1. receptors 2. enzymes 3. transporters

haroon pharmacology Flashcards by Areej Shahid

2 routes of administration

enteric - oral, rectal (GI TRACT INVOLVED)

parenteral - IM, IV, SC (NO GI TRACT INVOLVED)

others - inhaled and topical

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what do drugs target

receptors
enzymes
transporters

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what is a ligand

anythung that binds to a receptor - agonost or antagonist

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describe agonist

full affinity
full efficacy

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describe antagonist

full affinity
zero efficiacy

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wjhat is potency

how well a drug works and how much is needed to get a response

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example of selective b blocer

atenolol - only binds to b1

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example of non selective beta blockr

propanolol - binds to b1 and b2

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what do NSAIDS do

inhibit COX 1
prevent arachidonic acid
decrease prostaglandin production
affects GI mucosa
gastruc ulcer

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what dp ACE-I do

inhibit angiotension 1 to 2
antihypertensive

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what d PPIS do

irreversible inhibition of h+ k+ ATPase pumps
decrease gastric ph

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3 types of diuretics

loop
thiazides
spirooloactone

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where are loop dieutucs

ascending limb
inhibit NKCC2 symporter

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where are thiazde direuctis

DCT
inhibit nacl co transpter

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what us spironolactone

K+ SPARRING DIURETUC

inhibits aldosterne action BY INHIBITING ENAC CHANNELS IN COLLECTING DUCT SO MORE WATER AND SODUM EXCRETED AND POTASSIUM IS RETAINED

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describe process of pharmacokinetics

administration
distribution
metabolism
excretiin

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what is bioavailabulity

how fast and to what extent drug reaches systemic circulation

iv is always 100%

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where are drugs metabolised

kidneys - small water soluble

liver - hydrophic molecules

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phase 1 druf metabolism

microsomal enzymes increase hydrophlicity mildly

eg cyp450

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phase 2 drug metabolism

conjugation causes major increase in hydrophilicity

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describe autonomic PSNS

nicotinic ach at synpases

ach at nmj

mAch R muscarinic

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describe autonomic SNS

nicotinic ach at synpases

nAD at nmj

NAch R nicotinic

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descrive somatic ns

nicotinic ach at synpases

ach at nmj

NAch R nictonicc

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what happens to ach at nmj

synthesis
vesicle storage
release
breakdown
re uptake

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what drugs are there at nmj

1. botulinim toxin - negatuve 2. curative nach - r antagonist - negatuve 3. ach-ase inhibitors - positive

what causes cholinergic crisis

overstimulation of Ach at nmj - SLUDGE Salivatio Lacrimation Urination Defecation Gi distress Emesis vomiting

what neurotransmiiter in paraystmpathetic

ach

what neurotransmiiter in stmpathetic

nad

effect of paraympathetic

bronchoconcstricition increase gi motility and secretion bladder contraction penis points - erect

effect of sympathetic

bronchdilation decrease gi motility and secretion detrustor relaxes penis shoots - ejaculation

where are m1 receptrs

brain

where are m2 receptors

heart

where are m3 receptors

lumgs

what to give for CAP

amoxicillin/arithromycin

what to give for COPD exacerbation

amoxicclion/c;arithromycin doxyclcine

what. togive for HAP

co amoxiclav - 3x daily 500mg

what to give for cellulitis

floxacillin for group b strep or staph aureus

what to give for pyelonephritis

cefalexin, co amoxiclav

what to give for chalmidya

azithrromycin or doxyclcine

what. togive fo rgonorrhea

im ceftriazxone or azithromycin

what to give for syphillus

benzathinr penicil / benzylpeniccilin

what ti gve for gastrotenteritis

campylobacter --> clarithromycin salomella + shigells --> ciprofloxacin

what to give for. cdifficule

vancomycin 125 mg

what to give for ifnective endocardiiyis

stapj aureus --> vancomycin and rifampacin s viridans --> benzylpeniccilin and gentamicin

what to give fo rmeningitis in hos[ital

3rd gen cephalosporin ceftriaxone amoxicillin for listeria + steroids simulatenosuly

4 types of pain

acute cancer neuropathic chronic non cncer

what are ADRs reported to

MHRA yellow card scheme

name of drug classication for ADR

RAWLINS THOMPSN

WHAT IS ADR ABCDE

augmented bizarre chronic delayed end of use

what affects drug absorption

acidity motility solublity

what affects drug distrbution

protein binding

what affects drug metabolusm

1. cyp450- induction decreases therapteuc efecr 2. cyp450 inhibition increases theraptueic effecr

what affects drug excreetion

urine ph

2 types of opioids

naturally occuring - morhphone + codeine modified - dimorphine

opipid oral bioavaility

50%

tretament for resp distress

naloxone

what causes opioid tolerance

over stimulation of opipid receptor desensitises the effect

what causes opioid dependence

psychological state of craving how u feel

what does aspirin do

inhibits cox1(andcox 2 but 1 more) decrease thromboxane a2

what does clopidogrel do

inhibits p2y12

2 anti plateklts

aspirin. andclopidogrel

4 anticoagulamts

heparin warfarin DOAC thrombolysis eg altpease

what does heparin do

acrivates antithrombin 3 and inhibits factor 10

what does warfarin do

anti vtamin K inhibits vitamin k epoxide reducatse

what do doacs do

inhibitors of activated factor 10 eg apixaban

what do thrombolytics do

tissue plasminogen activatir activates plasmin to degrate fibrin

what to give if patient on wafatin is bleeding

vit k

impact of cox 1 inhibition

- decrease gastric mucosal potectant - increase somtach ph - increase risk f gastropathy

impact of cox 2 inhibition

anti inflmmatory

nsaids common SE

peptic ulcers or bleeds

ACE - I common se

DRY COUGH - due to bradykinin accumulation in lungs AKI due to decreased gFR due to dilation of glomerulus

ppi common SE

prolonges use increases fracture risk

opioids comon se

resp distress n+v tolerance +dependence

loop duiretcs and thiazides common se

hypokalaemia dehydration

spironolocatone common se

hyperkalsmeia

SIDE EFFECTS OF STEROIDS

cushingoid map cataracts ulcets striae hypertenson infection increases risk necrosis growth restriction osteoporosis increase icp T2DM myopathy adipose hypertrophy pancreatitis

haroon pharmacology Flashcards

(76 cards)