9/18 Flashcards

1
Q

Pralidoxime is what is going to be beneficial to someone who has

A

organophosphate overdose

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2
Q

If you have nicotine toxicity it is probably due to what type of ingestion?

A

eating them

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3
Q

if you have a muscarinic overdose, give

A

atropine

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4
Q

Why is there not much use for ganglion blockers?

A

It affects both the SNS and PNS because ACh is released in all ganglion

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5
Q

What is atropine derived from?

A

Belladona

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6
Q

ACh has what effect on the pupil?

A

constricts it

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7
Q

Atropine has what effect on the pupil?

A

dilates it

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8
Q

Atropine has L and D isomer but it is given as a

A

racemic mixture because the D isomer will switch to the L isomer which is 100X more potetent than d isomer

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9
Q

atropine is a

A

competitive inhibitor of muscarinic receptors for ACh

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10
Q

scopolamine is similar to

A

atropine

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11
Q

scopolamine is used to treat

A

nausea

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12
Q

What are examples of when we have an overproduction of parasympathetic response?

A

bradycardia
increased respiratory secretions
Increase in GI activity
constriction of airways
excessive eye watering
excessive urination (micturation)

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13
Q

What is cycloplegia?

A

the paralysis of ciliary muscle

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14
Q

scopolamine drops in the eye induce what? and reduces what?

A

cycloplegia
accommodation (flattening of the lens to adjust for near and far vision)
and eye watering

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15
Q

what is the difference between atropine, scopolamine, and tropicamide?

A

the duration
atropine: 7-10 days
scopolamine: 3-7 days
Tropicamide: 0.25 days

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16
Q

What is tropicamide used for?

A

short acting dilation of the pupil during a routine eye exam.

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17
Q

In low doses of atropine, pharmacologists assume that the dip in heart rate is due to

A

atropine effects the presynaptic muscarinic cell which releases ACh more than it’s effecting the effector cell.

Atropine comes in and increases the amount of ACh, slowing down the heart rate.
With larger doses we see the effect of atropine blocking the effector cell receptors and not allowing ACh to reach it, therefore speeding up heart rate

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18
Q

contraindications to atropine

A

glaucoma patients= blindness
elderly men (BPH)=Urinary retention

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19
Q

anticholinergic toxidrome

A

hot as a hare
blind as a bat
dry as a bone
red as a beet
mad as a hatter (confusion and hallucinations)

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20
Q

What is another name for antinicotinic drugs? if they target both Nm and Nn

A

ganglion blocking drugs

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21
Q

What is a ganglion?

A

a cluster of cell bodies in the PNS

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22
Q

Where do muscle relaxants work?

A

The nicotinic muscular receptors in the neuromuscular end plate of skeletal muscles

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23
Q

muscular relaxants work in 2 different ways

A
  1. depolarizing muscle relaxant
    -depolarizes the neuromuscular endplate and does not allow it to repolarize

2.nondepolarizing muscle relaxant
-block ACh receptors
- can have short, intermediate, or long effects
curare derivatives

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24
Q

Succinylcholine

A

acts as a really strong ACh receptor agonist
BECAUSE it doesn’t get broken down at the NMJ. This causes it to stay longer in the synapse and then push a phase 1block into a phase 2 block

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25
How is succs broken down?
by cholinesterase in the plasma within 5-15 minutes
26
What is phase 1 block?
depolarization and lack of repolarization
27
what is phase 2 block?
depolarization happens but the NMJ adapts and finally repolarizes
28
non-depolarizing muscle relaxants work by
blocking the effects of ACh
29
non-depolarizing muscle relaxants originated from
poisonous dart frogs in south America
30
non-depolarizing muscle relaxants are
competitive antagonists
31
What are the 2 non-depolarizing muscular blockage reversal agents?
Neostigmine Sugammadex - for roc and vec
32
How does sugammadex work to reverse vec and roc?
it is a cyclic molecule that wraps itself around the vec and/or roc and keeps it from interacting with the ACh receptor
33
How does neostigmine work?
It blocks AChE so that ACh is not broken down and therefore we have more ACh in the system
34
Where does epinephrine come from
adrenal medulla
35
what are the catacolamines?
epi norepi dopamine dobutamine isoproterenol
36
what is a catacol group?
a benzine ring with 2 OH groups
37
catecholamines have maximal activity at
adrenergic receptors (receptors that bind to epi, norepi, dopamine, isoproterenol)
38
substitution greatly reduces
potency
39
Why can't you take epi or norepi orally?
because catecholamines are inactivated by COMT (Catechol-O-methyltransferase) found in the stomach
40
What is COMT
Catechol-O-methyltransferase
41
How is phenylephrine different from epinephrine?
It is missing an OH group, making it NOT a catecholamine meaning it does NOT get broken down by Catechol-O-methyltransferase and can therefore be taken orally
42
What does a substitution at the alpha carbon do?
It changes the drug and give it a prolonged action by blocking oxidation by Monoamine oxidase (how NE is broken down)
43
what is the order of chatacholamine drugs that bind to alpha receptors strongest to weakest?
Epi>=norepi>isoproterenol
44
what is the order of chatacholamine drugs that bind to beta receptors strongest to weakest?
isoproterenol>epi>= norepi
45
when you see B2 think
lungs
46
beta 1 has equal affinity for
epi and norepi
47
beta 2 has greater affinity for ___ than ____
epi than norepi
48
Dopamine Gs
increases cAMP
49
Dopamine Gi
decreases cAMP
50
Overall effect of alpha 1
vasculature smooth muscle contraction = higher bp
51
Overall effect of alpha 2
adrenergic and cholinergic nerve terminal inhibition of transmitter release= relaxed
52
Overall effect of beta 1
heart, juxtaglomerular cells= increased force and rate of heart and increase renin
53
Overall effect of beta 2
respiratory, uterine, vascular smooth muscle= smooth muscle relaxation
54
Overall effect of dopamine
smooth muscle dilates renal blood vessels
55
with beta 3 think
fat
56
What is Cardiac output?
CO5L/min
57
What is the sterling law?
the more stretch that is applies, the more forceful the contraction will be
58
alpha agonist effects on vascular resistance, cardiac, and blood pressure?
Increased mixed increased
59
beta agonist effects on vascular resistance, cardiac, and blood pressure?
decreased increased decreased
60
mixed beta and alpha agonist effects on vascular resistance, cardiac, and blood pressure?
mixed increased increased
61
Blood vessel tone in most blood vessels vs. skeletal blood vessels
most blood vessels a primarily alpha 1-contract most skeletal vessels are primarily beta 2-relax
62
Blood vessel tone in most blood vessels vs. skeletal blood vessels during Sympathetic response
most blood vessels a primarily alpha 1- **contract** most skeletal vessels are primarily beta 2-**relax**
63
Blood vessel tone in most blood vessels vs. skeletal blood vessels during Parasympathetic response
most blood vessels a primarily alpha 1- **relax** most skeletal vessels are primarily beta 2-**relax**
64
the dilator muscle in the eye has what receptors?
alpha
65
what drug class decreases aqueous humor?
beta blocker eye drops
66
what receptors are in the bronchial smooth muscle?
beta2
67
what do beta 2 agonists do?
bronchodilation
68
both alpha and beta stimulation ____ the GI tract
relax
69
Epi works on both
beta1 and beta 2. mixed agonist
70
norepinephrine has less effects on________ than epi and therefore has little respiratory effects
beta 2
71
isoproterenol mainly effects
beta as a vasodilator very little alpha good if you want to increase cardiac output but not effect the bp this is a better option
72
Dopamine is a mixed agonist based on
dose. low dose= decrease peripheral resistance high dose= mimics action of epinephrine
73
Dobutamine is selective for which receptor?
Beta 1
74
Phenylephrine is selective for
alpa
75
what drug can be used for tetralogy of fallot?
phenylephrine raises BP -holes in the heart that allows oxygenated and deoxygenated blood to mix in the heart
76
What receptor does midodrine focus on?
alpha 1
77
examples of sympathomimetics?
Direct: Epinephrine Norepinephrine Isoproterenol Dopamine Dobutamine Phenylephrine Midodrine Clonidine Dexmedetomidine Ephedrine Indirect: Amphetamine Cocaine