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)
2
Q
Name 3 DOACs
A
o dabigatran
o apixaban
o rivaroxaban
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.
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
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.
6
Q
Indications: Warfarin
A
- Treatment of venous thromboembolism
* Thromboprophylaxis in: AF / metallic heart valves / cardiomyopathy
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”)
8
Q
Indication(s): Dabigatran
A
- Prophylaxis of venous thromboembolism (especially post-operative)
- Thromboprophylaxis in non-valvular AF
9
Q
Name 2 Factor Xa Antagonists
A
1) Rivaroxaban
2) Apixaban
Remember: RivaroXAban and ApiXAban are factor “Xa” inhibitors because they “ban” it
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.
11
Q
Indication(s): Rivaroxaban
A
- Prophylaxis of venous thromboembolism (especially post-operative)
- Thromboprophylaxis in non-valvular AF
- Treatment of venous thromboembolism
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.
13
Q
Indication(s): Epixaban
A
- Prophylaxis of venous thromboembolism following hip or knee replacement surgery.
- Thromboprophylaxis in non-valvular AF.
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.
15
Q
Indication(s): aspirin
A
- Secondary prevention of thrombotic events
* Pain relief
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.
17
Q
Indication(s): Clopidogrel
A
Secondary prevention of thrombotic events
Clopidogrel is not given after PCI.
18
Q
Mechanism of action: Ticagrelor
A
Prevents platelet activation and aggregation.
Ticagrelor is an antagonist of the P2Y₁₂ receptor.
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
20
Q
Contraindications: Ticagrelor
A
Active bleeding
history of intracranial haemorrhage
patients taking warfarin
patients weighing <60kg
21
Q
Classes of fibrinolytic drugs
A
1) Kinases
I. Streptokinase
II. Urokinase
2) Tissue plasminogen activators (tPA)
III. Alteplase
IV. Tenecteplase
V. Reteplase
22
Q
Mechanism of action: Tenecteplase/Alteplase
A
- Recombinant form of tissue plasminogen activator
- Catalyses conversion of plasminogen to plasmin
- Promotes fibrin clot lysis
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
24
Q
Name 2 Cardioselective Beta-Blockers
A
- Bisoprolol
* Atenolol
25
Mechanism of action: Bisoprolol/Atenolol
* 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
26
Indication(s): Bisoprolol/Atenolol
* Hypertension
* Angina
* Rate-control in atrial fibrillation
• Bisoprolol may be used as part of supportive therapy for mild / moderate heart failure
27
Name 2 Non-Cardioselective Beta-Blockers
* Propranolol
| * Carvedilol
28
Mechanism of action: Propanolol
Non-cardioselective beta-1-adrenoceptor antagonist.
Inhibits sympathetic stimulation in the heart
29
Mechanism of action: Carvedilol
Non-selective beta-1, beta-2 and alpha-1-adrenergic receptor antagonistic effects.
Inhibits sympathetic stimulation in the heart and vascular smooth muscle.
30
Indication(s): Propanolol/Carvedilol
* Hypertension
* Angina
* Anxiety
* Migraine prophylaxis
* Post-MI prophylaxis
Carvedilol may be used as part of supportive therapy for mild / moderate heart failure
31
Contraindication(s): Propanolol/Carvedilol
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.
32
Name 3 ACE Inhibitors
* Ramipril
* Enalapril
* Lisinopril
33
Mechanism of action: ACEi
* 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.
34
Indication(s): ACEi
* Hypertension
* Heart Failure
* Nephropathy
* Prevention of Cardiovascular events in high risk patients
35
Name 2 Nitrates
* Isosorbide Mononitrate
| * Glyceryl Trinitrate (GTN)
36
Mechanism of action: Nitrates
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.
37
Indication(s): Nitrates
* Treatment of Angina
| * Severe hypertension (intravenous GTN is sometimes used in this setting)
38
Name 2 Rate-limiting Calcium Channel Blockers
* Verapamil
| * Diltiazem
39
Mechanism of action: Verapamil/Diltiazem
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.
40
Indication(s): Verapamil/Diltiazem
* Supraventricular arrhythmias
* Treatment of angina
* Hypertension
41
Contraindication(s): Verapamil/Diltiazem
heart failure and left ventricular dysfunction due to potent negative inotropy.
Avoid in bradycardia and hypotension.
Do not use with beta-blockers.
42
Name 2 Non Rate-limiting Calcium Channel Blockers
* Amlodipine
| * Nifedipine
43
Mechanism of action: Amlodipine
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)
44
Indication(s): Amlodipine
* Hypertension
| * Treatment of Angina
45
Name 2 HMG CoA Reductase Inhibitors
* Simvastatin
| * Atorvastatin
46
Mechanism of action: statins
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.
47
Indication(s): statins
Familial hypercholesterolaemia
Prevention of cardiovascular events in high-risk patients.
48
Mechanism of action: Digoxin
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.
49
Indication(s): Digoxin
* Heart Failure
| * Rate control in Atrial fibrillation
50
Name an Anti-Arrhythmic Drug
Amiodarone
51
Mechanism of action: Amiodarone
Amiodarone blocks cardiac K+ channels, prolonging repolarization of the cardiac action potential.
Restores regular sinus rhythm.
slows atrioventricular nodal conduction.
52
Indication(s): Amiodarone
Supraventricular / ventricular arrhythmias.
NB: can affect thyroid gland due to high iodine content
53
Name 4 penicillins
* Flucloxacillin
* Amoxicillin
* Benzylpenicillin
* Penicillin V
54
Mechanism of action: penicillins
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.
55
Indication(s): penicillins
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
56
Name a Cephalosporin
• Ceftriaxone
57
Mechanism of action: Ceftriaxone
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
Indication(s): Ceftriaxone
Serious infection: septicaemia / pneumonia / meningitis
Provides both gram-positive and gram-negative cover.
NB: very C. differgic!
59
Name a Glycopeptide
Vancomycin
60
Mechanism of action: Vancomycin
Bactericidal
Inhibits cell-wall synthesis in Gram positive bacteria.
61
Indication(s): Vancomycin
* Severe gram positive infections
* MRSA
* Severe Clostridium difficile infection
62
Side Effects: Vancomycin
Nephrotoxicity
Ototoxicity (rare)
red-man syndrome
Remember: red man in the van
narrow therapeutic range, therapeutic drug monitoring is necessary
63
Name an Aminoglycoside
Gentamicin
64
Mechanism of action: Gentamicin
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
Indication(s): Gentamicin
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
Gentamicin dosing
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
Name a Quinolone
Ciprofloxacin
68
Mechanism of action: Ciprofloxacin
Interferes with bacterial DNA replication and repair.
69
Indication(s): Ciprofloxacin
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
Name 2 Macrolides
Erythromycin
| Clarithromycin
71
Mechanism of action: Macrolides
* Bind to 50s ribosomal subunit
| * Inhibit bacterial protein synthesis.
72
Indication(s): Macrolides
* 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
Name an Inhibitor of Folate Synthesis
Trimethoprim
74
Mechanism of Action: Trimethoprim
Inhibits folate metabolism pathway
leads to impaired nucleotide synthesis
Therefore interferes with bacterial DNA replication.
75
Indication(s): Trimethoprim
* 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
Name an Anti-Viral
acyclovir
77
Mechanism of Action: acyclovir
inhibits DNA polymerase, terminating the nucleotide chain and inhibiting viral DNA replication.
guanosine derivative
converted to triphosphate by infected host cells.
78
Indication(s): acyclovir
* Herpes simplex infection
| * Varicella zoster infection
79
Name a short-acting Beta-Adrenergic Bronchodilator
Salbutamol
80
Mechanism of action: Salbutamol
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
Indication(s): Salbutamol
* Asthma
| * COPD
82
Name a long-acting Beta-Adrenergic Bronchodilator
Salmeterol
83
Mechanism of action: Salmeterol
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
Indication(s): Salmeterol
* Asthma
| * COPD
85
Name 2 Anti-Muscarinic Bronchodilators
* Tiotropium
| * Ipratropium Bromide
86
Mechanism of action: Anti-Muscarinic Bronchodilators
M3 antagonists
produce bronchodilatory effects.
Reduce mucus secretion and may increase bronchial mucus clearance by stimulating cilia
87
Indication(s): Anti-Muscarinic Bronchodilators
* Asthma
* COPD
* Rhinitis
88
Name an Inhaled Corticosteroid
Beclomethasone
89
Mechanism of action: Beclomethasone
* Anti-inflammatory effect on the airways.
* Decrease formation of pro-inflammatory cytokines.
* Up-regulates beta-2-adrenoreceptors in airways
90
Indication(s): Beclomethasone
COPD
| Asthma
91
Name two H1 receptor antagonists
* Chlorpheniramine
| * Fexofenadine
92
Mechanism of action: Chlorpheniramine
* Antihistamine; H1 receptor antagonist.
| * Inhibits histamine-mediated contraction of the bronchial smooth muscle.
93
Indication(s): H1 receptor antagonists
* Anaphylaxis
* Hay fever
* Urticaria
* Sedation
94
What are Seretide and Symbicort?
inhaled preparations used in COPD and asthma containing both inhaled steroids and long acting bronchodilators
95
Name an oral steroid that is used as an immunomodulator
Prednisolone
96
Mechanism of action: Prednisolone
Bind to glucocorticoid receptors, which causes:
1) up-regulation of anti-inflammatory mediators
2) down regulation of pro-inflammatory mediators.
This provides immunosupression
97
Indication(s): Prednisolone
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
Mechanism of action: Etanercept
* Anti-TNF-α and anti-TNF-β
* Blocks its interactions with TNF cell receptors
* Reduces inflammation
99
Indication(s): Etanercept
* Rheumatoid arthritis
* Psoriatic arthritis
* Ankylosing spondylitis
* Juvenile arthritis
100
Which infections are patients on Etanercept predisposed to?
reactivation of latent TB --> disseminated TB
legionella
listeria
101
Mechanism of action: Methotrexate
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
Indication(s): Methotrexate
* Post transplantation immunosuppression
* Inflammatory bowel disease
* Renal vasculitis
* Paediatric leukaemia (methotrexate is used)
103
Mechanism of action: Azathioprine
* Disrupt DNA synthesis
| * blocks purine synthesis, mainly in lymphocytes
104
Indication(s): Azathioprine
* Post transplantation immunosuppression
* Inflammatory bowel disease
* Renal vasculitis
105
Mechanism of action: Codeine
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
Indication(s): Codeine
* Mild to moderate pain
* Persistent dry cough
* Diarrhoea
107
Mechanism of action: Morphine
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
Indication(s): morphine
* Acute severe pain (including in setting of myocardial infarction)
* Acute pulmonary oedema
* Chronic pain
109
Mechanism of action: oxycodone
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
Indication(s): oxycodone
* Moderate to severe pain relief in cancer patients
* Postoperative pain
* Severe pain
111
Name 2 NSAIDs
* Ibuprofen
| * Diclofenac
112
Mechanism of action: NSAIDs
Non-selective inhibition of cyclo-oxygenase (COX 1 and 2) enzymes, decreasing prostaglandin synthesis
Thereby reduces pain, inflammation and swelling.
113
Indication(s): NSAIDs
* Mild to moderate pain relief
* Rheumatic disorders (such as rheumatoid arthritis and osteoarthritis)
* Fever (anti-pyretic effect)
114
Mechanism of action: Celecoxib
* Selective inhibitor of COX-2
| * reduces pain, inflammation and swelling.
115
Indication(s): Celecoxib
• Pain and inflammation in: osteoarthritis / rheumatoid arthritis / ankylosing spondylitis
116
Mechanism of action: Paracetamol
* A weak cyclooxygenase (COX) inhibitor with selectivity for brain COX.
* lacks peripheral anti-inflammatory actions but inhibits prostaglandin synthesis and its effects centrally.
117
Indication(s): paracetamol
* Mild to moderate pain relief
| * Fever (anti-pyretic effect)
118
Mechanism of action: allopurinol
* Reduces synthesis of uric acid by competitively inhibiting xanthine oxidase.
* Reduces serum uric acid level
119
Indication(s): allopurinol
* Prophylaxis of gout
* Prophylaxis of calcium oxalate renal stones
* Hyperuricaemia associated with cancer chemotherapy
120
Name 2 Thiazide Diuretics
* Bendroflumethazide
| * Indapamide
121
Mechanism of action: Thiazide Diuretics
* Inhibit Na+/Cl- transporter at the distal convoluted tubule and collecting duct
* Increases Na+, Cl- and water excretion
122
Indication(s): Thiazide Diuretics
* Hypertension
| * Oedema
123
Name 2 Loop Diuretics
* Furosemide
| * Bumetanide
124
Mechanism of action: Loop Diuretics
* Na+/Cl-/K+ symporter antagonists
* Act on the thick ascending loop of Henle
* Increase secretion of Na+, K+, Cl- and water
125
Indication(s): Loop Diuretics
* Hypertension
* Hyperkalaemia
* Heart failure
* Cirrhosis of liver (fluid retention)
* Nephrotic syndrome
126
Mechanism of action: Omeprazole
Bind to H+/K+ ATPase pump on gastric parietal cells
Reduces HCl production and hence reduced gastric acidity
127
Indication(s): Omeprazole
* Peptic ulcers
* GORD
* H.Pylori infection
* Prophylaxis in patients receiving long term NSAIDs
128
Mechanism of action: Ranitidine
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
Indication(s): Ranitidine
* Peptic ulcer
| * GORD
130
Name 2 laxative drugs
* Lactulose
| * Senna
131
Mechanism of action: Lactulose
Bulk producing agent
reduces water reabsorption in intestine
pulls water into the bowel and thus promotes distention and movement
132
Mechanism of action: Senna
stimulant / irritant agent
acts on intestinal mucosa and alters water and electrolyte secretion
133
Name 3 anti-emetic drugs
Cyclizine
Metoclopramide
Prochlorperazine
134
Mechanism of action: Cyclizine
* Histamine H1 receptor antagonist
* Acts on vomiting centre in the medullary region
* Mild anti-cholinergic and anti-muscarinic effects
135
Indication(s): Cyclizine
* Nausea and vomiting
* Motion sickness
* Vertigo and dizziness
* Prophylaxis alongside chemotherapy and opiate analgesic use
136
Mechanism of action: Metoclopramide
* Dopamine (D2) receptor antagonist
* Also increases gastric emptying and intestinal transit
* Reduced oesophageal reflux
137
Indication(s): Metoclopramide
* Nausea
* Vomiting
* To increase gastric emptying
138
Mechanism of action: Prochlorperazine
• Dopamine (D2) receptor antagonist
139
Indication(s): Prochlorperazine
* Nausea and vomiting
| * Used as an adjunct in some psychotic disorders
