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stuff lecture 2 Flashcards

1
Q

M1 (acts on what, second messengers?)

A

sweat glands, CNS

Gq/11, PLC, IP3, DAG, increase Ca increase NT release/ excitatory

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2
Q

M2

A

Heart, SM, presynaptic

*stim Gi, inhibits adenylyl cyclase, inhibits cAMP/ inhibitory

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3
Q

M3

A

exocrine, SM, endothelium

Gq/11, PLC, IP3, DAG, increase Ca, increase NT release

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4
Q

Nicotinic

A

Na gated ion channel, Nn (brain and autonomic ganglia) and Nm (skeletal m), excitatory

  • brain, adrenal medulla, autonomic ganglia, NMJ
  • rapid desensitization
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5
Q

Alpha1

A

SM, excitatory

Gq, PLC, IP3, DAG, increase Ca, increase NT

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6
Q

alpha 2

A

presynaptic nerve terminal, some SM

Gi, inhibits adenylyl cyclase, inhibits cAMP

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7
Q

all beta receptors

A

stimulate Gs, stim adenylyl cylase, stimulate cAMP

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8
Q

B1

A

heart, increases rate and force

stim Gs, stim adenylyl cyclase

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9
Q

B2

A

bronchioles, heart, smooth m in skeletal blood vessel (vasodilation)
stim Gs, stim adenylyl cyclase

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10
Q

B3

A

lipolysis in fat cells

stim Gs, stim adenylyl cyclase

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11
Q

D1, 5

A

brain and vascular bed

ususally stim Gs, stim adenylyl cyclase, increase cAMP

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12
Q

D2,3,4

A

Brain and OTHER tissue

stim Gi, inhibits adenylyl cyclase, decrease cAMP

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13
Q

M2 on heart

A

decelerates SA node, decreases atrial contractility

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14
Q

M3 on eye

A

contracts iris circular m, contracts ciliary muscle

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15
Q

a1 on eye

A

contracts iris radial m

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16
Q

B on eye

A

relaxes ciliary m

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17
Q

B1 on heart

A

accelerates SA node, accelerates ectopic pacemakers, increases contractility

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18
Q

B2 on heart

A

accelerates SA node, accelerates ectopic pacemakers, increases contractility

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19
Q

alpha on skin, skeletal BV

A

contracts BV, contracts skeletal m BV

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20
Q

B2 on skeletal BV

A

relaxes (vasodilation)

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21
Q

M3, M5 stimulation by drug on BV

A

releases NO, vasodilation

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22
Q

B2 on lungs

A

bronchodilation

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23
Q

M3 on lungs

A

bronchoconstriction

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24
Q

a2 on GI

A

relaxes SM walls

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25
B2 on GI
relaxes EM wall
26
a1 on GI
contracts sphincters
27
SNS on GI secretion
na
28
M3 on GI
contracts SM walls, relaxes sphincters, increases secretion
29
B2 on GU
relaxes bladder wall, relaxes uterus preg
30
PNS on BV
na (except indired NO release via M3 stimulation)
31
PNS (M) on GU
erection
32
a1 on GU
contract sphincter
33
SNS on GU
ejaculation
34
M3 on GU
contract bladder wall, relax sphincter
35
SNS (a) on pilomotor SM
contracts
36
M on eccrine sweat glands
increase secretion
37
a on apocrine/stress sweat gland
increases secretion (a for apocrine)
38
B2 on metabolic function
gluconeogenesis and glycogenolysis in liver
39
a on metabolic function
gluconeogenesis and glycogenolysis in liver
40
B3 on metabolic function
lipolysis on fat cells
41
B1 on metabolic function
renin release in kidney
42
Direct Cholinergic agonists (M agonists)
ACh, Methacholine, Carbachol, Bethanechol (all esters, quaternary) then Pilocarpine and cevimeline
43
Direct Cholinergic agonsts (N agonists)
Nicotine, varenicline (varenicline is partial N agonist in brain)
44
M agonist activity on Brain
improve memory, alertness and arousal | tx: alzheimers
45
therapeutics M agonist eye
Glaucoma (pilocarpine) * revere narrow angle glaucoma attack * cause blurred vision, drug of last choice
46
Muscarinic/cholinergic SE
mushroom/muscarine poisoning: salivation, N/V, HA, visual disturbances, bronchospasm, bradycardia, shock tx: atropine (M antag) and albuterol (B2 agonist)
47
contraindication M agonist
PUD, asthma/COPD, bowel obstruction
48
N stimulation in brain
low dose = alert high = tremor, emesis, increased respiraiton toxic = convulsion
49
N stim in ganglia (Nn)
activates SNS and PNS SNS: HTN, tachycardia alt with vagal bradycardia PNS: N/V, diarrhea, urination
50
N stim at NMJ
muscle twitch/contraction then depolarizing block/paralysis aka desensitization
51
tx N toxicity
Atropine (block M, decrease PNS) anticonvulsants assist respiration
52
Cholinesterase inhibitors
Neostigmine (quarternary), Physostigmine (tert), Edrophonium, OP (DFP, Echothiphate, Soman, Sarin, Parathion, Malathion)
53
what are the carbamates of ACHe inhibitors
Neostigmine, Physostigmine *covalent bond, 30min - 6 hr slow AChE hydrolysis
54
Edrophonium vs OP
Edro reversible and short acting 5-10 min, inject | OP: long lasting, phosphorylate AChE can be irreversible so prevent with 2PAM
55
AChE inhibitor on CNS
alert, improve memory, convulsion, respiratory arrest
56
AChE inhibitor on heart
*all ganglia activated * in heart, PNS dominates (ganglia and M receptor stim) --> bradycardia, decrease contractility, decrease CO BP: little effect bc no cholinergic innervation
57
AChE at NMJ
low concentration: intensify/prolong ACh action, increase muscle strength (neo tx myasthenia) high: twitches, fasiculation, NMJ block, paralysis
58
Echothiophate
OP AChE inhibitor, quaternary, EYEDROP, long duration action, decrease IOP tx narrow angle glaucoma
59
soman, sarin, tabun
OP AChE inhibitor - n gases, more potent and faster than DFP
60
Glaucoma tx
direct M agonist (pilocarpine, carbachol) or AChE inhibitor (physostigmine, echothiophate) - SE bc activate ciliary m; near vision accomodation
61
Reversal of NMJ block
use AChE inhibitor ie neostigmine
62
AChE inhibitor toxicity
SLUDGE, bradycardia, hypotension, convulsion, NMJ stimulation then paralysis
63
OP AChE inhibitor toxicity tx
atropine til pupils dilate, 2PAM, respiration, Diazepam for convulsion
64
Carbamate (neostigmine, physostigmine AChE poisoning)
Carbaryl Propoxur Aldicarb 2PAM controversial
65
antimuscarinic (anticholinergic) drugs aka M antagonists
``` atropine, scopolamine tropicamide (eye), homatropine (eye) Ipratropium, tiotropium inhaled (lung) Dicyclomine (anti GI spasmodic) Lomotil (atropine +opiod tx diarrhea) Tolterodine, sarifenacin, darifenacin, fesoteridine, solifenacin, oxybutynin, trospium (bladder) ```
66
atropine absorption, scopolamine absorption
both good orally atropine in CNS only at high dose Scopolamine CNS easily (sedation, euphoria, amnesia) - motion sickness patch
67
effect of atropine on tissue related to dose
low: salivary, sweat gland, bronchiole medium: heart, eye, GI, GU high: CNS
68
anti M and parkinsons
antimuscarinics sometimes used for parkinsons
69
scopolamine on CNS
drowsiness, memory loss, relieves motion sickness, dies up secretion (pre-anesthetic) toxic: hallucinations, agitation, coma
70
M antagonist on eye
block iris circular m, mydriasis but inhibits ciliary so inhibits near vision, cycloplegia, photophobia, dry eyes, can cause narrow angle glaucoma! *tropicamide, homatropine
71
Normal conditions cholinergic input on heart vs with post-synaptic M2 antagonist/block
cholinergic input stimulate M2 receptors in atria, SA/AV node (no BP control) *PRESYNAPTIC M2 RECEPTORS DECREASE NE RELEASE thus HR is DECREASED aka VAGAL TONE so if give M2 antagonist like atropine, vagal tone will be inhibited, NE should increase, HR should increase aka TACHYCARDIA (slide 74 lecture 2)
72
post-synaptic M2 antagonist on heart rate and BP
increase NE bc M2 blocked, decreased vagal tone (vagal tone predominates in normal conditions), less vagal tones means TACHYCARDIA little effect on BV bc no cholinergic stimulants BUT since M3 stim can cause NO release (and thus vasodilation), blocking the M receptor prevents NO release and thus blocks vasodilation caused in response to M agonists
73
What affect might atropine OD have on the face
may cause vasodilation of face bc major route of perspiration is blocked, and if atropine is used excessively, perspiration (an M stimulated response) is inhibited (atropine is M antagonist). This inhibits heat loss via perspiration so the body responds by vasodilating the BV in face to decrease heat
74
overactive bladder meds
M3 antagonists (tolterodine, darifenacin, solifenacin, oxybutynin, trospium) *ocybutynin, tospium preven bladder spasm after prostrate surgery
75
how to remember the M antagonists
Mean antagonists. A troop gladly scoped [out] Ipra's tios home. The cyclone totally loaded Sarah's sole troubled ox. ``` meaning: Mean antagonists (M antagonists). A (atropine) troup (tropicamide) gladly (glycopyrrolate) scoped (scopolamine) [out] ipra's (ipratropium) tios (triotropium) home. (homatropine) The cyclone (dicyclomine) totally (tolterodine) loaded (lomotil) Sarah's (sarifenacin) sole (solifenacin) troubled (trospium) ox (oxybutynin) ```
76
M antagonist - cardiac uses
ATROPINE: decrease bradycardia due to vagal tone, reverse heart block, after MI GLYCOPYRROLATE: in surgery to prevent excessive vagal reflexes
77
M antagonist - Respiratory uses
IPATROPIUM (ATROVENT) or TIOTROPIUM (SPIRIVA): | improved breathing in COPD by blocking bronchoconstriction, some asthma help
78
M3 antagonist - overactive bladder use
Tolteridone, fesoterodine, darifenacin, solifenacin: *promote continence; SE dry mouth, blurred vision
79
M antagonist - post surgery bladder
Oxybutynin, trospium: * prevent bladder spasm after prostate survery by blocking muscarinic influence on bladder tone and spasm * dry mouth main SE
80
contraindications to using M antagonists
narrow angle glaucoma, BPH SE: dry mouth, decrease bronchial secretion, tachycardia, mydriasis, cycloplegia, decreased GI motility, urinary retention, dry kin, decreased sweating
81
Atropine OD and tx
dry as a bone, blind as bat, red as a beet, mad as a hatter | tx: AChE inhiitor (pysostigmine)
82
other drugs with anticholinergic effects to beware of for M antagonist OD
antihistamine (benadryl), TCA, antipsych, plants, eyedrops, anti-diarrheal prep
83
What types of NMJ blockers are there and what do they do?
block N receptor on skeletal m; used to produce paralysis during surgery * depolarizing: stim before blockade * non-depolarizing: competitive antagonist, produce direct block
84
How does Succinylcholine (a depolarizing NMJ blocker) work
two succ bin Nicotinic NMJ receptor, top gat opens, sodium flows through then time dep gate closure, channel BLOCKED *depolarizes before blocking, initial contraction before paralysis; brief action, rapid onset
85
how does non depolarizing block work
block receptor, prevent ACh effect (inhibit muscle contraction), competitive reversible, used in surgery to relax muscle *AChE inhibitor used to reverse effect
86
ganglion receptor blockers mode of action
block N receptor at autonomic ganglia, decrease ANS output, non depolarizing competitive antagonists *once used to tx HTN, not used now much
87
what are the ganglion blockers
hexamethonium | mecamylamine (competitive blocker, enters CNS, sedation, mental status affected, mvmt affected
88
hexamethonium man
pink, pale, warm dry, placid can't cry, doesn't blush or get pale, doesn't sweat,wears a corset and may fidget, dry mouth and throat, far sighted, blinded by light, eyes are red, doesn't belch, feels the cold, good BP, no ulcers, no hunger pangs, stomach doesn't rumble, constipated, urinary retention and impotence SNS
89
Ganglion blockers affect on body systems
mostly SNS: cycloplegia, mydriasis, vasodilation, decreased vagal tone, orthostatic hypotension, contractility blocked, decreased vagal tone - tachycardia, bladder tone decreased, urinary retention, erection/ejaculation reduced, no sweating
90
review
slides 100-111 on NMJ block

Pharm II (12 decks)

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