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Easter revision 2018 > Pharma > Flashcards

Pharma Flashcards

1
Q

First pass metabolism

A

Any metabolism before the blood i.e. gut lumen (acid), gut wall (P glycoprotein efflux), liver

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2
Q

Bioavailability =

A

the fraction of a drug reaching a particular body compartment

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3
Q

Vd=

A

How much volume we’d need to keep the total body conc equal to the plasma conc. Vd is low for drugs that stay in the blood and high for drugs that go to muscle/fat/etc

Vd = dose of drug given/ plasma conc

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4
Q

Factors affecting distribution

A 
Volume of distribution 
Protein binding (if bound then it can't have an effect)
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5
Q

Give examples of drugs with volumes of distributions from low to high

A 
Ibuprofen, warfarin (lowest Vd i.e. stay in blood)
Alcohol, insulin, dextrose
Paracetamol, caffeine
Cocaine, diazepam
Haloperidol, TCAs
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6
Q

Describe drug route from mouth to liver

A

Mouth, gut lumen, gut wall, portal vein, liver

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7
Q

Potency =

A

amount needed to produce a given effect (depends on efficacy and affinity)

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8
Q

Vd relates to our body fluid volumes- explain

A

Our plasma is 5%, about equal to heparin’s Vd so it stays in blood
ECV is 20%, about equal to gentamicin which stays outside cells and can’t enter very well
Total water is 55%, about equal to drugs that cross cells easily such as ethanol
Drugs with a Vd greater than our body volume go everywhere and are hard to remove by harm-dialysis e.g. TCAs, haloperidol

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9
Q

Vd is proportional to…

A

half life (higher Vd, longer half life)

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10
Q

Outline our fluid compartment numbers

A

42L total, 2/3 ICF 1/3 ECF

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11
Q

Why do drugs get conjugated

A

So they become water soluble to be eliminated

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12
Q

What is phase I and II metabolism

A

Both in liver
Phase I is oxidation, reduction, dealkylation and hydrolysis reactions. CYP450s carry out redox reactions (e.g. 2D6, absent in 7% white, hyperactive in 30% East African, metabolises codeine and inhibited by haloperidol)
Phase II is conjugation

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13
Q

What are first order and zero order kinetics

A

First order- elimination is proportional to amount of drug. Called linear

Zero order- elimination is at the same rate and does not vary with drug concentration. More likely to cause toxicity.

Some drugs have both e.g. paracetamol is linear and then non-linear when saturated

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14
Q

How many half lives to reach CpSS (concentration plasma steady state) and how many half lives to eliminate

A

4-5 half lives

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15
Q

What’s the point of loading doses

A

Allow us to get to CpSS without waiting for 4-5 half lives if the half lives are long
Loading dose = Vd / target CpSS

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16
Q

What is k?

A

Elimination constant
K = Clearance / Vd
T1/2 = Vd / Clearance

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17
Q

EC50 and Emax

A

EC50 is concentration at 50% effect

Emax is max effect

18
Q

What is Km

A

Concentration at half the Vmax (max velocity)

19
Q

Is the Vmax and Km different to the enzyme with:
a competitive inhibitor
a non-competitive inhibitor

A

Comp: same Vmax, different Km

Non-comp: different Vmax (lower), same Km

20
Q

Define affinity

A

How well it binds to receptor

21
Q

Efficacy

A

How much drug achieves its effect

22
Q

Potency

A

How much of a drug is needed to produce desired response

23
Q

Therapeutic index

A

EC50 of adverse effect / EC50 of desired effect
TD50 : ED50 (toxic to effective dose)
Used to quantify the therapeutic window (minimum toxic concentration - minimum effective concentration)

24
Q

What is P-glycoprotein

A

Efflux transporter, found in GI (moves back into gut lumen), kidneys (moves into urine), liver (moves into bile)
Grapefruit juice inhibits
St Johns wort induces

25
Q

What could affect metabolism

A

Genetics of CYP450s e.g. 2D6 (7% white absent 30% East African hyperactive for codeine)
Portal blood flow
Inducers (St Johns wort) or inhibitors (ethanol) of CYP450s

26
Q

Give a pharmacokinetic drug interaction example

A

I.e. affecting ADME.
Alginates (gaviscon) reduce absorption of other drugs

Or aspirin displaces warfarin from albumin –> excessive bleeding

27
Q

Give a pharmacodynamic drug interaction example

A

Agonism/antagonism at same receptor e.g. salbutamol is a beta agonist and stall is a beta blocker

28
Q

Describe disease-drug interactions

A

Renal disease: e.g. CKD impaired clearance so longer half life of renally excreted drugs e.g. digoxin
Hepatic disease: impaired clearance of hepatic cleared drugs e.g. opiates in cirrhosis can lead to coma
CVS disease: impaired hepatic and renal perfusion so impaired clearance

29
Q

What’s a normal QT interval and what can happen if its prolonged

A

350-450ms. If prolonged can cause torsades de pointes, a form of VT that can become VF. Sotalol, cocaine, TCAs can prolong QT

30
Q

Give examples of off target and on target ADRs

A

Beta blockers on-target ADR of bradycardia, off target bronchospasm

31
Q

Antagonists have affinity but no efficacy. Agonists have…

A

affinity and efficacy

32
Q

Grapefruit juice…

A

is a CYP450 inhibitor

33
Q

Obesity ____ Vd so need ___ dose

A

Increases Vd, need higher dose

34
Q

Kd

A

affinity between site and ligand

35
Q

Why is LDL bad for vessels

A

Enters arterial wall, becomes oxidised, oxidised LDL enters macrophages to become foam cells, activates T cells, mitogenic for SM cells, inhibits macrophages, increases platelet aggregation, toxic to endothelial cells.

36
Q

How do statins work? name one

A

Simvastatin. Inhibit cholesterol synthesis in hepatocytes via inhibiting HMG-CoA reductase

37
Q

When should you prescribe statins and name ADRs

A

When 20% 10yr risk of CVD or familial hypercholesterolemia.

ADRs myopathy, arthralgia

38
Q

What are fibric acid derivatives/ fibrates

A

PPAR agonists, treatment for hypertriglyceridemia by increasing LPL production to decrease TGs. As an adjunct to diet
ADRs cholelithiasis and abnormal LFTs (contraindicated in hepatic or renal or gallbladder disease)

39
Q

What does nicotinic acid do

A

Increase HDL-C
Decrease VLDL and coronary events
ADRs peptic ulcer activation, hepatotoxic, pruritus
Contraindicated in peptic ulcer disease, acute liver disease

40
Q

What does ezetimibe do

A

Inhibits GI LDL absorption and increases hepatic LDL Rs, circulating enterohepatically
ADRs abdo pain, diarrhoea
Adjunct to diet and statins in hypercholesterolemia

Easter revision 2018 (11 decks)

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