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BASIC - CARDIOVASCULAR + DERMATOLOGY Flashcards

1
Q

Names of loop diuretics?

A

Furosemide, bumetanide

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2
Q

Indications of loop diuretics?

A

Acute pulmonary oedema (with O2 and nitrates)
Chronic heart failure
Other oedematous states (renal and liver disease)

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3
Q

Mechanism of action of loop diuretics?

A
  • Act on ascending limb of loop of Henle – inhibit Na/K/2Cl co-transporter (from lumen to epithelial cell)
  • Stops water following by osmosis
  • Dilatation of capacitance veins – reduces preload and improves contractile function of heart failure
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4
Q

Side effects of loop diuretics?

A
  • Dehydration
  • Hypotension
  • Low electrolytes (Na, K, Cl, Ca, Mg)
  • Tinnitus and hearing loss
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5
Q

Contraindications of loop diuretics?

A
  • Dehydration/Hypovolaemia

- Hepatic encephalopathy (hypokalaemia cause/worsen coma)

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6
Q

Cautions of loop diuretics?

A
  • Electrolyte disturbances (low K, Na)

- Worsens gout – inhibit uric acid excretion

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7
Q

Interactions of loop diuretics?

A
  • Affect drugs excreted by kidneys
    o E.g. lithium levels increase and digoxin toxicity by hypokalaemia
  • Increase ototoxicity and nephrotoxicity of aminoglycosides
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8
Q

Dose of loop diuretics?

A

o Oral/IV furosemide 40g
o Oral 1mg bumetanide (500mg if elderly)
o Oral doses taken in morning (second dose in early afternoon when BDS) to avoid nocturia

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9
Q

Communication to patient of loop diuretics?

A

o Medicine will cause urine to be passed more

o Aim for weight loss of no more than 1kg/day

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10
Q

Monitoring of loop diuretics?

A

o U&Es during treatment

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11
Q

Names of thiazide diuretics?

A

Bendroflumethiazide, indapamide, chlortalidone, metolazone

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12
Q

Indications of thiazide diuretics?

A
  • Hypertension add-on (step 3)

- Alternative first-line hypertension when CCB cannot be used (HF, oedema)

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13
Q

Mechanism of action of thiazide diuretics?

A
  • Inhibit Na/Cl co-transporter in distal convoluted tubule

- Prevents sodium and water reabsorption

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14
Q

Side Effects of thiazide diuretics?

A
  • Hyponatraemia
  • Hypokalaemia
  • Cardiac arrhythmias
  • Increase glucose, HDLs and triglycerides
  • Impotence in men
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15
Q

Contraindications of thiazide diuretics?

A
  • Hypokalaemia
  • Hyponatraemia
  • Gout
  • Hypercalcaemia
  • Addison’s Disease
  • History of allergy to sulphonamides
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16
Q

Changes in renal failure of thiazide diuretics?

A
  • Ineffective in eGFR<30

- Metolazone effective if eGFR<30

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17
Q

Changes in liver failure of thiazide diuretics?

A
  • Caution mild-to-moderate

- Avoid in severe liver disease

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18
Q

Interactions of thiazide diuretics?

A
  • NSAIDs reduce effectiveness

- Combination of loop and thiazide diuretics lower serum K

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19
Q

Dose of thiazide diuretics?

A
  • Taken orally, regularly
  • Indapamide 2.5mg OD used for hypertension
  • Take in morning
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20
Q

Monitoring of thiazide diuretics?

A

U&Es before starting, 2-4 weeks into therapy and after change in dose

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21
Q

Names of K-sparing diuretics?

A

Amiloride (as co-amilofruse/co-amilozide), spironolactone, eplerenone

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22
Q

Indications of amiloride and spironolactone?

A

Amiloride - Hypokalaemia (arising from diuretic therapy)
Spironolactone - Ascites and oedema from liver cirrhosis, CHF, Hypertension (resistant), Nephrotic syndrome
Primary hyperaldosteronism

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23
Q

Mechanism of amiloride and spironolactone?

A
  • Amiloride
    o Weak diuretic but can counter-act potassium loss
    o Inhibits Na and water reabsorption by ENaC in distal convoluted tubule
  • Spironolactone
    o Competitively bind to aldosterone receptors affecting ENaC in distal convoluted tubule
    o Increases potassium retention and increases water and Na excretion
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24
Q

Side effects of K-sparing diuretics?

A
  • GI upset
  • Dizziness, hypotension and urinary symptoms
  • Hyperkalaemia
  • Spironolactone only – gynaecomastia, jaundice, liver impairment, SJS (bullous skin eruption)
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25
Q

Contraindications of K-sparing diuretics?

A
  • Severe renal impairment
  • Hyperkalaemia
  • Anuria
  • Spironolactone – Addison’s disease
  • Pregnancy and breast-feeding
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26
Q

Interactions of K-sparing diuretics?

A
  • Do not combine with potassium supplements, aldosterone antagonists, ACEi, ARBs – risk of hyperkalaemia
  • Dose adjustment of lithium and digoxin needed
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27
Q

Dose of K-sparing diuretics?

A

o Co-amilofruse tablet at strength 1:8 so state strength and dose as number of tablets taken daily
o Spironolactone = 100-200mg, increased up to 400mg
o Regular OD dose - take with food
o Take in morning to minimise nocturia

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28
Q

Communication to patients of K-sparing diuretics?

A

o Warn men possibility of growth and tenderness of tissue under the nipples and impotence - spironolactone
o Reversible

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29
Q

Monitoring of K-sparing diuretics?

A

o Serum potassium, U&Es
 1 week after initiation/dose increase
 Monthly for 3 months and then 3 monthly for a year
 Then every 6 months

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30
Q

Names of ACE inhibitors?

A

Ramipril, Lisinopril, Perindopril

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31
Q

Indications of ACE inhibitors?

A

Hypertension (1st or 2nd line Rx)
Heart Failure (1st line)
Ischaemic Heart Disease
CKD

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32
Q

Mechanism of ACE inhibitors?

A
  • Block action of ACE to prevent conversion of angiotensin 1 to angiotensin 2 (Angiotensin 2 is vasoconstriction and stimulates aldosterone secretion)
  • Reduces peripheral vascular resistance (BP), dilates efferent glomerular arteriole (reduces intraglomerular pressure – slows CKD)
  • Reduces aldosterone level – promotes sodium and water excretion (beneficial in HF)
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33
Q

Side effects of ACE inhibitors?

A
  • Dry cough (1 in 10) – due to increased bradykinin
  • Hypotension (especially with 1st dose – take in night)
  • Hyperkalaemia
  • Worsen renal failure
  • Angioedema
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34
Q

Contraindications of ACE inhibitors?

A
  • Renal artery stenosis
  • AKI
  • Pregnant and breastfeeding women
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35
Q

Dose changes in hepatic and renal impairment of ACE inhibitors?

A

Hepatic Impairment
- Caution
Renal Impairment
- Start with lower dose, adjust according to response

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36
Q

Interactions of ACE inhibitors?

A
  • Avoid in potassium-elevating drugs (K+ supplements, potassium sparing diuretics)
  • NSAIDs and ACEi – increased risk of renal failure
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37
Q

Dose of ACE inhibitors? (ramipril)

A
  • Orally
  • Starting dose 1.25-2.5mg ‘titrated up’ to a maximum 10 mg daily dose over a period of weeks
  • First dose before bed to reduce symptomatic hypotension
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38
Q

Communication to patient of ACE inhibitors?

A
  • Treatment to improve blood pressure and reduce strain on their heart
  • Advise patients about common side effects
  • Avoid taking over-the-counter anti-inflammatories (e.g. ibuprofen) due to the risk of kidney damage.
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39
Q

Monitoring of ACE inhibitors?

A

o Blood test monitoring as can interfere with their kidney function and upset potassium balance
o Check electrolytes and renal function before starting treatment
o Repeat these 1–2 weeks into treatment and after increasing the dose
If eGFR<25% increase and creatinine <30% increase - continue and recheck levels in 1-2 weeks
If eGFR>25% increase or creatinine >30% increase - stop drug or reduce dose to tolerated dose
If K>6 - stop ACEi

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40
Q

Names of beta-blockers?

A

Bisoprolol, Atenolol, Propranolol, Metoprolol

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41
Q

Indications of beta-blockers?

A
  • 1st line in Angina, ACS
  • CHF
  • AF
  • SVT
  • Hypertension (Step 4)
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42
Q

Mechanism of beta-blockers?

A
  • Beta1-adrenoreceptors found in heart mainly and Beta2-adrenoreceptors found in smooth muscle of airways and blood vessel
  • Beta-blockers non-specific
    o Atenolol, bisoprolol and metoprolol more B1 specific
    o Propranolol non-selective
  • Mechanism:
    o Reduce force of contraction and speed of conduction in the heart
    o Prolong refractory period in AV node
    o Reduce renin secretion
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43
Q

Side effects of beta-blockers?

A
  • Fatigue, cold extremities, headache and GI upset
  • Sleep disturbance
  • Impotence in men
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44
Q

Contraindications of beta-blockers?

A
  • Asthma (bronchospasm)
  • Cardiogenic shock
  • Hypotension
  • Metabolic acidosis
  • Prinzmetal angina
  • 2nd degree Heart block
  • Pregnancy
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45
Q

Cautions of beta-blockers?

A
  • 1st degree heart block
  • Hx of obstructive airway disease
  • Myasthenia gravis
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46
Q

Dose changes in hepatic and renal impairment of beta-blockers??

A

Hepatic Impairment
- Caution – maximum 10mg in severe

Renal Impairment
- Reduce dose (max 10mg) if eGFR<20

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47
Q

Interactions of beta-blockers?

A
  • Do not combine Beta-blockers and Non-DHP CCB – cause HF and bradycardia
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48
Q

Dose of beta-blockers?

A
  • Oral, start low dose
  • Bisoprolol in hypertension = 5-10mg
  • Bisoprolol in HF = 1.25mg increased by 1.25mg weekly up to 10mg
  • Take at same time each day OD
  • Aim for HR of 55-60bpm
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49
Q

Monitoring of beta-blockers?

A

o Lung function (in patients with Hx of obstructive airway disease)

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50
Q

Cessation of beta-blockers?

A

Avoid abrupt withdrawal, especially in IHD

Causes rebound worsening of myocardial ischaemia

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51
Q

Names of nitrates?

A

Isosorbide mononitrate

Glyceryl trinitrate

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52
Q

Indications of nitrates?

A
  • Acute angina, ACS
  • Prophylaxis of angina (where BB, CCB not tolerated)
  • IV nitrates in pulmonary oedema (with furosemide and oxygen)
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53
Q

Mechanism of nitrates?

A
  • Nitrates converted into NO
  • NO increases cGMP and reduces intracellular Ca in vascular smooth muscle cells
  • Relaxation of venous capacitance vessels reduces preload
  • Reduce cardiac work and myocardial oxygen demand
  • Relaxation of systemic arteries, reducing arterial resistance and afterload
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54
Q

Side effects of nitrates?

A
  • Flushing, headaches, light-headedness, hypotension, nausea and vomiting
  • Sustained use – tolerance
    o Nitrate free period important for 4-12 hours a day
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55
Q

Contraindications of nitrates?

A
  • Severe aortic stenosis
  • Cardiac Tamponade
  • Constrictive pericarditis
  • Cardiogenic shock
  • Hypotension
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56
Q

Cautions of nitrates?

A
  • HF due to obstruction
  • Hypothermia
  • Hypothyroidism
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57
Q

Dose changes in hepatic and renal impairment of nitrates?

A

Hepatic Impairment
- Caution in severe impairment

Renal Impairment
- Caution in severe impairment

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58
Q

Interactions of nitrates?

A
  • Avoid phosphodiesterase inhibitors (Sildenafil) – hypotension
  • Caution in antihypertensives – hypotension
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59
Q

Prescription of nitrates?

A

o GTN taken sublingually tablets or spray for immediate relief (half-life <5 mins)
o ISMN prescribed BDS/TDS for prevention of recurrent angina
o Available IR, MR, patches
o In ACS GTN given IVI:
 Usually given 1mg/mL (50mg in 50mL), express starting dose as rate 1mL/hr
 Increase GTN rate by 0.5mL/hr every 15-30 minutes until relieved

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60
Q

Communication to patients on nitrates?

A

o Take GTN before tasks to prevent angina
o Sit down and rest before and for 5 mins after taking GTN – hypotension
o GTN tablets need to be discarded after 8 weeks, so spray better for infrequent angina
o Ensure nitrate free period – usually overnight to prevent tolerance

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61
Q

Monitoring of nitrates?

A

o IV nitrates – measure BP and HR - >90mmHg systolic

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62
Q

Cessation of nitrates?

A

o Avoid abrupt withdrawal

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63
Q

Names of calcium channel blockers?

A

Dihydropyridines - Amlodipine, Nifedipine (vascular selective)
Non-dihydropyridines – Verapamil, Diltiazem (cardio-selective)

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64
Q

Indications of calcium channel blockers?

A
  • Hypertension – Amlodipine
  • Stable angina – amlodipine/Nifedipine
  • Supraventricular arrhythmias (diltiazem and verapamil) – SVT, Atrial flutter and fibrillation
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65
Q

Mechanism of action of calcium channel blockers?

A
  • Decrease Ca entry into vascular and cardiac cells
  • Causes
    o Relaxation and vasodilation in arterial smooth muscle (lowered blood pressure)
    o Reduced myocardial contractility
    o Reduce cardiac conduction (particularly AV node)
    o Reduce myocardial oxygen demand
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66
Q

Side effects of calcium channel blockers?

A
  • DHP
    o Ankle swelling, flushing, headache and palpitations (caused by vasodilatation and compensatory tachycardia)
    o Abdominal pain, nausea, vomiting
  • Verapamil
    o Constipation, bradycardia, hypotension, heart block, cardiac failure
  • Diltiazem – any of the above
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67
Q

Contraindications of calcium channel blockers?

A
  • Non-DHP – bradycardia, 2nd/3rd degree heart block, Wolf-Parkinson-White syndrome, hypotension, cardiogenic shock
  • DHP - unstable angina, cardiogenic shock and severe aortic stenosis
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68
Q

Dose change in hepatic impairment of calcium channel blockers?

A

Hepatic Impairment

- Caution – start at low dose

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69
Q

Interactions of calcium channel blockers?

A
  • Non-DHP – do not prescribe with Beta-blockers
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70
Q

Dose of amlodipine/diltiazem?

A
  • Oral, OD (amlodipine)
  • E.g. amlodipine 5-10mg OD for hypertension, diltiazem MR 90mg 12hr for angina
  • MR swallowed whole, not crushed or chewed
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71
Q

Names of angiotensin receptor antagonists (ARBs)?

A

Losartan, Candesartan, Irbesartan

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72
Q

Indications of angiotensin receptor antagonists (ARBs)?

A 
-	When ACEi not tolerated:
o	Hypertension
o	HF
o	IHD
o	CKD
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73
Q

Mechanism of angiotensin receptor antagonists (ARBs)?

A
  • ARBs block the action of angiotensin II on the AT1 receptor
  • Angiotensin II is a vasoconstrictor and stimulates aldosterone secretion
  • Blockage - reduces peripheral vascular resistance (Low BP), dilates the efferent glomerular arteriole (reduces intraglomerular pressure and slows the progression of CKD), reducing the aldosterone level promotes sodium and water excretion
  • Reduce venous return (preload), which has a beneficial effect in heart failure.
74
Q

Side effects of angiotensin receptor antagonists (ARBs)?

A
  • Hypotension (particularly first dose)
  • Hyperkalaemia
  • Renal Failure
75
Q

Contraindications of angiotensin receptor antagonists (ARBs)?

A
  • Renal artery stenosis
  • AKI
  • Avoid in pregnant or breast feeding women
76
Q

Dose changes in hepatic and renal impairment of angiotensin receptor antagonists (ARBs)?

A

Hepatic Impairment

  • Caution in mild to moderate – dose reduction
  • Avoid in severe

Renal Impairment
- Start low dose and adjust according to response

77
Q

Interactions of angiotensin receptor antagonists (ARBs)?

A
  • Avoid in potassium-elevating drugs (K+ supplements, potassium sparing diuretics)
  • NSAIDs and ACEi – increased risk of renal failure
78
Q

Prescription of angiotensin receptor antagonists (ARBs)?

A
  • Orally
  • Starting dose ‘titrated up’ to a maximum daily dose over a period of weeks
  • First dose before bed to reduce symptomatic hypotension
79
Q

Monitoring of angiotensin receptor antagonists (ARBs)?

A

o Check U&E before starting treatment
o Repeat these 1–2 weeks into treatment and after increasing the dose

If eGFR<25% increase and creatinine <30% increase - continue and recheck levels in 1-2 weeks
If eGFR>25% increase or creatinine >30% increase - stop drug or reduce dose to tolerated dose
If K>6 - stop ACEi

80
Q

Indications of aspirin?

A
  • Acute in ACS/CVA ischaemic
  • 2o prevention in CVD, CVA, PAD
  • AF (when warfarin or NOAC contraindicated)
  • Following coronary by-pass surgery
  • Pain (mild-to-moderate)
81
Q

Mechanism of aspirin?

A
  • Antiplatelets (along with clopidogrel, ticagrelor) – work on platelets in arterial systems
  • Irreversibly inhibits cyclooxygenase (COX) to reduce thromboxane production from arachidonic acid – reduces platelet aggregation
  • Antiplatelet effect at low doses and lasts lifetime of platelet
82
Q

Side effects of aspirin?

A
  • GI irritation, ulceration and haemorrhage
  • Bronchospasm
  • Tinnitus
83
Q

Overdose symptoms of aspirin?

A

o Hyperventilation, hearing changes, metabolic acidosis, confusion, collapse

84
Q

Contraindications of aspirin?

A
  • <16 years old (Reye’s syndrome)
  • Active peptic ulcer (and previous)
  • Bleeding disorders
  • Allergy to NSAIDs
85
Q

Cautions of aspirin?

A
  • Anaemia
  • Uncontrolled hypertension
  • Third trimester of pregnancy
  • Gout (may trigger acute attack)
86
Q

Dose changes in hepatic and renal impairment of aspirin?

A

Hepatic Impairment
- Avoid in severe impairment

Renal Impairment
- Avoid in severe

87
Q

Interactions of aspirin?

A
  • Synergistic increase risk of bleeding
88
Q

Doses of aspirin?

A

o ACS – Once-only loading dose 300mg followed by 75mg regularly
o Ischaemic CVA – 300mg for 2 weeks before switching to 75mg daily
o Long-term prevention – 75mg daily
- Gastroprotection in people at risk
- Take after food

89
Q

Indications of clopidogrel?

A

ACS
Coronary artery stents
2o prevention of CVD, CVA and PAD
AF (where warfarin or NOACs CI)

90
Q

Mechanism of clopidogrel?

A
  • Used when platelet-rich thrombus forms in atheromatous arteries
  • Prevents platelet aggregation by binding irreversibly to ADP receptors on platelet surface
91
Q

Side effects of clopidogrel?

A
  • Bleeding
  • GI upset – dyspepsia, abdominal pain, diarrhoea
  • Thrombocytopenia
92
Q

Contraindications of clopidogrel?

A
  • Active bleeding

- Stop 7 days before elective surgery

93
Q

Dose changes in hepatic and renal impairment of clopidogrel?

A

Hepatic Impairment
- Avoid in severe

Renal Impairment
- Caution

94
Q

Interactions of clopidogrel?

A
  • Pro-drug requires CYP450 enzymes hepatic to convert to active form
  • Efficacy affected by CYP450 inhibitors and inducers
  • Increased risk of bleeding – antiplatelets, anticoagulants, NSAIDs
95
Q

Dose of clopidogrel?

A
  • Doses require week to reach full antiplatelet effect
  • Loading dose – oral 300mg, maintenance dose 75mg OD
  • PPI used
96
Q

Names of LMWH?

A

Tinzaparin, enoxaparin, dalteparin, fondaparinux

97
Q

Indications of LMWH?

A

Prophylaxis of VTE (inpatients and initial treatment)
Treatment of DVT/PE
VTE in Pregnancy
ACS

98
Q

Mechanism of LMWH?

A
  • Unfractioned heparin – activates antithrombin that inactivates Factor 10a and thrombin
  • LMWH – similar but preferentially inhibit Factor 10a
  • Fondaparinux – synthetic compound inhibits Factor 10a only
99
Q

Side Effects of LMWH?

A
  • Bleeding
  • Injection site reaction
  • Heparin-induced thrombocytopenia
100
Q

Contraindications of LMWH?

A
  • Acute bacterial endocarditis
  • Major trauma
  • Epidural/Spinal anaesthesia/lumbar puncture (12hs after dose)
  • Haemophilia
  • Peptic ulcer
101
Q

Dose reduction in renal impairment of LMWH?

A

Dose reduction if eGFR <30 (use unfractioned heparin)

102
Q

Interactions of LMWH?

A
  • Combined antithrombotic drugs increase risk of bleeding

- Protamine can be given in major bleeding to reverse anticoagulation (effective for UFH mostly)

103
Q

Prescription of LMWH?

A
  • SC injection – dose dependent on patient weight and indication
  • Long-term therapy
  • Tinzaparin = prophylaxis 50U/kg, treatment 175U/kg
104
Q

Monitoring of LMWH?

A

o Baseline FBC and U&Es
o Platelet count monitored in therapy > 4 days
o U&Es regularly checked if >7 days

105
Q

Indications of warfarin?

A

Prophylaxis and treatment in DVT and PE

Prophylaxis in AF and heart valve replacement (lifelong after mechanical valve)

106
Q

Mechanism of warfarin?

A
  • Inhibits vitamin K epoxide reductase, preventing reactivation of vitamin K and coagulation factor synthesis (2, 7, 9, 10)
  • Vitamin K must be in reduced form for synthesis of coagulation factors, which it is then oxidised
  • Thins the blood
107
Q

Side effects of warfarin?

A
  • Bleeding (1-2%)

- Diarrhoea, nausea, rash

108
Q

Contraindications of warfarin?

A
  • Immediate risk of haemorrhage – stroke, bleeding
  • Pregnancy - <48 hours postpartum and not conceive (teratogenicity)
  • Women in 1st trimester
109
Q

Caution of warfarin?

A
  • Bacterial endocarditis
  • Hx of GI bleeding
  • Hyperthyroidism
110
Q

Dose changes in hepatic and renal impairment of warfarin?

A

Hepatic Impairment
- Avoid in severe

Renal Impairment
- Monitor INR more frequently

111
Q

Interactions of warfarin?

A
  • Low therapeutic index
  • Altered drug content by CYP450 inhibitors and inducers
  • Antibiotics kill gut flora which synthesis Vitamin K so increase anticoagulation
112
Q

Dose of warfarin?

A

o Oral OD – usually 6pm, same time
o 5-10mg on day 1
o Subsequent doses guided by INR
- If immediate effect needed – started on LMWH concomitantly

113
Q

Practicalities of warfarin?

A

o Patients receive anticoagulant book (yellow book) used to record doses and blood test results
o Always carry anticoagulant alert card with you

114
Q

Monitoring of warfarin?

A

o INR between 2-3 measured daily in hospital
 Initially be frequent (every 3-4 days until two consecutive readings are within range) then twice weekly for 1-2 weeks (again until two consecutive readings within range)
 Thereafter, testing can increase to longer periods (e.g. every 12 weeks)

115
Q

Missed dose rules of warfarin?

A

o Never double up on doses: If a dose is accidentally missed, they should continue with the regimen as prescribed, and never take a double dose (unless specifically advised)

116
Q

Lifestyle changes of warfarin?

A

o Avoid liver, spinach, cranberry juice, alcohol binges

o No NSAIDs/aspirin

117
Q

Names of NOACs?

A

Apixaban, Dabigatran, Rivaroxaban

118
Q

Indications of NOACs?

A

Prevention of VTE following knee/hip replacement surgery
DVT/PE – treatment and prophylaxis in recurrent
Prevention in AF
ACS (Rivaroxaban)

119
Q

Mechanism of NOACs?

A
  • Direct factor 10a inhibitor
120
Q

Side Effects of NOACs?

A
  • Bleeding
  • Abdominal pain, diarrhoea, constipation
  • Headache
121
Q

Contraindication of NOACs?

A
  • Antiphospholipid syndrome

- Active bleeding

122
Q

Cautions of NOACs?

A
  • Prosthetic heart valve

- Recent surgery (rivaroxaban

123
Q

Dose changes in hepatic and renal impairment of NOACs?

A
  • Avoid in severe
  • Avoid eGFR <15 (apixaban & rivaroxaban)
  • Reduce dose to 2.5mg BD if eGFR 15-29 (apixaban & rivaroxaban)
124
Q

Dose of NOACs?

A

Apixaban

  • Prophylaxis - 2.5mg
  • Treatment - 10mg

Dabigatran

  • Prophylaxis - 75mg
  • Treatment - 150-110mg

Rivaroxaban

  • Prophylaxis - 10mg
  • Treatment - 15mg
125
Q

Names & Indications of statins?

A

Simvastatin, Atorvastatin, Pravastatin, Rosuvastatin

  • 10 prevention of CVD (<84 years and with QRISK2 >10%)
  • 20 prevention of CVD
  • Offer in Type 1 diabetes, CKD, Primary hyperlipidaemia – in primary/familial hypercholesterolaemia, mixed dyslipidaemia
126
Q

Mechanism of statins?

A
  • Reduce serum cholesterol levels
  • Inhibit hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase
  • Decrease cholesterol production by liver and increase LDL clearance from blood
  • Reduce triglycerides and slightly increase HDL levels
127
Q

Side effects of statins?

A
  • Muscle aches (myopathy/rhabdomyolysis)
  • Headache and GI disturbances
  • Rise in ALT/CK
  • Drug-induced hepatitis
128
Q

Contraindications of statins?

A
  • Porphyria

- Pregnant or breastfeeding women – adequate contraception during treatment and for 1 month afterwards

129
Q

Caution of statins?

A
  • Elderly
  • High alcohol intake
  • Hepatic impairment – avoid in active or persistent elevated serum transaminases
  • Dose reduction starting at 20mg in renal impairment (excreted)
130
Q

Interactions of statins?

A

Metabolism reduced by CYP450 inhibitors – higher levels and risk of SE
- May have to withhold statin for period
- E.g. amiodarone, diltiazem, itraconazole, macrolides
- Avoid grapefruit juice
Maximum 10mg dose if using ciclosporin

131
Q

Prescription info of statins?

A
  • If myalgia – check CK
  • Oral OD
  • Atorvastatin - 20mg (primary prevention), 80mg (secondary prevention)
  • Taken in evening, after meal at same time per day
  • Avoid grapefruit juice (atorvastatin, simvastatin)
132
Q

Monitoring of statins?

A

o Baseline – Lipids profile, CK, LFTs, U&Es, HbA1c, TFTs
o CK – before treatment only measured if muscle aches – if >5x upper limit, repeat in 7 days and if >5x then do not start
o 3 months - Lipids screen (aim >40% reduction in non-HDLs), LFTs at 3 months and 12 months (if serum transaminases >3x upper limit then stop), HbA1c
o 12 months - LFTs
o Review annually
o Efficacy should be monitored in 20 prevention – specific target of total cholesterol <4mmol/L or LDL cholesterol <2mmol/L

133
Q

Indications of digoxin?

A
  • AF and Atrial flutter (usually after BB, CBB) – sedentary patients
  • HF
134
Q

Mechanism of digoxin?

A
  • Negatively chronotropic (reduced HR)
  • Positively ionotropic (increases force of contraction)
  • Increases vagal tone
  • Inhibits Na/K/ATPase pump, elevation of Na in cells causes Ca to accumulate (cannot be extruded by NaCa exchanger) in cell – increasing contraction
135
Q

Side effects of digoxin?

A
  • Bradycardia
  • GI upset
  • Rash
  • Dizziness
  • Blurred vision
  • Low therapeutic index so safety is paramount
136
Q

Contraindications of digoxin?

A
  • Intermittent complete heart block
  • 2nd degree heart block
  • SV arrhythmias (WPW)
  • Constrictive pericarditis
  • Hypertrophic Cardiomyopathy
  • Myocarditis
  • WPW syndrome
  • VT/VF
137
Q

Dose change in renal failure of digoxin??

A
  • Dose reduction in renal failure (eliminated by kidneys) – monitor plasma-digoxin concentration
138
Q

Interactions of digoxin?

A
  • Hypokalaemia
    o Loop and thiazide diuretics increase risk of toxicity
  • Increase plasma concentration of digoxin
    o Amiodarone, CCB, spironolactone, quinine – reduce dose by half
139
Q

Prescription of digoxin?

A
  • Oral administration common – effect seen after 2 hours
  • Loading dose needed if rapid effect
  • IV given slowly
140
Q

Monitoring of digoxin?

A 
o	Plasma digoxin concentration 6 hours after dose if toxicity suspected
o	ECG (ST segment depression – reverse tick - normal)
o	Electrolytes and U&amp;Es
141
Q

Indications of amiodarone?

A
  • Tachyarrhythmias (AF, AF, SVT, VT, VF) – when electrical CV not used
  • CPR algorithm
142
Q

Mechanism of amiodarone?

A
  • Blockage of Na, Ca and K channels
  • Antagonises of alpha and beta-adrenergic receptors
  • Effects
    o Reduce spontaneous depolarisation, conduction velocity
    o Increases refractoriness, including AV node
143
Q

Side effects of amiodarone?

A
  • Hypotension if IV
  • Pneumonitis
  • Bradycardia, AV block
  • Hepatitis
  • Photosensitivity and grey discolouration
  • Thyroid problems
144
Q

Contraindications of amiodarone?

A
  • Severe conduction disturbances
  • Iodine sensitivity
  • Heart block
  • Active thyroid disease
145
Q

Interactions of amiodarone?

A
  • Lots of interactions
  • Increases plasma concentration of digoxin, diltiazem and verapamil – risk of bradycardia and AV block
  • Long half-life – takes weeks to be eliminated
146
Q

Prescription of amiodarone?

A

o Senior involvement needed
o Usually needs loading dose and then maintenance dose so CHECK
o In cardiac arrest, given after third shock in ALS (300mg IV, followed by 20mL of 0.9% NaCl as a flush)
o If continuous IV needed – central line (can cause phlebitis)

147
Q

Communication of amiodarone?

A

o Advise the patient not to drink grapefruit juice, as this can increase the risk of side effects
o Avoid exposure of their skin to direct sunlight due to the risk of photosensitivity

148
Q

Monitoring of amiodarone?

A

o LFTs, TFTs done before and every 6 months
o U&Es done before treatment
o CXR
o IV – continuous ECG monitoring

149
Q

Definition of creams?

A

 Emulsions of oil and water and well absorbed into skin
 May also contain an antimicrobial preservative
 Less greasy and easier to apply than ointments

150
Q

Definition of gels?

A

 Active ingredients in suitable hydrophilic or hydrophobic bases
 High water content
 Face and scalp suitable

151
Q

Definition of lotions?

A

 Cooling effect and preferred over hairy areas

 Can sting broken skin

152
Q

Definition of ointment?

A

 Greasy preparations, more occlusive than creams
 Suitable for dry, chronic lesions
 Commonly used is soft paraffin or combination with hard paraffin

153
Q

Definition of pastes?

A

 Stiff preparations containing high proportion of finely powdered solids such as zinc oxide

154
Q

Quantity to prescribe for face?

Usually for an adult for BDS application for 1 week

A
  • Creams and ointments – 15-30g

* Lotions – 100ml

155
Q

Quantity to prescribe for both hands?

Usually for an adult for BDS application for 1 week

A
  • Creams and ointments – 25-50g

* Lotions – 200ml

156
Q

Quantity to prescribe for scalp?

Usually for an adult for BDS application for 1 week

A
  • Cream and ointments – 50-100g

* Lotions – 200ml

157
Q

Quantity to prescribe for both arms or legs?

Usually for an adult for BDS application for 1 week

A
  • Creams and ointments – 100-200g

* Lotions 200ml

158
Q

Quantity to prescribe for trunk?

Usually for an adult for BDS application for 1 week

A
  • Creams and ointments – 400g

* Lotions – 500ml

159
Q

Quantity to prescribe for groin/genitalia?

Usually for an adult for BDS application for 1 week

A
  • Creams and ointments – 15-25g

* Lotions – 100ml

160
Q

Names of emollients?

A

Aqueous cream, liquid paraffin

Examples - E45, Aveeno (colloidal oatmeal)

161
Q

Indications of emollients?

A
  • Topical treatment for all dry or scaling skin disorders

- Used alone or in combination with topical corticosteroids in the treatment of eczema

162
Q

Mechanism of emollients?

A
  • Emollients replace water content in dry skin
  • Contain oils or paraffin-based products that soften skin and reduce water loss by protecting against evaporation
  • Many preparations used as soap substitute (as soap is drying to the skin) and also bath or shower emollients
163
Q

Side effects of emollients?

A
  • Greasy on skin but this is part of therapeutic effect

- Exacerbate acne and folliculitis by blocking pores and hair follicles

164
Q

Interactions of emollients?

A
  • Space out topical emollients – usually apply emollient 15 minutes before application of steroid cream
165
Q

Contraindications of emollients?

A
  • Fire hazard when oil content high
166
Q

Properties of emollients?

A 
o	Emulsions of oil and water to make creams, lotions and ointments
o	Lotions (less oil, more water) and creams (50% oil and water) spread further
o	Ointments (80% oil, 20% water) are more occlusive and potent
167
Q

Directions of emollients?

A

o Applied BDS/TDS in active disease
o Give sufficient supply for frequent use – 500g
o Continue after improvement to prevent recurrence
o Apply emollients in the direction of hair growth
o If using other topical agents, apply 15 minutes after emollient

168
Q

Names of oral antihistamines?

A

Chlorphenamine (Piriton), Cetirizine, loratadine, fexofenadine

169
Q

Indications of oral antihistamines?

A
  • Symptomatic relief of allergy (hay fever, pruritus, urticaria, food allergy, drug reactions, itch)
  • Anaphylaxis emergency treatment
  • Relief of itch in chickenpox
170
Q

Mechanism of oral antihistamines?

A
  • Antagonism of H1 receptor, blocking effects of excess histamine
  • Histamine is released by mast cells as a result of IgE binding
    o Induces: wheals, flares, itch
    o In hay fever – nasal irritation, sneezing, rhinorrhoea, congestion, itch
    o Widespread histamine release – vasodilatation, vascular leakage and hypotension
171
Q

Side effects of oral antihistamines?

A
  • 1st gen (chlorphenamine) – sedation
  • 2nd gen (loratadine, cetirizine, fexofenadine) – do not cross blood brain barrier
  • General SE
    o Concentration impaired, dry mouth, fatigue, vision blurred
172
Q

Dose reduction of oral antihistamines?

A

o Avoid cetirizine if eGFR <10

o Half dose in eGFR 30-50

173
Q

Prescription of oral antihistamines?

A

o Cetirizine – 10mg tablets OD
o Loratadine – 10mg tablets OD
o Chlorphenamine – 4mg tablets and 2mg/5ml solution every 4-6 hours
o In anaphylaxis – chlorphenamine IV/IM 10mg
o Fexofenadine – 120mg OD

174
Q

Patient information for oral antihistamines?

A

o Chlorphenamine may make you sleepy and avoid with alcohol which can increase sedation

175
Q

Names of topical glucocorticoids?

A

Mild – Hydrocortisone 0.5-2.5%
Moderate – Eumovate (Clobetasone butyrate 0.05%)
Potent – Betnovate (betamethasone valerate 0.1%)
Very Potent – Dermovate (Clobetasol propionate 0.05%)

176
Q

Indications of topical glucocorticoids?

A
  • Inflammatory skin conditions, e.g. eczema, psoriasis where emollients are ineffective
177
Q

Mechanism of topical glucocorticoids?

A
  • Upregulate anti-inflammatory genes and downregulate pro-inflammatory genes (e.g. cytokines, tumour necrosis factor alpha)
  • Suppression of circulating monocytes and eosinophils
  • Increased gluconeogenesis from increased circulating amino and fatty acids, released by catabolism of muscle and fat
  • Mineralocorticoid effects, stimulating Na+ and water retention and K+ excretion in the renal tubule
  • Because topical, effects limited to site – need prolonged use of potent topical steroids for systemic effects
178
Q

Side effects of topical glucocorticoids?

A
  • Skin thinning
  • Telangiectasia
  • Skin depigmentation
  • Contact dermatitis
  • When used on face:
    o Perioral dermatitis
    o Exacerbate acne
179
Q

Contraindications of topical glucocorticoids?

A 
-	Contra-indications
o	Infection present
o	Perioral dermatitis
-	Avoid potent on face and course should be short
-	Keep away from eyes
180
Q

Prescription of topical glucocorticoids?

A
  • Use as mild as possible for as short a time
  • < 2 weeks (1 week for facial lesions)
  • Prescription
    o Name, strength, formulation, amount
181
Q

Application of topical glucocorticoids?

A

o One fingertip unit can be spread across two adult palms
o BDS applied thinly on affected area
o Wash hands after application
o 5 minutes between different preparations applied to same skin

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