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23 spring: pharm > Test 1: 14-16 > Flashcards

Test 1: 14-16 Flashcards

1
Q

where is ACh released

A
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2
Q

muscarine is considered to be a –

A

‘parasympathomimetic’

will cause vagal stimulation to the heart (decrease HR?)

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3
Q

how to make ACh

A
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4
Q

Choline synthesized from — supplied by diet and protein metabolism

A

serine

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5
Q

how is ACh made inside the nerve ending?

A

choline is brought into cell transporter (rate limiting step)

choline + Acetyle CoA (choline acetytransferase) = ACh

ACh moved into vesicle by VaCht(Vesicular acetylcholine transporter)

ACh is then moved out of nerve

there are no intracellular breakdown of ACh (unline NE)

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6
Q
A
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7
Q

what does botulinus toxin do?

A

blocks release of ACh into synapse

leads to flaccid paralysis

clostridium botulinum: cleaves synaptobrevin subunit to prevent export

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8
Q

how is ACh broken down

A

within the synaptic cleft
very fast reaction

water and acetylcholineterase(AChE)

will cleave/hydrolyze into acetic acid and choline

choline is then brought back into the nerve to be used again (this is rate limiting step)

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9
Q

how is NE vs ACh broken down in the synaptic cleft

A

NE: most NE will be taken back into the nerve to be recycled or broken down by MAO, anything left in the synaptic cleft will get eaten by COMT, bind to postsynaptic receptor, or bind to presynaptic autoreceptor(that stops reaction)

ACh: only gets broken down in the synapse, very fast hydrolization by AChE

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10
Q

— is not specific for ACh, but will hydrolyze it

A

Pseudocholinesterase (pseudo-/butyro-ChE)

non specific or serum cholinesterase

made by the liver and found in blood plasma

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11
Q

what is the rate limiting step of making ACh

A

choline reuptake into the nerve

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12
Q

where are nicotinic sites in PNS?

A

neuromuscular junctions(skeletal)
all preganglionic fibers (ANS and adrenal medulla)

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13
Q

where are the muscarinic sites in the PNS

A

where ACh is released at postganglionic fiber

all parasympathetics and sympathetic to the sweat gland

Muscarine is considered to be ‘parasympathomimetic’

nicotinic: both sympathetic and parasympathetic ganglia

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14
Q

what type of receptors are nicotinic?

A

ligand-gated ion channels
(ionotropic receptors)

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15
Q

what kind of receptors are muscarinic

A

GRCP
(metabotropic receptors)

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16
Q

Nicotinic — receptors are ligand-gated, nonselective cation ion channels

A

ACh

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17
Q

nicotinic ACh receptors will stimulate both the — and —

A

synpathetic and parasympathetic postganglionic neurons

ACh released all all pregranglionic site

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18
Q

4 effects of Nicotinic ACh receptors

A

stimulates ANS: sym and para postganglionic neurons

stimulate release of EPI/NE from adrenal medulla

cause contraction of skeletal muscle (Nm)

cause CNS effects: tremor, anxiety, respiratory and circulatory center effects

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19
Q

how does nicotinic receptor work?

A

5 subunits: 2⍺, 1 β𝛾δ

2 ACh binds to ⍺, pore opens, Na moves in and K moved out

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20
Q

— receptor works by Binding of 2 molecules of ACh causes opening of central pore allowing the flow of ions through the pore according to their concentration gradients (Na+ and K+)

A

nicotinic ACh

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21
Q

Muscarinic activation will cause:

— secretion
— contraction
relaxation of —
— of the heart

A

gland: sweat, salivary, tear, mucous

smooth muscle and pupillary constriction

sphincters: GI tract, urinary tract, biliary tract

slowing (bradycardia)

GPCR receptors

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22
Q

accronym to remember muscarinic activation

A

SLUMD

Salivation, Lacrimation, Urination, Miosis(pupils contract), Defecation,

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23
Q

M2 muscarinic receptors are found —

A

heart, smooth muscle, autonomic ganglia

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24
Q

where are M3 muscarinic receptors found

A

Exocrine glands, smooth muscle, blood vessels (endothelium)

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25
Q

Activation of M2 receptors are — in cardiac muscle

A

INHIBITORY

due to inhibition of adenylate cyclase (decrease cAMP in the cell) and activation of K+ channels (moves K out of cell)

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26
Q

Activation of M3 receptors are — in smooth muscle

A

EXCITATORY

due to the opening of plasma membrane and intracellular Ca2+ channels

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27
Q

how do M2 receptors cause inhibition of cardiac muscle

A

M2 will ativate K channels, this will cause K to leave making cell less negative (decreasing action potential)

M2 will also inhibit adenylate cyclase which leads to decrease in cAMP (cAMP used throughout the cell)

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28
Q

how does M3 receptors excitatory to smooth muscle?

A

M3 will open Ca channels, (Ca will come into cell, more positive= easier to cause impulse/contraction)

M3 will also open plasma membrane channel→ allow IP3 in which triggers more Ca into cell → contraction of cardiac muscle

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29
Q

what are some parasympathomimetics drugs

A

ACh
methacholine
carbachol
bethanecol

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30
Q

what happens when you give acetylcholine

A

No significant therapeutic applications

will trigger both nicotinic and muscarinic sites

poorly absorbed by GI or skin

if IV, rapidly hydrolyzed by plasma cholinesterase

no CNS effect, can’t get past BBB because it is + charged

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31
Q

— is a synthetic analog of acetylcholine that is more selective for Muscarinic vs Nicotinic receptor activity

A

methacholine (provocholine)

less susceptibile to getting hydrolyzed by AChE

used to diagnose asthma: will cause bronchial constriction

can cause bradycardia and hypotension

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32
Q

methacholine (provocholine) is more selective for — receptor activity

A

Muscarinic vs Nicotinic (M»N)

muscarinic ACh receptors: SLUMD
M2: inhibitory to cardiac muscle
M3: excitatory to smooth muscle

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33
Q

methacholine (provocholine) is used for

A

Used for diagnosis of asthma.
* Look for exaggerated bronchial constriction after methacholine administration

Cardiovascular side effects have limited its clinical use
* Potential for somewhat unpredictable bradycardia and hypotension

Muscarinic&raquo_space; Nicotinic
muscarinic ACh receptors: SLUMD
M2: inhibitory to cardiac muscle
M3: excitatory to smooth muscle

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34
Q

— are synthetic ACh that are Resistant to acetylcholinesterase (AChE) action

A

carbachol (carbamylcholine)

bethanecol (myotonachol)

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35
Q

what receptors do carbachol work on

A

Muscarinic and Nicotinic activity (M = N)

synthetic of ACh, that is resistant to AChE degredation

36
Q

what is carbachol used for

A
  • Selectively stimulates smooth muscle in the urinary and gastrointestinal tracts
  • Limited clinical use due to ganglionic stimulation (activates both para- and sympathetic side)
  • Used to induce miosis (pupil constriction)
  • Used in treatment of glaucoma to increase the outflow of aqueous humor from the eye

resistant to AChE
M=N

37
Q

bethanecol works on what receptors?

A

Muscarinic vs Nicotinic receptor activity (M&raquo_space; N)

38
Q

what is bethanecol used for

A

test pancreatic function since it increases secretions

Used to treat urinary retention by stimulating contraction of bladder

muscarinic: M3: found in exocrine glands, smooth muscle and blood vessels: is excitatory for smooth muscle

39
Q
A
40
Q

— is a Naturally Occurring Cholinergic Alkaloid from a south american shrub

A

pilocarpine

100x more potent then ACh
M>N

will cause sweating and increased salivation
will cause miosis, decreases intracoluclar pressuer by increasing drainage, increases BP and causes tachycardia

41
Q

pilocarpine will cause

A

(muscarinic effect) will cause sweating and increased salivation

will cause miosis

decreases intracoluclar pressuer by increasing drainage

(nictotinic effect) increases BP and causes tachycardia

south american shrub that acts as parasympathomimetic that is 100 x more potent then ACh with M>N activity

42
Q

— is made from the betel nut and turns teeth black

A

arecoline

M=N effect
previously used to treat tapeworm cause it increased GI movement

43
Q

arecoline is used for

A

no current uses

previously used to treat tapeworm infections

can be addictive and turn teeth black

made from betel nut

M=N receptors

44
Q

muscarine is made from —

A

mushroom amanita muscaria

poisonous from M»>N response

  • marked lacrimation, salivation, sweating, miosis
  • severe abdominal pain
  • frequent watery and painful bowel evacuations
  • cardiovascular collapse
  • vertigo, weakness, confusion, coma, convulsions
  • death in few hours

antidote atropine

45
Q

muscarine acts on what receptors?

A

M»>N

cause: marked lacrimation, salivation, sweating, miosis - severe abdominal pain - frequent watery and painful bowel evacuations - cardiovascular collapse - vertigo, weakness, confusion, coma, convulsions - death in few hours

poisionous mushroom

46
Q

what does muscarine cause

A
  • marked lacrimation, salivation, sweating, miosis
  • severe abdominal pain
  • frequent watery and painful bowel evacuations
  • cardiovascular collapse
  • vertigo, weakness, confusion, coma, convulsions
  • death in few hours
47
Q

antidote for muscarine

A

muscarinic receptor antagonist

atropine

muscarine is from poisonous mushroom

48
Q

side effects of atropine

A

Tachycardia
- Decreased intestinal contraction and motility
- Drying of airway and sinuses and brochodilation
- Pupillary dilation (mydriasis)
- Tremor
- CNS delusion ,excitement, life-like dreams

atropine is an anticholinergic with M»>N effects

49
Q

what receptors does atropine work on?

A

M»>N
with nonselective M1-6 activation

50
Q

— is made from deadly nightshade

A

atropine

51
Q

what are some therapeutic uses for atropine

A

atropine is a antimuscarinic agent:

decrease respiratory secretions after intubation

used in cold medications: decreases lacrimal and nasal gland secretions

antiasthmatic (blocks ACh mediated bronchoconstriction

52
Q

scopolamine is used for

A

motion sickness
sedate mentally ill patients

antimuscarinic agent

53
Q

tropicamide is used for

A

causes mydriasis (dilates pupil for very short time)

synthetic antimuscarinic agent: stops ACh receptors

54
Q

contraction of radial iris muscles causes

A

dilation (mydriasis)

innervated by SYM only

55
Q

contraction of the circular iris muscles will cause

A

constriction of pupil (miosis)

innervated by the PARA

56
Q

the iris is under both para and sym control, which one is stronger?

A

para

para controls circulear muscle (keeps eye slightly contricted at all times→ miosis)

57
Q

to cause miosis what kind of drug

A

muscarinic agonists

miosis/constriction controlled by PARA

58
Q

to cause mydriasis what type of drug

A

muscarinic antagonist

mydriasis/dilation controlled by SYM

tropicamide will cause short term dilation of the eye

59
Q

cililary muscle is controlled by —

A

PARA
muscle is always slightly contracted

60
Q

contraction of the ciliary muscle causes

A

lens to bulge, used for near vision

controlled by PARA: always slightly contracted

61
Q

relaxation of the ciliary muscle will cause the lens to —

A

flatten

used for far vision

under control of PARA

62
Q

— is paralysis of the ciliary muscles

A

cycloplegia

can be from to little or too much ACh

lens shape is controlled by contraction of ciliary muscle which is under PARA control and always slightly contracted

63
Q

paralysis of accommodation of the cililary muscle is caused by —

A

muscarinic antagonist= too little ACh

ciliary muscles kept slightly contracted by PARA, if you block this muscle relax and lens flattens= farsighted

64
Q

spasm of accomodation of the ciliary muscle is cause by

A

muscarinic agonist or AChE inhibtors or too much ACh

ciliary muscle under control of PARA, kept slightly contracted, if you increase stimulation will lead to constant state of max contraction= nearsighted

65
Q

farsightedness is caused by — of accommodation

A

paralysis

too littel Ach= relaxation and flat lens

66
Q

nearsightedness is caused by — of accomodation of the ciliary muscle

A

spasm

too much ACh= max contraction and lens bulges

67
Q

Inducing miosis with — and — drugs can increase drainage

A

pilocarpine (miosis= contraction controlled by PARA)

physostigmine

68
Q

β antagonist (—) decrease aqueous humor production

A

timolol

69
Q

nicotine causes —

A

a bunch of stuff- No significant therapeutic uses for nicotine

hard to determine cause nicotinic receptors( NM > NN) on PARA and SYM

nicotinic receptors also desensitize with increased dose

70
Q

— Specifically blocks ganglionic Nicotinic receptors (NN) not as active against NM

A

hexamethonium (C6)

Use is limited since it blocks both sympathetic and parasympathetic ganglia

71
Q

— is a ganglionic blocker of nictonic agents and Has been used in veterinary medicine to lower blood pressure during surgery

A

trimethaphan (arfonad)

72
Q

what will AChE inhibitors do

A

increase effect of ACh throughout, will have sym, somatic and para effects

73
Q

AChE inhibtors block the breakdown of ACh and are —

A

parasympathomimetics

will have more ACh activation of both muscarinic and nicotinic receptors

74
Q

— type of anti-AChE with Quaternary nitrogen that binds reversibly to the anionic site on AChE

A

reversible inhibitor

75
Q

— type of anti-AChE with Substrate for AChE and occupy active site for extended time

A

carbamylating inhibitor

76
Q

— type of anti-AChE that Covalently binds to and irreversibly inactivates AChE

A

phosphorylating inhibitors

77
Q

edrophonim (tensiolon) works as a reversible anti AcHE by —

A

competitive inhibitor for binding sites

no covalent attachment means rapidly reversible

used to diagnose myasthenia gravis

78
Q

edrophonium (tensilon) is used to diagnosis —

A

myasthenia gravis

reversible Anti- AChE- simple competitive inhibitor

Myasthenia Gravis is a neuromuscular disease characterized by weakness of skeletal muscle contraction as a result of a decrease in ACh receptor density at the neuromuscular junction

79
Q

how is edrophonium/tensilon used to diagnose myasthenia gravis

A

MG→ autoantibodies cause ACh receptors to be internalized

edrophonium will block the degrade of ACh allowing for a greater chance of ACh to bind to the receptor that are left

will have short response →transient improvement

increase ACh= increase muscle contraction

80
Q

how does carbamylated inhibitors of AChE work?

A

this drug will bind to same enzyme that breaks down ACh, but it will get stuck for 30 minutes

substrate will sit in active site of AChE for extended time

81
Q

how does physostigmine(eserine) work?

A

carbamylated inhibitor of AChE

will sit in AChE binding site and prevent it from working for 30 minutes

made from West African plant Physostigma venenosum

82
Q

physostigmine (eserine) was originally used to treat MG, — and — poisoning.

A

glaucoma
atropine

increases ACh available

physostigmine is a carbamylated inhibtor of AChE that sits in AChE binding site for extended period

83
Q

how does DFP work

A

phosphorylating inhibitor of AChE

will bind to AChE but will not let go, inactivating the enzyme → increases ACh avialable

84
Q

how to overcome phosphorylating inhibitors of AChE

A

these drugs break AChE by binding and never letting go

body needs to make new AChE enzymes which could take weeks.

toxic exposure when 80-90% of all AChE is inactivated

85
Q

nerve gas, sarin and VX gas work by

A

Phosphorylating Inhibitors of AChE

permently inactivate AChE

leads to overflow of ACh in the body →SLUMD and then paralysis and respiratory failure

86
Q

2-PA M does not work against — inhibitors

A

carbamylating AChE (PNPD)

does not cross BBB, only works on non-aged complex

will give atropine after to prevent extra ACh in mus. recp

23 spring: pharm (46 decks)

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