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Pharm II > stuff lecture 2 > Flashcards

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
Q

B2 on GI

A

relaxes EM wall

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26
Q

a1 on GI

A

contracts sphincters

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27
Q

SNS on GI secretion

A

na

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28
Q

M3 on GI

A

contracts SM walls, relaxes sphincters, increases secretion

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29
Q

B2 on GU

A

relaxes bladder wall, relaxes uterus preg

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30
Q

PNS on BV

A

na (except indired NO release via M3 stimulation)

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31
Q

PNS (M) on GU

A

erection

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32
Q

a1 on GU

A

contract sphincter

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33
Q

SNS on GU

A

ejaculation

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34
Q

M3 on GU

A

contract bladder wall, relax sphincter

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35
Q

SNS (a) on pilomotor SM

A

contracts

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36
Q

M on eccrine sweat glands

A

increase secretion

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37
Q

a on apocrine/stress sweat gland

A

increases secretion (a for apocrine)

38
Q

B2 on metabolic function

A

gluconeogenesis and glycogenolysis in liver

39
Q

a on metabolic function

A

gluconeogenesis and glycogenolysis in liver

40
Q

B3 on metabolic function

A

lipolysis on fat cells

41
Q

B1 on metabolic function

A

renin release in kidney

42
Q

Direct Cholinergic agonists (M agonists)

A

ACh, Methacholine, Carbachol, Bethanechol (all esters, quaternary) then Pilocarpine and cevimeline

43
Q

Direct Cholinergic agonsts (N agonists)

A

Nicotine, varenicline (varenicline is partial N agonist in brain)

44
Q

M agonist activity on Brain

A

improve memory, alertness and arousal

tx: alzheimers

45
Q

therapeutics M agonist eye

A

Glaucoma (pilocarpine)

  • revere narrow angle glaucoma attack
  • cause blurred vision, drug of last choice
46
Q

Muscarinic/cholinergic SE

A

mushroom/muscarine poisoning: salivation, N/V, HA, visual disturbances, bronchospasm, bradycardia, shock
tx: atropine (M antag) and albuterol (B2 agonist)

47
Q

contraindication M agonist

A

PUD, asthma/COPD, bowel obstruction

48
Q

N stimulation in brain

A

low dose = alert
high = tremor, emesis, increased respiraiton
toxic = convulsion

49
Q

N stim in ganglia (Nn)

A

activates SNS and PNS
SNS: HTN, tachycardia alt with vagal bradycardia
PNS: N/V, diarrhea, urination

50
Q

N stim at NMJ

A

muscle twitch/contraction then depolarizing block/paralysis aka desensitization

51
Q

tx N toxicity

A

Atropine (block M, decrease PNS)
anticonvulsants
assist respiration

52
Q

Cholinesterase inhibitors

A

Neostigmine (quarternary), Physostigmine (tert), Edrophonium, OP (DFP, Echothiphate, Soman, Sarin, Parathion, Malathion)

53
Q

what are the carbamates of ACHe inhibitors

A

Neostigmine, Physostigmine
*covalent bond, 30min - 6 hr
slow AChE hydrolysis

54
Q

Edrophonium vs OP

A

Edro reversible and short acting 5-10 min, inject

OP: long lasting, phosphorylate AChE can be irreversible so prevent with 2PAM

55
Q

AChE inhibitor on CNS

A

alert, improve memory, convulsion, respiratory arrest

56
Q

AChE inhibitor on heart

A

*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
Q

AChE at NMJ

A

low concentration: intensify/prolong ACh action, increase muscle strength (neo tx myasthenia)

high: twitches, fasiculation, NMJ block, paralysis

58
Q

Echothiophate

A

OP AChE inhibitor, quaternary, EYEDROP, long duration action, decrease IOP tx narrow angle glaucoma

59
Q

soman, sarin, tabun

A

OP AChE inhibitor - n gases, more potent and faster than DFP

60
Q

Glaucoma tx

A

direct M agonist (pilocarpine, carbachol) or AChE inhibitor (physostigmine, echothiophate) - SE bc activate ciliary m; near vision accomodation

61
Q

Reversal of NMJ block

A

use AChE inhibitor ie neostigmine

62
Q

AChE inhibitor toxicity

A

SLUDGE, bradycardia, hypotension, convulsion, NMJ stimulation then paralysis

63
Q

OP AChE inhibitor toxicity tx

A

atropine til pupils dilate, 2PAM, respiration, Diazepam for convulsion

64
Q

Carbamate (neostigmine, physostigmine AChE poisoning)

A

Carbaryl
Propoxur
Aldicarb
2PAM controversial

65
Q

antimuscarinic (anticholinergic) drugs aka M antagonists

A 
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
Q

atropine absorption, scopolamine absorption

A

both good orally
atropine in CNS only at high dose
Scopolamine CNS easily (sedation, euphoria, amnesia) - motion sickness patch

67
Q

effect of atropine on tissue related to dose

A

low: salivary, sweat gland, bronchiole
medium: heart, eye, GI, GU
high: CNS

68
Q

anti M and parkinsons

A

antimuscarinics sometimes used for parkinsons

69
Q

scopolamine on CNS

A

drowsiness, memory loss, relieves motion sickness, dies up secretion (pre-anesthetic)
toxic: hallucinations, agitation, coma

70
Q

M antagonist on eye

A

block iris circular m, mydriasis but inhibits ciliary so inhibits near vision, cycloplegia, photophobia, dry eyes, can cause narrow angle glaucoma!
*tropicamide, homatropine

71
Q

Normal conditions cholinergic input on heart vs with post-synaptic M2 antagonist/block

A

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
Q

post-synaptic M2 antagonist on heart rate and BP

A

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
Q

What affect might atropine OD have on the face

A

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
Q

overactive bladder meds

A

M3 antagonists (tolterodine, darifenacin, solifenacin, oxybutynin, trospium)

*ocybutynin, tospium preven bladder spasm after prostrate surgery

75
Q

how to remember the M antagonists

A

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
Q

M antagonist - cardiac uses

A

ATROPINE: decrease bradycardia due to vagal tone, reverse heart block, after MI

GLYCOPYRROLATE: in surgery to prevent excessive vagal reflexes

77
Q

M antagonist - Respiratory uses

A

IPATROPIUM (ATROVENT) or TIOTROPIUM (SPIRIVA):

improved breathing in COPD by blocking bronchoconstriction, some asthma help

78
Q

M3 antagonist - overactive bladder use

A

Tolteridone, fesoterodine, darifenacin, solifenacin: *promote continence; SE dry mouth, blurred vision

79
Q

M antagonist - post surgery bladder

A

Oxybutynin, trospium:

  • prevent bladder spasm after prostate survery by blocking muscarinic influence on bladder tone and spasm
  • dry mouth main SE
80
Q

contraindications to using M antagonists

A

narrow angle glaucoma, BPH

SE: dry mouth, decrease bronchial secretion, tachycardia, mydriasis, cycloplegia, decreased GI motility, urinary retention, dry kin, decreased sweating

81
Q

Atropine OD and tx

A

dry as a bone, blind as bat, red as a beet, mad as a hatter

tx: AChE inhiitor (pysostigmine)

82
Q

other drugs with anticholinergic effects to beware of for M antagonist OD

A

antihistamine (benadryl), TCA, antipsych, plants, eyedrops, anti-diarrheal prep

83
Q

What types of NMJ blockers are there and what do they do?

A

block N receptor on skeletal m; used to produce paralysis during surgery

  • depolarizing: stim before blockade
  • non-depolarizing: competitive antagonist, produce direct block
84
Q

How does Succinylcholine (a depolarizing NMJ blocker) work

A

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
Q

how does non depolarizing block work

A

block receptor, prevent ACh effect (inhibit muscle contraction), competitive reversible, used in surgery to relax muscle

*AChE inhibitor used to reverse effect

86
Q

ganglion receptor blockers mode of action

A

block N receptor at autonomic ganglia, decrease ANS output, non depolarizing competitive antagonists
*once used to tx HTN, not used now much

87
Q

what are the ganglion blockers

A

hexamethonium

mecamylamine (competitive blocker, enters CNS, sedation, mental status affected, mvmt affected

88
Q

hexamethonium man

A

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
Q

Ganglion blockers affect on body systems

A

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
Q

review

A

slides 100-111 on NMJ block

Pharm II (12 decks)

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