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Neuro Exam 4 > Pharm Kruse CIS > Flashcards

Pharm Kruse CIS Flashcards

1
Q

alpha 1 receptors

A

stimulate contraction of all sm. music.

glandular sm. m. secretion
vascular sm. m. –> vasoconstriction

sympathetic NS

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2
Q

beta 2 receptors

A

relax smooth muscle (vasodilation)

sympathetic nervous system

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3
Q

muscarinic receptors (G-protein coupled) do what to smooth muscle

A

Contract smooth muscle (different intracellular signal than α1 receptors)

GI tract for example

• Apparent discrepancy – ACh & muscarinic agonists given IV cause vasodilation due to release of nitric oxide (NO) (ach activating muscarinic releases NO and causes vasodilation)

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4
Q

parasympathetic response is what

A

cholinergic

salivation
decrease in HR
pupil constriction
increased secretion and motility

rest and digestion
smooth muscle contraction

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5
Q

sympathetic

A

adrenergic (anti-cholinergic)

cutaneous vasodilation
pupil dilation
increase in HR

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6
Q 
case- 2 year old 
overdose of antihistamines
pupils fixed and dilated
tachy
cutaneous vasodilation

overactivation of which division of the NS?

A

sympathetic NS

antihistamines have anti-cholinergic properties that is why they have sympathetic presentation (anti-cholinergic slows down secretions, etc. )

this drug acts at muscarinic receptors to inhibit them

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7
Q

how does cutaneous vasodilation occur?

are sweat glands under para or sympathetic innervation?

A

sympathetic

but this is an EXCEPTION
b/c the postganglionic neurotransmitter is ACH on a Muscarinic receptor on sweat glands

so the pt who overdosed on antihistamines is not sweating so she has a fever

this patient has vasodilation at the skin b/c she can’t sweat so she is trying to blow off heat at the skin

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8
Q

what receptor will correct the patients symptoms who overdosed on antihistamine?

what effects will occur with this activation?

A

muscarinic ACh Receptor (indirect mAChR)

  • effects–> heart rate would go down
  • M2 on heart
  • potentially release of NO
Not alpha-1 
not beta-1 
not nAChR
not beta-2
-will only make these symptoms worse
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9
Q

what other effects would you see in a patient with anti-cholinergic overdose

A

lack of urination
constipation
fever
rapid heart beat

lack of all rest and digest symptoms

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10
Q

how do you antagonize MAChr receptors

A

direct acting agonisht
-bind to receptor

indirect acting agonist
-bind to Acetylcholinesterase so that there would be increased ACh at all synapses

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11
Q 
case 2 61 year old male
double vision
droopy eyelids-ptosis
1 year ago noticed
worse during day

jaw muscles get tired
1-2 hours of rest it goes away

takes Aspirin everyday

after completion of 1 minute up-gaze demonstrating ptosis

antibodies to what would cause these symptoms??

how would you treat?

A

myesthenia gravis

antibodies to a receptor would cause there to be less receptors

antibodies against–> nicotinic acetylcholine receptor

treat with acetylcholinesterase inhibition–> increase the concentrations of ACh around the body, want this to work at the NMJ

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12
Q

what drug would inhibit the SNARE complex

A

botox (bottulin toxin)

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13
Q

do we have good selective mACHr agonists?

A

no

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14
Q

what would you see with a AChE inhibitor?

anhydrosis
decreased urination
diarrhea
dry mouth
mydriasis (pupil dilation)
A

diarrhea

b/c this is the only one that is parasympathetic overactivation

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15
Q

AChE inhibitor acute intoxication
parasymapthetic effects
SLUDGE

A 
slude 
salivation
lacrimation
urination
defecation
GI distress
Emesis
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16
Q

what will reduce symptoms of the patient (diarrhea)

A

mAChR antagonist

examples:
Lomotil
Atropine- military

17
Q

increased ACh at skeletal muscle junctions can cause what

A

paralysis of the skeletal muscles

18
Q 
Case 32 year old female
headache 
palpitations
anxiety
sweating
pending doom and tremors
after exercise or coffee

metanephrine test is positive

A

pheochromocytoma (too many catecholamines being produced)

overactive sympathetic response

triad:
headache
perspiration
palpitations

19
Q

if we give a beta receptor selective antagonist (blocks Beta 1 and beta 2) which will occur

would you get bronchial smooth muscle constriction

A

worsening of Hypertension and possible death

this is because we are blocking beta receptors
with beta yes we can slow the heart rate

so now there are alpha receptors that are also activated b/c of increased catecholamines
now there is unopposed alpha1 stimulation

bronchial smooth muscle constriction might happen but it is not the best choice

20
Q

which agent can be used to differentiate b/w false positive and actual pheochromocytoma

which agent will produce little to no physiological effects in a patient with pheochromocytoma

A

sympathetic division of the NS is the one releasing catecholamines

in the patient with pheochromocytoma,
centrally acting alpha 2 receptor agonist (Clonidine)
-these are found pre-synaptic !! so these would cause decreased release of NE and E and decreased sympathetic outflow

NOT mAChR antagonist-

NOT Beta-1 selective agonist–> No b/c this would make the beta receptors active, increase HR even more

Beta 2–> no b/c these are causing relaxation and would cause more vasoconstriction by alpha’s

Monoamine oxidase inhibitor–> breaks down catecholamines in the presynaptic neuron after reuptake

21
Q 
case 29 year old male
pinpoint pupils
oral foaming
incontinent
lacrimation
salivation
history of depression/suicide
muscle fasciculations, why? 
what receptor is involved?
an agent from which drug class is most likely ingested
A

parasympathetic signs so cholinergic receptors

drug ingested AChE inhibitor

why muscles fasciculations?
b/c of the nicotinic ACh receptors on skeletal muscles

SLUDGE
salivation
lacrimation
urination
defecation
gastrointestinal pain and gas
emesis

percutaneous absorption–> localized sweating, and muscle fasciculations

Lipid-soluble–> CNS involvement (organophosphates used in warfare)

Ingestion–> GI symptoms first

22
Q

antidote for AChE inhibitor toxicity

A

Atropine (muscarinic antagonist)

23
Q 
case 58 year old male
SOB
17 lb weight gain
dyspnea on exertion
orthopnea
ankle edema
PND
nocturia
cough- productive
HTN
diabetes in family history
tachy
NVD noted
hepatomegaly
rales and rhonchi

diagnosis?

on hydrochlorothiazide
ibuprofen
ranitidine

he is prescribed an agent that will decreased both the force and rate of cardiac conttraction- what agent is described?

A

ddx. CHF

agent for decreasing heart rate?
beta-1 selective antagonist

24
Q

CHF case

inhibition of which receptors on juxtaglomeruluar cells of the kidney will decrease renin secretion?

A

beta-1 - reduces preload and afterload on the heart
ALSO secondary benefit is reduce renin secretion and help mitigate HTN by reducing the formation of ANG II

these stimulate the release of renin from the kidney

renin helps form ANG II

ANG II increase will cause vasoconstriction in the body and ANG II blockers are used in the treatment of HTN

25
Q 
case 52 year old
20/40 right eye
20/80 left eye
IOP elevated in both eyes
nerve fiber bundle defect consistent with glaucoma

currently being treated for asthma

of the drugs listed which is contraindicated?
oral carbonic anhydrase inhibitor

oral nonselective beta receptor antagonist
topical selective beta-2 receptor antagonist

A

she has asthma so we want to keep her beta-2’s working

so an oral nonselective beta receptor antagonist would be BAD

26
Q

case 83 year old female
urinary incontinence
managed with adult diapers
which drug will help with her symptoms

A

muscarinic AChR antagonist (selective for M3 b/c this is more selective in the bladder)

inhibits bladder contraction

NOT beta-2 agonist b/c this will increase bladder capacity

27
Q

she is prescribed oxybutynin, nonselective MACh antagonist for urinary incontinence

what other symptoms b/c of blocking parasympathetics

A

dry mouth
dizziness
blurred vision
constipation

Neuro Exam 4 (1 decks)

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