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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
What are the key side effects of beta blockers?
- 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
Key contraindication of beta blockers ?
Asthma
27
What 2 drugs can beta blockers NOT be co-prescribed with? Why?
1) Amiodarone 2) Non-dihydripyridine CCBs (e.g. verapamil and diltiazem Can cause complete heart block.
28
Which CCBs can beta blockers be co-prescribed with?
dihydropyridine CCBs (e.g. amlodipine, felodipine)
29
What are pharmacokinetic drug interactions?
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
What is first pass metabolism?
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
Bioavailability of oral vs IV drugs?
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
What is the impact of oral iron on tetracycline antibiotics (e.g. doxycycline0?
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
How far apart should oral iron and tetracyclines be given?
At least 3 hours apart
34
What is the impact when heavily protein-bound drugs are displaced by another drug?
This can cause a sizeable increase in unbound free drug, resulting in a greater pharmacological effect.
35
What is the interaction between naproxen and warfarin?
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
Where & how does drug metabolism usually occur?
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
Is phenytoin an enzyme inhibitor or inducer?
Inducer
38
Are macrolide Abx enzyme inhibitors or inducers?
Inhibitors
39
What is the interaction between phenytoin & oral progesterone only contraceptives?
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
Is metronidazole an enzyme inhibitor or inducer?
Inhibitor
41
Is sodium valproate an enzyme inhibitor or inducer?
Inhibitor
42
What is the interaction between clarithromycin and simvastatin?
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
How do NSAIDs affect the excretion of methotrexate?
NSAIDs can increase methotrexate concentrations due to their nephrotoxic effects (due to reduced excretion).
44
Pharmacokinetic vs pharmacodynamic drug interactions?
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
How are ramipril and amlodipine for a beneficial additive/synergistic interaction?
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
How is the concurrent administration of enoxaparin (LMWH) with apixaban (DOAC) an example of a harmful additive/synergistic interaction?
The additive effects cause additive anti-Xa activity --> increases risk of bleeding. Concurrent administration is contraindicated.
47
Who should non-cardioselective beta-blockers (e.g. propanolol) be avoided in?
Asthma or COPD (due to risk of bronchospasm)
48
What are the 2 broad types of beta blockers?
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
Give some examples of cardioselective beta blockers
Bisoprolol Metoprolol Esmolol Atenolol
50
Interaction between NSAIDs and SSRIs?
SSRIs can increase the risk of upper gastrointestinal bleeding when given with NSAIDs
51
Interaction between methotrexate and trimethoprim?
Risk of severe bone marrow suppression & subsequent pancytopenia (may be fatal) when given concurrently.
52
Interaction between omeprazole with clopidogrel?
Omeprazole can decrease the antiplatelet effects of clopidogrel
53
Interaction between verapamil and beta-blockers?
Additive cardiac depression effects (leading to bradycardia, asystole, sinus arrest). This interaction can also occur with ocular beta blockers.
54
Interaction between ACEi and potassium-sparing diuretics (e.g. spironolactone / eplerenone)?
Concurrent use increases the risk of hyperkalaemia and AKI
55

Yr 4 - ACC (73 decks)

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