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Year 3 Drugs > Cardiovascular Drugs > Flashcards

Cardiovascular Drugs Flashcards

1
Q

Loop diuretics name

A

Furosemide, bumetanide

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2
Q

Loop diuretics indications

A
  1. Relief of breathlessness in acute pulmonary oedema in conjunction with oxygen and nitrates
  2. Symptomatic treatment of fluid overload in chronic heart failure
  3. Symptomatic treatment of fluid overload in other oedematous states: renal / hepatic disease - given in combination with other diuretics
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3
Q

Loop diuretics MOA

A
  • Act on ascending limb of Henlé
  • Inhibit Na+/K+/2Cl- co-transporter.
  • This normally transports sodium potassium and chloride ions from tubular lumen into epithelial cell, allowing water to follow by osmosis
  • Inhibiting this process leaves water in the lumen
  • Water then excreted in urine
  • Also cause dilation of capacitance veins - in HF this reduces preload and improves contractile function of overstretched cardiac muscle
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4
Q

Loop diuretics administration

A

IV: for acute pulmonary oedema - administered slowly
Oral: BD

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5
Q

Loop diuretics contraindications

A
  1. Severe dehydration or hypovolemia
  2. Caution in hepatic encephalopathy, hypokalaemia and hyponatraemia
  3. Gout: inhibit uric acid excretion so can worsen
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6
Q

Loop diuretics side effects

A
  • Diuresis can lead to dehydration and hypotension
  • Inhibiting Na+/K+/Cl- transporter increases urinary losses of sodium / potassium / chloride.
  • This also increases excretion of magnesium, calcium and hydrogen, so overall can cause low electrolyte state and metabolic alkalosis
  • Hearing loss / tinnitus: same co-transporter found in inner ear
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7
Q

Loop diuretics interactions

A
  1. Increase concentration of drugs metabolised by kidney especially lithium
  2. Digoxin: increased toxicity due to diuretic associated hypokalaemia
  3. Aminoglycosides: increase ototoxicity and nephrotoxicity
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8
Q

Loop diuretics patient info:

A

Avoid taking oral doses at night due to increased urinary output

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9
Q

Thiazide diuretics examples

A

Bendroflumethiazide, indapamide, chlorthalidone

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10
Q

Thiazide diuretics indications

A
  1. Hypertension: alternative where CCB would otherwise be used, but is unsuitable due to oedema or heart failure
  2. Hypertension additional treatment where BP is not controlled by CCB + ACEi / ARB
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11
Q

Thiazide diuretics MOA

A
  • Inhibit the Na+/Cl- co-transporter in the distal convoluted tubule
  • Prevents reabsorption of sodium and associated water
  • Resulting diuresis causes initial fall in extracellular fluid volume
  • Long-term, compensatory mechanisms such as RAAS tend to reverse this
  • Longer term mechanism may be due to vasodilation
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12
Q

Thiazide diuretics administration

A

Oral

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13
Q

Thiazide diuretics contraindications

A
  • CI in hypokalaemia
  • Avoid in hyponatraemia
  • Reduce uric acid excretion so caution in gout
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14
Q

Thiazide diuretics side effects

A
  • Prevention of sodium ion reabsorption can cause hyponatraemia
  • Increased delivery of sodium to distal tubule, where it can be exchanged for potassium, leads to hypokalaemia - cardiac arrhythmias
  • May increase plasma glucose, LDL and triglycerides
  • Impotence in men
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15
Q

Thiazide diuretics interactions

A
  • NSAIDs: may reduce effectiveness - low dose aspirin fine

- Other drugs that lower serum potassium concentration best avoided

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16
Q

Potassium-sparing diuretics name

A

Amiloride (co-amilofruse, amilozide)

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17
Q

Potassium-sparing diuretics indication

A
  1. Part of combination therapy for treatment of hypokalaemia during other diuretic treatment
    - Aldosterone antagonists e.g. spironolactone can be used as alternative
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18
Q

Potassium-sparing diuretics MOA

A
  • Weak diuretics alone but in combination can enhance diuresis while preventing hypokalaemia
  • Acts on distal convoluted tubule
  • Inhibits reabsorption of sodium (and therefore water) by epithelial sodium channels
  • Causes excretion of sodium and water and retention of potassium

Co-amilofruse: amiloride + furosemide
Co-amilozide: amiloride + hydrochlorothiazide

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19
Q

Potassium-sparing diuretics contraindications

A
  • Severe renal impairment and hyperkalaemia
  • Do not start in context of hypokalaemia as effect can be unpredictable
  • Avoid in states of volume depletion
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20
Q

Potassium-sparing diuretics side effects

A
  • Uncommon at low doses
  • GI upset may occur
  • In combination with other diuretics may cause dizziness, hypotension and urinary symptoms
  • Low electrolyte disturbance
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21
Q

Potassium-sparing diuretics interactions

A
  • Do not use in combination with other K+ sparing drugs due to risk of hyperkalaemia e.g. potassium supplements and aldosterone antagonists
  • Digoxin and lithium: alters renal clearance - adjust dose
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22
Q

Beta-blockers examples

A

Bisoprolol, propranolol, metoprolol, atenolol

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23
Q

Beta-blockers indications

A
  1. Ischaemic heart disease: first-line, to improve symptoms and prognosis associated with angina and ACS
  2. Chronic heart failure: first-line to improve prognosis
  3. AF: first line to reduce ventricular and maintain sinus rhythm in paroxysmal
  4. Supraventricular tachycardia: first-line option in patients without circulatory compromise to restore sinus rhythm
  5. Hypertension: when CCB / ACEi / thiazides are insufficient
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24
Q

Beta-blockers MOA

A
  • Block beta-1 receptor located in heart
  • Reduces force of contraction and speed of conduction
  • This reduces cardiac work + o2 demand and increases myocardial perfusion
  • Protect heart from effects of chronic sympathetic stimulation
  • Slow ventricular rate in AF by prolonged refractory period of AV node
  • Break self-perpetuating circuit of SVT and restore sinus rhythm
  • Hypertension: reduce renin secretion from kidney as this is mediated by beta-1
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25
Q

Beta-blockers administration

A
  • Oral, take at equal intervals throughout day

- IV preparations when rapid effect necessary

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26
Q

Beta-blockers contra-indications

A
  1. Asthma: can cause life-threatening bronchospasm due to beta-2 antagonism in airway smooth muscle
  2. COPD: usually safe but should chose cardioselective (not propranolol)
  3. Heart failure: start at low dose as may initially impair cardiac function
  4. Haemodynamic instability: avoid
  5. Heart block: contra-indication
  6. Hepatic failure: dose reduction
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27
Q

Beta-blockers side effects

A
  • fatigue
  • cold extremities
  • headache
  • GI disturbance
  • sleep disturbance and nightmares
  • impotence in men
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28
Q

Beta-blockers interactions

A
  1. DO NOT PRESCRIBE with non-dihydropine CCB - verapamil, diltiazem. Can cause heart failure, bradycardia and asystole/
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29
Q

Calcium channel blockers examples

A

Dihydropine: Amlodipine, nifedipine - vascular selective

Non-dihydrpine: diltiazem, verapamil - cardioselective

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30
Q

Calcium channel blockers indications

A
  1. Hypertension: Dihydropines 1st line in >55 or Afro-Caribbean
  2. Dihydropines reduce risk of stroke, MI or death from CVD
  3. All used to control symptoms of stable angina - beta-blockers main alternative
  4. Non-dihydropines control cardiac rate in those with SV arrhythmias (SVT, atrial flutter, AF)
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31
Q

Calcium channel blockers MOA

A
  • Decrease calcium entry in vascular and cardiac cells
  • Causes relaxation and vasodilation in arterial smooth muscle, lowering arterial pressure
  • Reduce myocardial contractility
  • Suppress cardiac conduction, particularly across AV node, slowing ventricular contraction
  • Reduced cardiac rate + contractility + afterload = reduced myocardial oxygen demand - prevents angina
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32
Q

Calcium channel blockers administration

A

Oral

Verapamil available IV for acute arrhythmias

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33
Q

Calcium channel blockers contra-indactions

A
  1. Poor LV function: non-dihydropines can precipitate HF
  2. AV nodal conduction delay: can provoke complete heart block
  3. Dihydropines contraindicated in patients with unstable angina: vasodilation causes increase in contractility and tachycardia, increasing myocardial oxygen demand
  4. Dihydropines contra-indicated in patients with severe aortic stenosis - can provoke collapse
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34
Q

Calcium channel blockers side effects

A
  • Dihydropines: ankle swelling, flushing, headache and palpitations due to vasodilation and compensatory tachycardia.
  • Verapamil: constipation, less often bradycardia, heart block and cardiac failure
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35
Q

Calcium channel blockers interactions

A
  1. DO NOT PRESCRIBE with non-dihydropine CCB - verapamil, diltiazem. Can cause heart failure, bradycardia and asystole as both negative chronotropes and inotropes
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36
Q

ACE Inhibitors examples

A

Ramipril, Lisinopril, Perindopril

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37
Q

ACE Inhibitors indications

A
  1. Hypertension: 1st / 2nd line treatment to reduce risk of cardiovascular events
  2. Chronic heart failure: 1st line treatment of all grades to improve symptoms and prognosis
  3. Ischaemic heart disease: reduce risk of subsequent cardio/cerebrovascular events
  4. Diabetic nephropathy and CKD with proteinuria: reduces proteinuria and progression
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38
Q

ACE Inhibitors MOA

A
  • Block ACE, preventing conversion of angiotensin I to angiotensin II
  • Angiotensin II causes vasoconstriction and stimulates aldosterone secretion
  • Blocking reduces afterload (PVR) which lowers blood pressure
  • Dilates efferent glomerular arteriole which reduces intraglomerular pressure and slows CKD progression
  • Reducing aldosterone promotes sodium and water excretion - this helps reduce preload which is beneficial in heart failure
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39
Q

ACE Inhibitors contra-indication

A
  • Renal artery stenosis
  • AKI
  • Pregnancy / breast-feeding
  • CKD: use lower doses and monitor effect on renal function closely
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40
Q

ACE Inhibitors side effects

A
  • Hypotension
  • Chronic dry cough due to increased bradykinin
  • Hyperkalaemia due to reduced aldosterone
  • Cause or worsen renal failure (dilation of arteriole needed to maintain renal perfusion)
  • Idiosyncratic angioedema, anaphylaxis
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41
Q

ACE Inhibitors interactions

A

-Avoid other drugs that increase potassium e.g. supplements, K+-sparing diuretics

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42
Q

Angiotensin receptor blockers examples

A

Losartan, Candesartan, Irbesartan

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43
Q

Angiotensin receptor blockers indications

A

Used 2nd line when ACEi not tolerated due to dry cough. Indications are the same:

  1. Hypertension: 1st / 2nd line treatment to reduce risk of cardiovascular events
  2. Chronic heart failure: 1st line treatment of all grades to improve symptoms and prognosis
  3. Ischaemic heart disease: reduce risk of subsequent cardio/cerebrovascular events
  4. Diabetic nephropathy and CKD with proteinuria: reduces proteinuria and progression
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44
Q

Angiotensin receptor blockers MOA

A
  • Block action of angiotensin II on AT1 receptor
  • Angiotensin II causes vasoconstriction and stimulates aldosterone secretion
  • Blocking reduces afterload (PVR) which lowers blood pressure
  • Dilates efferent glomerular arteriole which reduces intraglomerular pressure and slows CKD progression
  • Reducing aldosterone promotes sodium and water excretion - this helps reduce preload which is beneficial in heart failure
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45
Q

Angiotensin receptor blockers contra-indications

A
  • Renal artery stenosis
  • AKI
  • Pregnancy / breast-feeding
  • CKD: use lower doses and monitor effect on renal function closely
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46
Q

Angiotensin receptor blockers side effects

A
  • Hypotension
  • Hyperkalaemia
  • Cause or worsen renal failure
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47
Q

Angiotensin receptor blockers interactions

A
  • Potassium raising drugs
  • Diuretics: profound 1st dose hypotension
  • NSAIDs: increased risk renal failure
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48
Q

Nitrates examples

A

Isosorbide mononitrate, GTN

49
Q

Nitrates indications

A
  1. Short-acting (GTN) used in treatment of acute angina / ACS associated chest pain
  2. Long-acting (ISMN) used for angina prophylaxis where beta-blocker or CCB are insufficient / not tolerated
  3. IV nitrates used for pulmonary oedema, in combination with furosemide and oxygen
50
Q

Nitrates MOA

A
  • Converted to NO
  • NO increases cGMP synthesis and reduces Ca in vascular smooth muscle cells causing them to relax
  • This causes vasodilation
  • This reduces cardiac preload and left ventricular filling, which reduces cardiac work and myocardial oxygen demand
  • They also relieve coronary artery vasospasm and dilate collateral vessels, improving coronary perfusion
  • Also relax systemic arteries to reduce afterload (but most effects due to reduced preload)
51
Q

Nitrates administration

A
  • Stable angina: GTN sublingual as tablets or spray as immediate relief
  • ACS / HF: GTN continuous IV infusion
  • ISMN: oral, patches
52
Q

Nitrates contraindications

A
  1. Severe aortic stenosis: may cause collapse as heart unable to increase CO through narrow valve to maintain pressure
  2. Haemodynamic instability, especially hypotension
53
Q

Nitrates side effects

A

Vasodilators: common = flushing, headaches, dizziness, vasodilation

Sustained use leads to tolerance - reduced symptom relief. Don’t take doses overnight to prevent this.

54
Q

Nitrates interactions

A
  1. Phosphodiesterase inhibitors (sildenafil): enhance and prolong hypotensive effect
  2. Antihypertensives: cause hypotension
55
Q

Nitrates patient info

A

GTN spray should work after 5 mins - if no effect after 2 sprays ring ambulance

56
Q

Digoxin class

A

Cardiac glycoside

57
Q

Digoxin indication

A
  1. AF / Atrial flutter: reduces ventricular rate. Beta-blocker / NDCCB usually more effective.
  2. Severe heart failure: 3rd line when already taking ACEi, beta-blocker and aldosterone antagonist / ARB. (Used earlier if co-existing AF).
58
Q

Digoxin MOA

A
  • Negatively chronotropic (reduces heart rate)
  • Positively inotropic (increases force of contraction)
  • AF: increased parasympathetic tone reduces conduction at AV node, reducing ventricular rate
  • HF: directly effects myocytes through inhibition of Na+/K+ pumps, causing Na+ to accumulate in cell.
  • This causes Ca to accumulate in cell, which increases contractile force
59
Q

Digoxin administration

A

Oral: works within 2 hours
IV: works within 30 mins
Usually given loading dose

60
Q

Digoxin contra-indications

A
  1. Heart block: may worsen conduction abnormalities
  2. Ventricular arrhythmias
  3. Renal failure: dose reduction
  4. Electrolyte disturbance: hypokalaemia, hypomagnesia, hypercalcaemia: increased risk of toxicity - hypokalaemia is the worst as it competes to bind Na+/K+ pump, so when levels are low, digoxin is increased
61
Q

Digoxin side effects

A
  • Bradycardia
  • GI disturbance
  • Rash
  • Dizziness
  • Visual disturbance: blurred or yellow vision
  • Pro-arrhythmic and has a low therapeutic index - can cause a wide range of arrhythmias which can be fatal
62
Q

Digoxin interactions

A
  1. Loop and thiazide diuretics: cause hypokalaemia and increase risk of toxicity
  2. Amiodarone, CCB, spironolactone and quinine all increase plasma concentration and risk toxicity
63
Q

Amiodarone class

A

Anti-dysrhythmics

64
Q

Amiodarone indications

A
  1. Management of tachyarrhythmias: AF, atrial flutter, SVT, VT, ventricular fibrillation. Used when other therapeutic options - drugs are cardioversion - are ineffective or inappropriate
65
Q

Amiodarone MOA

A
  • Effects on myocardial cells: blockade of sodium, calcium and potassium channels, and antagonism of alpha + beta adrenergic receptors
  • This reduces spontaneous depolarisation, slows conduction velocity and increases resistance to depolarisation, including in AV node, which reduces ventricular rate
  • Increases chance of conversion to / maintenance of sinus rhythm
  • SVT: breaks self-perpetuating circuit to restore sinus rhythm
  • VT: suppresses spontaneous depolarisation
66
Q

Amiodarone administration

A

IV
Cardiac arrest: bolus
Other cases, given through central line

67
Q

Amiodarone contraindications

A
  • Dangerous drug, only give when benefits outweigh risks
  • severe hypotension
  • heart block
  • thyroid abnormalities
68
Q

Amiodarone side effects

A

-Hypotension during IV infusion
Taken chronically:
-pneumonitis
-bradycardia
-AV block
-hepatitis
-skin photosensitivity and discolouration
-hypo/hyperthyroid due to iodine content and structural similarities to thyroid hormone
-long half-life, takes months to be eliminated

69
Q

Amiodarone interactions

A

Increases concentration of: digoxin, diltiazem, verapamil - increases risk of bradycardia / AV block / HF. Doses of these should be halved.

70
Q

Aspirin class

A

Anti-platelet

71
Q

Aspirin indications

A
  1. ACS / acute ischaemic stroke where rapid platelet aggregation inhibition can limit thrombosis
  2. Long-term secondary prevention of thrombotic events in pts with CV / cerebrovascular / peripheral vascular disease
  3. Reduce risk of intra-cardiac thrombus and embolic stroke in AF where warfarin / DOACs are contraindicated
  4. Mild-moderate pain / fever
72
Q

Aspirin MOA

A
  • Inhibits COX to reduce production of thromboxane, a pro-coagulatory factor derived from arachidonic acid
  • Thromboxane inhibition reduces platelet aggregation
  • Effect occurs at low doses and lasts whole platelet lifetime as have no nuclei to produce new COX, so only wears off as new platelets formed
73
Q

Aspirin administration

A

Oral: 300mg loading dose, 75mg daily. Gastro-protection for daily dose.

Rectal at higher doses

74
Q

Aspirin contra-indications

A
  • Children < 16: Reye’s syndrome
  • Aspirin / NSAID hypersensitivity
  • 3rd trimester of pregnancy where prostaglandin inhibition leads to premature closure of ductus arteriosus
  • Caution in peptic ulcer or gout as can precipitate acute attack
75
Q

Aspirin side effects

A
  • GI irritation
  • Gastric ulceration
  • Haemorrhage
  • Hypersensitivity including bronchospasm
  • Tinnitus in regular high dose
  • OD: life-threatening. Hyperventilation, hearing changes, metabolic acidosis and confusion followed by convulsions, cardiovascular collapse and respiratory arrest
76
Q

Aspirin interactions

A

Synergistic with other anti-platelets - increased risk of hemorrhage. Caution when given with heparin / warfarin / clopidogrel.

77
Q

Clopidogrel class

A

Anti-platelet

78
Q

Clopidogrel indications

A

Generally prescribed with aspirin - may be prescribed alone where aspirin contraindicated
1. ACS / acute ischaemic stroke where rapid platelet aggregation inhibition can limit thrombosis

  1. Long-term secondary prevention of thrombotic events in pts with CV / cerebrovascular / peripheral vascular disease
  2. Reduce risk of intra-cardiac thrombus and embolic stroke in AF where warfarin / DOACs are contraindicated
  3. Mild-moderate pain / fever
  4. Prevent occlusion of coronary artery stents
79
Q

Clopidogrel MOA

A
  • Binds to ADP PY12 receptors on surface of platelets

- This is independent of COX pathway so action is synergistic with aspirin

80
Q

Clopidogrel contraindications

A
  1. Active bleeding
  2. Stop 7 days prior to surgery
  3. CAution in hepatic and renal impairment
81
Q

Clopidogrel side effects

A
  • Bleeding
  • GI upset
  • Thrombocytopenia
82
Q

Clopidogrel interactions

A
  • Pro-drug that requires metabolism by cP450 enzymes
  • Gastric protection with PPI: use lansoprazole pantoprazole so efficacy not reduced
  • Anti-coagulants / NSAIDs: increases bleeding risk
83
Q

Alteplase name and class

A

Tissue plasminogen activator

Thrombolytics (fibrinolytics)

84
Q

Alteplase indications

A
  1. Acute MI
  2. PE
  3. Acute ischaemic stroke
  4. Thrombolytic treatment of occluded central venous access devices
85
Q

Alteplase MOA

A
  • Activates plasminogen to form plasmin
  • Plasmin works to degrade fibrin, the main constituent of venous thrombi
  • Increased plasmin = degradation of thrombi
86
Q

Alteplase administration

A

IV, injection or infusion

87
Q

Alteplase contraindications

A
  • Pulmonary disease with cavitation
  • Acute pancreatitis
  • Aortic dissection
  • Endocarditis
  • Coagulation defects
  • Coma
  • Cerebrovascular disease history
  • Recent surgery / trauma
  • Hepatic impairment
  • 1st 18 weeks pregnancy due to risk of separation of placenta / foetal haemorrhage
88
Q

Alteplase side effects

A
  • Anaphylaxis
  • Haemorrhage
  • Cerebral oedema
  • Flushing + hypotension
  • Reperfusion arrhythmias
89
Q

Alteplase interactions

A

Increased risk of haemorrhage when used with other anti-coagulants

90
Q

Heparins and Fondaparinux examples

A

Enoxaparin, Dalteparin, Fondaparinux, Unfractionated heparin

91
Q

Heparins and Fondaparinux indaictions

A
  1. VTE: LMWH 1st line prophylaxis in inpatients and treatment of PE / DVT
  2. ACS: LMWH / fondaparinux part of 1st line to improve revascularisation and prevent intracoronary thrombus progression
92
Q

Heparins and Fondaparinux MOA

A

Thrombin + FXa part of coagulation pathway that leads to formation of fibrin clot.

  • Unfractionated heparin: activates anti-thrombin which inactivates FXa and thrombin
  • LMWH: dalteparin + enoxaparin. Preferentially inhibit FXa - more predictable and do not require monitoring.
  • Fondaparinux: synthetic compound similar to heparin, inhibits FXa only. 1st line anti-coagulant for ACS.
93
Q

Heparins and Fondaparinux administration

A

LMWH + fondaparinux: SC injection.

UFH: IV infusion

94
Q

Heparins and Fondaparinux contraindications

A
  1. Patients at increased risk of bleeding
  2. Avoid around time of invasive procedures
  3. LMWH + fondaparinux dose reduction in renal impairment
95
Q

Heparins and Fondaparinux side effects

A
  • Bleeding
  • Injection site reactions
  • Rare: heparin induced thrombocytopenia - most likely with UFH
96
Q

Heparins and Fondaparinux interactions

A

Anti-thrombotic drugs: increased bleeding risk. In bleeding associated with UFH, protamine can be given.

97
Q

Warfarin class

A

Oral anti-coagulant

98
Q

Warfarin indications

A
  1. To prevent clot extension and recurrence in VTE
  2. To prevent stroke in AF
  3. To prevent stroke after heart valve replacement - short-term after tissue replacement, life-long after mechanical replacement

**Not used to prevent arterial thrombosis as this is driven by platelet aggregation, so antiplatelet agents needed instead

99
Q

Warfarin MOA

A
  • Vitamin K must be reduced for synthesis of coagulation factors, and is then oxidised during synthesis.
  • Vitamin K epoxide reductase enzyme reduces vitamin K to reactivate it
  • Warfarin inhibits vitamin K epoxide reductase enzyme
  • This Inhibits hepatic production of vitamin-K coagulation factors and co-factors
100
Q

Warfarin administration

A

Oral, OD. 5-10mg initially, subsequent doses guided by INR

Initiate with heparin until full anti-coagulation achieved

101
Q

Warfarin contraindications

A
  1. Patients at risk of immediate bleeding
  2. Hepatic impairment - risk of bleeding
  3. 1st trimester pregnancy and towards term
102
Q

Warfarin side effects

A
  1. Bleeding, slight excess increases risk from existing abnormalities e.g. peptic ulcer. Large excess can cause spontaneous hemorrhage.
103
Q

Warfarin interactions

A

-Metabolised by cP450
Low therapeutic index so inducers / inhibitors have significant effect.
-Antibiotics: kill gut flora which synthesise vitamin K so increase anti-coagulation

104
Q

Warfarin patient info

A

Take at 18:00 to allow consistent INR readings.

105
Q

Rivaroxaban class

A

DOAC

106
Q

Rivaroxaban indications

A
  1. Initial treatment of VTE
  2. Prophylaxis of VTE following surgery / recurrent VTE
  3. Prophylaxis of stroke and systemic embolism in patients with AF
  4. Prophylaxis of atherothrombotic events following ACS with elevated cardiac biomarkers, in combination with aspirin ± clopidogrel
107
Q

Rivaroxaban MOA

A

Direct inhibitor of FXa (other DOACs inhibit thrombin directly)

108
Q

Rivaroxaban administration

A

Oral, 2.5-20mg OD

109
Q

Rivaroxaban contraindications

A
  • Active / risk of bleeding
  • Previous stroke
  • TIA
110
Q

Rivaroxaban side effects

A
  • GI upset
  • Dizziness, headache, hypotension
  • Pruritis, rash

Rare: jaundice, oedema

111
Q

Rivaroxaban interactions

A
  • Anti-coagulants: bleeding risk

- Metabolised by cP450 enzymes

112
Q

Statins examples

A

Simvastatin, Atorvastatin, Pravastatin, Rosuvastatin

113
Q

Statins indications

A
  1. Primary prevention of cardiovascular events in people > 40 with 10 year history of >20% CVS risk
114
Q

Statins MOA

A
  • Inhibit HMG CoA reductase enzyme which is involved in cholesterol production
  • Decrease hepatic cholesterol synthesis
  • Increase clearance of LDL
  • Indirectly they reduce triglycerides and increase HDL
  • These effects slow / reverse atheroscloertic process
115
Q

Statins administration

A

Oral, OD. Simvastatin 40mg, Atorvastatin 10mg for primary prevention. 80mg for secondary prevention.

116
Q

Statins contraindications

A
  1. Caution in hepatic and renal failure

2. Avoid in pregnancy / breastfeeding as cholesterol essential for development

117
Q

Statins side effects

A
  • Generally safe and well tolerated
  • Muscle and headaches most common
  • GI upset
  • Rarer: myopathy / rhabdomyolysis
  • Increase liver enzymes - drug induced hepatitis
118
Q

Statins interactions

A

Metabolised by cP450 enzymes

Amlodipine also causes statin to accumulate

119
Q

Statins patient info

A

Take in evening as evidence shows effects greatest when dietary intake low

Year 3 Drugs (9 decks)

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