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The Principles of Prescribing Flashcards

1
Q

Cmax

A

Peak Plasma Concentration

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2
Q

Tmax

A

Time to peak plasma concentration

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3
Q

Steady State Concentration

A

When the inflow of the drug into plasma is equal to the rate of removal

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4
Q

How many half-lives does it take to reach 95% clearance of a drug?

A

Approximately 5 half-lives

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5
Q

What ionisation state are drugs best absorbed in?

A

Unionised
Hence, acidic drugs best absorbed in stomach, while basic drugs best absorbed in small intestines.

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6
Q

Examples of pro-drugs

A

Codeine -> morphine
Azathioprine -> mercaptopurine
Enalapril -> enalaprilat
Cyclophosphamide -> phosphoramide mustard

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7
Q

How does phenytoin affect other medications?

A

It can affect the concentration of concomitant antiseizure medicines by inducing the metabolism of other drugs and reducing their serum/plasma concentration.

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8
Q

Volume of Distribution Definition

A

The theoretical volume of fluid that would be needed to achieve the actual plasma drug concentration.

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9
Q

Volume of Distribution Calculation

A

Vd = (total amount of drug in the body) / (plasma-drug concentration)

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10
Q

How does Vd affect plasma concentration?

A

High Vd will give a low plasma concentration

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11
Q

Low Vd

A

Highly water soluble drugs (e.g. gentamicin, atenolol, insulin)
Extensively protein-bound drugs (e.g. warfarin)
Due to drugs staying in the plasma

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12
Q

High Vd

A

Highly lipid soluble (e.g. digoxin, morphine, diazepam)
Due to drugs moving out of the plasma into the tissues and organs

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13
Q

How does pregnancy affect Vd?

A

Increase total body water therefore water soluble drugs have a higher Vd and lower plasma concentrations

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14
Q

How does dehydration affect Vd?

A

Water soluble drugs will have a lower Vd
Lipid soluble drugs will have a higher Vd

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15
Q

Why do fat-soluble drugs tend to have longer half-lives?

A

Some drug is taken up into fat and when the drug is stopped being given the plasma concentration lowers and the drug moves from the fat back into the plasma. The fat acts as a reservoir with ‘slow release’.

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16
Q

What plasma protein do acidic drugs bind to?

A

Albumin

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17
Q

What plasma protein do basic drugs bind to?

A

alpha-1-acid-glycoprotein

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18
Q

Total Clearance (CL)

A

CL = CLH + CLR
Hypothetical volume of blood from which the drug is completely removed per unit time.

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19
Q

Elimination rate constant (k)

A

k = CL / Vd

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20
Q

Half-life calculation

A

t1/2 = 0.693/k
t1/2 = ln(2) / k

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21
Q

Phase 1 Liver Metabolism

A

Renders the drug more polar by oxidation, reduction or methylation so it can combine with another molecule.
Cytochrome P450 group of enzymes are responsible for the majority of Phase 1 reactions.

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22
Q

Phase 2 Liver Metabolism

A

Conjugation - results in a water soluble compound which is usually inactive and more easily excreted in the urine or bile.
Some mechanisms of Phase 2 reactions (e.g. glucuronidation and sulphation) have been shown to be impaired in liver disease

23
Q

P450 Inducers

A

E.g. phenytoin.
Accelerate the metabolism of concomitant drugs

24
Q

P450 Inhibitor

A

E.g. erythromycin.
Slows down the metabolism of other drugs.

25
What drugs are routine TDM recommended?
Digoxin Gentamicin Lithium Salts Vancomycin
26
What level of digoxin indicates toxicity?
>3 micrograms/litre
27
How does muscle mass affect volume of distribution?
Lower muscle mass lowers distributable space for water soluble drugs within the body and therefore reduces the volume of distribution. This leads to higher serum levels with a smaller dose.
28
Affinity
Measure of how well a drug binds to a receptor.
29
Proportion of receptors occupied calculation
p = ([D]) / ([D]+Kd) Where Kd is the ratio of k-/k+
30
How does a competitive antagonist affect the drug concentration curve?
Right shift
31
Agonist
A chemical that binds to its target to increase its activity
32
Antagonist
A chemical that opposes the action of another chemical therefore should have no action on their targets in the absence of an agonist
33
Competitive antagonist
Competes with an agonist for the same binding sites. Causes right shift in the relationship between agonist conc and binding. Reversed by increasing conc of agonist to 'out-compete' antagonist
34
Non-competitive antagonist
Prevents the agonist from producing a response at its receptor Effects cannot be overcome by increasing the conc of the agonist The maximum response of the agonist is reduced
35
Efficacy
How well an agonist achieves a response
36
Potency
Often described by the concentration or dose that is able to elicit 50% of the maximal response (ED50) A drug with a higher potency will have a lower ED50
37
Partial Agonist
A drug that has a lower maximal response resulting from lower efficacy
38
Allosteric Modulators
Bind to proteins at sites other than the binding site for the principal agonist
39
What effects can allosteric modulators elicit?
Alter the affinity of the binding sites for its agonists OR change the efficacy of the response when the agonist binds Their action can be either positive (increase potency of the agonists) or negative (decrease the potency of the agonists)
40
How many alpha subunits genes are there for calcium channels?
10
41
How many alpha subunits genes are there for potassium channels?
40 - very few examples of drugs targeting this channel type
42
How many alpha subunits genes are there for sodium channels?
9
43
When is the HMG-CoA reductase enzyme most active?
At night - therefore statins with short half-lives should be taken at bedtime for the most benefit
44
According to the GMC when is prescribing an unlicensed medicine potentially necessary?
1) There is not suitable licensed alternative that would meet the patients needs 2) There is a suitable licensed medicine that would meet the patients needs but it is not available 3) Prescribing is part of a properly approved research project 4) Serious risk to public health and the MHRA has temporarily authorised the sale or supply of an unlicensed medicine (e.g. vaccine or treatment) in response 5) A POM that is unlicensed in Northern Ireland has been supplied under the NIMHRA Authorised Route
45
AWaRe
Access Watch Reserve
46
Start SMART (AIPD)
Assess - for clear evidence of infection to establish if antimicrobial therapy is likely to be beneficial Investigate - obtain appropriate cultures prior to starting treatment (where appropriate) and undertake other investigations as per local policy Prescribe - start antimicrobials within ONE HOUR of recognition of red flag sepsis, septic shock or life-threatening infections Document - document evidence of infection, indication for treatment, antimicrobial prescribed (dose, route and frequency) and state a review or stop date
47
Then Focus (CARES)
At 48-72 hours, review and revise the diagnose and need for continuing antimicrobials. Document a clear management plan including one of the following five review outcomes: 1) Cease treatment (i.e. if no evidence of infection) 2) Amend antimicrobials (i.e. based on sensitivities) 3) Refer for Complex Outpatient Parenteral Antibiotic Therapy (COPAT) or virtual ward 4) Extend current treatment and document next review or stop date 5) Switch antimicrobials from IV to oral route
48
Bacteriostatic Agents
Macrolides Tetracyclines
49
Efflux Pumps
Pump any antibacterial which has passed through the outer membrane back out before they reach the target site (e.g. P. aeruginosa)
50
Antibacterial-modifying enzymes
Destroy the antibacterial before it reaches its target within the cell (e.g. beta-lactamase or aminoglycoside-modifying enzymes)
51
What information should you provide when calling for advice on infection management?
- Any known previous colonisation and/or infection with an organism with antibacterial susceptibilities - Any known allergies - especially to antibacterials - Any recent hospitalisation - Any recent procedures or surgery - Any recent travel or any relevant social history - Any obvious source of current infection
52
What antibiotic is used for empirical treatment of suspected C. diff?
Metronidazole
53
What 4 acute infections do NICE recommend the majority of patients do not require antibacterials for?
Acute cough Acute otitis media Acute sinusitis Acute sore throat

PSA (7 decks)

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