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KNES 372 > lec 16 - drugs and pharmacology > Flashcards

lec 16 - drugs and pharmacology Flashcards

1
Q

what is pharmacokinetics

A

how the body affects a drug
- time course of a drug and its metabolites after administration

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2
Q

what are the 4 main steps of pharmacokinetics

A
  • absorption
  • distribution
  • metabolism
  • excretion / elimination
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3
Q

what are the most common forms of administration

A

oral, topical, injection

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4
Q

what are the drug factors that affect absorption

A

formulation (delayed release, aerosol, etc)
solubility (lipid vs water)
particle size
pH
drug ionisation

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5
Q

what are the host factors that affect absorption

A

motiliy of gut
food in stomach
vomiting / diarrhea
amt of circulatino to the administration site
SA at the administration site
degrees of first pass metabolism

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6
Q

what are the patterns in tissue distribution

A

blood gets to the brain the fastest out of anywhere in the body

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7
Q

what are the mechanical / biochemical factors involved in distribution

A

mechanical
- blood flow
- barriers (placenta, blood brain barrier, etc)

biochemical
- lipid solubility
- binding to plasma proteins
- accumulation in tissues
- pH

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8
Q

what is the process of metabolism (biotransformation)

A

conversion by enzymes to generally more polar (less lipid soluble) forms
- occurs in the smooth ER of cells in the liver (also kidneys, GI, lung, and plasma)

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9
Q

how can drugs be metabolised

A

activated
changed to another active metabolite
changed to a toxic metabolite
inactivated

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10
Q

what are the phase I and II reactions in drug metabolism

A

phase I
- conversion to polar metabolite (oxidation, reduction, hydrolysis)

phase II
- coupling of drug (or polar metabolite) with an endogenous substance

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11
Q

what are the factors affecting metabolism

A

genetics
environment (drug interactions)
physiological (age, disease, nutrition, alcohol, smoking)

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12
Q

what are the main ways of excretion

A

kidneys (main)
GI tracts
exhalation
saliva

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13
Q

what are the elimination kinetics

A

half life = time taken for the serum drug level to fall 50% during elimination

1st order kinetics = 5 half lives to reach steady state

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14
Q

what is bioavailability

A

fraction of the dose that reaches the systemic circulation in an unchanged state

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15
Q

what are the methods of drug transport

A

passive = diffusion and facilitated diffusion
active = uses ATP to move drug

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16
Q

what are pharmacodynamics

A

how the drug affects the body (physiological effects)

17
Q

what are the different types of drug antagonists

A

chemical
functional - acting independently at different receptors and have opposite physiological effects
competitive - binds to same site
non competitive - binds to different site to change the effect

18
Q

what are the upper and lower limits of the therapeutic window

A

lower limit
- concentration that produces half the greatest possible effect

upper limit
- no more than 5-10% of patients experience a harmful side effect

19
Q

what is the effective vs toxic dose

A

effective dose = dose that gives the required response in 50% of subjects

toxic dose = dose that produces harmful side effects in 50% of subjects

20
Q

what is the therapeutic index

A

toxic dose divided by effective dose
- reflects margin of safety (larger = safety)

21
Q

what are the effects of tylenol (acetaminophen)

A

analgesic and antipyretic (anti fever)

22
Q

what are the pharmacokinetics of acetaminophen

A
  • high absoprtion in SI
  • metabolism in liver
  • eliminated through urine as metabolites

time to peak = 10-60 mins
half life = 2-3 hours

23
Q

what are the effects of NSAIDs

A

anti inflammatory
anti pyretic
anti platelet
analgesic (better than tylenol)

24
Q

how do NSAIDs act

A

acts by inhibiting cyclo oxygenase (COX)

25
Q

what are the pharmacokinetics of NSAIDs

A
  • absorbed rapidly from the stomach and upper SI
  • distribution throughout most body tissues
  • metabolised in liver
  • excreted through liver

time to peak = 1-2 hours
half life = 2 hours

26
Q

what are the side effects of NSAIDs

A

stomach = nausea, pain, gastritis, ulcer
kidneys = hypertension, fluid retention, failure
platelets = dysfunction - inhibit clotting
vessels = vasconstriction
other = tinnitus

27
Q

what are the implications for injury from NSAIDs

A

inhibit protein synthesis and muscle repair / regeneration
inhibit tenocytes proliferation and collagen formation
(may be useful in acute / reactive tendinopathy)
impair bone healing

28
Q

what is the benefit of topical NSAIDs

A

avoids systemic effects
- way less plasma concentration than oral form

29
Q

what are cortisone injections commonly used for

A

bursitis
tenosynovitis
OA

30
Q

what are contraindications to cortisone injections

A

infection, prosthetic joint, fracture
don’t give to achilles or patellar tendinopathies
anticoagulant, IDDM, TB, hemarthrothis, immunosuppression

31
Q

what are possible adverse drug reactions from cortisone injections

A

damage to cartilage / tendon
infection
post infection flare
skin atrophy
tendon rupture
bleeding

32
Q

what are the medical uses for opoids

A

pain relief (acute and chronic)
sedation, anasthesia
cough
diarrhea
dyspnea

33
Q

what are the side effects of opoids

A

nausea, dizziness, constipation, sedation, confusion

34
Q

what occurs during opoid overdose

A

respiratory depression

35
Q

what are the two main compounds of cannabinoids

A

CBD = non psychoactive
THC = psychoactive

36
Q

what are the pharmacokinetics of cannabinoids

A

oral absorption = lower peak concen and slower onset
distribution mainly to fatty tissues
metabolised in liver
elimination mainly through feces

37
Q

what can cannabinoids be used for

A

chemo effects, spasticity, neuropathic pain, seizures, wasting syndromes (HIV/AIDS)

no supportive evidence for acute pain, headache, fibromyalgia, arthritis

38
Q

what are the acute vs chronic adverse effects of cannabinoids

A

acute = “high symptoms”
chronic (correlation not necessarily causation)
= more mental health conditions

KNES 372 (24 decks)

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