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Phase 4 > PSA - drugs > Flashcards

PSA - drugs Flashcards

1
Q

Name 3 weak opioids

A

codeine, dihydrocodeine, tramadol

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2
Q

What are the clinical implications for weak opioids?

A

Mild to moderate pain
Diarrhoea
Cough suppression

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3
Q

Prescribing doses and frequency for weak opioids used to manage pain

A

30-60mg every 4 hours as required (maximum 240mg daily)

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4
Q

Common adverse effects of weak opioids?

A

Constipation, biliary/ureteric spasm, dysphoria, sweating

Nausea/vomiting, drowsiness

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5
Q

Important adverse effects of weak opioids?

A 
Respiratory depression (high doses)
Hypotension (high doses)
Paralytic ileus (dihydrocodeine)
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6
Q

In who should you avoid using weak opioids?

A

Avoid in COPD, acute asthma attack, acute respiratory depression, comatose patients and those at risk of paralytic ileus

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7
Q

What do weak opioids interact with?

A

CNS depressants (increased risk of respiratory depression) – alcohol, sedatives, hypnotics, general anaesthetics

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8
Q

What do you need to communicate to the patient when prescribing weak opioids?

A

Explain to patients that this medication could cause them to feel drowsy and that if this happens they should not drive or operate machinery. Patients should also be advised to avoid drinking alcohol while taking this medication

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9
Q

Name a few strong opioids

A

Buprenorphine, diamorphine, fentanyl, methadone,

oxycodone

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10
Q

Clinical indications for strong opioids?

A

Moderate to severe pain (including use in palliative care)
Acute diarrhoea (not first line)
Cough in terminal care

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11
Q

Dose and frequency of morphine administration

A

Morphine: 10mg s/c or IM every 4 hours (5mg every 4 hours if elderly, reduce dose in hepatic or renal impairment) , adjust according to response
Can also be administered by syringe driver or patient controlled analgesia (PCA) system

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12
Q

Adverse effects of strong opioids (same as weak)

A

Constipation, biliary/ureteric spasm, dysphoria, sweating

Nausea/vomiting, drowsiness

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13
Q

Important adverse effects of strong opioids

A 
Respiratory depression
Hypotension
Sedation and coma
Tolerance
Physical and psychological dependence
Overdose – this is reversed with naloxone
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14
Q

Who to avoid use of strong opioids in?

A

Avoid in acute respiratory depression, coma, head injury or raised ICP (opioids interfere with pupillary responses used in neurological assessment) and those at risk of paralytic ileus

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15
Q

What interacts with strong opioids?

A 
CNS depressants (increased risk of respiratory depression) – alcohol, sedatives, hypnotics, general anaesthetics
MAOIs (potentiate action of morphine)
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16
Q

What do you need to communicate to the patient when prescribing strong opioids? (same as weak)

A

Explain to patients that this medication could cause them to feel drowsy and that if this happens they should not drive or operate machinery. Patients should also be advised to avoid drinking alcohol while taking this medication.

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17
Q

Name two LMWHs

A

Dalteparin, Tinzaparin

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18
Q

What is the mechanism of action of LMWHs?

A

LMWH binds to antithrombin 3 and accelerates its action: Inhibition of factor Xa in the common pathway of the clotting cascade
Factor Xa is needed to convert prothrombin to thrombin, therefore LMWHs inhibit coagulation

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19
Q

What are the clinical indications for LMWHs?

A

Prophylaxis of venous thromboembolism (VTE)
Treatment of VTE before adequate oral anticoagulation (with warfarin) is established
Treatment of acute MI and unstable coronary artery disease, PE, DVT

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20
Q

Important adverse effects of LMWHs?

A

Haemorrhage
Heparin-induced thrombocytopenia (discontinue in these patients)
Hyperkalaemia

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21
Q

Who should you avoid giving LMWHs to?

A

Avoid in haemophilia and other haemorrhagic disorders, thrombocytopenia, recent cerebral haemorrhage, severe hypertension, peptic ulcer disease, acute bacterial endocarditis, following major trauma and in patients with known hypersensitivity to heparins

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22
Q

What do LMWH interact with?

A

NSAIDs (increased risk of haemorrhage)
ACE inhibitors, ARBs (increased risk of hyperkalaemia)
Antiplatelet agents (increased risk of haemorrhage)

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23
Q

What do you need to advise the patient of when taking LMWHs?

A

Advise the patient to avoid OTC NSAIDS

24
Q

What type of drug is Warfarin?

A

Vit K competitive inhibitor
Depletion of active clotting factors II, VII, IX and X
The onset of warfarin’s anticoagulant effect is delayed for several days until already formed active clotting factors have been degraded

25
Q

Clinical indications for Warfarin

A

Prophylaxis of embolisation in rheumatic heart disease and AF
Prophylaxis after insertion of prosthetic heart valve
Prophylaxis and treatment of VT and PE
Transient ischaemic attack (TIA)

26
Q

What are the usual doses for Warfarin?

A

Loading dose 5-10mg
Daily maintenance dose 3-9mg at the same time each day
Dose depends on patient’s prothrombin time (INR), wide interindividual variation in dose

27
Q

Common adverse effects of Warfarin?

A

Haemorrhage and bruising

28
Q

Important adverse effects of Warfarin?

A

Skin necrosis, hypersensitivity, liver dysfunction, jaundice, pyrexia

29
Q

Who should you avoid giving Warfarin to?

A

Avoid in pregnancy, peptic ulcer disease, severe hypertension and those with hepatic impairment (especially if prothrombin time already prolonged)

30
Q

How do you monitor Warfarin?

A

Regular INR - begin with daily/alternate days

Can extend up to 12 week intervals

31
Q

What do you need to communicate to the patient?

A

Do not take ASPIRIN without speaking to pharmacist
Use contraception - warfarin is damaging to pregnancy
Avoid cranberry juice, major diet changes (leafy veg), excess alcohol
Take Warfarin at the same time each day
Attend appts for INR checks

32
Q

Additional Warfarin notes

A

As the onset of the anticoagulant effect of Warfarin is delayed by several days, patients should be given a LMWH to cover them during this period

33
Q

What enhances the effect of Warfarin?

A

Alcohol
NSAIDs incl. aspirin
Anti-arrhythmics - amiodarone etc
Antibacterials – chloramphenicol, ciprofloxacin, co-trimoxazole, erythromycin, metronidazole, ofloxacin and sulphonamides
Experience from anticoagulant clinics suggests that any broad-spectrum antibiotic, especially ampicillin, can increase the INR
Antifungals – fluconazole, itraconazole, ketoconazole, miconazole
Lipid-lowering drugs – fibrates and simvastatin
Ulcer-healing drugs – cimetidine, omeprazole

34
Q

What reduces the effect of Warfarin?

A

Antiepileptics – carbamazepine, primidone, phenytoin
Antifungals – griseofulvin
oCP
Vitamin K – high intake of vitamin K can counteract warfarin activity
Retinoids – acitretin
Antidepressants – St. John’s Wort

35
Q

What is Rivaroxaban and what is its MoA?

A

Factor Xa inhibitor
Inhibits activated factor Xa, which is required for the conversion of prothrombin to thrombin in the common pathway of the coagulation cascade
Lack of thrombin prevents conversion of fibrinogen to fibrin and therefore inhibits thrombus formation

36
Q

What is the clinical indication of Rivaroxaban?

A

Prophylaxis of venous thromboembolism (VTE) following hip/knee replacement surgery Treatment of DVT & prophylaxis of recurrent DVT & PE

37
Q

What dose of Rivaroxaban/Dabigatran?

A

Rivaroxaban – 10mg once daily for 2 weeks after knee replacement (5 weeks after hip replacement)
Dabigatran – 220mg once daily for 9 days after knee replacement (27-34 days after hip replacement) Reduce dose in renal impairment

38
Q

Common adverse effects of Rivaroxaban?

A

Haemorrhage (no reversal agent liscensed at present)
Abdominal pain; constipation; diarrhoea; dizziness; dyspepsia;
headache; hypotension; nausea; pain in extremities; pruritus; rash; renal impairment; vomiting

39
Q

Important adverse effects of Dabigatran?

A

Hepatobiliary disorders (dabigatran)

40
Q

Interactions of Rivaroxaban?

A 
NSAIDs (increased risk of bleeding)
Amiodarone (increased plasma dabigatran concentration – reduce dose of dabigatran)
Verapamil (increased plasma dabigatran concentration – reduce dose of dabigatran)
Triazole antifungals (avoid combination with rivaroxaban)
41
Q

Additional notes for NOACs

A

These novel anticoagulants have a much broader therapeutic index than the traditionally-used oral anticoagulant warfarin – this allows for fixed drug dosing without the need for coagulation monitoring. However, at present no specific antidotes to these drugs exist.
Tablets should be taken with food.

42
Q

What type of drug is aspirin?

A

Antiplatelet

43
Q

What is the MoA of aspirin?

A

COX enzyme inhibitor

Impairs synthesis of thromboxane A2 + prostacyclin within plts

44
Q

Clinical indication for aspirin

A

Secondary prevention of CVD after MI/ACS/stroke

45
Q

Dose of aspirin?

A

75mg OD

46
Q

Important adverse effects of aspirin?

A

GI irritation, ulceration and breathing

Bronchospasm

47
Q

CI of aspirin?

A

Avoid in active peptic ulcer, haemophilia, known hypersensitivity

48
Q

Interactions with aspirin?

A

Increased bleeding risk with:

NSAIDs, anticoagulants, SSRIs

49
Q

What is clopidogrel?

A

Antiplatelet

50
Q

What is the MoA of clopidogrel?

A

Inhibits binding of ADP to its platelet receptor

51
Q

Clinical indications for clopidogrel use?

A

Secondary prevention of atherothrombotic event - following MI/stroke/PAD
With aspirin in ACS + for 1yr following coronary artery procedures

52
Q

Doses of clopidogrel?

A

Secondary prevention following MI/stroke: 75mg once daily Acute coronary syndrome: Loading dose – 300-600mg
Maintenance dose – 75mg daily

53
Q

Common adverse effects of clopidogrel?

A

GI disturbance, bleeding disorders

54
Q

Important adverse effects of clopidogrel?

A

gastric + duodenal ulcers

55
Q

Who should avoid using clopidogrel?

A

Pregnant women, active bleeding, discontinue for 7 days before elective surgery

56
Q

What interacts with clopidogrel?

A

Increased risk of bleeding: other antiplatelet drugs, anticoagulants, fibrinolytic, NSAIDs
Decreased risk: ulcer healing drugs

Phase 4 (13 decks)

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