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J3 > Bane of my life > Flashcards

Bane of my life Flashcards

1
Q

What are the 3 broad categories of Anticoagulants?

A
  • Heparins and Fondaparinux
  • Oral warfarin – vitamin K antagonist,
  • Newer direct oral anticoagulants (DOACs)
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2
Q

Name 3 DOACs

A

o dabigatran
o apixaban
o rivaroxaban

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3
Q

Mechanism of action: Unfractionated Heparin

A
  • Enhances activity of antithrombin III (indirect IIa inhibitor)
  • Antithrombin III inhibits thrombin.
  • Heparins also inhibit multiple other factors of the coagulation cascade.
  • This produces its anticoagulant effect.
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4
Q

Indications: Unfractionated Heparin

A
  • Treatment and prophylaxis of thromboembolic diseases, including induction of vitamin K antagonists.
  • Renal dialysis (haemodialysis)
  • Acute Coronary Syndrome treatment
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5
Q

Mechanism of action: Warfarin

A
  • Inhibits vitamin K epoxide reductase.
  • Prevents recycling of vitamin K to reduced form after carboxylation of coagulation factors II, VII, IX and X.
  • Prevents thrombus formation.
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6
Q

Indications: Warfarin

A
  • Treatment of venous thromboembolism

* Thromboprophylaxis in: AF / metallic heart valves / cardiomyopathy

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7
Q

Mechanism of action: Dabigatran

A
  • Direct thrombin inhibitor; prevents conversion of fibrinogen to fibrin.
  • Factor IIa inhibitor
  • This prevents thrombus formation.

Remember: daBIgatran inhibits factor II (“BI”)

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8
Q

Indication(s): Dabigatran

A
  • Prophylaxis of venous thromboembolism (especially post-operative)
  • Thromboprophylaxis in non-valvular AF
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9
Q

Name 2 Factor Xa Antagonists

A

1) Rivaroxaban
2) Apixaban

Remember: RivaroXAban and ApiXAban are factor “Xa” inhibitors because they “ban” it

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10
Q

Mechanism of action: Rivaroxaban

A
  • Inhibits conversion of prothrombin to thrombin, reducing concentrations of thrombin in the blood.
  • This inhibits the formation of fibrin clots.
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11
Q

Indication(s): Rivaroxaban

A
  • Prophylaxis of venous thromboembolism (especially post-operative)
  • Thromboprophylaxis in non-valvular AF
  • Treatment of venous thromboembolism
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12
Q

Mechanism of action: Epixaban

A
  • Inhibits conversion of prothrombin to thrombin, reducing concentrations of thrombin in the blood.
  • This inhibits the formation of fibrin clots.
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13
Q

Indication(s): Epixaban

A
  • Prophylaxis of venous thromboembolism following hip or knee replacement surgery.
  • Thromboprophylaxis in non-valvular AF.
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14
Q

Mechanism of action: Aspirin (Acetylsalicylic acid)

A
  • Irreversible inactivation of cyclooxygenase (COX) enzyme.
  • This reduces production of platelet thromboxane (TXA2) and endothelial prostaglandin (PGI2)
  • Reduced thromboxane production reduces platelet aggregation and thrombus formation
  • Reduced prostaglandin synthesis decreases nociceptive sensitisation and inflammation.
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15
Q

Indication(s): aspirin

A
  • Secondary prevention of thrombotic events

* Pain relief

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16
Q

Mechanism of action: Clopidogrel

A
  • Irreversibly blocks the ADP-receptor on platelet cell membranes.
  • Consequently inhibits formation of GPIIb/IIIa complex, required for platelet aggregation.
  • Decreased thrombus formation.
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17
Q

Indication(s): Clopidogrel

A

Secondary prevention of thrombotic events

Clopidogrel is not given after PCI.

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18
Q

Mechanism of action: Ticagrelor

A

Prevents platelet activation and aggregation.

Ticagrelor is an antagonist of the P2Y₁₂ receptor.

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19
Q

Indication(s): Ticagrelor

A

Used in combination with aspirin for the prevention of atherothrombotic events in patients with acute coronary syndrome

prevents re-infarction post-MI, in addition to aspirin

Shown to improve outcome compared to clopidogrel in acute coronary syndrome. Clopidogrel is not given after PCI.

Ticagrelor, in combination with low-dose aspirin, is recommended for up to 12 months as a treatment option in adults with acute coronary syndromes

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20
Q

Contraindications: Ticagrelor

A

Active bleeding
history of intracranial haemorrhage
patients taking warfarin
patients weighing <60kg

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21
Q

Classes of fibrinolytic drugs

A

1) Kinases
I. Streptokinase
II. Urokinase

2) Tissue plasminogen activators (tPA)
III. Alteplase
IV. Tenecteplase
V. Reteplase

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22
Q

Mechanism of action: Tenecteplase/Alteplase

A
  • Recombinant form of tissue plasminogen activator
  • Catalyses conversion of plasminogen to plasmin
  • Promotes fibrin clot lysis
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23
Q

Indication(s): Tenecteplase/Alteplase

A
  • Acute ischaemic stroke within 4.5 hours of onset
  • Myocardial infarction within 12 hours of onset
  • Massive pulmonary embolism
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24
Q

Name 2 Cardioselective Beta-Blockers

A
  • Bisoprolol

* Atenolol

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25
Q

Mechanism of action: Bisoprolol/Atenolol

A
  • blocks beta-1 receptors in cardiac and renal tissue.
  • Inhibits sympathetic stimulation of the heart and renal vasculature.
  • Blockade of SAN reduces HR (negative chronotrope)
  • blockade of receptors in the myocardium depresses cardiac contractility (negative inotrope)
  • blockade of beta-1 adrenoceptors in renal tissue inhibits the release of renin
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26
Q

Indication(s): Bisoprolol/Atenolol

A
  • Hypertension
  • Angina
  • Rate-control in atrial fibrillation

• Bisoprolol may be used as part of supportive therapy for mild / moderate heart failure

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27
Q

Name 2 Non-Cardioselective Beta-Blockers

A
  • Propranolol

* Carvedilol

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28
Q

Mechanism of action: Propanolol

A

Non-cardioselective beta-1-adrenoceptor antagonist.

Inhibits sympathetic stimulation in the heart

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29
Q

Mechanism of action: Carvedilol

A

Non-selective beta-1, beta-2 and alpha-1-adrenergic receptor antagonistic effects.

Inhibits sympathetic stimulation in the heart and vascular smooth muscle.

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30
Q

Indication(s): Propanolol/Carvedilol

A
  • Hypertension
  • Angina
  • Anxiety
  • Migraine prophylaxis
  • Post-MI prophylaxis

Carvedilol may be used as part of supportive therapy for mild / moderate heart failure

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31
Q

Contraindication(s): Propanolol/Carvedilol

A

diabetic patients – risk of deranged carbohydrate metabolism

Asthma and COPD – risk of bronchospasm

Do not combine Beta-Blockers with rate-limiting Ca2+-Channel-Blockers (Verapamil / Diltiazem) in anti-hypertensive therapy (risk of heart block)

Propanolol is lipid-soluble and is predominantly cleared by the liver. Avoid in liver impairment. Avoid abrupt withdrawal – risk of liver impairment.

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32
Q

Name 3 ACE Inhibitors

A
  • Ramipril
  • Enalapril
  • Lisinopril
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33
Q

Mechanism of action: ACEi

A
  • Inhibits conversion of Angiotensin I to Angiotensin II (a more potent systemic vasoconstrictor).
  • This subsequently inhibits Aldosterone release from the adrenal cortex, depressing renal sodium and fluid retention, thereby decreasing blood volume.
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34
Q

Indication(s): ACEi

A
  • Hypertension
  • Heart Failure
  • Nephropathy
  • Prevention of Cardiovascular events in high risk patients
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35
Q

Name 2 Nitrates

A
  • Isosorbide Mononitrate

* Glyceryl Trinitrate (GTN)

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36
Q

Mechanism of action: Nitrates

A

Converted to Nitric Oxide (NO), a potent vasodilator.

Cardioselective, acting predominantly on coronary blood vessels, enhancing flow of blood to ischaemic areas of the myocardium.

Reduces myocardial oxygen consumption by reducing cardiac preload and afterload.

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37
Q

Indication(s): Nitrates

A
  • Treatment of Angina

* Severe hypertension (intravenous GTN is sometimes used in this setting)

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38
Q

Name 2 Rate-limiting Calcium Channel Blockers

A
  • Verapamil

* Diltiazem

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39
Q

Mechanism of action: Verapamil/Diltiazem

A

Prevent cellular entry of Ca2+ by blocking L-type calcium channels.

Myocardial and Smooth muscle contractility depressed. Cardiac contractility will be reduced.

Dilate coronary blood vessels and reduce afterload.

Antidysrhythmic actions due to prolonged atrioventricular node conduction – depresses heart rate.

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40
Q

Indication(s): Verapamil/Diltiazem

A
  • Supraventricular arrhythmias
  • Treatment of angina
  • Hypertension
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41
Q

Contraindication(s): Verapamil/Diltiazem

A

heart failure and left ventricular dysfunction due to potent negative inotropy.

Avoid in bradycardia and hypotension.

Do not use with beta-blockers.

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42
Q

Name 2 Non Rate-limiting Calcium Channel Blockers

A
  • Amlodipine

* Nifedipine

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43
Q

Mechanism of action: Amlodipine

A

Prevents cellular entry of Ca2+ by blocking L-type calcium channels.

Myocardial and smooth muscle contractility depressed – mainly affects smooth muscle.

Dilates coronary blood vessels and reduce afterload

Does not lower heart rate (heart rate may increase)

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44
Q

Indication(s): Amlodipine

A
  • Hypertension

* Treatment of Angina

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45
Q

Name 2 HMG CoA Reductase Inhibitors

A
  • Simvastatin

* Atorvastatin

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46
Q

Mechanism of action: statins

A

Competitively inhibits HMG CoA Reductase; the rate-determining enzyme in the synthesis of cholesterol.

This causes an increase in LDL-receptor expression, on the surface of hepatocytes.

Increases hepatic uptake of cholesterol, reducing plasma cholesterol levels.

Reduces development of atherosclerotic plaques.

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47
Q

Indication(s): statins

A

Familial hypercholesterolaemia

Prevention of cardiovascular events in high-risk patients.

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48
Q

Mechanism of action: Digoxin

A

Inhibits the Na+/K+ pump, causing a buildup of Na+ intracellularly.

In an effort to remove Na+, more Ca2+ is brought into the cell by the action of Na+/Ca2+ exchangers.

The buildup of Ca2+ is responsible for the increased force of contraction and reduced rate of conduction through the AV node.

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49
Q

Indication(s): Digoxin

A
  • Heart Failure

* Rate control in Atrial fibrillation

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50
Q

Name an Anti-Arrhythmic Drug

A

Amiodarone

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51
Q

Mechanism of action: Amiodarone

A

Amiodarone blocks cardiac K+ channels, prolonging repolarization of the cardiac action potential.

Restores regular sinus rhythm.

slows atrioventricular nodal conduction.

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52
Q

Indication(s): Amiodarone

A

Supraventricular / ventricular arrhythmias.

NB: can affect thyroid gland due to high iodine content

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53
Q

Name 4 penicillins

A
  • Flucloxacillin
  • Amoxicillin
  • Benzylpenicillin
  • Penicillin V
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54
Q

Mechanism of action: penicillins

A

Attaches to penicillin-binding-proteins on forming bacterial cell walls.

This inhibits the transpeptidase enzyme which cross-links the bacterial cell wall.

Failure to cross-link induces bacterial cell autolysis.

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55
Q

Indication(s): penicillins

A

Flucloxacillin provides Staphylococcus aureus cover, amoxicillin does not

Amoxicillin provides some amount of gram-negative cover in addition to gram-positive drugs

Flucloxacillin:
• Soft tissue infection
• Staphylococcal endocarditis
• Otitis externa

Amoxicillin:
• Non-severe community acquired pneumonia

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56
Q

Name a Cephalosporin

A

• Ceftriaxone

57
Q

Mechanism of action: Ceftriaxone

A

Attaches to penicillin-binding-proteins on forming bacterial cell walls.

This inhibits the transpeptidase enzyme which cross-links the bacterial cell wall.

Failure to cross-link induces bacterial cell autolysis.

Less susceptible to beta-lactamases than penicillins

58
Q

Indication(s): Ceftriaxone

A

Serious infection: septicaemia / pneumonia / meningitis

Provides both gram-positive and gram-negative cover.

NB: very C. differgic!

59
Q

Name a Glycopeptide

A

Vancomycin

60
Q

Mechanism of action: Vancomycin

A

Bactericidal

Inhibits cell-wall synthesis in Gram positive bacteria.

61
Q

Indication(s): Vancomycin

A
  • Severe gram positive infections
  • MRSA
  • Severe Clostridium difficile infection
62
Q

Side Effects: Vancomycin

A

Nephrotoxicity
Ototoxicity (rare)
red-man syndrome

Remember: red man in the van

narrow therapeutic range, therapeutic drug monitoring is necessary

63
Q

Name an Aminoglycoside

A

Gentamicin

64
Q

Mechanism of action: Gentamicin

A

Binds to 30s ribosomal subunit, inhibiting protein synthesis. This induces a prolonged post-antibiotic bacteriostatic effect.

bactericidal action on bacterial cell wall results in rapid killing early in dosing interval and is prominent at high doses.

provides a synergistic effect when used alongside other antibiotics (such as flucloxacillin or vancomycin in gram-positive infections).

65
Q

Indication(s): Gentamicin

A

Severe gram-negative infections (such as biliary tract infection, pyelonephritis, hospital-acquired pneumonia).

Some severe gram-positive infections (such as soft tissue infection and endocarditis).

66
Q

Gentamicin dosing

A

Give high initial dose to take advantage of rapid killing

Leave long dosing interval to minimise toxicity

Measure trough level to ensure gentamicin is not accumulating. Only prescribe further doses once this is confirmed.

limit use to approximately 3 days to minimise risk of side-effects.

67
Q

Name a Quinolone

A

Ciprofloxacin

68
Q

Mechanism of action: Ciprofloxacin

A

Interferes with bacterial DNA replication and repair.

69
Q

Indication(s): Ciprofloxacin

A

Broad-spectrum bactericidal antibiotic

provides both gram-positive and gram-negative cover.

  • Gram negative bacterial infection
  • Respiratory tract infection
  • Upper urinary tract infection
  • Peritoneal infection
  • Gonorrhoea
  • Prostatitis
70
Q

Name 2 Macrolides

A

Erythromycin

Clarithromycin

71
Q

Mechanism of action: Macrolides

A
  • Bind to 50s ribosomal subunit

* Inhibit bacterial protein synthesis.

72
Q

Indication(s): Macrolides

A
  • Atypical organisms causing pneumonia / Severe CAP
  • Severe campylobacter infection
  • Mild / moderate skin and soft-tissue infection
  • Otitis media
  • Lyme disease
  • Helicobacter pylori eradication therapy
73
Q

Name an Inhibitor of Folate Synthesis

A

Trimethoprim

74
Q

Mechanism of Action: Trimethoprim

A

Inhibits folate metabolism pathway
leads to impaired nucleotide synthesis

Therefore interferes with bacterial DNA replication.

75
Q

Indication(s): Trimethoprim

A
  • First line antibiotic in uncomplicated UTI.
  • Acute / chronic bronchitis
  • Pneumocystis pneumonia (PCP)
  • Good range of action against gram -/+ bacteria. Including some MRSA cover.

• Avoid in the first trimester of pregnancy

76
Q

Name an Anti-Viral

A

acyclovir

77
Q

Mechanism of Action: acyclovir

A

inhibits DNA polymerase, terminating the nucleotide chain and inhibiting viral DNA replication.

guanosine derivative
converted to triphosphate by infected host cells.

78
Q

Indication(s): acyclovir

A
  • Herpes simplex infection

* Varicella zoster infection

79
Q

Name a short-acting Beta-Adrenergic Bronchodilator

A

Salbutamol

80
Q

Mechanism of action: Salbutamol

A

Short-acting Beta-2 adrenoceptor agonists (SABA)

Relaxes bronchial smooth muscle –> bronchodilation.

Inhibits pro-inflammatory cytokine release from mast cells and TNF-α release from monocytes, reducing airway inflammation.

Increase mucus clearance from the airways by stimulating cilia action.

81
Q

Indication(s): Salbutamol

A
  • Asthma

* COPD

82
Q

Name a long-acting Beta-Adrenergic Bronchodilator

A

Salmeterol

83
Q

Mechanism of action: Salmeterol

A

long-acting Beta-2 adrenoceptor agonists (SABA)

Relaxes bronchial smooth muscle –> bronchodilation.

Inhibits pro-inflammatory cytokine release from mast cells and TNF-α release from monocytes, reducing airway inflammation.

Increase mucus clearance from the airways by stimulating cilia action.

84
Q

Indication(s): Salmeterol

A
  • Asthma

* COPD

85
Q

Name 2 Anti-Muscarinic Bronchodilators

A
  • Tiotropium

* Ipratropium Bromide

86
Q

Mechanism of action: Anti-Muscarinic Bronchodilators

A

M3 antagonists

produce bronchodilatory effects.

Reduce mucus secretion and may increase bronchial mucus clearance by stimulating cilia

87
Q

Indication(s): Anti-Muscarinic Bronchodilators

A
  • Asthma
  • COPD
  • Rhinitis
88
Q

Name an Inhaled Corticosteroid

A

Beclomethasone

89
Q

Mechanism of action: Beclomethasone

A
  • Anti-inflammatory effect on the airways.
  • Decrease formation of pro-inflammatory cytokines.
  • Up-regulates beta-2-adrenoreceptors in airways
90
Q

Indication(s): Beclomethasone

A

COPD

Asthma

91
Q

Name two H1 receptor antagonists

A
  • Chlorpheniramine

* Fexofenadine

92
Q

Mechanism of action: Chlorpheniramine

A
  • Antihistamine; H1 receptor antagonist.

* Inhibits histamine-mediated contraction of the bronchial smooth muscle.

93
Q

Indication(s): H1 receptor antagonists

A
  • Anaphylaxis
  • Hay fever
  • Urticaria
  • Sedation
94
Q

What are Seretide and Symbicort?

A

inhaled preparations used in COPD and asthma containing both inhaled steroids and long acting bronchodilators

95
Q

Name an oral steroid that is used as an immunomodulator

A

Prednisolone

96
Q

Mechanism of action: Prednisolone

A

Bind to glucocorticoid receptors, which causes:

1) up-regulation of anti-inflammatory mediators
2) down regulation of pro-inflammatory mediators.

This provides immunosupression

97
Q

Indication(s): Prednisolone

A

Replacement therapy in adrenal insufficiency

Post-transplantion immunosupression

Treatment of exacerbations many inflammatory conditions (including eczema, RA, IBD, and MS).

Treatment of acute asthma

98
Q

Mechanism of action: Etanercept

A
  • Anti-TNF-α and anti-TNF-β
  • Blocks its interactions with TNF cell receptors
  • Reduces inflammation
99
Q

Indication(s): Etanercept

A
  • Rheumatoid arthritis
  • Psoriatic arthritis
  • Ankylosing spondylitis
  • Juvenile arthritis
100
Q

Which infections are patients on Etanercept predisposed to?

A

reactivation of latent TB –> disseminated TB
legionella
listeria

101
Q

Mechanism of action: Methotrexate

A

stops the action of the enzyme dihydrofolate needed for production of DNA

thereby disrupts DNA synthesis

supplementation with folic acid is important to prevent deficiency

102
Q

Indication(s): Methotrexate

A
  • Post transplantation immunosuppression
  • Inflammatory bowel disease
  • Renal vasculitis
  • Paediatric leukaemia (methotrexate is used)
103
Q

Mechanism of action: Azathioprine

A
  • Disrupt DNA synthesis

* blocks purine synthesis, mainly in lymphocytes

104
Q

Indication(s): Azathioprine

A
  • Post transplantation immunosuppression
  • Inflammatory bowel disease
  • Renal vasculitis
105
Q

Mechanism of action: Codeine

A

Opioid receptor agonist; acts on mu, kappa and delta on presynaptic neurones.

This gives numerous effects that increase nociceptive thresholds throughout the central and peripheral nervous system.

Metabolised to morphine, which is responsible for analgesic effects.

106
Q

Indication(s): Codeine

A
  • Mild to moderate pain
  • Persistent dry cough
  • Diarrhoea
107
Q

Mechanism of action: Morphine

A

Opioid receptor agonist; acts on mu, kappa and delta on presynaptic neurones.

This gives numerous effects that increase nociceptive thresholds throughout the central and peripheral nervous system.

108
Q

Indication(s): morphine

A
  • Acute severe pain (including in setting of myocardial infarction)
  • Acute pulmonary oedema
  • Chronic pain
109
Q

Mechanism of action: oxycodone

A

Opioid receptor agonist; acts on mu, kappa and delta on presynaptic neurones.

This gives numerous effects that increase nociceptive thresholds throughout the central and peripheral nervous system.

110
Q

Indication(s): oxycodone

A
  • Moderate to severe pain relief in cancer patients
  • Postoperative pain
  • Severe pain
111
Q

Name 2 NSAIDs

A
  • Ibuprofen

* Diclofenac

112
Q

Mechanism of action: NSAIDs

A

Non-selective inhibition of cyclo-oxygenase (COX 1 and 2) enzymes, decreasing prostaglandin synthesis

Thereby reduces pain, inflammation and swelling.

113
Q

Indication(s): NSAIDs

A
  • Mild to moderate pain relief
  • Rheumatic disorders (such as rheumatoid arthritis and osteoarthritis)
  • Fever (anti-pyretic effect)
114
Q

Mechanism of action: Celecoxib

A
  • Selective inhibitor of COX-2

* reduces pain, inflammation and swelling.

115
Q

Indication(s): Celecoxib

A

• Pain and inflammation in: osteoarthritis / rheumatoid arthritis / ankylosing spondylitis

116
Q

Mechanism of action: Paracetamol

A
  • A weak cyclooxygenase (COX) inhibitor with selectivity for brain COX.
  • lacks peripheral anti-inflammatory actions but inhibits prostaglandin synthesis and its effects centrally.
117
Q

Indication(s): paracetamol

A
  • Mild to moderate pain relief

* Fever (anti-pyretic effect)

118
Q

Mechanism of action: allopurinol

A
  • Reduces synthesis of uric acid by competitively inhibiting xanthine oxidase.
  • Reduces serum uric acid level
119
Q

Indication(s): allopurinol

A
  • Prophylaxis of gout
  • Prophylaxis of calcium oxalate renal stones
  • Hyperuricaemia associated with cancer chemotherapy
120
Q

Name 2 Thiazide Diuretics

A
  • Bendroflumethazide

* Indapamide

121
Q

Mechanism of action: Thiazide Diuretics

A
  • Inhibit Na+/Cl- transporter at the distal convoluted tubule and collecting duct
  • Increases Na+, Cl- and water excretion
122
Q

Indication(s): Thiazide Diuretics

A
  • Hypertension

* Oedema

123
Q

Name 2 Loop Diuretics

A
  • Furosemide

* Bumetanide

124
Q

Mechanism of action: Loop Diuretics

A
  • Na+/Cl-/K+ symporter antagonists
  • Act on the thick ascending loop of Henle
  • Increase secretion of Na+, K+, Cl- and water
125
Q

Indication(s): Loop Diuretics

A
  • Hypertension
  • Hyperkalaemia
  • Heart failure
  • Cirrhosis of liver (fluid retention)
  • Nephrotic syndrome
126
Q

Mechanism of action: Omeprazole

A

Bind to H+/K+ ATPase pump on gastric parietal cells

Reduces HCl production and hence reduced gastric acidity

127
Q

Indication(s): Omeprazole

A
  • Peptic ulcers
  • GORD
  • H.Pylori infection
  • Prophylaxis in patients receiving long term NSAIDs
128
Q

Mechanism of action: Ranitidine

A

antagonises the effect of histamine at H2 receptors on gastric parietal cells

Reduced cAMP and thereby reduced activity of H+/K+ ATPase pump

reduces gastric acid secretion

129
Q

Indication(s): Ranitidine

A
  • Peptic ulcer

* GORD

130
Q

Name 2 laxative drugs

A
  • Lactulose

* Senna

131
Q

Mechanism of action: Lactulose

A

Bulk producing agent

reduces water reabsorption in intestine

pulls water into the bowel and thus promotes distention and movement

132
Q

Mechanism of action: Senna

A

stimulant / irritant agent

acts on intestinal mucosa and alters water and electrolyte secretion

133
Q

Name 3 anti-emetic drugs

A

Cyclizine
Metoclopramide
Prochlorperazine

134
Q

Mechanism of action: Cyclizine

A
  • Histamine H1 receptor antagonist
  • Acts on vomiting centre in the medullary region
  • Mild anti-cholinergic and anti-muscarinic effects
135
Q

Indication(s): Cyclizine

A
  • Nausea and vomiting
  • Motion sickness
  • Vertigo and dizziness
  • Prophylaxis alongside chemotherapy and opiate analgesic use
136
Q

Mechanism of action: Metoclopramide

A
  • Dopamine (D2) receptor antagonist
  • Also increases gastric emptying and intestinal transit
  • Reduced oesophageal reflux
137
Q

Indication(s): Metoclopramide

A
  • Nausea
  • Vomiting
  • To increase gastric emptying
138
Q

Mechanism of action: Prochlorperazine

A

• Dopamine (D2) receptor antagonist

139
Q

Indication(s): Prochlorperazine

A
  • Nausea and vomiting

* Used as an adjunct in some psychotic disorders

J3 (18 decks)

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