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Yr 4 - ACC > Prescribing > Flashcards

Prescribing Flashcards

1
Q

What are the common P450 enzyme inducers?

Acronym: PC BRAS

A

P - Phenytoin
C - Carbamazepine

B - Barbiturates
R - Rifampicin
A - Alcohol (chronic excess)
S - Sulphonylureas

Others: topiramate, St John’s Wort, and smoking.

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2
Q

Is smoking an enzyme inducer or inhibitor?

A

Inducer

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3
Q

What are the common P450 enzyme inhibitors?

Acronym: AO DEVICES

A

A - Allopurinol
O - Omeprazole

D - Disulfram
E - Erythromycin
V - Valproate
I - Isoniazid
C - Ciprofloxacin
E - Ethanol (acute intoxication)
S - Sulphonamides

Others: grapefruit juice, amiodarone, and SSRIs (fluoxetine, sertraline).

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4
Q

How can alcohol affect P450 enzymes?

A

Chronic excess –> inducer

Acute intoxication –> inhibitor

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5
Q

What bloods tests are required before and after starting statins?

A

Before –> cholesterol levels & LFTs (baseline)

After –> LFTs 3 months and 12 months

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6
Q

Mechanism of statins?

A

Its primary mechanism of action is to inhibit 5-HMG-CoA reductase, an enzyme used to synthesise cholesterol.

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7
Q

What baseline tests are required before starting statins?

A
  • lipid profile
  • triglyceride concentrations
  • LFTs
  • TFTs
  • renal function
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8
Q

What LFT results indicate that statins should be stopped?

A

If the ALT rise to and persist >3 times above the upper limit of normal

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9
Q

What atorvastatin dose is recommended for 1ary prevention?

A

20mg

increase the dose if non-HDL has not reduced for >= 40%

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10
Q

What atorvastatin dose is recommended for 2ary prevention?

A

80mg

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11
Q

What are side effects of levothyroxine usually due to?

A

Usually due to excess dosing of levothyroxine which causes symptoms of hyperthyroidism: anxiety, restlessness, flushing/sweating, fine tremors, diarrhoea, nausea & vomiting.

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12
Q

When should levothyroxine be taken?

A

In the morning, 30 minutes before breakfast and drinks containing caffeine.

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13
Q

What reduces the absorption of levothyroxine?

A
  • Caffeine & food
  • Antacids
  • Calcium supplements
  • Iron supplements
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14
Q

How does caffeine affect levothyroxine?

A

Reduces absorption

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15
Q

Which 2 supplements reduce the absorption of levothyroxine?

A

Calcium & iron

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16
Q

How far apart should levothyroxine and calcium/iron supplements be taken?

A

At least 4 hours apart

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17
Q

Monitoring of TSH after treatment with levothyroxine?

A

TSH is monitored every three months until stable, with dosing adjustment if required.

Afterwards, TSH is then monitored once yearly.

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18
Q

Mechanism of PPIs?

A

irreversibly binds to the H+/K+ ATPase pump, inhibiting acid (H+) secretion

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19
Q

What are the key long-term side effects of omeprazole?

A

1) increased risk of osteoporosis

2) increased risk of C. diff infection

3) hypomagnesaemia

4) vit B12 deficiency

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20
Q

How can PPIs affect Mg level?

A

Can cause hypomagnesaemia

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21
Q

What 3 key drugs can omeprazole interact with?

A

1) SSRIs

2) Clopidogrel

3) Methotrexate

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22
Q

Impact of omeprazole on SSRIs?

A

omeprazole increases SSRI exposure (as the same enzyme metabolises them both)

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23
Q

Impact of omeprazole on clopidogrel?

A

omeprazole reduces effectiveness of clopidogrel

24
Q

Impact of omeprazole on methotrexate?

A

omeprazole increases exposure to methotrexate as it inhibits renal elimination

25
Q

What are the key side effects of beta blockers?

A
  • Dizziness & syncope
  • Hypotension
  • Erectile dysfunction
  • Coldness of peripheries
  • Headaches
  • Sleep disturbances e.g. waking up and nightmares (as they cross the BBB)

Safety netting:
- Bronchospasm
- Masking of hypoglycaemia symptoms e.g. tachycardia, palpitations & tremor

26
Q

Key contraindication of beta blockers ?

A

Asthma

27
Q

What 2 drugs can beta blockers NOT be co-prescribed with?

Why?

A

1) Amiodarone

2) Non-dihydripyridine CCBs (e.g. verapamil and diltiazem

Can cause complete heart block.

28
Q

Which CCBs can beta blockers be co-prescribed with?

A

dihydropyridine CCBs (e.g. amlodipine, felodipine)

29
Q

What are pharmacokinetic drug interactions?

A

When one drug alters the absorption, distribution, metabolism or excretion of another, resulting in either an increase or decrease of the available drug to produce a pharmacological effect.

30
Q

What is first pass metabolism?

A

Drug metabolism in the gut or liver, which leads to a reduction in the concentration of the active drug before it reaches the site of action or systemic circulation.

Oral drugs will have varied bioavailability due to the extent of first-pass metabolism.

31
Q

Bioavailability of oral vs IV drugs?

A

Oral drugs will have varied bioavailability due to the extent of first-pass metabolism.

IV drugs will have 100% bioavailability as they bypass the gastrointestinal tract.

32
Q

What is the impact of oral iron on tetracycline antibiotics (e.g. doxycycline0?

A

Oral iron can DECREASE the absorption of tetracycline Abx.

Tetracyclines have a strong affinity for iron, creating a poorly soluble chelate that is less readily absorbed by the GI tract, resulting in much lower serum concentrations of the antibiotic.

33
Q

How far apart should oral iron and tetracyclines be given?

A

At least 3 hours apart

34
Q

What is the impact when heavily protein-bound drugs are displaced by another drug?

A

This can cause a sizeable increase in unbound free drug, resulting in a greater pharmacological effect.

35
Q

What is the interaction between naproxen and warfarin?

A

Naproxen can displace warfarin from plasma protein binding sites, leading to more unbound warfarin available, increasing its pharmacological effect (as well as toxic effects).

  • Warfarin is 99% protein bound, and 1% is unbound (free)
  • If naproxen displaces warfarin by just 1%, it will result in warfarin being 98% protein bound and 2% unbound
  • This effect causes a 100% increase in the free-form drug (from 1% to 2%)
36
Q

Where & how does drug metabolism usually occur?

A

Cmmonly occurs in the liver through phase I reactions (oxidation, reduction, or hydrolysis) or phase II reactions (e.g. glucuronidation).

Most drug metabolism is carried out by phase I reactions involving the isoenzyme cytochrome P450 (CYP450).

37
Q

Is phenytoin an enzyme inhibitor or inducer?

A

Inducer

38
Q

Are macrolide Abx enzyme inhibitors or inducers?

A

Inhibitors

39
Q

What is the interaction between phenytoin & oral progesterone only contraceptives?

A

Phenytoin is a potent CYP3A4 inducer which induces the metabolism of PIP (e.g. desogestrel), reducing their effect.

Contraceptive exposure can be reduced by up to 50% and may cause intermenstrual breakthrough bleeding and spotting.

Use alternative methods of contraception (intrauterine devices, depots or barrier methods).

40
Q

Is metronidazole an enzyme inhibitor or inducer?

A

Inhibitor

41
Q

Is sodium valproate an enzyme inhibitor or inducer?

A

Inhibitor

42
Q

What is the interaction between clarithromycin and simvastatin?

A

Clarithromycin induces the CYP3A4 enzyme responsible for metabolising simvastatin, increasing the plasma concentrations of simvastatin.

This interaction can potentially cause toxicity, leading to myopathies and rhabdomyolysis.

Concurrent use is contraindicated; withhold simvastatin while administering clarithromycin.

43
Q

How do NSAIDs affect the excretion of methotrexate?

A

NSAIDs can increase methotrexate concentrations due to their nephrotoxic effects (due to reduced excretion).

44
Q

Pharmacokinetic vs pharmacodynamic drug interactions?

A

Pharmacokinetic: take place when one drug interacts with another at the level of metabolism, absorption or excretion.

Pharmacodynamic: take place at the level of receptor sites, where they may have additive or potentiating effects.

45
Q

How are ramipril and amlodipine for a beneficial additive/synergistic interaction?

A

Ramipril and amlodipine work synergistically to reduce blood pressure at an enhanced level due to the different mechanisms of action:

1) Ramipril inhibits the ACE enzyme from converting angiotensin I to angiotensin II (causing increased vasodilation due to inhibition of bradykinin breakdown)

2) Amlodipine exhibits its antihypertensive effects due to the direct relaxation of the vascular smooth muscles

46
Q

How is the concurrent administration of enoxaparin (LMWH) with apixaban (DOAC) an example of a harmful additive/synergistic interaction?

A

The additive effects cause additive anti-Xa activity –> increases risk of bleeding.

Concurrent administration is contraindicated.

47
Q

Who should non-cardioselective beta-blockers (e.g. propanolol) be avoided in?

A

Asthma or COPD (due to risk of bronchospasm)

48
Q

What are the 2 broad types of beta blockers?

A

1) Cardioselective: acting on the beta-1 receptors in the heart (therefore reducing bronchoconstriction in the lungs)

2) Non-cardioselective: acting on the beta-2 receptors on heart and lung receptors.

49
Q

Give some examples of cardioselective beta blockers

A

Bisoprolol
Metoprolol
Esmolol
Atenolol

50
Q

Interaction between NSAIDs and SSRIs?

A

SSRIs can increase the risk of upper gastrointestinal bleeding when given with NSAIDs

51
Q

Interaction between methotrexate and trimethoprim?

A

Risk of severe bone marrow suppression & subsequent pancytopenia (may be fatal) when given concurrently.

52
Q

Interaction between omeprazole with clopidogrel?

A

Omeprazole can decrease the antiplatelet effects of clopidogrel

53
Q

Interaction between verapamil and beta-blockers?

A

Additive cardiac depression effects (leading to bradycardia, asystole, sinus arrest).

This interaction can also occur with ocular beta blockers.

54
Q

Interaction between ACEi and potassium-sparing diuretics (e.g. spironolactone / eplerenone)?

A

Concurrent use increases the risk of hyperkalaemia and AKI

55
Q
A

Yr 4 - ACC (73 decks)

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