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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

46
Q

Indications for thiazide-like diuretics (& TD)?

A

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

47
Q

What type of diuretics are better for reducing overload?

A

Loop

48
Q

Examples of thiazide-like diuretics?

A

Idapamide, chlortalidone

bendroflumethiazide (thiazide diuretic)

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

50
Q

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

A

thrombocytopaenia
agranulocytosis
photosensitivity rash
pancreatitis

51
Q

thiazide-like diuretics vs thiazide diuretics?

A

Same effect, different chemical structure.
Pretty much same.

52
Q

Thiazide diuretics (& T-L) cause increased…

A

urine output

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.

54
Q

Examples of aminosalicylate drugs?

A

sulphasalazine
mesalazine
olsalazine

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
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
57
Q

Aminosalicylate drugs: olsalazine?

A

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

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

59
Q

Antidiarrhoeal agents: opioid agonists include?

A

loperamide and diphenoxylayte

60
Q

Cholestyramine?

A

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

61
Q

Indications for cholestyramine?

A

1) hyperlipidaemia= reduces LDL cholesterol

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

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

63
Q

Adverse effects of cholestyramine?

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

Metoclopramide class?

A

D2 receptor antagonist

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
66
Q

Adverse effects of metoclopramide?

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

What should metoclopramide be avoided in?

A

bowel obstruction, but helpful in paralytic ileus

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
69
Q

Mechanism of action of proton pump inhibitors (PPI)?

A

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

70
Q

Examples of PPI?

A

omeprazole and lansoprazole

71
Q

Adverse effects of PPI?

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

Vitamin A?

A

aka retinol
Fat soluble vitamin

73
Q

Functions of Vitamin A (retinol)?

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

Consequences of vit A def?

A

night blindness

75
Q

Vitamin B1?

A

aka thiamine
Water soluble vit of B complex group

76
Q

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

A

Thiamine pyrophosphate (TPP) coenzyme

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
78
Q

Vit B1 (thiamine) is important for what?

A

catabolism of sugars and aminoacids

79
Q

Clinical consequence of thiamine def is seen first where?

A

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

80
Q

Causes of vit B1 (thiamine) def?

A
  • alcohol XS (alcoholics recommended to supplement)
  • malnutrition
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
82
Q

Vitamin B2?

A

aka riboflavin

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

83
Q

Consequences of Vit B2 (riboflavin) def?

A

angular cheilitis

84
Q

Vitamin B3?

A

aka niacin
Water soluble vitamin of B complex group.

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

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
87
Q

Consequences of Vit B3 (niacin) def?

A
  • pellagra= dermatitis, diarrhoea, dementia
88
Q

Vitamin B6?

A

aka pyridoxine

Water soluble vitamin of B complex group.

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

90
Q

Causes of Vit B6 (pyridoxine) def?

A

isoniazid therapy

91
Q

Consequences of Vit B6 (pyridoxine) def?

A
  • peripheral neuropathy
  • sideroblastic anaemia
92
Q

Vitamin C?

A

aka ascorbic acid

Water soluble

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
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).

95
Q

Features of Vit C (ascorbic acid) def?

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

What vitamins are water soluble?

A

B and C

97
Q

What is rifampicin used for?

A

TB

98
Q

MOA of rifampicin?

A

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

99
Q
A
100
Q

S/Es of rifampicin?

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

potent liver enzyme inducer

101
Q

What is isoniazid used for?

A

TB

102
Q

MOA of isoniazid?

A

inhibits mycolic acid synthesis

103
Q

S/Es of isoniazid?

A
  • peripheral neuropathy
  • hepatitis
  • agranulocytosis

liver enzyme inhibitor

104
Q

What must be given with isoniazid for TB?

A

pyridoxine (Vit B6) as prevents peripheral neuropathy

105
Q

What is pyrazinamide used for?

A

TB

106
Q

MOA of pyrazinamide?

A

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

107
Q

S/Es of pyrazinamide?

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

What is ethambutol used for?

A

TB

109
Q

MOA of ethambutol?

A

inhibits the enzyme arabinosyl transferase which polymerises arabinose into arabinan

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
A

FINALS (32 decks)

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