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Flashcards in Pharmacology Deck (43)
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1
Q

what are local anaesthetics used for

A

to reduce awareness of pain

2
Q

how do local anaesthetics work

A

by blocking ion channels, preventing propagation of AP

3
Q

give examples of antibiotics used in dentistry

A

amoxycillin

4
Q

give examples of anti-virals

A

aciclovir

5
Q

give examples of anti fungals

A

topical - nystatin systemic - fluconazole

6
Q

how do anti-inflammatories work

A

by inhibiting arachidonic acid binding to either COX 1 or 2, prevents prostaglandin production

7
Q

what are common side effects with NSAID

A

increased risk of bleeding, increased gastric ulcer production, exacerbate asthma

8
Q

what causes the side effects caused by NSAID

A

inhibiting COX 1 or 2 results in blocking thromboxane production, prevents platelet aggregation - more prone to bleeding

9
Q

what drug interacts with aspirin and ibruprofen

A

warfarin

10
Q

what is the difference between aspirin and ibruprofen

A

aspirin has much more severe side effects, aspirin blocks COX 1, ibruprofen blocks COX 2

11
Q

what is diclofenac

A

an NSAID that can only be prescribed with prescription

12
Q

what is a positive of using aspirin

A

if people have heart problems, blood is thinner

13
Q

how do corticosteroids work

A

inhibits capillary permeability, bradykinin formation and white blood cell migration, suppresses inflammation but doesnt target the cause

14
Q

give examples of corticosteroids

A

beclomethasone - inhaler, prednisolone - oral, hydrocortisone - topical

15
Q

what are the side effects of corticosteroids

A

high blood pressure, diabetes, weight gain, adrenal suppression, gastric ulceration

16
Q

what drugs are used in sedation

A

nitrous oxide and diazepan

17
Q

how is nitrous oxide administered

A

inhaled as a gas but should be avoided in pregnancy - interacts with folic acid

18
Q

name 3 ways in which a drug can exert its effect on the body

A

activating an ion channel, activating/inhibiting an enzyme, coupled to G-protein receptors

19
Q

what is the result of activating a g protein

A

this activates an enzyme which results in production of a second messenger, acts within the cell to bring about change e.g. protein production

20
Q

give an example of a drug altering ion channels

A

local anaesthetic blocks ion channels to prevent AP conduction

21
Q

give an example of a drug that alters enzyme activity

A

aspirin, inhibits COX 1 preventing arachiodonic acid from binding

22
Q

what effects a drugs efficacy

A

affinity and occupancy

23
Q

when might a drugs affinity for a receptor be lowered

A

if the drug is only a partial agonist, doesnt fit as well into the binding site so wont work as well

24
Q

what can be done to increase the efficacy of partial agonists

A

increase the concentration, increases occupancy, however, doesnt work for all drugs

25
Q

name different types of antagonists and give explanations

A

reversible - unbinds to the receptor, leaving it unchanged
irreversible - permanent change to receptor
competitive and non-competitive - depends on whereabouts it exerts it’s effect

26
Q

what are the phases of drug action

A

absorption, clinical effect, metabolism, excretion

27
Q

what are the routes of administration for drugs

A

oral, subcutaneous, intravenous, intramuscular

28
Q

what are the advantages of oral administration

A

socially acceptable

29
Q

what are the disadvantages of oral administration

A

slow onset, variable absorption, unpredictable bioavailability, must have functioning GI tract and liver, drug must be lipophillic (unionised) to get through the membrane but then active part is ionised

30
Q

describe first pass metabolism

A

oral drugs go through the GI tract and into hepatic portal vein into the liver before reaching the systemic circulation. therefore, before they reach the area they are targeting, a proportion of the drug is already lost. makes us unsure of how much drug is actually reaching the desired area and also a bigger dose is required

31
Q

what routes of administration are unaffected by first pass metabolism

A

injection via muscle or vein, sublingual or rectal absorption

32
Q

what organs must be working well for drugs to be given

A

liver and kidney

33
Q

what is bioavailability

A

the proportion of drug exerting the clinical effect

34
Q

what factors affect bioavailability

A

absorption, first pass metabolism, dosage, destruction in gut

35
Q

how is the drug distributed amongst the body

A

lipid binding - accumulation and slow release

plasma protein binding

36
Q

how does plasma protein binding work in drug distribution

A

drug bound to plasma protein is inactive, however, it frees up more space in the plasma to carry more drug. the drug in the plasma free is active and available. when this diffuses out to tissue, the drug unbinds from plasma protein and moves into plasma to be available.

37
Q

give an example of drug interaction via plasma protein binding

A

aspirin and warfarin - one has a higher affinity to the plasma protein so this binds, making the other available

38
Q

describe the 2 phases of drug metabolism

A

phase 1 - inactivation of drug via oxidation, hydrolysis, reduction
phase 2 - conjugation with a molecule being excreted

39
Q

describe first order kinetics in terms of drug clearance

A

the amount of drug cleared is proportional to the concentration of drug. is a passive process, drug has a half life - for a given time half the concentration is cleared

40
Q

describe zero order kinetics in terms of drug clearance

A

the amount of drug cleared in a given time is fixed. is an active process involving enzymes. when the enzyme is saturated, unable to clear any more drug, has to wait until space becomes available

41
Q

how can plasma toxicity occur

A

if there is high levels of drug in the plasma and not enough being cleared, give more drug and building on plasma levels already there

42
Q

how can drugs be excreted

A

through the kidney and liver then passed through GI tract, or through lungs with breathing or sweat

43
Q

what is meant by a dosing schedule

A

knowing when and how much drug to give for the clinical effect to be seen but preventing plasma toxicity