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FINALS > Drugs > Flashcards

Drugs Flashcards

1
Q

What does ACE inhibitor stand for?

A

Angiotensin-converting enzyme inhibitors

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2
Q

Indications for ACE inhibitors?

A

HTN (less effective in Afro-Caribbean pts), HF, diabetic nephropathy, secondary prevention of IHD

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3
Q

Mechanism of action of ACE inhibitors

A

Inhibits the conversion of angiotensin I to angiotensin II

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4
Q

Mechanism of action of ACE inhibitors explained for reducing BP?

A

Inhibits the conversion of angiotensin I to angiotensin II

→ decrease in angiotensin II levels → vasodilation and reduced blood pressure

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5
Q

Mechanism of action of ACE inhibitors explained in relation to the kidneys?

A

Inhibits coversion of angiotensin I to angiotensin II
→ decrease in angiotensin II levels → reduced stimulation for aldosterone release → decrease in sodium and water retention by the kidneys

AND

renoprotective mechanism: decrease in angiotensin II -> dilation of efferent glomerular arterioles -> reduced glomerular capillary pressure -> decreased mechanical stress on the delicate filtration barriers of the glomeruli (important in diabetic nephropathy)

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6
Q

Role of ADH?

A

Helps body retain water.

Dehydrated or high salt -> ADH released by pituitary gland -> acts on collecting duct -> reabsorb more water into the blood.
Therefore causes:
Water retention.

High levels ADH= less urine.

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7
Q

Role of aldosterone?

A

Helps control balance of sodium and potassium in blood.

BP drops or sodium low -> aldosterone released by adrenal glands -> kidneys reabsorb more sodium (and so water) and excrete potassium.
Therefore: increases blood volume and pressure.

High levels aldosterone: increased BP and loss of potassium.

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8
Q

Role of angiotensin II?

A

1) Constricts arterioles (increase BP).
2) Constricts efferent glomerular arterioles (increase BP).
3) Triggers adrenal glands to release aldosterone and pituitary to release ADH.

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9
Q

ACE inhibitors are acivated by what?

A

Phase 1 metabolism in the liver

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10
Q

Side effects of ACE inhibitors?

A

cough (15% and up to 1yr after starting), angioedema (up to 1yr), hyperkalaemia, first dose-hypotension (common if taking diuretics)

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11
Q

Why can ACE inhibitors cause a cough?

A

increases bradykinin levels

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12
Q

Why do ACE inhibitors cause hyperkalaemia?

A

decrease in angiotensin II -> reduced aldosterone excretion -> decreased uptake of sodium and less potassium excreted.

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13
Q

Cautions and contraindications of ACE inhibitors?

A
  • AVOID: pregnancy and breastfeeding
  • Renovascular disease: may result in renal impairment
  • Aortic stenosis: may result in hypotension
  • hereditary of idiopathic angioedema
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14
Q

Specialist advice should be sought before starting ACE inhibitors in pts with what?

A

potassium >=50mmol/L

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15
Q

ACE inhibitor interactions?

A

pts receiving high dose diuretic therapy (more than 80mg furosemdie a day)= signif increases risk of hypotension

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16
Q

What should you monitor in pts taking ACE inhibitors?

A

U&Es: rise in creatinine and K+ may be expected after starting

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17
Q

Acceptable changes in an increase in serum creatinine and potassium for pts who have just started an ECE inhibitor?

A

increase in creatinine up to 30% from baseline and potassium up to 5.5mmol/l

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18
Q

Significant renal impairment may occur in pts who take ACE inhibitor and have what?

A

undiagnosed bilateral renal artery stenosis

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19
Q

Examples of ACE inhibitors?

A

ramipril
enalapril
lisinopril

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20
Q

What are calcium channel blockers primarily used in the management of?

A

CVD

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21
Q

Voltage-gated calcium channels are present where?

A

In myocardial cells, cells of the conduction system and vascular smooth muscle

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22
Q

Different types of CCBs affect…

A

different areas: myocardial cells, cells of conduction system or vascular smooth muscle

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23
Q

Examples of CCBs?

A

1) nifedipine, amlodipine, felodipine (dihydropyridines)
2) verapamil
3) diltiazem

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24
Q

CCBs: indications for dihydropyridines eg. amlodipine and nifedipine?

A

HTN, angina, Raynaud’s

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25
Q

CCBs: dihydropyridines eg. amlodipine and nifedipine affect what?

A

Peripheral smooth muscle more than myocardium so don’t result in worsening HF but may therefore cause ankle swelling.

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26
Q

CCBs: shorter acting dihydropyridines eg. nifedipine cause what?

A

peripheral vasodilation which may result in reflex tachycardia

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27
Q

CCBs: S/Es for dihydropyridines eg. amlodipine and nifedipine?

A

flushing, headache, ankle swelling

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28
Q

CCBs: verapamil indications?

A

angina, HTN, arrhythmias

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29
Q

CCBs: vreapamil is highly…

A

negatively inotropic (keep heart muscle from working too hard by beating with less force)

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30
Q

CCBs: verapamil should not be given with what?

A

Beta blockers as may cause heart block

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31
Q

CCBs: S/Es of verapamil?

A

HF, constipation, hypotension, bradycardia, flushing

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32
Q

CCBs: indications for diltiazem?

A

angina, HTN

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33
Q

CCBs: diltiazem is less negatively inotropic than verapamil but should be used in caution in pts with…

A

HF or taking BBs

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34
Q

CCBs: S/Es of diltiazem?

A

hypotension, bradycardia, HF, ankle swelling

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35
Q

What CCB most likely to cause ankle and do NOT worsen HF?

A

Dihydropyridines eg. amlodipine, nifedipine

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36
Q

What CCBs should be not given/used in caution in pts with HF or on BBs?

A

Verapamil (NOT)
Diltiazem (caution)

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37
Q

What CCBs more likely to cause bradycardia, hypotension and HF?

A

verapamil and diltiazem

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38
Q

What does ARB stand for?

A

Angiotensin II receptor blockers

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39
Q

Mechanism of action of ARB?

A

block effects of angiotensin II at the AT1 receptor

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40
Q

Common side effect of ARB?

A

Hyperkalaemia

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41
Q

When are ARB used?

A

Usually when ACEi not tolerated eg. cough

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42
Q

Example of ARB?

A

Ends in ‘-sartan’
eg. candesartan

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43
Q

Mechanism of action of Thiazide diuretics (and thiazide-like diuretics)?

A

Inhibit sodium absorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive sodium chloride symporter. Potassium is lost as a result of more sodium reaching the collecting ducts.

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44
Q

Common side-effects of thiazide diuretics (& T-L)?

A

Hyponatraemia, hypokalaemia, dehydration, postural hypotension, hypercalcaemia & hypocalciuria, gout, impaired glucose tolerance, impotence (ED)

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45
Q

Do thiazide diuretics have a strong or weak diuretic action? (& T-L)

A

Weak

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46
Q

Indications for thiazide-like diuretics (& TD)?

A

HTN
mild HF (loop diuretics are better for reducing overload)

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47
Q

What type of diuretics are better for reducing overload?

A

Loop

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48
Q

Examples of thiazide-like diuretics?

A

Idapamide, chlortalidone

bendroflumethiazide (thiazide diuretic)

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49
Q

Why can thiazide diuretics cause hypokalaemia? (& T-L)

A

Due to increased delivery of Na+ to distal part of DCT -> increased sodium reabsorption in exchange for potassium and hydrogen ions

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50
Q

Rare adverse effects of thiazide diuretics? (& T-L)

A

thrombocytopaenia
agranulocytosis
photosensitivity rash
pancreatitis

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51
Q

thiazide-like diuretics vs thiazide diuretics?

A

Same effect, different chemical structure.
Pretty much same.

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52
Q

Thiazide diuretics (& T-L) cause increased…

A

urine output

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53
Q

Mechanism of action of aminosalicylate drugs?

A

5-aminosalicyclic acid (5-ASA) is released in the colon and not absorbed. It acts locally as an anti-inflam. MOA not fully understood but 5-ASA may inhibit prostaglandin synthesis.

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54
Q

Examples of aminosalicylate drugs?

A

sulphasalazine
mesalazine
olsalazine

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55
Q

Aminosalicylate drugs: sulphasalazine?

A
  • 5-ASA + suphapydridine (a sulphonamide)
  • many S/Es due to sulphapyridine moiety: rashes, oligospermia, headache, Heinz body anaemia, megaloblastic anaemia, lung fibrosis
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56
Q

Aminosalicylate drugs: mesalazine?

A
  • a delayed release form of 5-ASA
  • no sulphapyridine S/Es
  • S/Es: GI upset, headache, agranulocytosis, pancreatitis, intestinal nephritis
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57
Q

Aminosalicylate drugs: olsalazine?

A

2 molecules of 5-ASA linked by a diazo bond, which is broked by colonic bacteria

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58
Q

Key Ix in an unwell pt taking aminosalicylate drugs?

A

FBC as they are associated with vairety of haem adverse effects eg. agranulocytosis

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59
Q

Antidiarrhoeal agents: opioid agonists include?

A

loperamide and diphenoxylayte

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60
Q

Cholestyramine?

A

Bile acid sequestrant used in Mx of hyperlipidaemia to reduce LDL cholesterol.

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61
Q

Indications for cholestyramine?

A

1) hyperlipidaemia= reduces LDL cholesterol

2) Crohn’s for treatment of diarrhoea following bowel resection

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62
Q

Mechanism of action of cholestyramine?

A

decreases bile acid reabsorption in small intestine therefore upregulating the amount of cholesterol converted to bile acid

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63
Q

Adverse effects of cholestyramine?

A
  • abdo cramps and constiption
  • decreases absorption of fat-soluble vitamins
  • cholesterol gallstones
  • may raise level of triglycerides
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64
Q

Metoclopramide class?

A

D2 receptor antagonist

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65
Q

Indications for metoclopramide?

A
  • main= nausea
  • GORD
  • prokinetic action good for gastroparesis secondary to diabetic neuropathy
  • combined with analgesics for Mx of migraine (migraine attacks result in gastroparesis, slowing absoprtion of analgesics)
  • paralytic ileus
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66
Q

Adverse effects of metoclopramide?

A
  • extrapyramidal= acute dystonia eg. oculogyric crisis (more in children and young adults)
  • diarrhoea
  • hyperprolactinaemia
  • tardive dyskinesia
  • parkinsonism
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67
Q

What should metoclopramide be avoided in?

A

bowel obstruction, but helpful in paralytic ileus

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68
Q

Mechanism of action of metoclopramide?

A
  • Primarily D2 receptor antagonist
  • also a mixed 5-HT3 receptor antagonist/5-HT4 receptor agonist
  • antiemetic action due to anatgonisitic activity at D2 receptors in chemoreceptor trigger zone. At higher doses the 5-HT3 receptor antagonist also has an effect
  • gastroprokinetic activity is mediated by D2 receptor antagonist activity and 5-HT4 receptor agonist activity
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69
Q

Mechanism of action of proton pump inhibitors (PPI)?

A

irreversible blockage of the H+/K+ ATPase of the gastric parietal cell

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70
Q

Examples of PPI?

A

omeprazole and lansoprazole

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71
Q

Adverse effects of PPI?

A
  • hyponatraemia, hypomagnesaemia
  • osteoporosis -> increased risk of fractures
  • micoscopic colitis
  • increased risk of c.diff infections
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72
Q

Vitamin A?

A

aka retinol
Fat soluble vitamin

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73
Q

Functions of Vitamin A (retinol)?

A
  • converted to retinal, an important visual pigment
  • important in epithelial cell differentiation
  • antioxidant
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74
Q

Consequences of vit A def?

A

night blindness

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75
Q

Vitamin B1?

A

aka thiamine
Water soluble vit of B complex group

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76
Q

One of Vitamins B1’s (thiamine) phosphate derivates?

A

Thiamine pyrophosphate (TPP) coenzyme

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77
Q

Thiamine pyrophosphate (TTP, vit B phosphate derivates) is a coenzyme in what reactions?

A
  • pyruvate dehydrogenase complex
  • pyruvate decarboxylase in ethanol fermentation
  • alpha-ketoglutarate dehydrogenase complex
  • branched-chain amino acid dehydrogenase complex
  • 2-hydroxyphytanoyl-CoA lyase
  • transketolase
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78
Q

Vit B1 (thiamine) is important for what?

A

catabolism of sugars and aminoacids

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79
Q

Clinical consequence of thiamine def is seen first where?

A

highly aerobic tissues eg. brain (Wenicke-Koraskoff syndrome) and heart (wet beriberi)

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80
Q

Causes of vit B1 (thiamine) def?

A
  • alcohol XS (alcoholics recommended to supplement)
  • malnutrition
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81
Q

Conditions associated with Vit B1 (thiamine) def?

A
  • Wernicke’s encephalopathy: nystagmus, ophthalmoplegia and ataxia
  • Korsakoff’s syndrome: amnesia, confabulation
  • dry beriberi: peripheral neuropathy
  • wet beriberi: dilated cardiomyopathy
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82
Q

Vitamin B2?

A

aka riboflavin

A cofactor of flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN) and is important in energy metabolism.

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83
Q

Consequences of Vit B2 (riboflavin) def?

A

angular cheilitis

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84
Q

Vitamin B3?

A

aka niacin
Water soluble vitamin of B complex group.

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85
Q

Role of Vit B3 (niacin)?

A

it’s a precursor to NAD+ and NADP+ and so plays an essential metabolic role in cells

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86
Q

Biosynthesis of Vit B3 (niacin)?

A
  • Hartnup’s disease= hereditary disorder which reduces absorption of tryptophan
  • Carcinoid syndrome= increased tryptophan metabolism to serotonin
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87
Q

Consequences of Vit B3 (niacin) def?

A
  • pellagra= dermatitis, diarrhoea, dementia
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88
Q

Vitamin B6?

A

aka pyridoxine

Water soluble vitamin of B complex group.

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89
Q

Role of Vit B6 (pyridoxine)?

A

converted to pyridoxal phosphate (PLP) which is a cofactor for many reactions incl. transamination, deamination and decarboxylation

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90
Q

Causes of Vit B6 (pyridoxine) def?

A

isoniazid therapy

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91
Q

Consequences of Vit B6 (pyridoxine) def?

A
  • peripheral neuropathy
  • sideroblastic anaemia
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92
Q

Vitamin C?

A

aka ascorbic acid

Water soluble

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93
Q

Functions of Vit C (ascorbic acid)?

A
  • antioxidant
  • collagen synthesis: acts as cofactor for enzymes that are needed for hydroxylation proline and lysine in synthesis of collagen
  • facilitates iron absorption
  • cofactor for norepinephrine synthesis
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94
Q

What can Vit C (ascorbic acid) def lead to?

A

Vit C def= scurvy

Vit C def (scurvey) leads to defective synthesis of collagen resulting in capillary fragility (bleeding tendency) and poor wound healing).

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95
Q

Features of Vit C (ascorbic acid) def?

A
  • gingivitis, loose teeth
  • poor wound healing
  • bleeding from gums, haematuria, epistaxis
  • general malaise
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96
Q

What vitamins are water soluble?

A

B and C

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97
Q

What is rifampicin used for?

A

TB

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98
Q

MOA of rifampicin?

A

inhibits bacterial DNA dependent RNA polymerase preventing transcription of DNA into mRNA

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99
Q
A
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100
Q

S/Es of rifampicin?

A
  • hepatitis
  • orange secretions (eg. red urine)
  • flu-like symptoms

potent liver enzyme inducer

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101
Q

What is isoniazid used for?

A

TB

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102
Q

MOA of isoniazid?

A

inhibits mycolic acid synthesis

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103
Q

S/Es of isoniazid?

A
  • peripheral neuropathy
  • hepatitis
  • agranulocytosis

liver enzyme inhibitor

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104
Q

What must be given with isoniazid for TB?

A

pyridoxine (Vit B6) as prevents peripheral neuropathy

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105
Q

What is pyrazinamide used for?

A

TB

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106
Q

MOA of pyrazinamide?

A

converted by pyrazinamidase into pyrazinoic acid which in turn inhibits fatty acid sythase (FAS) I

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107
Q

S/Es of pyrazinamide?

A
  • hyperuricaemia causing gout
  • arthralgia, myalgia
  • hepatitis
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108
Q

What is ethambutol used for?

A

TB

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109
Q

MOA of ethambutol?

A

inhibits the enzyme arabinosyl transferase which polymerises arabinose into arabinan

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110
Q

S/Es of ethambutol?

A

optic neuritis (check visual acuity before and during Tx)

dose needs adjusting in pts with renal impairment

111
Q

What TB drugs are renally excreted?

A

ethambutol and pyrazinamide

so altered Tx regimens may be needed in pts with renal impairment

112
Q

Example of short-acting inhaled bronchodilator?

A

salbutamol (SABA)

113
Q

Mechanism of action of SABA?

A

Beta receptor agonist- relaxes bronchial smooth muscle through effects on beta 2 receptors

114
Q

What has similar effects to salbutamol but is long-acting?

A

salmetrol (LABA)

115
Q

Mechanism of action of corticosteroids?

A

anti-inflam

116
Q

Inhaled vs oral or IV corticosteroids for asthma/COPD?

A

inhaled= maintenance

oral/IV= acute exacerbation

117
Q

Example of a SAMA (short-acting muscarinic antagonist)?

A

ipratropium

118
Q

Mechanism of ipratropium?

A

SAMA
blocks the muscarinic acetylcholine receptors

119
Q

What is similar to ipratropium but is long-acting?

A

tiotropium (LAMA)

120
Q

When is ipratropium (SAMA) used?

A

primarily in COPD

short acting inhaled bronchodilator that relaxes bronchial smooth muscle

121
Q

Mechanism of action of methylxanthines eg. theophylline?

A

non-specific inhibitor of phosphodiesterase resulting in an increase in cAMP

122
Q

Indications for methylxanthines eg. theophylline?

A

asthma (acute and long term) and in neonates (apnea and help them extubate from ventillation)

123
Q

Mechanism of monteleukast, zafirlukast?

A

blocks leukotriene receptors (LTRA)

124
Q

Example of leukotriene receptor antagonist (LTRA)?

A

montelukast

125
Q

What is montelukast (LTRA) useful in?

A

aspirin-induced asthma

usually taken orally

126
Q

What is dabigatran contraindicated in?

A

use in pts with prosthetic and mechanical heart valve replacements- higher bleeding and thrombotic events

127
Q

What does DOAC stand for?

A

direct oral anticoagulants

128
Q

Indications for DOACs?

A
  • prevention of stroke in non-valvular AF (generally need at least one also to be present: prior stroke/TIA; 75yrs+; HTN; DM; HF)
  • prevention of VTE following hip/knee surgery
  • Tx of DVT and PE
129
Q

Name 4 examples of a DOAC

A

dabigatran
rivaroxaban
apixaban
edoxaban

130
Q

DOACs: MOA of dabigatran?

A

direct thrombin inhibitor

131
Q

DOACs: MOA of rivaroxaban?

A

direct factor Xa inhibitor

132
Q

DOACs: MOA of apixaban?

A

direct factor Xa inhibitor

133
Q

DOACs: MOA of edoxaban?

A

direct factor Xa inhibitor

134
Q

DOACs: excretion of dabigatran?

A

majority renal

135
Q

DOACs: excretion of rivaroxaban?

A

majority liver

136
Q

DOACs: excretion of apixaban?

A

majority faecal

137
Q

DOACs: excretion of edoxaban?

A

majority faecal

138
Q

DOACs: reversal agent for dabigatran?

A

idarucizumab

139
Q

DOACs: reversal agent for rivaroxaban?

A

andexanet alfa

(a recombinant form of human factor Xa protein)

140
Q

DOACs: reversal agent for apixaban?

A

andexanet alfa

(a recombinant form of human factor Xa protein)

141
Q

DOACs: reversal agent for edoxaban?

A

No authorised reversal agent, although andexanet alfa has been studied

142
Q

2 types of heparin?

A

unfractionated ‘standard’ heparin

low molecular weight heparin (LMWH)

143
Q

How do heparins generally act?

A

by activating antithrombin III

144
Q

Adverse effects of heparins?

A
  • bleeding
  • thrombocytopenia
  • osteoporosis and an increased risk of fractures
  • hyperkalaemia - this is thought to be caused by inhibition of aldosterone secretion
145
Q

Unfractionated heparin: administration?

A

IV

146
Q

Unfractionated heparin: duration of action?

A

short

147
Q

Unfractionated heparin: MOA?

A

activates antithrombin III

forms a complex that inhibits thrombin, factors Xa, IXa, Iia and XIIIa

148
Q

Unfractionated heparin: side effects?

A
  • bleeding
  • heparin-induced thrombocytopaenia (HIT)
  • osteoporosis
149
Q

Unfractionated heparin: monitoring?

A

activated partial thromboplastin time (APTT)

150
Q

Unfractionated heparin: indications?

A

useful in situations where there is a high risk of bleeding as anticoag can be terminated rapidly

also useful in renal failure

151
Q

LMWH: administration?

A

subcut

152
Q

LMWH: duration of action?

A

long

153
Q

LMWH: MOA?

A

activates antithrombin III.

Forms a complex that inhibits factor Xa

154
Q

LMWH: side-effects?

A
  • bleeding
  • lower risk of HIT and osteoporosis with LMWH
155
Q

LMWH: monitoring?

A

anti-factor Xa
BUT routine monitoring is NOT required

156
Q

LMWH: indications?

A

standard Mx of VTE treatment and prophylaxis
and ACS

157
Q

Heparin-induced thrombocytopaenia (HIT) pathophysiology?

A

immune mediated- antibodies form against complexes of platelet factor 4 (PF4) and heparin

these antibodies bind to PF4-heparin complexes on the platelet surface and induce platelet activation by cross linking FcγIIA receptors

158
Q

Heparin-induced thrombocytopaenia (HIT) may develop when?

A

after 5-10 days of treatment

159
Q

What is Heparin-induced thrombocytopaenia (HIT)?

A

despite being associated with low platelets it is actually a PROTHROMBOTIC condition

160
Q

Features of Heparin-induced thrombocytopaenia (HIT)?

A

> 50% reduction in platelets, thrombosis and skin allergy

161
Q

Heparin-induced thrombocytopaenia (HIT) Mx?

A

need ongoing anticoag:
- direct thrombin inhibitor eg. argatroban
- danaparoid

162
Q

How can heparin overdose be reversed?

A

protamin sulphate

only partially reverses the effect of LMWH

163
Q

Examples of parenteral anticoag?

A

unfractionated heparin
LMWH
fondaparinux
direct thrombin inhibitors

164
Q

Parenteral anticoags are used for what?

A

prevention of VTE and Mx of ACS

165
Q

MOA of fonaparinux?

A

Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa. It is given subcutaneously.

166
Q

Examples of direct thrombin inhibitors?

A

bivalirudin

generally given intravenously

167
Q

What is dabiggatran?

A

Dabigatran is a type of direct thrombin inhibitor that is taken orally. It is often grouped alongside the direct oral anticoagulants (DOACs).

168
Q

What is now mainly used instead of warfarin?

A

DOACs as don’t need same level of monitoring

169
Q

Warfarin drug class?

A

oral anticoag

170
Q

Mechanism of action of warfarin?

A

inhibits epoxide reductase preventing the reduction of vitamin K to its active hydroquinone form

this in turn acts as a cofactor in the carboxylation of clotting factor II, VII, IX and X (mnemonic = 1972) and protein C.

171
Q

Indications for warfarin?

A
  • mechanical heart valves
  • second line after DOACs: VTE and AF
172
Q

Target INR for warfarin for mechanical heart valves?

A

depends on valve type and location

mitral valves generally require higher INR than aortic

173
Q

Target INR for warfarin (used 2nd line after DOACs)?

A

VTE= target INR 2.5, if recurrent 3.5

AF= target INR 2.5

174
Q

How are patients on warfarin monitored?

A

using INR

175
Q

What does INR stand for?

A

international normalised ratio

176
Q

What is INR?

A

the ratio of prothrombin time for the pt over the normal prothrombin time

used to monitor pts on warfarin

177
Q

How long might it take to achieve a stable INR in a pt on warfarin?

A

warfarin has a long half-life and achieving stable INR may take several days

variety of loading regimens and computer software is now often used to alter the dose

178
Q

Factors that may potentiate warfarin (enhance the effect of warfarin leading to an increased risk of bleeding)?

A
  • liver disease
  • P450 enzyme inhibitors, e.g.: amiodarone, ciprofloxacin
  • cranberry juice
  • drugs which displace warfarin from plasma albumin, e.g. NSAIDs
  • inhibit platelet function: NSAIDs
179
Q

Examples of P450 enzyme inhibitors?

A

amiodarone
ciprofloxacin

180
Q

Side-effects of warfain?

A
  • haemorrhage
  • teratogenic, but can be used in breastfeeding mothers
  • skin necrosis
  • purple toes
181
Q

Why is a side-effect of warfarin skin necrosis?

A
  • when warfarin is first started biosynthesis of protein C is reduced
  • this results in temporary procoagulant state after initially starting warfarin, normally avoided by concurrent heparin administration
    thrombosis may occur in venules leading to skin necrosis
182
Q

Drugs which either inhibit or induce what may affect the metabolism of warfarin and hence the INR?

A

P450 system

183
Q

Induces of the P450 system will do what to the INR?

A

increased (faster) metabolism of warfarin and so decreases INR

184
Q

What is warfarin metabolised by?

A

cytochrome P450 (CYP450) enzyme system

inducers of this system increase the activity of these enzymes, leading to faster metabolism which reduces anticoag effect

185
Q

Effects of CYP450 inducers on warfarin and INR?

A
  • speed up breakdown of warfarin causing its levels in blood to decrease more quickly
  • this reduces the anticoag effect of warfarin, making it less effective at preventing blood clots
  • when warfarin is metabolised more quickly its anticoag effect diminishes resulting in lower INR
  • lower INR means blood is clotting fasting, increasing the risk of blood clots
186
Q

Effects of CYP450 inhibitors on warfarin and INR?

A
  • blocks the enzymes responsible for warfarin metabolism (break down)
  • leads to higher levels of warfarin in blood becuase its metabolised more slowly
  • warfarin’s anticoag effect is enhanced so blood less likely to clot, but risk of XS bleeding increases
  • inhibitors increase anticoag effect of warfarin causing INR to rise
  • higher INR can result in dangerous bleeding: GI haemorrhage, internal bleeding, intracranial haemorrhage
187
Q

INR reflects what?

A

how long it takes the blood to clot

higher INR indicates that blood clotting is delayed so higher risk of bleeding

low INR indicated that blood clotting is faster so increased risk of blood clots

188
Q

Examples ofI nducers of the P450 system include - INR will decrease?

A

antiepileptics: phenytoin, carbamazepine

barbiturates: phenobarbitone

rifampicin

St John’s Wort

chronic alcohol intake

griseofulvin

smoking (affects CYP1A2, reason why smokers require more aminophylline)

189
Q

Examples of Inhibitors of the P450 system include - INR will increase?

A

antibiotics: ciprofloxacin, clarithromycine/erythromycin

isoniazid

cimetidine,omeprazole

amiodarone

allopurinol

imidazoles: ketoconazole, fluconazole

SSRIs: fluoxetine, sertraline
ritonavir

sodium valproate

acute alcohol intake

quinupristin

190
Q

Mx for Major bleeding (eg. variceal haemorrhage, intracranial haemorrhage)

A
  • stop warfarin
  • IV vit K 5mg
  • Prothrombin complex concentrate: in not available then FFP

(FFP can take time to defrost, prothrombin complex conc should be used in intracranial H)

191
Q

Mx for INR >8.0 and minor bleeding?

A
  • stop warfarin
  • IV vit K 1-3mg
  • repeat dose of vit K if INR still too high after 24hrs
  • restart warfarin when INR <5
192
Q

Mx for INR >8 and no bleeding?

A
  • stop warfarin
  • vit K 1-5mg by mouth, using IV prep orally
  • repeat dose of vit K if INR still too high after 24hrs
  • restart when INR <5.0
193
Q

Mx for INR 5.0-8.0 and minor bleeding?

A
  • stop warfarin
  • IV kit K 1-3mg
  • restart when INR <5.0
194
Q

Mx if INR 5.0-8.0 and no bleeding?

A
  • withhold 1 or 2 doses of warfarin
  • reduce subsequent maintenance dose
195
Q

Typical INR range?

A

2.0-3.0

196
Q

INR >4.0
INR >5.0-9.0
INR <1.5

A

INR > 4.0: Significantly increases the risk of major bleeding. Medical attention is often required to lower INR.

INR > 5.0–9.0: Requires careful management and possibly administration of vitamin K or withholding warfarin doses to reduce the risk of life-threatening bleeding.

INR < 1.5: Increases the risk of clot formation, particularly in patients with conditions like atrial fibrillation, mechanical heart valves, or a history of thromboembolism.

197
Q

Why is dabigatran a good alternative to wardarin?

A

doesn’t need regular monitoring

198
Q

2 indications for dabigatran?

A

1) VTE prophylaxis following hip or knee replacement

2) Stroke prophylaxis for pts with non-valvular AF with 1 or more RFs present:
- previous stroke, TIA or systemic embolism
- left ventricular ejection fraction below 40%
- symptomatic heart failure of NYHA class 2 or above
- age 75 years or older
- age 65 years or older with one of the following: diabetes mellitus, coronary artery disease or hypertension

199
Q

Side effects of dabigatran?

A

Haemorrhage

200
Q

Doses of dabigatran should be reduced in who?

A

pts with CKD

201
Q

When to not prescribe dabigatran?

A

if creatinine clearance <30

202
Q

Reversal of anticoag effects of dabigatran?

A

Idarucizumab

203
Q

Examples of Adenosine diphosphate receptor inhibitors (ADP)?

A

Clopidogrel
Prasugrel
Ticagrelor
Ticlopidine

204
Q

What does ADP receptor inhibitors stand for?

A

adenosine diphosphate

205
Q

MOA of ADP receptor inhibitors eg. clopidogrel?

A

ADP is one of the main platelet activation factors, mediated by G-coupled receptors P2Y1 and P2Y12.

The main target of ADP receptor inhibition is the P2Y12 receptor, as it is the one which leads to sustained platelet aggregation and stabilisation of the platelet plaque.

206
Q

How do aspirin and ADP inhibitors work?

A

blocking different platelet aggregation pathways

207
Q

Most commonly used ADP inhibitor?

A

clopidogrel; prasugrel and ticagrelor newer

208
Q

Use of ADP inhibitors in ACS?

A

DAPT= aspirin (75mg daily) and ticagrelor (90mg twice daily) for 12m as secondary prevention

(trials show marked reduction compared to clopidogrel in high risk pts)

209
Q

Use of ADP inhibitors in pt with ACS undergoing PCI?

A

aspirin (75-100mg daily) in combination with either prasugrel (10mg daily), ticagrelor (90mg twice daily), or clopidogrel (75mg daily, if prasugrel or ticagrelor are not suitable) for 12 months, with aspirin alone thereafter

210
Q

Adverse effects of ADP inhibitors?

A

Tricagrelor= may cause dyspnoea due to impaired clearance of adenosine

211
Q

Interactions of clopidogrel (ADP inhibitor)?

A

with PPI eg. omeprazole and esomeprazole leading to reduced antiplatelet effects

212
Q

Contraindications of ADP inhibitors?

A

1) Prior stroke or TIAk, high risk of bleeding, and prasugrel hypersensitivity are absolute contraindications to prasugrel use.

2) Ticagrelor is contraindicated in patients with a high risk of bleeding, those with a history of intracranial haemorrhage, and those with severe hepatic dysfunction. Used with caution in those with acute asthma or COPD, as ticagrelor-treated patients experience higher rates of dyspnoea.

213
Q

ACS 1st line medical Mx and 2nd line?

A

1st= aspirin (lifelong) & ticagrelor (12m)

2nd= if aspirin contraindicated, clopidogrel (lifelong)

214
Q

PCI 1st and 2nd line medical Mx?

A

1st= Aspirin (lifelong) & prasurgrel or ticagrelor (12 months)

2nd= If aspirin contraindicated, clopidogrel (lifelong)

215
Q

TIA medical Mx 1st and 2nd line?

A

1st= Clopidogrel 75mg daily (lifelong)
sometimes and aspirin (DAPT- for 3-4w)

2nd= Aspirin (lifelong) & dipyridamole (lifelong)

216
Q

Ischaemic stroke medical Mx 1st and 2nd line?

A

1st= Clopidogrel 75mg daily (lifelong)
sometimes and aspirin (DAPT- for 3-4w if minor)

2nd= Aspirin (lifelong) & dipyridamole (lifelong)

217
Q

PAD medical Mx 1st and 2nd line?

A

1st= Clopidogrel 75mg daily (lifelong)

2nd= Aspirin (lifelong)

218
Q

What do antiplatelets do?

A

decrease platelet aggregation and inhibit thrombus formation in arterial circulation

219
Q

4 types of antiplatelet drugs?

A

1) Aspirin

2) ADP receptor inhibitors= clopidogrel, prasugrel and ticagrelor

3) Dipyridamole

4) Glycoprotein IIb/IIIa inhibitors= abciximab, eptifibatide, tirofiban

220
Q

Aspirin MOA?

A

irreversibly inhibits cyclo-oxygenase-1 and 2 and blocks the production of thromboxane

221
Q

MOA of ADP receptor inhibitors= clopidogrel, prasugrel and ticagrelor?

A

block the platelet P2Y12 receptor. They inhibit the binding of adenosine diphosphate or triphosphate to their platelet receptor, thereby blocking platelet activation and aggregation.

222
Q

MOA of dipyridamole?

A

has both antiplatelet and vasodilatory properties. It is a phosphodiesterase III inhibitor, and suppresses cyclic AMP (cAMP) degradation, leading to increased cAMP in platelets and blood vessels, inhibiting aggregation.

223
Q

MOA of Glycoprotein IIb/IIIa inhibitors= abciximab, eptifibatide, tirofiban?

A

block the binding of fibrinogen to glycoprotein IIb/IIIa receptors on the platelet. They are given intravenously in secondary care.

224
Q

Main indications for antiplatelet Tx?

A

The secondary prevention of atherothrombotic events in people with acute coronary syndrome (ACS), angina, peripheral arterial disease (PAD), and atrial fibrillation (AF) (although anticoagulants are usually used).

The secondary prevention of atherothrombotic events in people after myocardial infarction (MI), percutaneous coronary intervention (PCI), stroke, or transient ischaemic attack (TIA).

225
Q

Antiplatelets should not be prescribed routinely for primary prevention of CVD but they may be considered in who?

A

people at v high risk of stroke or MI

226
Q

When should long-term antiplatelet monotherapy with one agent be prescribed?

A

for secondary prevention of CVD for people with stable conditions

227
Q

Evidene suggests that what with aspirin gives added benefit in people with stable CV and PAD?

A

low dose rivaroxaban

228
Q

How to reduce risk of dyspepsia on antiplatelet agents?

A

Use low-dose aspirin where recommended (75 mg).

Consider testing for and treating H.pylori if the person has a history of ulcer disease or upper gastrointestinal (GI) bleeding, unless previously tested and treated for this.

Proton pump inhibitors (PPIs) may be used to protect against GI adverse effects if the person is at high risk (Avoid omeprazole and esomeprazole with clopidogrel.)

Refer if persistent despite Tx

229
Q

What to advise people taking antiplatelet meds to do?

A

inform dental or surgical teams before any procedures

230
Q

What is cyclooxygenase responsible for? (aspirin blocks this)

A

prostaglandin, prostacylin and thromboxane synthesis

231
Q

What reduces the ability of platelets to aggreggate?

A

blocking of thromboxane A 2 formation in platelets (by aspirin)

232
Q

Aspirin potentiates?

A

oral hypoglycaemics
warfarin
steroids

233
Q

What age group should aspirin not be used in and why?

A

children <16 due to risk of Reye’s sndrome

Exception is Kawasaki disease- benefits outweigh risks

234
Q

What is Reye’s syndrome?

A

Reye’s syndrome is a rare but serious illness that affects the brain and liver, and can be life-threatening. It’s most common in children ages 4 to 14 who have taken aspirin and esp if recovering from a viral infection, such as the flu or chickenpox, and

tired, lethargic, irritability, tachypnoeic, seizures, loss of consciousness, difficult to clot,

235
Q

What is clopidogrel?

A

antiplatelet

236
Q

Clopidogrel drug class?

A

Thienopyridines (ADP receptor inhibitors)

237
Q

Another name for ADP receptor inhibitors?

A

thienopyridines

238
Q

Clopidogrel MOA?

A

antagonist of the P2Y12 adenosine diphosphate (ADP) receptor, inhibiting the activation of platelets

239
Q

Interactions with clopidogrel?

A

concurrent use of proton pump inhibitors (PPIs) may make clopidogrel less effective, esp omeprazole and esomeprazole (lansoprazole should be OK)

240
Q

When may pt need combination of antiplatelet and anticoag?

A

Antiplatlet eg for CVD and anticoag for eg. AF, VTE or valvular heart disease

241
Q

Combination therapy of antiplatelet and anticoag increases risk of?

A

bleeding

may not be needed in all cases

242
Q

What if pt needs secondary prevention of stable CVS with also an indication for anticoag?

A

Normally recommend starting antiplatelet

If have indication for anticoag eg. AF then indicated that anticoag monotherapy is given without the addition of antiplatelets (as high risk of bleeding giving both)

243
Q

If pt on antiplatelet develops a VTE they are likely prescribed what?

A

anticoag 3-6m

ORBIT score should be calculated:
- low risk of bleeding= can continue antiplatelets
- intermediate or high= stop antiplatelet

244
Q

5-HT3 antagonists class?

A

antiemetic, used mainly in Mx of chemo related nausea

245
Q

5-HT3 antagonists MOA?

A

act in chemoreceptor trigger zone of medulla oblongata

246
Q

5-HT3 antagonists examples?

A
  • ondansetron

-palonosetron= second gen 5-HT3 antagonists, main advantage is reduced effect on QT interval

247
Q

5-HT3 antagonists adverse effects?

A

prolonged QT interval
constipation

248
Q

Carbamazepine class?

A

anticonvulsant
chemically similar to tricyclic antidepressants

249
Q

Carbamazepine indications?

A
  • epilepsy (esp partial seizures)
  • trigeminal neuralgia
  • bipolar
250
Q

Carbamazepine MOA?

A

binds to sodium channels increases their refractory period

251
Q

Carbamazepine adverse effects?

A

P450 enzyme inducer

dizziness and ataxia

drowsiness

headache

visual disturbances
(especially diplopia)

Steven-Johnson syndrome

leucopenia and agranulocytosis

hyponatraemia secondary to syndrome of inappropriate ADH secretion

252
Q

Carbamazepine is known to exhibit autoinduction, this means?

A

when pts start Carbamazepine they may see a return of seizures after 3-4w of Tx

253
Q

Drugs that can cause peripheral neuropathy?

A

amiodarone
isoniazid
vincristine
nitrofurantoin
metronidazole

254
Q

Lamotrigine class and indications?

A

antiepileptic
epilepsy

255
Q

Lamotrigine MOA?

A

sodium channel blocker

256
Q

Lamotrigine adverse effects?

A

Stevens-Johnson syndrome

257
Q

What is levodopa combines with and why?

A

decarboxylase inhibitor (e.g. carbidopa or benserazide) to prevent peripheral metabolism of L-dopa to dopamine

258
Q

2 facts about levodopa?

A

reduced effectiveness with time (usually by 2 years)

no use in neuroleptic induced parkinsonism

259
Q

Adverse effects of levodopa?

A

dyskinesia
‘on-off’ effect
postural hypotension
cardiac arrhythmias
nausea & vomiting
psychosis
reddish discolouration of urine upon standing

260
Q

Indication of pheytoin?

A

Mx of seizures

261
Q

Phenytoin MOA?

A

binds to sodium channels increasing their refractory period

262
Q

Phenytoin is an…

A

inducer of the P450 system

263
Q

acute adverse effects of phenytoin?

A

initially: dizziness, diplopia, nystagmus, slurred speech, ataxia
later: confusion, seizures

264
Q

Chronic adverse effects of phenytoin?

A

common: gingival hyperplasia (secondary to increased expression of platelet derived growth factor, PDGF), hirsutism, coarsening of facial features, drowsiness

megaloblastic anaemia (secondary to altered folate metabolism)

peripheral neuropathy
enhanced vitamin D metabolism causing osteomalacia
lymphadenopathy
dyskinesia

265
Q

Idiosyncratic meaning?

A

adverse effects that cannot be explained by the known mechanisms of action of the offending agent, do not occur at any dose in most patients, and develop mostly unpredictably in susceptible individuals only

266
Q

Idiosyncratic adverse effects of phenytoin?

A

fever
rashes, including severe reactions such as toxic epidermal necrolysis
hepatitis
Dupuytren’s contracture
aplastic anaemia
drug-induced lupus

267
Q

Teratogenic adverse effects of phenytoin?

A

associated with cleft palate and congenital heart disease

268
Q

Monitoring of phenytoin?

A

Phenytoin levels do not need to be monitored routinely but trough levels, immediately before dose should be checked if:
adjustment of phenytoin dose
suspected toxicity
detection of non-adherence to the prescribed medication

269
Q

Class of triptans?

A

specific 5-HT1B and 5-HT1D agonists

270
Q

Indications for triptans?

A

acute Tx of migraine

generally used 1st line in combination therapy with NSAID or paracetamol

271
Q

Prescribing points for triptans?

A

should be taken as soon as possible after the onset of headache, rather than at onset of aura

oral, orodispersible, nasal spray and subcutaneous injections are available

272
Q

Adverse effects of triptans?

A

‘triptan sensations’ - tingling, heat, tightness (e.g. throat and chest), heaviness, pressure

273
Q

Contraindications of triptans?

A

pts with a history of, or significant risk factors for, ischaemic heart disease or cerebrovascular disease

FINALS (36 decks)

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