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HHD 2 > ADRs important in dentistry > Flashcards

ADRs important in dentistry Flashcards

1
Q

An additional drug at the same molecular site of action causes either __________ or __________ effect

A

antagonists
additive (enhanced)

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2
Q

What is an antagonistic effect?

A

this is when two drugs have opposing pharmacological effects leading to the reduced effectiveness of one or both drugs

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3
Q

Give an example of a drug with an antagonistic effect on another

A

NSAIDs (tend to increase blood pressure) inhibit the antihypertensive effect of ACE inhibitors or diuretics

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4
Q

What is the possible result of two drugs with the same pharmacodynamic profile?

A

may result in an excessive respinse of the target tissue and toxicity

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5
Q

What does additive synergy refer to?

A

effect equals the sum of effects of the 2 drugs

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6
Q

What does enhanced synergy refer to ? Give an example of this

A

potentiation; the effect is greater
benzodiazepine and opiods could result in respiratory depression

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7
Q

What antibiotic can be prescribed in penicillinase producing bacteria?

A

-beta lactamase producing bacteria
-coamoxiclav can be prescribed as clavaulanic acid is an inhibitor of betalactamse

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8
Q

What is the effects of pharmacokinetic interactions on drugs?

A

they alter the concentration of a drug that reaches its site of action

they can increase or decrease the concentration of a drug at the site of action

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9
Q

What are the pharmacokinetic processes that affect the concentration of a drug at its site of action?

A
  • absorption
  • distribution
  • metabolism
  • excretion
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10
Q

What is the effect of penicillin based antimicrobials that can alter the gut flora?

A
  • some of the gut flora is vital for the production of vitamin K
  • vitamin K is essential for the producion of clotting factors II, VII, IX, X
  • this can result in an increased INR - increased bleeding tendency
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11
Q

What clotting factors have the shortest and longest half lives?

A
  • factor VII has the shortest half life
  • factor IX has the shortest half-life
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12
Q

Why are antacids, PPIs and H2 receptor blockers contraindicated for use with antifungals like ketoconazole ?

Azole antibiotics prevent formation of ergosterol
polyene antibiotics disrupt the cell membrane and cause it to become more leaking

Antacid- CaCo3
PPI- omeprazole
H2 receptor blocker ranitidine

A
  • this is because ketoconazole can only be absorbed in acidic conditions therefore their asborption is reduced
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13
Q

Drugs that are bound to plasma proteins are …

A

inert/inactive

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14
Q

Unbound drugs are active because…

A

they are free to bind to target receptor binidng sites

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15
Q

Why is the use of aspirin contraindicated for a patient on warfarin?

A

this is because warfarin and aspirin are predominantly proteins bound and thus compete for the same binidng site on albumin

In the presence of aspirin, warfarin remains unbound and thus there is an increase in its pharmacological effects
There will be an increase in INR and bleeding tendency as a result of this

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16
Q

Why is the use of antibiotic rimfapicin contraindicated with the use of the contraceptive pill?

A

this is because rimfapicin causes the induction of the CYP450 enzymes in the liver
this leads to an increase in the metabolism of the oral contraceptive pill and therefore its failure

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17
Q

What is the antibiotic rimfapicin used to treat?

A
  • mainly tuberculosis
  • brucellosis
  • legionnaires disease
  • serious staphylococcal infection
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18
Q

There is potential for interaction when two drugs share the sam excretion site. What is the consequence of this?

A

there is a reduced rate of excretion for one or both drug
this means that the drug is in circulation for longer meaning that the therapeutic effect is prolonged and can potentially be harmful

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19
Q

Why is NSAID use contraindicated with methrotrexate?

A

they share the same site of excretion (kidneys); this can leads to methotrexate toxicity as there is a reduced rate of excretion of methotrexate

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20
Q

What are the consequences of methotrexate toxicity?

A
  • bone marrow suppression (sore throat, bruising, mouth ulcers)
  • liver, pulmonary and GI toxicity
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21
Q

What is the MOA of methotrexate?

A

inhibits dihydrofolate reductase (DHFR)
which is essential for synthesis of purines and pyrimidines

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22
Q

What is the function of a therapeutic index?

A

it is a measure of drug safety
gives an indication of how safe the drug is

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23
Q

What is a narrow therapeutic index?

A

a small reduction or increase of the active drug availability can mean the loss of efficacy or potential toxicity for the drug (a narrow margin of safety)

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24
Q

What does a wide therapeutic index refer to ?

A

changes in drug availabiliyy unlikely to produce a clinical effect due to a wide margin of safety

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25
Q

Give an example of a drug with a low therapeutic index

A

digoxin

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26
Q

Give an example of a drug with a higher therapeutic index

A

amytriptilline

TCA

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27
Q

How are people on drugs with narrow therapeutic indices managed?

A

they are monitored more regularly

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28
Q

Give examples of lipid regulating drugs

A

simvastatin
atorvastatin

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29
Q

Give examples of PPIs

A

omeprazole
iansoprazole

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30
Q

Give example of a non opioid and opioid analgesic

A

non opioid: paracetamol
opioid: co-codamol

31
Q

Give an example of a ACE inhibitor

A

ramipril

32
Q

Give examples of antiplatelet drugs

A

aspirin
clopidogrel

33
Q

Give examples of beta-adrenoceptor blockers

A

atenolol
propanolol

34
Q

Give an example of thyroid hormone replacement therapy

A

levothyroxine

35
Q

Give exampls of biguanides and sulphonureas

A

biguanide: metformin
sulfonylureas: glicazide

36
Q

Give examples of beta-2 agonist

A

salbutamol - SABA
salmeterol - LABA

37
Q

Give an example of a thiazide diuretic

A

bendroflumethiazide

38
Q

Give an example of a loop diuretic

A

Furosemide

heart failure medication

39
Q

Give an example of a calcium channel blocker

A

amlodipine
nifedipine

40
Q

Give an example of an oral anticoagulant

A

warfarin

41
Q

Give an example of an antihistamine

A

cetrizine

42
Q

What are the most commonly prescribed drugs in GDP care

A
  • amoxicillin- 250/500 mg doses
  • metronidazole- 200mg/400mg dose
  • chlorhexidine- acts on oropharynx
  • duraphate 2800/5000 ppm- minerals
  • erythromycin (macrolide)
  • ibuprofen, diclofenac and other NSAIDs
  • difflam and benzyamine oral rinses- benzydamine hydrochloride
  • co-amoxiclav 125/250mg oral doese
    1. * daktarin gen- miconazole antifungal
43
Q

List some interacting drugs for macrolide antibiotics (include the risk of interaction and the potential management option for each drug)

A
  • CCBs- increased and prolonged hypotensive effects of CCBs
  • simvastatin- increased change of muscle toxicity
  • clopidogrel- increased risk of bleeding
  • warfarin- increased risk of bleeding

Management- avoid macrolides

44
Q

List some interacting drugs for metronidazole (include the risk of interaction and the potential management option for each drug)

A
  • warfarin- increased risk of bleeding - avoid metronidazole
  • NSAIDs- increased risk of bleeding- avoid NSAIDs
  • phenytoin- effect of phenytoin may be increased- monitor closely or give another antibiotic
45
Q

List some interacting drugs for azole antifungals (include the risk of interaction and the potential management option for each drug)

A
  • warfarin- increased risk of bleeding
  • simvastatin- risk of muscle tocixity
  • avoid azoles, give nystatin instead
  • avoid azoles- prescribe alternative antifungal
46
Q

List some interacting drugs for penicillin based antibiotics (include the risk of interaction and the potential management option for each drug)

A
  • oral contraceptive pill -decreased contraceptive effect
  • warfarin- may increase risk of bleeding
  • methotrexate; increase methotrexate toxicity
  • use barrier contraceptives
  • vigilant for increased bleeding
  • risk is with high dose penicillins, give lower dose
47
Q

List some interacting drugs for LA with adrenaline (include the risk of interaction and the potential management option for each drug)

A
  • beta-blockcers- hypertensive response is possible
  • TCAs- increased sympathetic respnse
  • GA agents (propofol)- potentiates anti-hypertensive drugs leads to hypotension
  • limit LA to 3-4 cartridge/use adrenaline free x2
  • anaesthetist will manage this
48
Q

List some interacting drugs for NSAIDs (include the risk of interaction and the potential management option for each drug)

A
  • anticoagulants/coumarins- increased bleeding risk
  • ACE inhibitors, Beta blockers, diuretics- NSAIDs increase hypotensive effects of these drugs
  • Aspirin- increased bleeding risk
  • MTX- increased MTX toxicity
  • SSRIs- increased bleeding risk
  • careful use of NSAIDs, consult GP x2
  • avoid aspirin/consult GP
  • consult GP
  • careful advice on use of NSAIDs
49
Q

What is the consequence of endogenous agonist binding to alpha-1 receptors?

A

vasoconstriction

50
Q

What are the effects of adrenaline on adrenergic receptors?

A
  • adrenaline binds to alpha receptors in peripheral vasculature and cause vasoconstriction
  • adrenaline also binds to B1 receptors in the heart wall and cause increased heart rate
51
Q

What is the effect of adrenaline on the CVS?

A

tachycardia
peripheral vasoconstriction
increased BP

52
Q

B1 adrenergic receptors are found in the …

A

heart wall

53
Q

B2 adrenergic receptors are found in …

A

smooth muscle cells

54
Q

List classes of anti-hypertensive drugs

A

calcium channel blockers
ACE inhibitors
Beta blockers
Angiotensin II receptor agonist
Loop diuretics- furesemide

55
Q

NSAIDs are contraindicated with the use of antihypertensive drugs. Explain why this is the case

A
  • inhibiton of COX2 enzymes leads to reduced prostaglanding synthesis (PG12, PGE2, PGD2)
  • This leads to less vasodilation, increased vascular resistance in kidneys and reduced renal perfusion
  • as a result of this there is increased retention of urinary sodium, vasoconstriction also causes increased fluid retention exarcebating pre-existing hypertension
56
Q

What are the 3 ways in which NSAIDs interact with diuretics?

A

nephrotoxicity
antagonise diuretic effect
increases risk of hyperkalaemia

57
Q

What is the advice for NSAID use with antihypertensive drugs?

A

controlled acute use of ibuprofen for 4-5 days is okay

58
Q

Why are macrolide antimicrobials contraindicated for use with CCBs?

A

macrolides are inhibitorts of the CYP3A4 enzyme which is responsible for metabolising CCBs
this results in a rise in serum CCBs and a dangerous hypotenisve effect

59
Q

What macrolide does not cause the hypotensive effects observed with concomitant use of CCBs?

A

azithromycin

60
Q

Why are statins contraindicated for use with macrolides and azole antifungals?

A

this is because statins are metabolised by CYP3A4 enzyme
macrolide and azole antifungals leads to inhibition of CYP3A4 enzyme thus, serum statin concentration increases

This can lead to muscle toxicity- rhabdomyolosis and muscle myopathy

61
Q

What is the difference between aspirin and other NSAID drugs? (MOA)

A

aspirin provide an irreversible COX block
NSAIDs are reversible, need to be replaced every 6 hours

aspirin therefore completely halts TXA2 production in platelets and prevents platelet aggregation

62
Q

Why is aspirin use with other NSAIDs contraindicated?

A

they can antagonise the antiplatelet effect of aspirin
NSAIDs and aspirin are competitive agonists for the same binding sites on COX1
When NSAIDs are bound, thromboxane A2 is still formed and this platelet aggregation is normal; risk of stroke or TIA maintained

63
Q

COX-2 specific NSAIDs are associated with an increased risk of …

A

MI

64
Q

Clopidogrel interacts significantly with NSAIDs, what kind of effect is observed and what is the consequence?

A

additive effect
causes an increased bleeding risk

65
Q

Clopidogrel effects are antagonised by macrolides and azole antifungals. Briefly explain why this is

A

macrolides and azole antifungals could potentiate effect of CYP450 enzymes leads to metabolism and this inhibition of its effect

66
Q

What is the effect of warfarin?

A

prevent thromboembolic disease
inhibition of synthesis of vitamin K dependent clotting factors II, VII, IX, X

67
Q

What is the effect of metronidazole on warfarin?

A

metronidazole increase inhibition of CYP2C9 which metabolises warfarin
Inhibition of warfarin means more is available
increased bleeding risk

CYP2C9 metabolises warfarin

68
Q

What is the effect of macrolides on warfarin?

A

macrolides inhibit metabolism of warfarin
increasing bleeding risk

do they bind CYP2C9??

69
Q

What is the effect of using broad spectrum antibiotics and warfarin ?

A

further increased risk of bleeding
broad spectrum antibiotic can affect gut flora; this affects bacteria that are important in vitamin K synthesis
vitamin K dependent clotting factors are further affected

70
Q

What is the effect of azole antifungals on warfarin?

A

azoles inhibit CYP450 enzymes
warfarin stays active longer
INR, bleeding risk increases
use nystatin instead
if using micoazole, liase with GP for INR monitoring

71
Q

TCAs have a narrow therapeutic index. What is their MOA?

A
  • at neuronal synaptic junctions, block re-uptake of NA
  • elevation of NA at synapses and 5-HT at cholinergic neurons enhances transmission
72
Q

What consideration should you make when delivering LA to patients on TCAs?

A
  • enhanced neuronal transmission (NA, 5-HT)
    PLUS adrenaline in LA could initiate hazardous CVS effects- arrhythmias,hypertension

Use aspirating synringes, no more than 3 cartridges in one session

73
Q

Citalopram (SSRI) has a wider therapeutic index however its use with NSAIDs is contraindicated. Why is this ?

A

-increased risk of GI bleeding
5-HT acts a vasoconstrictor in normal platelet clotting
SSRIs block the reuptake of 5-HT in platelets therefore there is an increased risk of bleeding; less serotonin in platelets to be released at site of injury; less vasoconstriction; therefore increased risk of bleeding

HHD 2 (37 decks)

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