Session 1 - Intro and Pharmacokinetic concepts Flashcards Preview

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

Flashcards in Session 1 - Intro and Pharmacokinetic concepts Deck (53):
1

What instance would require brand prescription over generic prescription?

When bioavailability of drugs differs significantly.

2

What is a black triangle drug?

Drug being intensively monitored for adverse effects

3

What is pharmacokinetics?

What body does to drug

4

What is pharmacodynamics?

What drug does to the body

5

What is pharmacogenetics?

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

6

What are the 4 pharmacokinetic processes?

ADME

Absorption, Distribution, Metabolism, Elimination

7

What is bioavailability?

Fraction of a dose which finds its way into the circulation

8

What is the bioavailability percentage of IV infusions?

100%

9

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

Area under the curve = total drug exposure

Oral bioavailability = AUC oral / AUC iv

10

What 5 factors affect the bioavailability of a drug?

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

11

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

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

12

What circulation proteins do these drugs bind to:

a) acidic drugs

b) basic drugs

c) hormones

a) albumin

b) lipoproteins and/or acid glycoproteins

c) globulins

13

What 4 factors affect protein binding of drugs?

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

14

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

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.

15

How are drugs differently distributed in the body?

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

16

How does volume of distribution relate to half life?

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

17

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

4-5 half lives

18

What 3 processes determine renal excretion of drugs?

  1. Glomerular filtration
  2. passive tubular reabsorption
  3. active tubular secretion

19

How does reduced GFR affect clearance rate of drugs?

Reduced GFR results in reduced clearance which increases half life

20

Explain zero order and first order kinetics

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.

21

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

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

22

limitations of phase 1 to 3 trials

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

23

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

v common - 10

common - 100 then goes up in x10

24

ADR types A to E

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

When should ADRs be reported via yellow card scheme?

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

established drug - serious illnesses or death

26

Pros and cons of yellow card scheme

pros - low cost, generates ADR hypothesis

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

27

legal requirements for prescription

legible, signed and dated, 2 forms of pt ID

28

where does 1st pass metabolism occur

gut wall, lumen, liver

29

CYP inhibitors

G-COMICS

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

30

how is T1/2 differnet in children

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

31

Monophasic and multiphasic COCP?

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

32

COCP ADRs

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

decrease risk of ovarian cancer, endometrial and colorectal

33

high ldl effects on blood?

increase platelet aggreg therefore atherogenic

34

obesity effects on lipids in blod

increase cholesterol and TG, decrease HDL

35

why acei different in blacks and older ppl

dye to reduced RAS activity

36

what is type A and B ADR according to pharmacogenetics

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

MoA of corticosteroids

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

38

effects of glucocorticoids (GC) and in excess

increase blood glucose, AAs, and TGs

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

39

how are GCs elminated in liver

what is steroid sparing drug

how monitor steroid usage

phase 1 and 2

DMARD

peak flow, ALT, CRP

40

how should GCs be stopped?

gradually tapered off to prevent adrenal insufficiency

41

symptoms of mineralocorticoud deficiency?

hy[ptension, dehydration, hypoNa, hyper K+

42

what is time dependent and conc dependent killing

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

severe asthma and life threatening asthma criteria

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

life threatejning - less than 33% PEFR

44

how treat acute asthma 

O2, nebulised salbutamol, oral prednisolone

45

what is autacoid and eg.

ocal hormones e.g. No, histamine

46

schedule 2 and 5 drugs

2 - storage and locked, prescription and destruction conditions

5 - just keep invoice of prescription

47

difference unfractionated and LMWH

unfractionated more effective but needs more monitoring. APTT monitor

48

nephrotoxic drugs

ACEi, NSAIDs, metformin, aminoglycosides

MANA

49

ADRs of aspirin

ASPIRIN

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

50

parkinson drugs

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

51

sodium valproate ADR

VALPROATE

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

52

steroid ADRs

CUSHINGOID

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

53

WPW pathophysiology

reentry through bundle of kent