Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BPT > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What drugs alter Digoxin clearance, and what is the mechanism?

A

Clearance decreased due to increased MDR1 transporter activity

Drugs that cause this: amiodarone, dronedarone, quinidine, ritonavir, ranolazine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

St John’s Wort acts on which CYP, and in which way?

A

Induce 3A4

Ciclosporin is key drug that is metabolised more

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Celecoxib and Warfarin

A

Celecoxib inhibits CYP2C9, leading to raised s-Warfarin and thus increased warfarin effect. Can double INR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What transporter variant is associated with Imatinib resistance?

A

ABCG2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Furosemide and Lithium

A

Furosemide will increase serum lithium levels

As will HCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Valproate and Lamotrigone

A

If used together, Lamotrigine needs dose adjustment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Ciclosporin metabolism

A

CYP3A4 in liver
Metabolism also occurs in small intestine via same CYP3A4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pharmacokinetics

A

What the body does to a given drug (absorption, distribution, metabolism, elimination)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pharmacodynamics

A

What the drug does to the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Best measure of overall exposure to a drug

A

Area under the curve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

For what drugs is Cmax most important?

A

Those with low therapeutic index - i.e. toxicity develops easily above therapeutic range

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Bioavailability and hepatic extraction ratio

A

Hepatic extraction ratio = 1 - bioavailability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Volume of Distribution

A

Conceptual not actual volume. Would be the volume of fluid required to contain all of the drug in the body at the concentration it exists in plasma. More in the cells = bigger volume of distribution

Volume of distribution = total amount of drug in body/plasma drug concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How to determine a loading dose

A

Volume of distribution multiplied by target plasma concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What binds with highest affinity to albumin?

A

Acidic drugs

Salicyclic acid, warfarin, phenylbutazone, penicillins, sulphonamides

Has lower affinity for basic and neutral drugs, but high capacity for these which can cause displacement. Digitoxin, bilirubin and fatty acids can all bind.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Bioavailability versus clearance for drug metabolism

A

Drug with low bioavailability will be more affected by changes in metabolism or transporters in bowel than changes in clearance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Calculation for half life

A

half life = 0.693 x Volume of distribution/clearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

First order versus zero order kinetics

A

First order: constant proportion of drug eliminated per unit time
Zero order: constant amount of drug eliminated per unit time

19
Q

What is the therapeutic index?

A

Difference between dose at which adverse effect and therapeutic effects occur

Therapeutic index = adverse effect EC50/Therapeutic effect EC50

(EC50 = concentration of drug required to give half maximal response)

20
Q

Tachyphylaxis

A

Rapid tolerance to drug - response to same plasma concentration decreases rapidly

Results in hysteresis loop.

21
Q

Reverse Hysteresis Loop

A

Delay in onset and duration of effect due to:
- Prodrug/active metabolite
- Secondary messengers
- Redistribution phase

22
Q

Potency

A

Measure of dose required to produce a response

NOT a measure of maximum response

So the lower the dose required, trhe higher the potency. Usually based on dose required to produce 50% of maximal effect/dose required to produce response in 50% of population

23
Q

Dosing aims for Vancomycin

A

Measure with 24h AUC/MIC
Essentially give as much antibiotic as possible without causing toxicity

24
Q

Aminoglycoside dosing aims

A

Target peak level >10x MIC
Measure Cmax/MIC
Concentration dependent and some post antibiotic effect

25
Q

Fluoroquinolone dosing aims

A

Aim AUC >125
Measure with AUC/MIC
Concentration dependent and post antibiotic effect

26
Q

Dosing aims for beta lactams

A

Time ? MIC
Aiming to be above MIC 40-70% of the time

27
Q

Type 1 Error

A

False outcome by chance

28
Q

Type 2 Error

A

Rejecting a true outcome by chance (sample size key)

29
Q

Phase 1 drug trial:

A

Assessing safety, bioavailability, maximum tolerated dose, side effects

30
Q

Phase 2 drug trial

A

Dose selection
Effect

31
Q

Phase 3 drug trial

A

Efficacy in target population
Survival benefit

32
Q

Common CYP Inducers

A

Rifampicin (1A2, 2B6, 2C8, 2C9, 2C19, 3A4/5) - so all but 2D6
Phenytoin ( 1A2, 2B6, 3A4/5)

33
Q

Do -azoles typically inhibit or induce CYP enzymes?

A

Typically inhibit

34
Q

Clopidogrel and CYP Enzymes

A

Inhibits: 2B6, 2C8
Substrate for 2B6, 2C19

35
Q

Antibiotics and CYP enzymes

A

Mostly inhibitors other than Rifampicin

Cipro: 1A2 inhibitor
Clarithromycin: 2C19 inhibitor, 3A4/5 inhibitor
Erythromycin: 3A4/5 inhibitor

36
Q

Inhibition or Induction of which CYP enzymes will influence Warfarin levels?

A

1A2, 2C9, 2C19, 3A4/5

37
Q

Bioavailability Calculation

A

Two key calculations:

AUC of oral / AUC of IV

Also Bioavailability = 1 - hepatic extraction ratio

When using AUC, need to ensure have considered the doses in the question

38
Q

Key clinical features of Serotonin Syndrome

A

Rapid onset within 24hr of commencing causative drug (i.e. whichever drug tips patient over into SS)

Autonomic dysfunction: diaphoresis, tachycardia
Neuromuscular excitability: hyperreflexia, clonus, increased tone
Altered mental state
Nausea, vomiting, diarrhoea

MAOI can cause hypotension (whereas hypertension overall more typical)

39
Q

Acute management of Serotonin Syndrome

A

Discontinue all serotonergic drugs
Benzodiazepines for agitation/excessive muscle activity
Active cooling for hyperthermia
Antihypertensives
Cardiac monitoring
Consider need for intubation/sedation

40
Q

Temperature indication for sedation/intubation in Serotonin Syndrome

A

> 41.1 degrees
Use non depolarising agent for paralysis, e.g. rocuronium. So don’t use Sux

41
Q

Mechanism and key causes of Neuroleptic Malignant Syndrome

A

Dopamine blockade is key. Central C2 receptor blockade in nigrostriatal pathway and hypothalamus -> movement disorders, impaired thermoregulation, increases sympathetic tone, disrupted autonomic regulation, calcium release from muscle

First generation antipsychotics, second generation antipsychotics, metoclopramide, promethazine

42
Q

Presentation of NMS

A

Insidious onset, can take 2-4 weeks
Cognitive changes early
Catatonia
Parkinsonism
Hyperthermia
Autonomic instability
Raised CK

No clonus or hyperreflexia

43
Q

Management of NMS

A

Discontinue cause
Supportive
Dantrolene if severe
Dopamine agonists
ECT for refractory disease

44
Q
A

BPT (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions