pc term 1 Flashcards

1
Q

the 2 categories of antiulcer drugs are
1. reducing acid in stomach
2. mucosal protective agents
what are 3 ways to reduce acid in stomach?

A
  1. antacids to neutralise gastric acid
  2. H2 blockers to reduce acid secretion
  3. PPIs to irreversibly inhibit gastric acid secretion
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2
Q

the 2 categories of antiulcer drugs are
1. reducing acid in stomach
2. mucosal protective agents
what are the 3 mucosal protective agents?

A
  1. sucralfate forms viscous gel that acts a protective barrier in stomach
  2. bismuth compounds that form a protective layer to coat ulcer beds + anti microbial activity against H. Pylori
  3. misoprostol which is a synthetic PGE1 to promote bicarb & mucus secretion, enhance mucosal blood flow, inhib gastric acid secretion
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3
Q

what is in triple therapy for H. pylori infection?

A

PPI
metronidazole (antibiotic)
clarithromycin or amoxicilin (antibiotic)

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4
Q

what is in quadruple therapy for H. pylori infection?

A

PPI metronidazole clarithromycin amoxicilin (antibiotics)
or
PPI bismuth-subcitrate metronidazole tetracycline

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5
Q

why is H pylori a toxigg bitch

A

it enters stomach and attach to epithelial layer -> has enzymes that can convert urea into NH3 to neutralise gastric acid -> H pylori just hang ard the stomach and cause a shit ton of infection & mucosal cell death

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6
Q

what is the mechanism of omeprazole

A
  • a PPI
  • targets parietal cells, inhibs H+ K+ ATPase
  • in prodrug form -> absorbed by parietal cells to form covalent disulphide bond w H+ K+ ATPase
  • irreversibly inhibit gastric acid secretion
  • slight antimicrobial activity against H. pylori
  • PPIs need to be given on empty stomach
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7
Q

what is therapeutic index and how is it measured

A

TI = TD50/ED50

measures safety of drug

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8
Q

what is efficacy

A

efficacy = likelihood of activating effector and eliciting a response
higher efficacy = higher E max

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9
Q

what is efficacy of

a) full agonist
b) partial agoist
c) antagonist

A

a) a = 1
b) 0 < a < 1
c) a = 0 since antagonist do not produce a direct response

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10
Q

what is E max

A

emax = maximum response of a system

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11
Q

what is potency

A

potency = dose required to produce a given degree of response
lower dose = higher potency

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12
Q

what is EC50

A

EC50 = drug dose required to produce 50% of the fx

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13
Q

what are the 3 types of antagonism

A
  1. chemcial antagonism in which antagonist itself cancels out the fx of active drug
  2. pharmacological antagonism in which antagonist binds to receptor to prevent active drug from forming DRC
  3. physiological antagonism in which antagonist causes and opposing fx to active drug via different mechanism
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14
Q

how will [drug] - dose curve shift when non competitive antagonist is added

A

curve shift down
Emax decreases
EC50 remains same

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15
Q

how will [drug] - dose curve shift when competitive agonist is added

A

curve shift right
Emax same
EC50 increases

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16
Q

How will [drug] - dose curve shift when agonist is added

A

curve shift left
emax same
EC50 decreases

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17
Q

steady state of drug concentration is received after how many t1/2?

A

after 5 t1/2

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18
Q

MOA of antihistamines?

A

competitive H1 receptor antagonist

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19
Q

what does alpha 1 receptor control

A
dilate pupils (midriasis)
increase aq humour secretion
increase glycogenolysis 
piss less
(alpha in general) vasocon for viscera bv, decrease GIT motility and secretion
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20
Q

what does alpha 2 receptor control

A

reduce salivary production

(alpha in general) vasocon for viscera bv, decrease GIT motility and secretion

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21
Q

what does beta 1 receptor control

A

increase HR and contractility
increase renin release in kidney
(beta in general) increase aq humour secretion

22
Q

what does beta 2 receptor control

A
bronchodilation
increase glycogenolysis 
decrease GIT motility and secretion
vasodilation of skeletal mm bv
(beta in general) increase aq humour secretion
23
Q

what does beta 3 receptor control

A

increase lipolysis
piss less
(beta in general) increase aq humour secretion

24
Q

what does M1 receptor control

A

increase stomach secretion

25
Q

what does M2 receptor control

A

decrease heart rate and contractility
increase GIT motility and secretion
piss more
arterial dilation & erection

26
Q

what does M3 receptor control

A
constrict iris (miosis)
decrease IOP
increase salivary production 
increase bronchoconstriction and secretions 
increase GIT motility and secretion 
piss more 
arterial dilation & erection

tldr = lungs, glands, GIT

27
Q

how beta blockers decrease blood pressure

A
  1. reduce hr and contractility

2. reduce renin, reduce water retention, reduce vasoconstriction

28
Q

what does M4 M5 receptors control

A

something in the CNS

29
Q

MAChR MOA?

A

metabotropic, via GPCR

30
Q

NAChR MOA?

A

ionotropic, via ligand gated Na channels

31
Q

NT for symp postG eccrine sweat glands

A

cholinergic!!!

32
Q

common ADR of cholinergic

A
diarrhea
sweat
miosis 
nausea
pissssss
contraindications for asthma & peptic ulcers
33
Q

what is the association btwn sarin, pralidoxime, atropine

A
sarin = the poison that irreversibly inhib CE
pralidoxime = the antidote to regenerate CE
atropine = MAChR blocker
34
Q

common ADR of anticholinergic

A
a confused man [confusion]
cant see [mydriasis]
cant piss [urinary retention]
cant shit [constipation]
cant spit [xerostomia]
35
Q

beta blockers used to treat what

A
high bp
irregular heart beat
angina
heart failure / attack
reduce symptoms of hyperthyroidism
36
Q

drug for COPD

A

ipratropium bromide

37
Q

drug for ophthalmic examination

A

atropine

cyclopentolate

38
Q

drug for parkinsons

A

benzatropine

39
Q

drug for skeletal mm paralysis for surgery

A

pancuronium (non depol NMBA)

succinylcholine (depol NMBA)

40
Q

drug for sedation

A

dexmedetomidine

41
Q

drug for glaucoma

A

pilocarpine (direct)
physostigmine (not rly,..this is more for atropine od)
betaxolol (b1 selective)
timolol (b non selective)

42
Q

drug to come out of GA

A

neostigmine

43
Q

drug for alzheimers

A

donepezil

44
Q

pharmacodynamics vs pharmacokinetics?

A
pd = what drug does to body [MOA]
pk = how body processes drug via ADME
45
Q

what is first pass elimination

A

a phenomenon of drug metabolism whereby the concentration of a drug, specifically when administered orally, is greatly reduced before it reaches the systemic circulation.

sublingual route bypasses the first-pass metabolism

46
Q

in a plasma conc against time curve, what does AUC represent

A

bioavailability

47
Q

what does metabolism of drug involve

A

phase 1 - functionalization (CYPs)

phase 2 - conjugation (lipophilic -> hydrophilic for easy excretion)

48
Q

what inhibits CYP 3a4

A

grapefruit juice

49
Q

smoking and drugs??

A

smoking induces CYPs -> bd drug faster -> drug lack intended effect

50
Q

what is affinity

A

probability that a drug molecule will interact w its receptor to form a DRC

  • agonist and antagonist must both have an affinity for receptor
  • higher Kd = higher affinity
51
Q

dose response curve equation??

A

[DR] = [Rt][D] / (Kd + [D])