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Pharmacology > Autonomic NS > Flashcards

Autonomic NS Flashcards

1
Q

methyldopa

A

adrenergic

  • effects metabolic transformation
  • results in displacement of NE by false neurotransmitter
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2
Q

cocaine

A

adrenergic

  • blocks transport system at the nerve terminal
  • results in accumulation of NE at the receptors
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3
Q

reserpine

A

adrenergic

  • blockade of transport system of storage granule membrane
  • results in destruction of NE by mitochondrial MAO and depletion from adrenergic terminals

depletes NE by blocking vesicular transporter (thus there is no NE in membrane vesicles)

  • decreases CO, and is the last choice for antihypertensive medication
  • not used clinically any longer
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4
Q

amphetamine,tyramine

A
  • adrenergic
  • displaces transmitter from axonal terminal
  • sympathomimetic
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5
Q

botulinum toxin

A
  • prevents release of ACh transmitter
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6
Q

muscarine, methacholine

A

mimics muscarinic NT of postsynaptic receptor and works as a cholinomimetic

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7
Q

nicotine

A

mimics nicotinic NT and is cholinomimetic

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8
Q

anti-ChE agents

A

physostigmine, diisopropyl phosphorofluoridate (DFP) - inhibit the enzymatic breakdown of ACh

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9
Q

MAO inhibitors

A

inhibit the breakdown

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10
Q

glaucoma treatment

A

muscarinic stimulants cause contraction ofciliary body, facilitating outflow of aqeous humor and reducing intraocular pressure
- thus can be tx w/ direct-acting cholinergic agonists, but more often treated now with topical beta blockers

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11
Q

accomodative esotropia

A

young children who are farsighted overcorrect for farsightedness and eyes become corssed
- treated with cholinomimetic agonists

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12
Q

contraindications of use of mACHR agonists

A

asthma, hyperthrydoidism, coronary insufficiency, acid-peptic disease

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13
Q

tx for xs muscarinic stimulation

A

atropine, for CNS stimulation use diazepam

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14
Q

enteral

A

via GI tract: oral, sublingual, rectal

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15
Q

parenteral

A

non-oral route

SQ, IM, IV, inhalation, intranasal, intraarticular

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16
Q

quaternary salts

A

permanently charged, thus can’t cross BBB

  • good tx for myasthenia gravis
  • neostigmine, physostigmine
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17
Q

Vd

A

plasma = 4 L
EC fluid = 14 L
total body water = 42 L

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18
Q

where are bases and acids best absorbed?

A

weak acid is unionized in low pH thus better absorbed in stomach

weak base is unionized at high pH thus better absorbed in intestine

the opposite is true for excretion

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19
Q

which drugs are more likely to bind in plasma?

A

weak acids and lipid-soluble drugs

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20
Q

catabolic

A

breakdown rxns

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21
Q

anabolic

A

build up rxns

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22
Q

phase 1 rxns

A

biological inactivation

  • catabolic
  • made more polar via oxidation, reduction, hydrolysis
  • mixed function oxidases (MFO’s) and Cytochrome P450’s (P450 CYP) carry out this process
  • enzymes located in lipophilic ER membranes of liver
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23
Q

phase 2 rxns

A
  • metabolite w/ increased water solubility and molecular weight
  • conjugation reactions
  • anabolic
  • polar molecules
  • occurs in liver
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24
Q

CYPs

A

CYP3A4 is most abundant

- use molecular O2 and NADPH to carry out oxidation of substrates

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25
Q

pseudocholinesterase

A
  • metabolizes succinylcholine.
  • succin. deplarizes skeletal mm = relaxant
  • individs w/ genetic defect in this enzyme can metabolize it at 50% less
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26
Q

slow acetylator phenotype

A

individs w/ this autosomal recessive trait have decrease in N-acetyltransferase levels in liver

  • results in isoniazids, hydralazine (HTN), caffeine and other amines to be metabolized slower and can cause hepatitis (esp. w/ isoniazids, tx of TB)
  • problem with Phase I metabolism and responsible of drug induced SLE
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27
Q

grapefruit juice effect

A

irreversibly inhibits intestinal CYP3A4 - decreases oralavailability of many drugs

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28
Q

enzyme induction

A

some P450 substrates can induce the activity and thus increase the rate or reduce the rate of degredation of other drugs

inducers:
- phenobarbital
- ethanol
tobacco smoke
- isoniazids, glucocorticoids

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29
Q

potency

A
  • drugs affinity for the receptor
  • amount of drug needed to obtain particular effect
  • on x axis, represents dose - more potent drugs lie to the left of the LDR
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30
Q

intrinsic activity

A

if the drug can activate the receptor, antagonists have no intrinsic activity though cthey can have efficacy

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31
Q

kd

A

equilibrium dissociation constant - measures affinity for the drug

low kd = high affinity

= concentration at which half the maximal binding occurs

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32
Q

ED50, EC50

A

ED = effective dose to see 50% response (in vivo)

EC = effective concentration to see 50% response (in vitro)

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33
Q

efficacy

A

capacity of drug to produce pharmacologic response

partial agonists/antagonists are less effecacious

34
Q

therapeutic index

A

LD50/ED50

increased TI usually means safer

35
Q

TD50

A

toxicity dose

36
Q

first and zero order

A
  • first order kinetics = exponential: rate is dependent on drug concentration. K and t1/2 don’t change with drug concentration, but the rate does. the rate is proportional to the concentration of the drug
  • zero order: linear, rate is independent of the concentration of the drug and remains steady - usually encountered when mechanism of absorption becomes saturated
  • at drug concentrations that exceed saturation of the system zero-order kinetics prevail, in between a mixed order prevails
37
Q

bioavailability

A

F - fraction of dose that is absorbed and reaches the systemic circulation

= ratio of the area under the curve for IV versus oral administration

38
Q

C0

A

= initial plasma concentration

hypothetical drug concentration predicted if the distribution had been acheived instantly

where the constant line meets the Y axis

Vd = dose/C0

39
Q

clearance

A

apparent volume of fluid from which drug is totally removed per unit time

40
Q

G6PD deficiency

A

G6PD produces NADPH reqd for protecting RBC’s against oxid. damage (through the reduction of glutathione)

w/out G6PD protection via NADPH RBCs are susceptible to oxidant drugs like primaquine, cauisng hemolysis

ingestion of fava bean, favism

41
Q

Warfarin therapy (coumadin)

A

anticoagulant used for prevention of thromboembolism via blocking enzyme Vit K epoxide reductase complext, VKORC1 - results in decreased Vit K factor needed for clotting

Warfarin therapy is dependent upon diet changes in Vit K, meds that interfere, genetic VKORC1 variability, CYP2C9 amounts = all results in individual differences in Warfarin dosage

42
Q

crossover design

A

consists of pateints receiving each therapy in sequence so that the patients serve as their own controls

43
Q

Phase 0

A

clinical trial of microdosing to provide early pharmacokinetic data

44
Q

Phase 1

A

determines whether humans and animals show significantly different responses

small number of healthy volunteers

absorption, half life and metabolism

45
Q

Phase II

A

test to determine its efficacy

larger group: 100-200 pt

tests efficacy, dosing reqs, toxicities (to test toxicity and pharmacokinetics)

done in clinical centers

drug failure usually occurs here

46
Q

PHase III

A

large group of patientsto further establish drug safety and efficacy 300-3,000 people

crossover and double blind techniques used here

evaluates overall benefit risk: efficacy and toxicitiy

47
Q

Phase IV

A

post marketing study w/ purpose of continual monitoring of safety

48
Q

malignant hyperthermia

A

problem with ryanodine receptor mutations

when inhalation of anesthetics and succinycholine, results in elevation of calcium in the sarcoplasm of muscle causing muscle rigidity, elevation of body temp and rhabdomyolysis

49
Q

organ system effects of cholinergic agonists

A

Eye: miosis, accomodation

CV: through M2 see vasodilation with minimal doses and resulting tachycardia. With larger doses see bradycardia and decreased conduction along w/ hypotension

GI: M3 mACHR’s cause smooth mm. contraction, M2 mACHR’s reduce relaxation caused by adrenergic effects

CNS: excitatry mACHR’s involved in increased cog. fn, inhibitory mACHRs play role in tremors, hypothermia and analgesia

PNS: nACHR agonist predominates here, results in increased discharge of both PS and Symp (Symp effects on heart, PS on GI)

50
Q

what are two classes of cholinergic agonists?

A

choline esters: permanencly charged: ACh (Most rapid)> methacholine >carbachol = bethanecol (least rapid)

Alkaloids: uncharged tertiary amines (muscarine, pilocarpine, nocotine)

51
Q

clinical uses of direct acting cholinergic agonists?

A
  1. glaucoma (miosis causes contraction of ciliary body, causing outflow of vitreous humor)
  2. acccommodative esotropia
  3. GI/GU disorders: Bethanecol for increased GI motility, Pilocarpine/cevimeline for Sjogrens and increased secretions
52
Q

contraindications of mACHR agonists

A

asthma, hyperthyroidism, coronary insufficiency, acid-peptic disease

53
Q

Nicotinic toxicity

A

seen in insecticides, results in skeletal mm and plate depolarization leading to resp. paralysis, hypertension and cardiac arrythmias

54
Q

three types of indirect-acting cholinergic agonists

A

“cholinesterase inhibitors”
1. alcohols: alcohol group + quaternary ammonium ion (charged) - binding is noncovalent and reversible, and short lived (edrophonium)

  1. carbamic acid esters (carbamates): quaternary ammonium groups (pos. charged or neutral) - binding to AChE is noncovalent and reversible, and lasts 1-6 hours (ex. pysostigmine, neostigmine, pyridostigmine, carbaryl)
    pyrid and neo = charged
    physo= uncharged
  2. organophosphates: charge neutral and highly lipid soluble - binding is covalent and irreversible and can last 100 hours (ex. insecticides, nerve gases). Regeneration of ACHE is reqd in order to reestablish termination of ACh signaling at NMJ
    * After initial binding, the enzyme complex may undergo aging, and the complex is even more stable and difficult to break
55
Q

organ effects of AChE inhibitors?

A

Quaternary AChE inibitors are absorbed poorly from GI tract and excluded from CNS - work preferentially at the NMJ and have less effect at autonomic sites

Organophosphates and tertiary AChE inhibitors act at peripheral and central sites and may be sequestered fro a long time

  1. stimulate mACHRs at autonomic effector organs
  2. stimulate all autonomic ganglia and nACHR’s resulting in paralysis
  3. stimulate cholinergic receptor sites in CNS with occasional depression
56
Q

myasthenia gravis

A

therapeutic doses of AChE inhibitors prolong intensity oif ACh and can be used to treat MG

57
Q

therapeutic uses of AChE inhibitors?

A

diseases of eye (glaucoma, accomodative esotropia),

GI And urinary tracts (postoperative atony, neurogenic bladder),

the NMJ (myasthenia gravis, curare-induced nm paralysis) - reverse surgical paralysis

Atrial arrhythmias

CNS: dementia and alzhemiers

58
Q

cholinergic antagonists

A

antinicotinic = influence at NMJ and ganglia
mACHR blockers block PS discharge

ex. atropine: tertiary amine exerts effects on eye or CNS - antagonizes mACHR’s

59
Q

organ effects of cholinergic antagonists?

A

CNS: treat tremor assoc with parkinsons, decreased drowsiness and motion sickness

EYE: unopposed mydriasis, useful for opthamologic exams, reduced lacrimal secretion

CV: prevent CV effects of direct muscarinics: high doses of atropine cause tachycardia and blockade of vagal slowing

Resp: bronchodilation and reduced secretion

GI: decreased salivary secretion, decreased gastric emptyping, treatment for urinary incontinence, decreased sweating

60
Q

clinical uses of cholinergic antagonists?

A
  1. PD- Parkinson disease, reduce tremor
  2. Motion sickness
  3. Anesthesia: blocks vagal reflexes induced by surgical manipulations
  4. opthalamic disorders uveitisis and iritis along with mydriasis for surgeries
  5. respiratory disorders: treat asthma and COPD
  6. CV: acts against reflex vagal discharge
  7. GI: traveller’s diarrhea
  8. Urinary disorders: oxygutynin, darifenacin, solifenacin, tolterodine
  9. cholinergic poisoning: insecticides, wild mushrooms, chemical warfare
61
Q

adverse effects of mACHR antagonists

A

high concentration of atropine blocks all PS- dry, blind, red, mad, hot

overdoses treated w/ cholinesterase inhibitors

62
Q

contraindications of mAChR antagonists?

A

glaucoma, prostatic hyperplasia, acid-peptic disease

63
Q

alpha1 adrenergic effects?

A

constriction of blood vessels, mydriasis, smooth mm. contraction, glycogenolysis in the liver

64
Q

glycogenolysis in liver

A

alpha1 and beta2 (thus for nonspecific beta blockers, must be careful when giving to diabetic patients)

65
Q

Beta1 effects?

A

increased chronotropic, increased inotropic, renin release

66
Q

Beta2 effects?

A

smoooth mm. relaxation, glycogenolysis in liver, insulin release

67
Q

Beta3 effects?

A

lipolysis

68
Q

epi, NE, Iso compared

A

alpha1: epi>NE»>iso
beta2: iso>epi»>NE (epi has greater affinity for beta2, so at low doses it results in vasodilation)
beta1: iso>epi=NE

69
Q

clinical use for epi?

A
  1. bronchial asthma in children (B2)
  2. anaphylactic shock: bronchodilation, decreased edema, decreased spread of ag, alleviation of hypotension (efficacy is on a1 and B2)
  3. glaucoma - lowers intraoc pressure through unknown mechanism
  4. infiltration with local anesthetics
  5. topical hemostatic
70
Q

adverse effects of epi?

A

BP: cerebral hemorrhage
CV: arrhythmias
CNS: fear, anxiety, h/a

71
Q

contraindications of epi?

A

HTN,
shock w/ compromised bloodflow to organs
hyperthyroidism- increased incidence of arryhthmias
angina pectoris: increased work and demand on heart
asthamatics w/ degenerative heart disease

72
Q

what does blocking alpha2 do?

A

results in enhnaced release of NE from symp. nn. this often causes tachycardia at the heart when it is due to a nonspecific alphablocker.

73
Q

tyramine

A

found in beer, red wine, cheese

  • normally rapidly degraded by MAO in GI tract and liver
  • Patients taking MAO inhibitor have high levels
  • Tyr displaces NE from nerve terminal –> hyptertensive crisis, MI, stroke
74
Q

Cocaine

A

blocks reuptake of NE

75
Q

Ephedrine

A

mixed acting agonist
direct B receptor agonist, indirectly releases NE
- no substrate for COMT or MAO Thus is long lasting
- use: pressor agent, bronchospasm, nasal decongestant

76
Q

clonidine**

A
  • alpha2 agonist
  • centrally acting hypotensive agent that works at the brainstem
  • decreses symp outflow and regulates NT release
  • clinical use: hypertension and off-label uses
  • third line tx to HTN
  • b/c it can block symp outflow it is used offlabel for help from narcotic withdrawal
77
Q

methyldopa

A
  • False neurotransmitter concept
  • Converted to methyl-NE
    stored in vesicles instead of NE
  • released & acts as a centrally acting a2-agonist
  • compare with clonidine
  • Considered a drug of choice for treating hypertension in pregnant females
78
Q

why alpha 1 selective blocker?

A

don’t block alpha 2, thus reflex tachycardia is less prevalent

used to treat HTN, and BPH

79
Q

why use beta blockers?

A

angina pectoris - reduce CO and work

HTN: decreases CO And produces slow decrease in peripheral resistance due to blockade of renin

migraine headaches

arrhythmias

pheochromocytoma

panic attacks

CHF

80
Q

uses of NE and epi?

A 
cardiac arrest
adjunct to local anesthetic
hypotension
anaphylaxis (epi only)
asthma (epi only)
81
Q

two types of treatment for glaucoma?

A

beta blockers to decrease formation of fluid by ciliary epithelial cells

muscarinic agonist to improve drainage

82
Q

Dumbbells

A 
Diarrhoea
Urination
Miosis/muscle weakness
Bronchorrhea
Bradycardia
Emesis
Lacrimation
Salivation/sweating

Pharmacology (2 decks)

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