Interactions COPY Flashcards Preview

Pharmacy Pre-Registration 20/21 > Interactions COPY > Flashcards

Flashcards in Interactions COPY Deck (131)
Loading flashcards...
1
Q

Name the enzyme inhibitors (SICKFACES.COM)

A
Sodium valproate
Isoniazid / itraconazole
Cimetidine
Ketoconazole
Fluconazole / fluoxetine
Alcohol (acute, binge) / Amiodarone
Chloramphenicol
Erythromycin + clarithromycin
Sulphonamides (co-trimoxazole)
Ciprofloxacin
Omeprazole
Metronidazole

Also:
Grapefruit juice

2
Q

Name the enzyme inducers (SCRAP GPSS)

A
Sulphonylureas
Carbamazepine
Rifampicin
Alcohol (chronic)
Phenytoin

Griseofulvin
Phenobarbital
St John’s Wort
Smoking

3
Q

What are the main interactions with amiodarone?

A
  1. Amiodarone inhibits warfarin metabolism- enhanced anticoagulant effect
  2. Increased risk of bradycardia, AV block, myocardial depression with beta blockers
  3. Risk of ventricular arrhythmias with lithium
  4. Plasma concentration of digoxin increased by amiodarone

Amiodarone has a very long half life so there is potential for drug interactions to occur weeks/months after stopping treatment

4
Q

What are the common interactions with digoxin?

A
  1. Plasma conc of digoxin increased by amiodarone (enzyme inhibitor)
  2. Plasma conc of digoxin increased by erythromycin (enzyme inhibitor)
  3. . Plasma conc of digoxin reduced by rifampicin (enzyme inducer)
  4. Plasma conc of digoxin reduced by St John’s Worst (enzyme inducer)
  5. Increased toxicity of digoxin if hypokalaemia occurs with loop and thiazide diuretics
  6. Plasma conc of digoxin increased by CCBs
5
Q

What are the common interactions with lithium?

A
  1. Risk of lithium toxicity with ACEi (excretion reduced)
  2. Risk of lithium toxicity with NSAIDs (excretion reduced)
  3. Sodium depletion with loop and thiazide diuretics (excretion of lithium reduced)
  4. Risk of ventricular arrhythmias with amiodarone
6
Q

What are the common interactions with methotrexate?

A
  1. Increased risk of infection with vaccines
  2. PPIs at high doses reduce clearance of methotrexate increasing risk of toxicity
  3. Penicillins increases risk of methotrexate toxicity
  4. Trimethoprim- both folate antagonists, increased risk of side effects and nephrotoxicity
7
Q

What are the common interactions with phenytoin?

A
  1. Effects of phenytoin enhanced by NSAIDs
  2. Amiodarone inhibits phenytoin metabolism
  3. Phenytoin accelerates metabolism of warfarin
  4. Cimeditine inhibits metabolism of phenytoin
  5. Plasma conc of phenytoin increased by fluoxetine
  6. St John’s Wort reduces plasma conc of phenytoin
  7. Ciprofloxacin affects the concentration of phenytoin
  8. Decreases efficacy of combined contraceptive pill
  9. Phenytoin decreases exposure to NOACS
8
Q

What are the common interactions with theophylline?

A
  1. Increased risk of convulsions with quinolones e.g. ciprofloxacin
  2. Plasma conc of theophylline reduced by St John’s Wort
  3. Plasma conc of theophylline reduced by rifampicin
  4. Plasma conc of theophylline increased by cimetidine
  5. Plasma conc of theophylline increased by fluconazole
  6. Smoking can increase theophylline clearance and increased doses of theophylline are therefore required
9
Q

What are the common interactions with warfarin?

A
  1. Anticoagulant effect increased by NSAIDs
  2. Anticoagulant effect increased by fluconazole
  3. Anticoagulant effect increased by statins
  4. Anticoagulant effect increased by ciprofloxacin, erythromycin, metronidazole
  5. Anticoagulant effect reduced by griseofulvin
  6. Anticoagulant effect reduced by antiepileptics
  7. Alcohol effects anticoagulant control
  8. Anticoagulant effect antagonised by Vitamin K
  9. Anticoagulant effect enhanced by cranberry juice
10
Q

What is the risk of consuming tyramine based food and drink e.g. cheese if on MAOIs?

A

Hypertensive crisis

11
Q

How does alcohol interact with TCAs and mirtazapine?

A

Increased sedative effect

12
Q

What are the main interactions with combined oral contraceptives?

A
  • Enzyme inducing drugs increase metabolism of contraceptives. Additional contraceptive precautions should be taken for 4-8 weeks after stopping treatment
  • Some ABX may reduce efficacy of the pill by impairing bacterial flora responsible for recycling ethinylestradiol e.g. ampicillin, amoxicillin, doxycycline. Additional precautions are required for duration of treatment and for 7 days after stopping
13
Q

What are the main interactions with progesterone only contraceptives?

A

Efficacy reduced by enzyme inducers

Additional protection is needed for duration of treatment and 4 weeks after

14
Q

What are the main interactions with sympathomimetics e.g. pseudoephedrine?

A
  • MAOI- hypertensive crisis

- Beta blockers- hypertension risk

15
Q

What are the main interactions with Orlistat?

A
  • Orlistat reduces plasma conc of amiodarone
  • Anticoagulants- monitor
  • Acarbose for diabetes due to its GI effects
  • Reduces absorption of ciclosporin
16
Q

What is a pharmacokinetic interaction?

A

These occur when one drug alters the absorption, distribution, metabolism, or
excretion of another drug, thus increasing or reducing the amount of drug available
to produce its pharmacological effects.

17
Q

What is a pharmacodynamic interaction?

A

This is where effects of one drug are changed by the presence of another drug at its
pharmacological site of action.

e.g. electrolyte imbalance, combined toxicity, antagonising effects

18
Q

What PPI does clopidogrel interact with and what would be an alternative?

A

Omeprazole and esomeprazole

Lansoprazole would be an alternative

19
Q

What drug can cause blue vision and which drug can cause yellow vision in overdose

A

Blue vision can be cause by slidenafil and yellow vision is a sign of digoxin toxicity alongside nausea and vomiting

20
Q

Which SGLT is not licensed to be used with pioglitazone for triple therapy

A

Dapagflozin

21
Q

What is drug interaction?

A

the modifications of effects of one drug by another drug (poly-pharmacy)

22
Q

What is drug interaction? Pharmacodynamics (PD)

A

(“what the drug does to the body”)
related to the pharmacological activity of the interacting drugs leading to either:
synergistic effect, 1+1 > 2
or antagonistic effect, 1+1 < 2

23
Q

What is drug interaction? Pharmacokinetic (PK)

A
(“what the body does to the drug”)
related to the effect of a drug on another on physical disposition of the drug, i.e. movement of drug thru the body
absorption
distribution
metabolism
elimination
24
Q

Effects of drug interaction
Increased effect: Additive or Synergistic
effect

A
BAD - Increased toxic effect
GOOD - Increased therapeutic effect
to produce synergistic therapeutic effects
e.g. several antibiotic combinations
Penicillin-Streptomycin
25
Q

PD interactions arise when one drug changes the response of target or non-target tissues to another drug:
• Synergism

A

– Penicillin-Streptomycin

– Digoxin toxicity with diuretic induced potassium wasting

26
Q

PD interactions arise when one drug changes the response of target or non-target tissues to another drug:
• Antagonism

A

– Beta adrenoceptor antagonist diminish the effectiveness of b-adrenoceptor agonists such as salbutamol
– Antidote: agents with a specific action against the activity or effect of drugs involved in poisoning cases

27
Q

PK absorption eg. Altered pH; The non-ionized form of a drug is more lipid soluble and more readily absorbed from GIT than the
ionized form does.
-Ex1., antacids (aluminum or magnesium
hydroxide) Increase the pH and Reduce absorption of acidic drugs

A
digoxin (heart conditions),
phenytoin (epilepsy),
chlorpromazine (schizophrenia)
isoniazid (tuberculosis)
Therefore, these drugs must be separated by at least 2h in the time of administration of both.
28
Q

PK absorption eg H2 antagonists increase the pH and Reduce absorption of acidic drugs:

A
digoxin (heart conditions),
phenytoin (epilepsy),
chlorpromazine (schizophrenia)
isoniazid (tuberculosis)
Therefore, these drugs must be separated by at least 2h in the time of administration of both.
29
Q
Altered motility: Atropine (non-selective muscarinic blocker) Increase absorption of cyclosporine due to the increase of stomach emptying time and Increase the toxicity of cyclosporine
example of 
- PD 
- PK absorption
- PK excretion
- PK metabolism
- PK distribution
A

PK absorption

30
Q
Chelation - Iron may chelate ciprofloxacin, resulting in decreased absorption
example of 
- PD 
- PK absorption
- PK excretion
- PK metabolism
- PK distribution
A

PK absorption

31
Q

PK interactions (2): Distribution

A

• Drugs in bloodstream often bound to plasma proteins;
• Only unbound drugs can leave blood to affect target organs;
• Low albumin levels can increase availability of drugs and potentiate their effects;
• Competitive: drugs with higher affinity to albumin are capable to displace others, leading to increase concentration of free
drug (therefore yield more drug response):
Phenytoin (90%)
Tolbutamide (96%)
Warfarin (99%) –>
Aspirin
Sulfonamides
Phenylbutazone

32
Q

PK interaction (3):Metabolism

A

the most drug-drug interactions are metabolism based (diagram)
Phase I metabolism: involves oxidative metabolism via the Cytochrome P450 (CYP) family of enzymes

33
Q

Enzymatic induction

A

Inducer: Drug that will increase the synthesis of CYP450 enzymes
e.g. barbiturates, bzd, hydantoin antiepileptics, glucocorticoids, rifampicin, griseofulvin, St. John´s wort, smoking, grilled meat, chronic alcohol
intake – increase
SCRAP GPSS
-Decrease the effect of several drugs, e.g.
cardiotonics, steroid hormones, coumarin
anticoagulants
N.B enzyme induction involves protein synthesis. Therefore, it needs time up to 3 weeks to reach a maximal effect

34
Q

Enzymatic inhibition

A

SICKFACES.COM
Inhibitor: Drug that will decrease the metabolism of a substrate
e.g. some macrolides, quinolones, sulfonamides, some antimycotics (e.g. ketoconazole, fluconazole), isoniazid, metronidazole, chloramphenicol,
amiodarone, verapamil, diltiazem, quinidine, SSRI, proton pump inhibitors, cimetidine, garlic, ginkgo, grapefruit juice

-Increase the effect of several drugs
Inhibition of the enzyme may be due to the competition on its binding sites , so the onset of action is short may be within 24h.

35
Q

When an enzyme inducer (e.g.carbamazepine) is administered with an inhibitor (verapamil) -> the effect of the __________ will be predominant

A

inhibitor

36
Q
Omeprazole Inhibits oxidative metabolism of 
A. aspirin
B. diazepam
C. sertraline
D. clarithromycin
A

B. diazepam

Omeprazole has actual adverse influences on the pharmacokinetics of medications such as diazepam, carbamazepine, clozapine, indinavir, methotrexate, tacrolimus, mycophenolate mofetil, clopidogrel, digoxin, itraconazole, posaconazole, and oral iron supplementation.

37
Q

PK interaction (4): Excretion

A

Drugs are eliminated from the body as an unchanged drug or metabolite
– Renal excretion is the major route of
elimination;
– affected by renal function and urinary pH

38
Q

Drug-Food

interactions

A

Tetracycline interacts with Milk (Ca2+ ) -> Unabsorpable complex

Warfarin (diagram)
Vitamin K-containing foods

39
Q

Drug-Disease interactions

A

HEART : b1 adrenergic receptors - Heart rate & Contractility

SMOOTH MUSCLE -airway & vasculature:
b2 adrenergic receptors -> Relaxation & dilation

Drug ADR: homologous targets
•Non-selective b antagonists, e.g. Propranolol, are contraindicated in patients with asthma

40
Q

Drug-Disease interactions:

Contraindications of atropine

A

1- Patients with angle closure glaucoma
2- Patients with shallow anterior chamber
3- Senile hyperplasia of the prostate
4- Patients with gastric ulcer
(increase symptoms due to slowing gastric emptying)

41
Q

Changes in absorption

Alteration -GI motility

A

Alteration/ action

GI motility - Increased GI motility caused by metoclopramide may decrease cefprozil absorption (2nd gen cephalosporin)

42
Q
GI alkalinization by omeprazole may decrease absorption of 
A. amantadine
B. dapsone
C. metronidazole
D. ketoconazole
A

D. ketoconazole

changes in absorption PK

43
Q

GI flora - Decreased GI bacterial flora caused by an antibiotic admin could decrease bacterial production of vitamin K augmenting anticoagulant effect of

A

warfarin

44
Q

Changes in absorption

Alteration -Drug metabolism in wall of intestine

A

Drug metabolism in wall of intestine -
certain antidepressants is that phenylephrine could potentiate a spike in blood pressure; TCAs and MAOI

MAO acts to break down neurotransmitters like norepinephrine (and dopamine and serotonin); thus, MAOIs act to increase the amount of these chemicals in our synapses. Monoamine oxidases (MAO) are in the wall of GI tract. NE = main neurotransmitter of SNS and works to immediately increase our BP. Thus, a sympathomimetic like phenylephrine + MAOI, which is also stimulating the sympathetic system, has the potential to elevate BP into a hypertensive crisis.

45
Q

Incidentally, MOA is involved in other body processes including the breakdown of tyramine, an amino acid involved in BP regulation. Tyramine helps release more NE. Thus, to prevent hypertensive crises, patients who take MAOIs should stay away from..

A

foods rich in tyramine like strong/aged cheeses, cured meats, yeasts, beers and dried fruits.

46
Q

Phase II metabolism

A

conjugates the previously oxidized molecule with a water soluble weak acid (glucouronic acid, tauric acid, etc) enhancing overall water solubility

47
Q

How to do drug-drug interactions occur

A

Drug-drug interaction always due to interaction at phase I enzymes (i.e. cytochrome P450)

48
Q

Passive tubular reabsorption example

A

Sodium bicarbonate. Increases lithium clearance and decreases its action

Antacids Increases salicylates clearance and decreases its action

49
Q

What happens when pH increases

A

Ionisation doesn’t occur as it only occurs at acidic pH

50
Q
PK interactions: Absorption
a)
b)
c)
d)
A

a) altered pH
b) altered motility
c) altered intestinal bacteria flora
d) chelation

51
Q

which drugs have strong affinity to protein binding

A

Phenytoin (90%)
Tolbutamide (96%)
Warfarin (99%)

52
Q

which drugs have weak affinity

A

Aspirin
Sufonamides
Phenylbutazone

53
Q

Non selective antimuscarinic drugs should never be used to

A

Non selective antimuscarinic drugs should never be used to treat acid-peptic disease.

54
Q

Active tubular secretion

A

-It occurs in the proximal tubules. The drug combines with a specific protein to pass through the proximal tubules.
-When a drug has a competitive reactivity to the protein that is responsible for active transport of another drug, this drug will reduce such a drug excretion increasing
its con. and hence its toxicity.
-Probenecid decreases tubular secretion of methotrexate.

55
Q

Passive tubular reabsorption

A
  • Excretion and reabsorption of drugs occur in the tubules by passive diffusion which is regulated by concentration and lipid solubility.
  • N.B., Ionized drugs are reabsorbed lower than non-ionized ones
56
Q

Pharmacokinetic drug interactions

A
• Changes in GI absorption
• Displacement from plasma protein binding
• P450 Mediated
– Enzyme inhibition
– Enzyme induction
• Decreased renal elimination
57
Q

Drug-Herb interactions

A
• St John’s Wort
e.g. cyclosporin
• Ginkgo biloba
• Kava
• Garlic
58
Q

Clinically significant to pharmacist perspective for interactions – what to look for

A
1. Vulnerable patient groups
– Elderly
– Multiple drug therapies (poly-pharmacy)
– Renal or hepatic impairment
– Chronic or serious illness
2. Particular groups of drugs:
• Narrow therapeutic index
• Enzyme inducers
• Enzyme inhibitors
59
Q

Sirolimus & grapefruit juice

A

Plasma concentration of sirolimus increases by grapefruit juice

60
Q

Clozapine & cytotoxics

A

Avoid use of cytotoxics with clozapine due to possible increased risk of ventricular arrhythmias

61
Q

Theophylline & phenobarbital

A

Metabolism of theophylline accelerated by phenobarbital

62
Q

Tetracyclines & zinc

A

Absorption of tetracyclines possibly reduced by zinc (give atleast 2-3 hours apart)

63
Q

Lithium & metronidazole

A

Increased risk of lithium toxicity when given with metronidazole
SICKFACES.COM

64
Q

Narrow therapeutic index

A

digoxin, theophylline, warfarin, ciclosporin, phenytoin, carbamazepine

65
Q
Enzyme inducers out of the following:
A. Carbamazepine
B. Ciprofloxacin
C. Warfarin
D. Amiodarone
E. Ketoconazole
F. Phenytoin
G. Diltiazem
H. Rifampicin
A

carbamazepine
phenytoin
rifampicin

66
Q
Enzyme inhibitors out of the following:
A. Amiodarone
B. Ciprofloxacin
C. St Johns Wort
D. Verapamil
E. Fluoxetine
F. Omeprazole
G. Ketoconazole
H. Diltiazem
A

amiodarone, ciprofloxacin, diltiazem, fluoxetine, verapamil, ketoconazole

67
Q

Phenytoin and Amiodarone

A

Amiodarone increases phenytoin concentration

NB: Amiodarone is an enzyme inhibitor.
Due to amiodarones long half life: potential for interaction several months after discontinuation

68
Q

Phenytoin and Warfarin

A

Phenytoin (p450 enzyme INDUCER) induces warfarins metabolism, decreases warfarin concentration, reduced anti-coagulation effect, decreases INR

69
Q

Phenytoin and COC

A

Phenytoin (a p450 enzyme inducer) accelerates metabolism of Oestrogens, reducing their effectiveness

Patient should be changed to an IUD

70
Q

Phenytoin and Fluoxetine

A

Fluoxetine increases phenytoin concentration

71
Q

Phenytoin and Theophylline

A

Theophylline decreases phenytoin concentration

72
Q

Phenytoin and St Johns Wort

A

St Johns Wort decreases phenytoin concentration

St Johns Wort is an enzyme inducer

73
Q

Phenytoin and Fluconazole

A

Fluconazole increases phenytoin concentration (Fluconazole enzyme inhibitor part of SICKFACES)

74
Q

Phenytoin and Cimetidine

A

Cimetidine increases phenytoin concentration (Cimetidine enzyme inhibitor part of SICKFACES)

75
Q

Phenytoin and Diltiazem

A

Diltiazem increases phenytoin levels, and diltiazems own effects are decreased by phenytoin

76
Q

Phenytoin and Rate limiting CCB’s

A

Phenytoin decreases effects of Verapamil and Diltiazem and also Felodipine

77
Q

Amiodarone and Grapefruit Juice

A

Grapefruit Juice increases levels of Amiodarone

Grapefruit Juice is an enzyme inhibitor

78
Q

Amiodarone and warfarin

A

Amiodarone increases warfarin levels
Enhances anti-coagulant effects, increased bleed risk

Amiodarone is an inhibitor of some of the CYP450 enzymes.

79
Q

Amiodarone and Simvastatin

A

Increased risk of Myopathy
Max dose of Simvastatin: 20mg

This is not the same with Atorvastatin etc but still monitor for mypopathy

80
Q

Amiodarone and beta blockers and Rate-limiting CCB’s diltiazem and verapamil

A

Increased risk of
Bradycardia
Myocardial depression
AV block

When given with beta blockers/ rate limiting CCB

81
Q

Amiodarone and Lithium

A

Increased risk of Ventricular Arrhythmias
(poss associated with QT prolongation)

Also both effect THYROID function

82
Q

Theophylline + enzyme inhibitors:

Cimetidine, Fluconazole, Ketoconazole, Ciprofloxcin, Erythromycin

A

Theophylline levels increased as it is metabolised by the CYP450 enzymes

83
Q

Theophylline + enzyme Inducers:
Carbamazepine, Alcohol, Phenobarbital, Phenytoin, Rifampicin, St Johns Wort
(SCRAP GP’s)

A

Theophylline levels decreased

84
Q

Theophylline and Quinolone antibiotics e.g. Ciprofloxaxin, Levofloxacin

A

Increased risk of SEIZURES

These BOTH lower seizure threshold

85
Q

What do diltiazem and Verapamil (rate limiting CCBs) do to Theophyllines concentration?

A

Increase it

these are CYP3A4 enzyme inhibitors!

86
Q

NSAIDs and warfarin/ phenindione

A

NSAIDs increase warfarin levels- increased anticoagulant effect

NSAIDs, like warfarin, have a high affinty for Albumin. They displace warfarin off the protein= more free warfarin

So remember the interaction is not because both drugs can increase bleed risk- NSAIDs actually increase the levels of warfarin

87
Q

SSRI’s and TCA’s and warfarin

A

SSRI’s and TCA’s will increase warfarin levels- increased anticoagulant effect

88
Q

Statins and warfarin

A

Only statin that interacts: Rosuvastatin

Increased effects of warfarin

89
Q

Clopidogrel and warfarin

A

Anti-coagulant effect enhance (both thin blood)- increased risk of bleeds

90
Q

Orlistat + Antiepileptics

A

Possible increased risk of convulsions- orlistat lowers seizure threshold

91
Q

Methotrexate and Phenytoin

A

Do not use together- both deplete Folate

92
Q

Methotrexate and Trimethoprim/ Co-trimoxazole (trimethoprim + Sulfamethoxazole)

A

Do not use together- both deplete folate- haematological blood toxicity risk

Sulfamethoxazole also increases methotrexate toxicity

93
Q

Methotrexate and Ibuprofen

A

Methotrexate toxicity increased by NSAIDs due to decreased renal excretion

94
Q

Methotrexate and Flucloxacillin

A

Methotrexate toxicity increased by all penicillins due to decreased renal excretion

95
Q

Methotrexate and Clozapine

A

Neutropenia risk increased

96
Q

PPI’s and Methotrexate

A

Increased risk of Methotrexate toxcity as excretion decreased

97
Q

ALOT of antibiotics interact with Methotrexate. Can you think of any?

A

Trimethoprim/ co-trimoxazole (folate depletion)

The following increase methotrexate toxicity:
Ciprfloxacin
Doxycycline
Tetracycline
Sulfonamide (Sulfamethoxazole)
98
Q

If in doubt, whats that ONE DRUG that seems to have interactions with everything?!

A

CICLOSPORIN

an immunosuppressant

99
Q

Which OTC medication can possibly interact with ANTI-EPILEPTICS and increase the risk of CONVULSIONS?

A

ORLISTAT (Alli)

100
Q

Carbamazepine is an enzyme inducer, but is itself metabolised by the CYP450 system. Which other enzyme inducers may reduce the concentration of carbamazepine?

A

Phenytoin (May also reduce phenytoins conc)
Rifabutin
St Johns Wort

101
Q

What drugs, used in hypertension, can increase the risk of Myopathy?

A

Diltiazem
Verapamil
Amlodipine
Ranolazine

MAX SIMVASTATIN DOSE= 20mg for all of these!!

102
Q

Drugs interacting with Gentamicin/ Vancomycin?

A

NEPHROTOXIC DRUGS:
Ciclosporin (immunosuppressant)
Tacrolimus (immunosuppressant)
Cephalosporins

OTOTOXICITY:
Loop diuretics (furosemide)
103
Q

What kind of OTC products should patients with high BP avoid?

A

SOLUBLE preparations e.g. effervescent

Due to high SODIUM content

104
Q

Spironolactone + ACEi/ARB

A

Potassium sparing diuretic given with postassium elevating drugs: HYPERKALEAMIA

105
Q

Spironolactone + Tacrolimus

A

Potassium sparing diuretic given with postassium elevating drug Tacrolimus: Hyperkaleamia

106
Q

Furosemide + Vancomycin

A

Increased risk of Ototoxicity

107
Q

Digoxin + Diuretics

A

Diuretics (thiazides and loops) can cause Hypokaleamia
Digoxin toxicity is precipitated by low potassium!!

Give potassium sparing diuretics/ potassium chloride to manage

108
Q

Eplerenone (potassium sparing diuretic) is metabolised by the CYP450 enzyme system

A

Its concentration is increased by clarithromycin and itraconazole only

Its concentration is reduced by all the enzyme inducers

109
Q

What drugs may cause hypoglyceamia and therefore reduce the amount of insulin a patient needs?

A

ACE inhibitors!

Other oral antidiabetics

110
Q

NSAID + quinolone (ciprofloxacin, Levofloxacin)

A

Possible increased risk of seizures

111
Q

NSAID + Diuretics

A

Increased risk of nephrotoxicity

NSAIDs will also antagonise the diuretic effects: Fluid retention! Can cause ankle swelling and high blood pressure with chronic use

112
Q

NSAIDs + anti-hypertensives (beta-blockers, CCB’s, ACE inhibitors, alpha-blockers [tamsulosin, doxazosin] nitrates)

A

NSAIDs themselves can cause high BP

They antagonise the hypotensive effects of these drugs

113
Q

Which opioid can enhance the anticoagulant effect of coumarins (warfarin)

A

Tramadol

114
Q

Which antibiotic can reduce the effectiveness of most of the opioids, including fentanyl, morphine, codeine, methadone?

A

RIFAMPICIN!! (enzyme inducer)

115
Q

Opioids can reduce BP (hypotensive)

Their hypotensive and sedative effects are increased by alcohol. What happens if given with MAOIs?

A

Possible CNS excitation or depression
Hypotension or hypertension can occur
(remember MAOIs can cause hypotensive crisis)

116
Q

Clopidogrel + enzyme inhibitors

A

Some of the enzyme inhibitors (erythromycin, cimetidine, ciprofloxacin, fluconazole, ketoconazole) actually REDUCE clopidogrels antiplatelet effect!- dont get confused in exam!

117
Q

Clopidogrel + PPI’s

A

Antiplatelet effect REDUCED by omeprazole and esomeprazole

Pantoprazole safest PPI to use, or H2 antagonist

118
Q

Sotalol + loop or thiazide diuretics

A

risk of ventricular arrhythmias caused by sotolol is increased by diuretics due to their hypokaleamia effect

119
Q

Lithium + ACE inhibitors

A

ACE inhibitors will decrease the excretion of lithium!

Nothing to do with electrolyte disturbance

120
Q

Lithium + Beta blockers

A

No interaction!

121
Q

Lithium + Aminophylline/ Theophylline

A

These will increase the excretion of lithium, reducing its levels

122
Q

NSAIDs + Lithium

A

Excretion of lithium reduced by NSAIDs so increased risk of Lithium Toxicity!

123
Q

Lithium + SSRIs

A

Increased risk of CNS effects, lithium toxicity

think SSRI’s cause hyponatreamia- sodium levels effect lithium

124
Q

Methotrexate and Aspirin

A

Methotrexate toxicity increased

As Aspirin and NSAIDs decrease methotrexate excretion

125
Q

Doxycycline + Isotretinoin

A

Severe headache/ visual disturbance due to cranial (brain) hypertension

126
Q

Atorvastatin and clarithromycin

A

increased risk of myopathy

127
Q

Co-trimoxazole + Spironolactone

A

Increased risk of hyperkaleamia

128
Q

Metronidazole + Mebendazole

A

severe skin reaction

129
Q

Baclofen + ACE inhibitors

A

Baclofen enhances hypotensive effect

130
Q

Baclofen + beta blockers

A

Baclofen enhances hypotensive effect

131
Q

Alpha blockers (sildenafil) + nitrates (isosorbide mononitrate)

A

Enhanced hypotension effects

Decks in Pharmacy Pre-Registration 20/21 Class (82):