Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PB+T > ANS > Flashcards

ANS Flashcards

0
Q

M1,M2,M3: G-protein activation

A

M1 and M3: Gq - Phospholipase C

M2: Gi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Sympathetic vs. parasympathetic

A

Sympathetic: t1-L2, short preganglionic (ACh nicotinic), long post (Epi)
Parasympathetic C1-C8 + L3-S5, long preganglionic (ACh) short post (muscarinic ACh)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

M2 receptor locations

A 
M2 is the heart of med school)
M2 - Gi (decrease cAMP) 
- SA node
- AV node
- cardiac myocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

M1/M3: location and activation

A

Phospholipase C

  • vascular sm. muscle
  • sm. muscle of GI (walls, sphincters)
  • GI secretions
  • urogenital: bladder walls, sphincters, uterus, seminal vesicles
  • eye: iris, ciliary muscle, lacrimal glands
  • M1 are CNS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Direct muscarine agonists

A

Non-selectively activates M1,2 and 3. Cevimaline is more selective for M3 (civilized people drive M3s)
Choline esters:
- methacholine: asthma diagnosis
- carbachol: glaucoma(constricts pupils) meiosis induction
- bethanachol: urinary retention/GI dysmotility

Alkaloids:

  • pilocarpine (muscarine analog) xerostomia
  • cevimaline - glaucoma, miosis induction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Cholinergic effects:9 DUMBBELLS

A 
Blurred vision
N/V/D
Sweating 
Hypersalivation
Flushing
Bradycardia
Reflex tachycardia 
Bronchoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Natural alkaloid amines:

A

in NAAM the AK shot (antagonize) AT you with a SCOPE)
Direct muscarinic antagonists: nicotinic ACh poisoning, N/V (motion sickness)
Atropine, scopolamine
Tertiary amines : high CNS penetrance
Quaternary amines: lower CNS penetrance than tertiary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Atropine

A

No selective muscarinic antagonist

  • antidote for muscarinic ACh toxicity
  • bronchi, salivary and sweat glands most effective
  • ACLS algorithm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Scopolamine

A

Nonselective muscarinic antagonist

  • Substantial CNS effects
  • prevention of motion sickness N/V
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Benzotropine and triphenidyl

A
  • M1 selective
  • decrease tremor in early Parkinson’s (park your benz, with the triprop logo, benzs are thrilling cars)
  • treat extra pyramidal symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

hyoscyamine and dicyclomine

A
  • Nonselective muscarinic antagonist (hyoscyamine)
  • M1/3 selective (dicyclomine)
  • decreases GI motility in IBS
    (hyo rode a cycle back from the bathroom)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Tertiary and quaternary amines: indications for urinary incontinence

A 
Urinary incontinence
- high M3 selectivity tertiary amines:
    ~ Darifenacin
    ~ solifenacin 
- low M3 selectivity tertiary amines:
    ~ oxybutynin
    ~ tolterodine
    ~ fesoterodine
- quaternary amines
    ~ Trospium
  (Don't Soil (high) Old Trousers For (low) the 4th Time (quaternary))
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Quaternary amines for COPD/asthma

A
  • Nonselective muscarine antagonists
  • first line for COPD
  • not first line for emergency management of airways
    Ipratroprium (brats are short and high energy: short acting, muscarinic agonist) and tiotropium (long acting)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Direct nicotinic agonist

A

Acetylcholine/nicotine: agonists (Varen Succed DAN: direct nicotinic agonists)

  • varenicline (partial nicotinic agonist)
  • succinylcholine (paradoxical action: brief fasiculation followed by flaccid paralysis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Direct nicotinic agonist toxicity: cause

A 
nicotine and varenicline
Nicotine: 
- acute
    ~ N/V/D
    ~ Cardiac (HTN, arrythmias) 
    ~ CNS: seizures, depolarizing blockade 
- chronic CV and GI risk
Varenicline
- nausea
- CNS: insomnia, abnormal dreams psych
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Direct nicotinic agonist toxicity: succinylcholine

A
  • paralysis (prolonged)
  • malignant hyperthermia
  • myopathy
  • hyperkalemia (continue depolarization causes continuous efflux of K)
    (Hypnotize My Mind Please)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

AChE inhibitors: general

A

Indirect cholinergic agonist (inhibits degradation in the synapse)
- treatment for myasthenia gravis (edro, neo and phyo caused ester agony)
- edrophonium (short acting: non-covalent bond)
- neostygmine
- phyostigmine
~ stigmines: nonlabile covalent bond long lasting (Stygmines styck around)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Organophosphate poisoning: MOA and trt

A
  • Covalent bonding
  • muscarinc and nicotinic toxicity
  • trt: atropine and pralidoxamine (ACH antagonism and AChE regeneration)
    (spray at toxic at bugs: atropine + pralidoxamine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Central AChE inhibitors (DRG): examples (3), indications, toxicities

A
  • indicated in dementia esp. Alzheimer’s
  • relatively selective for CNS AChE (DRG)
  • toxicity: GI, dizziness, bradycardia, hepatotoxicity
  • e.g.
    ~ Donepezil
    ~ galantamine
    ~ rivastimine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Adrenergic receptor: general

A

G-protein linked

  • a1: Gq (Phospholipase C)
  • a2: Gi (decrease cAMP)
  • B1/2: Gs (increase cAMP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Dopamine pathway

A

Tyrosine -THB-> L-dopa -pyridoxal phosphate-> dopamine -vitamin C-> norepi -s-adenysylmethionine-> epi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Catecholamine affinity

A 
NE: high for a1/2 and lower for B1
Epi: dose dependent
- low dose B predominates 
- high dose a predominates 
DA: also dose dependent 
- low dose: dopamine 
- moderate dose: high affinity to B1, lower for a1 and dopamine
- high dose: a1 over B1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Alpha Agonists

A

a1: vasoconstriction
- systemic: phenylepherine, midorine
- local: phenylepherine, oxymetazoline, tetrahydrazoline

a2: negative feedback on central and peripheral adrenergic *note-even though its adrenergic, stimulating it decreases symp.
- neurons - decrease NE release/sympathetic outflow
- Clonadine, methyldopa, dexmedetomidine, tizanidine

AA is for potheads) (sMoking local POT causes agony, Come To My Drugstore: drugstore will help you take less)

23
Q

Non-selective alpha antagonists

A

Phenoxybenzamine (irreversible)
Phentolamine (reversible)
- pro-op pheo management
(NSAA popt into space to get iron from a meteor)

24
Q

a1-antagonists

A
  • inhibit vasoconstriction (a1med) and prostate sm. muscle contrxn.
  • terazosin
  • tamulosin

Alpha An: a ninja

25
Q

Clinical indications for a1 inhibitors

A
  • blockade of a1 vasoconstriction, vascular and prostatic for BHP and 2nd line for HTN
  • terazosin, doxazosin, prazosin
  • a1a antagonist: tamulosin for BHP
  • risk of hypotension

alpha: elite ninjas Put Tangos Down)

26
Q

a2 antagonists:

A

Minimal clinical utility: increases sympathetic outflow

- mirtazapine (antidepressant) exhibits central a2 antagonism as one MOA

27
Q

Non-selective B agonist: 1

A

Isoproteronol (terrornol)
- B1: increases HR/contractility (B1)
- B2: induces vascular and bronchial sm. muscle realaxation
- rarely clinically used: tachyarrythmias, palpitations
Doberman causes terror

28
Q

B1 adrenergic AGonist

A

Dobutamine:
- enatiomers have competing B1 and a1 effects -> B1 antagonism
- causes positive inotropy with minimal increase in HR and without vasoconstriction (Doberman causes terror, less hr increase/vasodilation)
BAG): they put 1BAG over the dobermans head to make it less frightening)

29
Q

Clinical indications for dobutamine and toxicity

A

Phamacological Cardiac stress test
Acute decompensating heart failure
Cardiogenic shock
Toxicity: arrythmias, HTN and tremors

30
Q

B2 adrenergic agonists: short and long acting

A 
(2 Bags of alcohOL)
Short: albuterol et al
- 5-15 min onset; 3-4 hour duration
- acute asthma trt (1st line)
- COPD, hyperkalemia (2nd line) (IV albuterol)

Long: salmeterol et al

  • 15-50 minute onset; 12-24 hour duration
  • chronic asthma trt (prevents bronchospasm)
31
Q

B3 - adrenergic agonists

A

Mirabegron (miraBegron, Bladder, Beta = 3)

  • over active bladder
  • toxicity: HTN, Tachycardia
  • drug interactions: CYP3A4, 2D6
32
Q

B blockers: 4 types

A

Non-selective
B1 selective
Selective vasodilators
Sympathomimetics

33
Q

Non-selective B antagonists

A

Tim antagonized the Pro and got kicked in the Nads. The boys (beta) lolled)
LOLs: propranolol, nadolol, timolol
- B1 blockade: decreases heart contractility
- decrease in renin release
- B2 blockade: many non-cardiac symptoms, tremor and glaucoma
- highly lipophilic, on the way out for CV indications

34
Q

Vasodilation B blockers:

A

a/B blockers: carvedilol, labetalol

  • vasodilation
  • more commonly used for CV indications

B blockers with NO (nitrous oxide) effect: Nebivolol

  • B1 selective
  • increases NO release from endothelium
  • NO B Nebivolol
35
Q

B- sympathomimetics

A

they pinned a medal on the ace mime
Acebutolol, pindolol
- partial B1 agonist with or without B2 activity
- for PTs. With CV indications who can’t tolerate Beta blockade
- rarely used (less effective than full antagonists)

36
Q

Indications for B blockers

A

HTN: 1st line only for PTs. With additions CV indications
Ischemic HD
Chronic HF
Arrythmias

37
Q

B blocker toxicity

A 
CV: 
- bradycardia, or block
- hypotension
- worsening of acute HF
Peripheral
- bronchospasm
- masked hypoglycemia 
- worsening PVD
- impotence 
CNS
- fatigue 
- depression (assoc with lipophilicity) 
Decreaseed exercise tolerance
Management of overdose: IsoproTERRORnol, glucagon
38
Q

Catecholamine storage inhibitor: use, MOA, toxicities

A

Reserpine

  • irreversible inhibitor of VMAT
  • depletes: norepi, epi, serotonin and dopamine
  • used to be used for HTN
  • toxicities: depression, anxiety, psychosis
39
Q

Catecholamine Storage inhibitors

A

MOA: promotes release of stored catecholamines

clinical indication: ADHD, narcolepsy, obesity (phentermine only)

40
Q

False neurotransmitters:

A

Tyramine: many food and drug interactions with MAOIs
- in beer, wine, aged cheese, live, fave beans
- displaces NE -> can lead to HTN crisis
Tyr is a false god, but encountering him will raise your BP

41
Q

Storage inhibitors: mixed action sympathomimetics; MOA, Indications (mimics are false: pseudo)

A

Ephedrine, pseudoephedrine

  • MOA: Nonselective a/B agonist
  • enhanced norepi release
  • MOA: decongestant (Sudafed)
42
Q

Catecholamines reuptake inhibitors

A 
Amy and Velna were a pain when they cockblocked atom from picking up Sarah Tonin because atom was hyper) 
Cocaine: potent NET inhibitor
- c-II controlled substance
Atomoxerine
- less potent that cocaine 
- used to trt ADHD
- minimal CV risk (Clonadine like effect) 
SSRIs/SNRIs
- amitriptyline (SS)
- venlafaxine (SN) 
- for depression and neuropathic pain
43
Q

MAOIs: function, interactions, SE

A

MOA: inhibition of MAO increases available catecholamines for release
- effects both a and B receptors
- interaction with tryramine -> HTN crisis
- serotonin syndrome
~ anti-depressants and seretonergic meds (tramadol, meperidine, dex, St. John wort)
~ hyperthermia, HTN, myoclonus, rigidity, autonomic instability, and mental status changes

44
Q

Chol

A

Direct ACh agonist: choline esters

  • carbachol
  • bethanachol
45
Q

Receptor locations: a1

A

Iris radial smooth muscle
Vascular smooth muscle; skin, mucosa, viscera
GI/UG sphincters, (contraction: pressure builds)
Pilomotor
- Gq (act Phospholipase C - IP3/DAG)

46
Q

Receptor locations: a2

A

GI walls: activation (auto receptors decrease sympathetic flow)
Sympathetic preganglionic auto receptors (decrease NE) (MAIN)
Pancreatic islet cells (decrease secretion)
- Gi (decrease cAMP)

47
Q

B1 receptor locations

A

Heart (increase contractility, CO)
Kidneys: (increase renin release-> increase BP)
- Gs (increase cAMP)

48
Q

B2 receptor locations

A
  • AIRWAY: vaso/bronchodilation
  • All other Sm. muscle
  • Gs (increase cAMP)
49
Q

M1: receptor location

A

CNS, parasympathetic

- Gq (Phospholipase C-> IP3/DAG)

50
Q

M2 receptor locations

A

Heart

-Gi (decrease Phospholipase C - IP3/DAG)

51
Q

M3 receptor locations

A

Et al

- Gq (act Phospholipase C - IP3/DAG)

52
Q

Zosin

A

Alpha-1 antagonists

54
Q

Cycloplegia

A
  • Loss of parasympathetic accommodation reflex

- blurred vision sans Diplopia

82
Q

ANS receptor for which there are no drugs (or of little clinical significance)

A

Nonspecific alpha agonist
Alpha-2 Antagonist
Beta-2 Antagonist

PB+T (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions