, Dopamine.

22
Q

Indirect sympathomimetics

A

Mimic sympathetic function. Displaces NE in synapse. Example: amphetamine gets taken up by storage vesicle, so NE is pushed out of synapse (cannot be stored) and will see increased effects.

23
Q

Adrenoceptors

A
  1. 2 alpha, 3 beta.
24
Q

NANC

A

Nonadrenergic, noncholinergic neurons. Autonomic effector tissue containing nerve fibers that have no adrenergic or cholinergic fibers. Both motor and sensory. Peptides are the most common transmitter substances. Poorly understood, most studied in Enteric NS.

25
Q

Muscarinic agonists

A

Different ways they work. Either increase second messengers, or open ion channels.

26
Q

Nicotonic agonists

A

Prolonged agonist receptor occupancy: Contraction in skeletal muscle due to opening of ion channels and depolarization. Not in cardiac muscle. Example: succinylcholine, paralyzes because it over stimulates the receptor until it can no longer respond.

27
Q

Cholinergic agonists CNS effects

A

M1 receptors richly expressed in brain areas involving cognition.
Nicotine stimulates ACH receptors on dopamine-containing neurons: Mesolimbic system, reward system, pleasure/positive feedback. (Tobacco nicotine, highly lipid soluble, crosses BBB)

28
Q

Indirect acting cholinomimetics

A

Mimic ACH activity in the body, do not stimulate the receptor. Some have direct actions at nicotine receptors. Block acetylcholinesterase.
“-mine’s”, donepezil, edrophonium. Irreversible: “-phate’s” echothiophate, organophosphates

29
Q

Glaucoma

A

Aqueous humor is secreted by the epithelium of the ciliary body, flows into space in front of iris, exits via the canal of Schlemm.

30
Q

Glaucoma: Iris circular muscle

A

contracts, m3

31
Q

Glaucoma: Cilliary muscle

A

contracts, m3

32
Q

Myasthenia Gravis

A

An autoimmune disease affecting skeletal muscle neuromuscular junctions. Autoantibodies against a1 at nicotinic receptor, bind to receptor and ACH cannot bind. Competitive receptor interaction. Ptosis, diplopia, difficulty speaking and swallowing, extremity weakness.

33
Q

Diagnosis of MG

A

Edrophonium administered after baseline muscle strength measured, if no reaction occurs after 45 sedconds, an additional dose is given. If patient has MG, an improvement in muscle strength lasts about 5 minutes. Edrophonium inhibits metabolism of ACH, increasing activity.

34
Q

Treatment of MG

A

Ocular may be treated with cholinesterase inhibitors alone. Pyridostigmine or neostigmine used for long term. Additional therapy of immunosuppresssants for widespread muscle weakness. Immunoglobulins, plasmapharesis and thymus removal for severe disease.

35
Q

MG treatment side effects

A

Can have muscarinic side effects, treat with antimuscarinics (atropine). Bradycardia, diarrhea.

36
Q

Donepezil

A

Reversible indirect-acting cholinomimetic. Used for dementia, mild to moderate Alzheimer’s.

37
Q

Edrophonium

A

Reversible indirect-acting cholinomimetic. Diagnosis of MG, reversal of nondepolarizing neuromuscular blockade.

38
Q

Neostigmine

A

Reversible indirect-acting cholinomimetic. Reversal of nondepolarizing neuromuscular blockade.

39
Q

Oxybutynin

A

M1-4. First line for OAB. Also for bladder spasm after urologic surgery, reducing involuntary voiding in neuro disease.

Undergoes 1st pass metabolism. Metabolized by liver. 6% bioavailability. t1/2: IR 2 h, ER 13.2 +- 6.2 h.

Cross BBB more than other OAB drugs. Lipophilic, small, neutral.

Multiple forms.

40
Q

Oxybutynin metabolite

A

DEO. N-desethyloxybutynin. Responsible for unwanted SE.

ER released slowly over 24h, decreasing first pass metabolism and DEO production. Transdermal patch further decrease DEO, decrease dry mouth, associated with local skin rash/pruritus.

41
Q

Transdermal Oxybutinin

A

Up to 96 hours, steady state reached within 1 week. Significantly reduces urge incontinence, frequency.

42
Q

Toletrodine

A

OAB. Tertiary-amine (BUT low lipophilic). Nonselective M1-3, 5. First pass metabolism, hepatic metabolism. 77% bioavailability. t1/2: 2-3 h.

Limited ability to cross BBB. Efficacy similar to oxybutynin, but less SE (dry mouth).

43
Q

Trospium

A

OAB. Quaternary-amine, non selective. M1-5. First pass, RENAL excretion. (may be good for poly-pharmacy). 4-16% bioavailability. IR, ER.

60% excreted unchanged in the urine.

P-gp substrate, actively transported out of the brain

44
Q

Fesoterodine

A

OAB. Tertiary-amine. Non selective. M1-3, 5. First pass metabolism, hepatic. 50% bioavailability.

Active metabolite 5-hydroxymethyl tolterodine. 70% RENAL excretion as active/inactive metabolites. CrCl <30 adjust dose. Fine for 30-80.

Low lipophilic, limited crossing BBB. P-gp substrate, transported out of brain

45
Q

Darifenacin

A

OAB. Tertiary-amine. M3 SELECTIVE ANTAGONIST.
First pass, 15-20% bioavailability.
98% protein bound.
60% renal excretion, 3% unchanged.

High lipophilicity, substrate for P-gp out of brain.

46
Q

Solifenacin

A

OAB. Quaternary-amine. Non-selective M2-3. First pass, hepatic. 90% bioavailability.
Active metabolite 4R-hydroxy solifenacin.
LONG HALF LIFE, longer in elderly. 45-68 hours.
Only 3-6% excreted unchanged renally.

Low lipophilicity, P-gp substrate.

Pharmacology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions