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Neuro > PNP Mini Module > Flashcards

PNP Mini Module Flashcards

1
Q

Hemicholinium

Category

A

NMJ presynaptic blocker

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2
Q 
Myasthenia Gravis (MG)
(CP, cause, pathophys)
A

Antibodies against postsynaptic NMJ nicotinic ACH receptors
Scooped-out post-synaptic membrane with less scalloping (low #nAChRs)
CP: easily fatigued skeletal m. - lid ptosis, normal initial muscle strength but fatigues too easily
Fatigue due to depression of ACh release (runs out) and lacking safety factor for contraction = more likely to run out = less muscle strength

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3
Q

TTX

mechanism

A

presynaptic - blocks Na Channel in AP propagation
post-synaptic - blocks Na Channel in AP propagation

AKA tetrodotoxin

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4
Q

Mg2+ and other polyvalent cations

mechanism

A

Presynaptic NMJ competitive inhibitor for Ca2+ channel (reduces Ca entry)

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5
Q

Aminoglycosides ABx (side effect)

A

Presynaptic NMJ block of V-gated Ca Channels

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6
Q

Lambert-Eaton Myasthenic Syndrome (LEMS)

cause, assoc, CP

A

Antibodies against presynaptic Ca channels
Assoc: 50% pts suffer from small lung cell carcinoma (muscle sx present before cancer)
CP: muscles initially weak (less Ca channels impair ACh release, reduce EPPs)
ACh release and muscle contraction IMPROVES with REPETITIVE motor nerve activation (raises intracell Ca)

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7
Q

Black Widow Spider Venom (Iatrotoxin)

Mechanism, Effect

A

M: forms Ca channel in nerve presynaptic terminal
E: asynchronous muscle twitching -> flatline paralysis (run out of ACh)

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8
Q

Botulinum toxin Type A

Mechanism, Uses, SE, antidote

A

M: cleave SNAP-25 snare - reduced Ca sensitivity of secretory apparatus (cleaves near binding site of Ca to synaptotagmin), inhibits ACh secretion (less EPP without changing MEPP)
CU: Blepharospasm (Orbicularis oculi m spasm), Cosmetic (excessive facial m. contraction), Hemifacial spasms, Laryngeal Problems (Stuttering, spasmodic dysphoria - target thyroarytenoid m.), Cerebral Palsy/Stroke (reduce spasticity), Musician’s/Writer’s Cramp (reduce spasms with repetitive activity)
SE: risk weakening breathing/swallowing muscles; bioterrorism
Antidote: Heptavalent antitoxin (only works when toxin is not yet bound to nerve terminals)

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9
Q

How to use electrophysiology to determine mechanism (pre vs. post synaptic)?

A

Post-synaptic: EPP, MEPP, and response to exogenous ACh ALL DECREASE IN PARALLEL
Pre-Synaptic: EPP decrease without change in MEPP amplitudes (affects vesicle release, not amount of ACh in vesicle)

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10
Q

Botox B (mechanism)

A

cleaves synaptoBrevin - the only snare that attaches to the vesicle

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11
Q

Tubocurarine
Pancuronium
(Category)

A

NMJ Postsynaptic Non Depolarizing Blockers

-curoniums

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12
Q

Vecuronium

Mechanism, SE, elimination, use

A

M: non-depolarizing nAChR block
SE: no CV effects (tachy/hist release hypotension)
Elimination: Liver (good for pt in renal failure)
U: duration of surgery

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13
Q

Rocuronium

Mechanism, SE, use, eliimination

A 
"Fast vecuronium"
M: non-depolarizing nAChR block
SE: no CV effects
use: intubation, surgery duration (1.5 min onset)
elimination: liver
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14
Q

Succinylcholine

structure, mechanism, use, SE, contraindications

A

S: 2 ACh mLc = 2 step hydrolysis by ChE
M: depolarizing nAChR block
U: early anesthesia for intubation/rapid airway (phase 1 block)
SE: low dose - bradycardia (activates mAChR), malignant hyperthermia (opens RyR in muscle - high body temp, massive skeletal muscle contraction)
CI: conditions where new AChRs form along entire muscle surface (burn pts - high serum K can cause CV collapse), pts with cardiac arrhythmias (heart block worry), liver disease/ChE deficiency, not used for duration of surgery (can cause post op muscle pain)

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15
Q

Nicotine (Category)

A

Exogenous ACh - Depolarizing nAChR blocker

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16
Q

Edrophonium (Tensilon)

Mechanism, use, SE

A

M: short acting anti-ChE
U: TEST for MG (cause sx improvement! for brief time)
SE: muscarinic mAChR effects

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17
Q

Sugammadex

Mechanism, SE, use

A

M: encapsulates curoniums and inactivates them (donut-shape)
SE: hypersensitivity rxn, and reduces steroids effect (anti-contraceptive)
Use: reverse non-depolarizing block after surgery

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18
Q

What is synergy?

A

2 drugs with same effect but different mechanism of action = compounded and enhanced effect greater than the sum of the two medications individually

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19
Q

Mechanism of Phase I and Phase II block

A

Phase I: block by receptor depolarization (Na channel inactivated, membrane depolarized at E(ACh))

Phase II: block by desensitization (Na not inactivated, but nAChR blocked)

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20
Q

How does rocuronium cause NMJ depression?

A

curonium = nondepolarizing block nAChR = removes spare receptors

now inhibited NT release via ATP in vesicles from repeated stim will cause depression in EPPs

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21
Q

How does SUX act in phase I and phase II block in response to high freq stim?

A

Phase I: depolarizing block - high freq stim = no depression, but whole response is scaled down (less nAChRs activated)

Phase II: desensitizing block - high freq stim = depression (spare receptors gone)

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22
Q

How do you observe full recovery from a neuromuscular block?

A

All 4/4 impulses in a train crease a twitch

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23
Q

Effects of ANS on Pupil Dilator, Bronchiolar Smooth Muscle, GI tract/Urinary Bladder, Cardiac Fx, Liver and Fat, Blood vessels, Sexual Fx, Hair, Spleen, Secretions, Pancreas, Accommodation

A

Symp: Mydriasis (dilation of pupils), bronchiodilation (open airway), less GI/bladder wall tone more sphincter tone, Cardiac: high HR, more contraction force, more glycogenolysis/gluconeogenesis/fatty acid release, VC via A1 = high BP (VD in skeletal muscle/liver B2 - less important for BP), Sex Fx: more smooth muscle contraction/secretions, piloerector contraction (hair), more release of erythrocytes from spleen, viscous salivary secretions, inhibits insulin secretion

Parasymp: opposite with accommodation

24
Q

Acetylcholine

  • effects (2)
  • low dose vs. high dose
A

Acts on Parasymp mAChRs (parasympathomimetic)

  1. CV: decrease HR at SA Node
  2. Vessels: VD (via NO release) = low TPR = low BP

Low dose: not enough ACh in SA Node - low BP compensated by higher HR (reflex tachycardia - barostatic reflex via B1 receptors)

High dose: huge VD and lower HR (overcomes reflex)

25
Q

Metacholine

-use

A

Parasympathomimetic (agonist mAChRs)

-use for bronchial asthma (constricts airway)

26
Q

Bethanechol

- uses (2)

A

Parasympathomimetic (agonism mAChR)

  1. GI Tract - improve mobility
  2. Urinary Bladder - tx urinary retention
27
Q

Pilocarpine

-uses (2)

A

Parasympathomimetic (agonist mAChR)

  1. tx Glaucoma: both types by increasing flow through meshwork/uncrowding angle
  2. tx Sjogren’s: stimulates saliva secretion to tx dry mouth from autoimmune attack on exocrine glands
28
Q

What are the sx of anticholinesterase poisoning? How to tx it?

A

SLUD: Salivation, Lacrimation, Urination, Defecation

tx: Atropine: blocks mAChR activity; Pralidoxime (2-PAM, Protopam) - anti-ChE antagonist

29
Q

Physostigmine

  • type
  • use
A

Indirect parasympathomimetic (reversible)

  • anticholinesterase (more ACh)
  • tx Glaucoma
  • antidote for reversing NMJ blocks
30
Q

Neostigmine

  • type
  • use

Pyridostigmine
-use

Edrophonium
-use

A

All are anticholinesterases (reversible)

Neo: tx MG, and GI stasis

Pyrido: main MG tx

Edro: Tensilon test for MG (short duration)

31
Q

How do the following toxic gases or insecticides work:

DFP, Parathion, Malathion, Chlorpyrifos, Sarin, VX

A

Irreversible anticholinesterases - cause SLUD

32
Q

Atropine, Homatropine, Scopolamine, Glycopyrrolate

  • uses
  • mechanism
A

General anticholinergic agents - block parasympathetic mAChR
use: cause sympathetic effects - tx GI spasm, block accommodation (cyclospasm), increase HR during anesthesia, antidote for anti-ChE poisoning, CNS depressant (anti-emetic scopolamine, sedation), block secretions

33
Q

Mechanism/Uses for “-terodine” and “-fenacin” drugs and oxybutynin

A

Parasympathetic mAChR antagonist specific to urinary bladder - tx overactive bladder

34
Q

Mechanism/Uses for Tropicamide and Cyclopentolate

A

Parasympathetic mAChR antagonist specific to eye

cause dilation, cycloplegia (paralyze accommodation to determine refractive errors)

35
Q

Signs of anti-muscarinic toxicity (5)

tx for toxicity

A 
DRY as a bone (less secretions)
HOT as a stove (high body temp)
RED as a beet (VD, high body temp)
BLIND as a bat (dilation, cycloplegia)
MAD as a hatter (delirium)
tx: activated charcoal - salt of physostigmine (antilirium)
36
Q

What are the effects of the following receptors:

A1, A2, B1, B2, B3

A 
A1: VC (HTN)
A2: Cell inhibition
B1: STIM HEART (high HR, contraction)
B2: RELAXES smooth muscle (bronchodilation, hypotension)
B3: RELAXES bladder
37
Q

What receptors are activated by the following:

EPI, NE, ISO

A

EPI: all receptors
NE: no B2
ISO: B only

38
Q

EPI reversal:

  • what happens with high dose EPI
  • what happens with high dose EPI and adding an a1 blocker (ergotoxin)?
A

EPI: VC = high BP (a1)

EPI + a1 block: VD = low BP (b2)

39
Q

Describe how TPR, HR, and BP change with NE, ISO, and EPI use

A

NE: act only on a1, a2, b1

  • TPR: increases (a1)
  • DBP: increases (a1)
  • SBP: increases (b1)
  • BP: increases (SBP, DBP)
  • HR: decreases (barostatic reflex wins due to high MAP)

ISO: acts only b1, b2

  • TPR: decreases (b2)
  • DBP: decreases (b2)
  • SBP: increases (b1)
  • BP: decreases (DBP > SBP)
  • HR: increases (b1 + reflex tachycardia)

EPI: low dose

  • TPR: decreases (b2)
  • DBP: decreases (b2)
  • SBP: increases (b1)
  • BP: little to no change
  • HR: increases (b1)

EPI: high dose

  • HR: initially high (b1 on SA node), then lowers (barostatic reflex takes over)
  • BP: initially high (b1 contractility), then rises more (a1 VC)
40
Q

Uses of Epi (4), NE (1), ISO

A

Epi: Cardiac arrest (a1, b1), VC (a1), Rescue inhaler (b2), anaphylaxis (b2, b1, a1)

NE: tx severe hypotension in ICU

ISO: rarely used

41
Q

Phenylephrine

  • type
  • use
A

a1 agonist

use: nasal decongestant (VC), pupil dilation, raise BP during surgery (VC)

42
Q

ImidaZOLINEs

  • type
  • use
A

a1 agonist

long acting nasal decongestant (reactive hyperemia - rebound congestion)

43
Q

Midodrine

  • type
  • use
A

a1 agonist

tx orthostatic hypotension (VC), POTS (VC prevents further increases in HR)

44
Q

Cl”ONIDINE”

  • type
  • use
A

a2a agonist

tx: anti-HTN (low TPR/HR), opioid withdrawal

45
Q

alpha-methyldopa

  • type
  • use
A

a2a agonist

tx: anti-HTN during pregnancy (not used at NMH)

46
Q

dobutamine

  • type
  • use
A

b1 agonist

tx: acute HF (increase CO), mimic exercise in stress echo

47
Q 
Albuterol
Salmetrol
Formoterol
Terbutaline
-type
-use
A

All b2 agonists
Albuterol - SABA (rescue inhaler)
Salmeterol/Formoterol - LABA (inhaler need to use with CS)
Terbutaline: for uterine relaxation (premature labor)

48
Q

Mirabegron

  • type
  • use
A

B3 agonist

tx overactive bladder (relaxes bladder)

49
Q

tyramine and amphetamines

-mechanism

A

cause NE release!! (indirect agonist of a1/a2/b1 by kicking NE from nerve terminal)

50
Q

Ephedrine-Pseudoephedrine

  • type
  • use
A

causes NE release by kicking it out of nerve terminal and b2 agonist
use: nasal decongestant (a1), anti-asthma (b2) - watch for toxicity

51
Q

Phenoxybenzamine and Phentolamine

  • mechanism
  • use
A

A1 and A2 antagonists

-lower HTN, manage pheochromocytoma during surgery

52
Q

“ZOSINs” and “LOSINs”

  • mechanism
  • use
A

A1 blockers

tx: benign prostatic hypertrophy (decrease resistance to urine outflow)

53
Q

Yohimbine

  • mechanism
  • use
A 
A2 blocker (selective)
- tx impotence in DM
54
Q

How can we use pharm to control sexual dysfx?

A

A2 blocker
- increase Ca entry to parasymp (less a2) = more NO release = more cGMP in smooth muscle = VD/erectile response

Sildenafil
-PDE5 inhibitor = blocks cGMP breakdown = more effects of NO = VD/erectile response

55
Q

List the 1st gen, 2nd gen, and 3rd gen beta blockers and their selectivities

A

1st gen: Timolol (glaucoma) and Propanolol - both b1 block

2nd gen: Metoprolol, Atenolol, Betaxolol, Esmolol (block b1 only)

3rd gen: Labetalol (b1 and a1), Carvedilol (b1, b2, a1, CCB, antioxidant), Nebivolol (b1, NO)

Neuro (36 decks)

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