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ESA 5 - Pharmacology > Session 1 - Intro and Pharmacokinetic concepts > Flashcards

Session 1 - Intro and Pharmacokinetic concepts Flashcards

1
Q

What instance would require brand prescription over generic prescription?

A

When bioavailability of drugs differs significantly.

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2
Q

What is a black triangle drug?

A

Drug being intensively monitored for adverse effects

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3
Q

What is pharmacokinetics?

A

What body does to drug

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4
Q

What is pharmacodynamics?

A

What drug does to the body

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5
Q

What is pharmacogenetics?

A

Effect of genetic variability on pharmacokinetics of a drug on an individual

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6
Q

What are the 4 pharmacokinetic processes?

A

ADME

Absorption, Distribution, Metabolism, Elimination

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7
Q

What is bioavailability?

A

Fraction of a dose which finds its way into the circulation

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8
Q

What is the bioavailability percentage of IV infusions?

A

100%

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9
Q

In this picture, how would you calculate the total drug exposure? How would you calculate oral bioavailability?

A

Area under the curve = total drug exposure

Oral bioavailability = AUC oral / AUC iv

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10
Q

What 5 factors affect the bioavailability of a drug?

A
  1. Drug formulation
  2. Age
  3. Food - lipid soluble or water soluble drug
  4. Vomiting or malabsorption
  5. First pass effect
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11
Q

What is the advantage of modified release over immediate release drug?

A

modified release spends more time in the therapeutic window than immediate release

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12
Q

What circulation proteins do these drugs bind to:

a) acidic drugs
b) basic drugs
c) hormones

A

a) albumin
b) lipoproteins and/or acid glycoproteins
c) globulins

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13
Q

What 4 factors affect protein binding of drugs?

A
  1. Hypoalbuminaema
  2. pregnancy
  3. renal failure
  4. displacement by other drugs
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14
Q

How does protein binding displacement by drug B affect drug A which is usually bound to the protein?

A

Preferential binding of protein to drug B means drug A is displaced and results in greater concentration of drug A in plasma, can have serious consequences.

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15
Q

How are drugs differently distributed in the body?

A

Some drugs bound to tissues, others remain only in circulation AKA volume of distribution

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16
Q

How does volume of distribution relate to half life?

A

Larger volume of distribution means longer half life because drug resides in tissues and has to diffuse into plasma to be eliminated

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17
Q

How many half lives does it take for a drug to reach steady state?

A

4-5 half lives

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18
Q

What 3 processes determine renal excretion of drugs?

A
  1. Glomerular filtration
  2. passive tubular reabsorption
  3. active tubular secretion
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19
Q

How does reduced GFR affect clearance rate of drugs?

A

Reduced GFR results in reduced clearance which increases half life

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20
Q

Explain zero order and first order kinetics

A

First order - Half lives. Most drugs display first order kinetics unless high doses are given in which case they display zero order

Zero order - Set amount of drug eliminated per unit time.

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21
Q

Which drugs are more likely to be toxic? first order or zero order and why?

A

zero order as it has a fixed rate of elimination. Small dose changes can lead to toxicity and large increments in dose

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22
Q

limitations of phase 1 to 3 trials

A

small number of patients, controlled nature of trials, exclusion of patients at greater risk of ADRs

23
Q

Freq of adverse events of v common, common, uncommon, rare, v rare

A

v common - 10

common - 100 then goes up in x10

24
Q

ADR types A to E

A

A - causally related to drug pharmacology. common

B - idiosyncratic response. rare

C - chronic

D - delayed e.g. steroid and osteoporosis

E - end of treatment effects

25
Q

When should ADRs be reported via yellow card scheme?

A

All ADRs - if associated with new med (black triangle) or with child (below 18) or pregnent

established drug - serious illnesses or death

26
Q

Pros and cons of yellow card scheme

A

pros - low cost, generates ADR hypothesis

cons - poor compliance, absence of control groups, coincidence or causal relationship?

27
Q

legal requirements for prescription

A

legible, signed and dated, 2 forms of pt ID

28
Q

where does 1st pass metabolism occur

A

gut wall, lumen, liver

29
Q

CYP inhibitors

A

G-COMICS

Grapefruit - cranberry, omeprazole, metronidazole, isoniazide, cimetidine, sodium valproate

30
Q

how is T1/2 differnet in children

A

longer as Vd is lower as more of their body is ECF

31
Q

Monophasic and multiphasic COCP?

A

monophasic - same dose of oest and prog on each of 21 days

32
Q

COCP ADRs

A

increase risk of PE, stroke, DVT, headache, depression

decrease risk of ovarian cancer, endometrial and colorectal

33
Q

high ldl effects on blood?

A

increase platelet aggreg therefore atherogenic

34
Q

obesity effects on lipids in blod

A

increase cholesterol and TG, decrease HDL

35
Q

why acei different in blacks and older ppl

A

dye to reduced RAS activity

36
Q

what is type A and B ADR according to pharmacogenetics

A

A - polymorphism in affected structure increase or decrease effect

B - presence of gene leads to abnormal interaction e.g. hepatic porphyria induced by alcohol

37
Q

MoA of corticosteroids

A

binds with intracellular receptor and complex forms dimer with another one then binds to clucocorticoid response element (GRE) in nucleus and modulats transcription

38
Q

effects of glucocorticoids (GC) and in excess

A

increase blood glucose, AAs, and TGs

excess - atrophy, increase bone resorption (osteoporosis), DM (prolonged increase glucose)

39
Q

how are GCs elminated in liver

what is steroid sparing drug

how monitor steroid usage

A

phase 1 and 2

DMARD

peak flow, ALT, CRP

40
Q

how should GCs be stopped?

A

gradually tapered off to prevent adrenal insufficiency

41
Q

symptoms of mineralocorticoud deficiency?

A

hy[ptension, dehydration, hypoNa, hyper K+

42
Q

what is time dependent and conc dependent killing

A

time dependent - requires drug exceed a certain conc for a prolonged period of time to work

conc dependent - needs to exceed certain conc to kill bacteria

43
Q

severe asthma and life threatening asthma criteria

A

severe - unable to complete sentences, HR 110+, RR 25+, PEFR 33-55% of best

life threatejning - less than 33% PEFR

44
Q

how treat acute asthma

A

O2, nebulised salbutamol, oral prednisolone

45
Q

what is autacoid and eg.

A

ocal hormones e.g. No, histamine

46
Q

schedule 2 and 5 drugs

A

2 - storage and locked, prescription and destruction conditions

5 - just keep invoice of prescription

47
Q

difference unfractionated and LMWH

A

unfractionated more effective but needs more monitoring. APTT monitor

48
Q

nephrotoxic drugs

A

ACEi, NSAIDs, metformin, aminoglycosides

MANA

49
Q

ADRs of aspirin

A

ASPIRIN

asthma, salicyalism, peptic ulcer disease, intestinal bleeding, reyes syndrome, idiosyncracy, noise (tinnititus)

50
Q

parkinson drugs

A

SALAD - selegeline, anticholinergics, L-DOPA + DCT, amantadine, dopamine agonist

51
Q

sodium valproate ADR

A

VALPROATE

vomiting, alopecia, liver toxic, pancytopenia, retention of fats (weight gain), oedema, appetite increase, teratogen, enzyme inducer

52
Q

steroid ADRs

A

CUSHINGOID

cataracts, ulcers, skin straie, hypertension and hyperglyc, infections, n.., g..,osteoporosis + obesity, immunosuppression, diabetes + depression

53
Q

WPW pathophysiology

A

reentry through bundle of kent

ESA 5 - Pharmacology (22 decks)

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