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Applied Pharmacology > CVS > Flashcards

CVS Flashcards

1
Q

Aspirin - Main Indications

A

1)

  • ACS: Angina
  • Acute ischaemic stroke

2) Long-term secondary prevention of thrombotic arterial events in patients with :
- Cardivascular
- Cerebovascular
- Peripheral arterial disease

Historically, used to control mild-to-moderate pain and fever

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2
Q

Aspirin - MOA

A
  • Thrombotic events occur when platelet-rich thrombus forms in atheromatous arteries and occludes circulation.
  • Aspirin irreversibly inhibits cyclooxygenase (COX) to reduce production of the pro-aggregator factor thromboxane from arachidonic acid, reducing platelet aggregation and the risk of arterial occlusion.
  • Effect of aspirin occurs at low dose and lasts for lifetime of the platelet.
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3
Q

Aspirin - Side Effects

A 
GI irritation:
- Peptic ulceration + Haemorrhage
Hypersensitivity reactions:
- Bronchospasm
Regular high-dose - tinnitus
Life-threatening in overdose:
-hyperventilation, hearing changes, metabolic acidosis, confusion, convulsions , CVS collapse, reps arrest
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4
Q

Aspirin - Contraindications

A

Should not be given:

  • Children under 16 years (risk of Reye’s syndrome)
  • People with aspirin hypersensitivity
  • 3rd trimester of pregnancy
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5
Q

Aspirin - Caution

A
  • Peptic ulceration
  • Gout (may trigger attack)
  • Elderly
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6
Q

Aspirin - Key interactions

A

Acts synergistically with antiplatelets and anticoagulants

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8
Q

Aspirin - Monitoring

A

Enquire about side effects

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8
Q

Aspirin - Patient Education

A

To minimise GI irritation taken after food.

Enteric-coated may help further but not useful in medical emergencies due to slower absorption

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9
Q

Clopidogrel - Class of drug and Other examples

A

Anti-platelet drugs , ADP-receptor antagonists

E.g : Ticagrelor, Prasugrel

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10
Q

Clopidogrel - Main Indications

A

1) ACS usually in combination with aspirin
2) Prevent occlusion of coronary artery stents - with aspirin

3) Long-term secondary prevention of thrombotic arterial events in patients with :
- Cardiovascular
- Cerebrovascular
- Peripheral arterial disease - alone or with aspirin

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11
Q

Clopidogrel - MOA

A
  • Prevent platelet aggregation and reduce risk of arterial occlusion by binding irreversibly to adenosine diphosphate (ADP) receptor .
  • Synergistic with aspirin
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12
Q

Clopidogrel - Side effects

A
  • Bleeding
  • GI upset - dyspepsia, abdominal pain & diarrhoea
  • Can cause thrombocytopenia
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13
Q

Clopidogrel - Contraindications

A
  • Active bleeding
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14
Q

Clopidogrel - Caution

A
  • Must be stopped 7 days before elective surgery

- Renal and haptic impairment

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15
Q

Clopidogrel - Key interactions

A
  • Clopidogrel is pro-drug that requires metabolism by hepatic cytochrome P450 enzymes to its active form to have an anti-platelet effect..
  • -> Efficacy maybe reduced by CYP inhibitors by inhibiting activation.
  • Antiplatelets and anticoagulants - increase risk of bleeding
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16
Q

Clopidogrel - Monitoring

A

Clinical monitoring for adverse effect

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17
Q

Clopidogrel - Patient Education

A
  • Can be given with or without food
  • Purpose of the treatment is to reduce risk of heart attacks or strokes
  • Usually taken for 12 months
  • stop if there is any active bleeding
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18
Q

Statins - Main indications

A

1) Primary prevention of CVS events: to prevent CVS in people over 40 years with QRISK tool of >10%
2) Secondary prevention CVS events: 1st line along with lifestyle changes, to prevent CVS disease
3) Primary hyperlipidaemia: 1st line

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19
Q

Statins - Examples

A

Simvastatin
Atorvastatin
Pravastatin
Rosuvastatin

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20
Q

Statins - MOA

A

Reduce serum cholesterol levels by:

  • Inhibit 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG CoA) reductase - enzyme involved in making cholesterol
  • Decrease cholesterol production by the liver and increase clearance lof LDL from blood.
  • Also reduce triglycerides and slightly increase HDL
  • These effects slow the atherosclerotic process.
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21
Q

Statins - Side effects

A
  • Headache
  • GI disturbances
  • Aches to serious myopathy; or rarely rhabdomyolysis
  • rise in liver enzymes ; drug-induced hepatitis
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22
Q

Statins - Contraindications

A

None

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23
Q

Statins - Caution

A
  • Hepatic impairment
  • Renal impairment
  • Pregnant (cholesterol essential in foetal development)
  • Breastfeeding
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24
Q

Statins - Key interactions

A

Metabolism of statins reduced by cytochrome P450 inhibitors:
- amiodarone
- diltiazem
- macrolides
- protease inhibitors
These lead to accumulation of the statin in the body which can increase risk of adverse effects.

Amlodipine

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25
Q

Statins - Monitoring

A

Primary prevention :
- Check lipid profile before treatment and 3 months after treatment : aim for 40% reduction in non-HDL levels.

Secondary prevention:
- Check for target cholesterol levels.

Safety:

  • Check liver enzymes at baseline and 3 & 12 months.
  • Rise in ALT is normal upto 3 times upper limit of normal.
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26
Q

Statins - Patient Education

A
  • Simvastatin is traditionally taken in the evening.

- Inform patient that the medication is to reduce risk of heart attack or stroke

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27
Q

Warfarin - Main indications

A

1) Venous thromboembolism - Treatment and prevention of recurrence
2) To prevent arterial embolism in patients with AF or prosthetic valves.
- short- term for tissue valve replacement
- lifelong for mechanical valve replacement

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28
Q

Warfarin - MOA

A

Clot formation is driven by coagulation cascade.

  • Warfarin inhibits hepatic production of vitamin K-dependent coagulation factors.
  • It does this by inhibiting vitamin K epoxide reductase.
  • the enzyme responsible for restoring vitamin K to its reduced form, necessary as a co-factor in the synthesis of these clotting factors.
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29
Q

Warfarin - How can it be reversed?

A
  • Can be reversed by phytomenadione (vitamin K) or dried prothrombin complex
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30
Q

Warfarin - Side effects

A
  • Bleeding

- Epistaxis or retroperitoneal haemorrhage

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31
Q

Warfarin - Contraindications

A
  • Immediate risk of haemorrhage

- 1st trimester of pregnancy

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32
Q

Warfarin - Caution

A
  • Liver disease : patients who are less able to metabolise the drug at risk
  • later on pregnancy due to the risk of peripartum haemorrhage
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32
Q

Warfarin - Key interactions

A
  • CYP inducers e.g phenytoin, carbamazpine, rifampicin : increases warfarin metabolism + risk of clots
  • CYP inhibitors e.g. fluconazole, macrolides : decrease warfarin metabolism + increase bleeding risk
  • Antibiotics - increase warfarin effect by killing gut flora that synthesise vitamin K.
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34
Q

Warfarin - Patient Education

A
  • Advice patients it is balance between benefits (prevent clot) and risks (bleeding)
  • Patient receive an anticoagulant book (‘Yellow Book’)
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35
Q

Warfarin - Prescription

A
  • Usually taken with heparin (fast onset action). Heparin should. be stopped once INR is in target range.
  • Doses are guided by INR
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36
Q

Warfarin - Monitoring

A
  • INR is the prothrombin time of a person on warfarin divided by that of a non-warfarinised ‘control’.
  • Target INR varies by indication.
  • Once stable dose of warfarin is established, INR measurement is less frequent.
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37
Q

Heparin - Types and Examples

A

Types:

  • unfractionated heparin (UFH)
  • low molecular weight heparin (LMWH)

Examples:
LMWH:
- enoxaparin
- dalteparin

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38
Q

Heparin - Main indications

A

1) Usually LMWH - primary prevention of DVT and PE (VTE).
- An option for VTE until oral anticoagulation is established.
2) ACS : LMWH is used with anti-platelet agents to reduce clot progression or maintain revascularisation

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39
Q

Heparin - MOA

A
  • Antithrombin (AT) inactivates clotting factors (esp : IIa - thrombin and Xa), providing a natural break to the clotting process.
  • Heparin act by enhancing the anticoagulant effect of AT.

Size of heparin molecule determines the specificity :

  • UFH (large & small) - promotes inactivation of both IIa and Xa
  • LMWH (smaller) - specific for factor Xa
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40
Q

Heparin - Side effects

A
  • Main SE : haemorrhage
  • Bruising at injection at site
  • Hyperkalaemia
  • Rare : immune reaction to heparin resulting in low platelet count and thrombosis (heparin-induced thrombocytopenia, HIT) - less likely with LMWH than UFH
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41
Q

Heparin - Contraindication

A

N/A

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42
Q

Heparin - Caution

A

Increased risk of bleeding:

  • clotting disorders
  • severe uncontrolled hypertension
  • recent surgery or trauma

Withheld before and after invasive procedures : lumbar puncture & spinal anaesthesia.

Renal impairment : LMWH accumulate so low dose UFH should be used

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43
Q

Heparin - Key interactions

A

Combing with other antithrombotic drugs (warfarin) has an additive effect.
- Desired in ACS but has increased risk of bleeding so should be otherwise avoided

In major bleeding, protamine is an option to reverse heparin anticoagulation.
- Effective for UFH but less for LMWH

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44
Q

Heparin - Prescription

A
  • Usually given SC

- Depends on indication and body weight

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45
Q

Heparin - Monitoring

A

LMWH’s effect is predictable
- In pregnancy and renal impairment : antifactor Xa activity is measured.

UFH is not predicatble

  • Dosage is titrated against the activated partial thromboplastin ration (APTR: 1.5-2.5 target)
  • FBC, baseline clotting and renal profiles done before treatment.

In prolonged therapy (>4 days) : platelet count and serum potassium concentration should be monitored.
- Risk of thrombocytopenia and hyperkalaemia increases with duration of therapy.

-Seek medical advice if platelt count drop significanlty : can signify HIT

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46
Q

Heparin - Patient Education

A
  • In VTE prophylaxis, explain that you are offering a daily injection to reduce the risk of blood clots.
  • Avoid activities that may increase their risk of bleeding
  • Patient must be trained to take SC injection, or district nurse must administer.
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47
Q

Direct Oral Anticoagulants - Examples

A
  • Apixaban
  • Dabigatran
  • Edoxaban
  • Rivaroxaban
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48
Q

Direct Oral Anticoagulants - Main Indications

A

1) Venous thromboembolism : as treatment and prevention of recurrence. (secondary prevention)
2) Atrial Fibrillation : Prevent stroke and systemic embolism in patients with non-vulvular AF with at least 1 risk factor (prev stoke, symptomatic HF, DM or HTN)

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49
Q

Direct Oral Anticoagulants - MOA

A

The DOACs act on the final common pathway of the coagulation cascade, comprising factor X, thrombin and fibrin.

  • Apixaban, edoxaban and rivaroxaban directly inhibit activated factor X (Xa), preventing conversion of prothrombin to thrombin.
  • Dabigatran directly inhibits thrombin, preventing the conversion of fibrinogen to fibrin.

–> less effective in the arterial circulation as clots are mainly platelet driven - better prevented by antiplatelets

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50
Q

Direct Oral Anticoagulants - Adverse Effects

A

Most common : bleeding
- epistaxis, GI and GU haemorrhage
- increased risk of GI bleeding
(intraluminal drug accumulation causing local anticoagulant effect )

Other AE :

  • Anaemia
  • GI upset
  • Dizziness
  • Elevated liver enzymes
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51
Q

Direct Oral Anticoagulants - Contraindication

A
  • Active, clinically significant bleeding
  • Risk factors for major bleeding : peptic ulceration, cancer, and recent surgery or trauma.
  • Pregnancy
  • Breastfeeding
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52
Q

Direct Oral Anticoagulants - Caution

A

Hepatic or renal disease

  • DOACs are excreted by mulptiple routes, including CYP enzyme metabolism and elimination in faeces and urine.
  • So may need dose reduction or alternative .
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53
Q

Direct Oral Anticoagulants - Interactions

A

Other antithrombotic agents:

  • increased risk bleeding
  • e.g. heparin, antiplatelets and NSAIDs.

Macrolides, protease inhibitors, flucanazole.
- increased the effect of DOACs by affecting their metabolism and excretion.

Rifampicin and phenytoin
- decreased effect

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54
Q

Direct Oral Anticoagulants - Prescription

A
  • Dosage and duration depends on indication.

- Can be started without heparin treatment

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55
Q

Direct Oral Anticoagulants - Monitoring

A

Do not require monitoring

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56
Q

Direct Oral Anticoagulants - Patient Education

A
  • Patient should have alert card.
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57
Q

Loop Diuretics - Examples

A
  • Furosemide

- Bumetanide

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58
Q

Loop Diuretics - Indications

A

1) Acute pulmonary oedema :
- for relief of breathlessness
- in conjunction with oxygen and nitrates

2) Chronic heart failure : symptomatic treatment of fluid overload

3) Other oedematous states: :
- e.g. due to renal disease or liver failure
- in combination with other diuretics

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59
Q

Loop Diuretics - MOA

A
  • Acts on the ascending limb of the loop of henle
  • inhibit the Na+/K+/2Cl- co-transporter.
  • This protein is responsible for transporting sodium, potassium and chloride ions from the tubular lumen into the epithelial cell.
    Water then follows by osmosis.
  • loop diuretics prevents this effect.
  • Also causes dilatation of capacitance veins.
  • In acute HF : this reduces preload and improves contractile function of the ‘overstretched’ heart muscle.
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60
Q

Loop Diuretics - Adverse Effects

A
  • Dehydration
  • Hypotension
  • Low electrolyte state
  • Hearing loss & tinnitus
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61
Q

Loop Diuretics - Contraindication

A
  • Hypovolaemia

- Dehydration

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62
Q

Loop Diuretics- Caution

A
  • Hepatic encephalopathy
  • Hypokalaemia and/or hyponatraemia
  • Gout (inhibited uric acid excretion)
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63
Q

Loop Diuretics - Interactions

A

Affect drugs that are excreted by the kidneys. E.g:

  • Lithium levels are increased due to reduced excretion
  • increased risk of digoxin toxicity - diuretic associated hypokalaemia
  • increase the ototoxicity and nephrotoxicity of amino-glycosides
64
Q

Loop Diuretics - Prescription

A
  • oral and IV preparations
65
Q

Loop Diuretics - Monitoring

A

For efficacy:

  • Acute management: monitor symptoms (tachycardia, hypertension & oxygen requirement)
  • Long-term therapy: monitor symptoms, signs and body weight (body loss of no more than 1kg/day)

For safety:
- periodic monitoring of serum sodium, potassium and renal function in first few weeks of therapy

66
Q

Loop Diuretics - Patient Education

A

Explain:

  • body is overloaded with water
  • treatment will increase urine flow
  • pass water more often
  • provided doses are not taken late in the day, it should not affect them at night
67
Q

Thiazide and Thiazide- Like Diuretics - Examples

A
  • Bendroflumethazide
  • Indapamide
  • Chlortalidone
68
Q

Thiazide and Thiazide- Like Diuretics - Indications

A

1) Hypertension : alternative 1st line when CCB would otherwise be used
2) Hypertension: add-on in patients whose BP not controlled by CCB plus ACEi or ARB

69
Q

Thiazide and Thiazide- Like Diuretics - MOA

A
  • Inhibit the Na+/Cl- co-transporter in the distal convoluted tubule of the nephron
  • Prevents reabsorption of sodium and osmotically related water.
70
Q

Thiazide and Thiazide- Like Diuretics - Adverse Effects

A
  • Hyponatraemia
  • Hypokalaemia
  • Cardiac arrhytmias
  • (may increase plasma conc of glucose, LDL and triglycerides)
  • Impotence in men
71
Q

Thiazide and Thiazide- Like Diuretics - Contraindications

A
  • Hypokalaemia
72
Q

Thiazide and Thiazide- Like Diuretics - Caution

A
  • Hyponatraemia

- Gout

73
Q

Thiazide and Thiazide- Like Diuretics - Interactions

A
  • Effectiveness may reduce NSAIDs (low dose aspirin is not a concern)
  • Avoid loop diuretics (lower serum k+ conc)
74
Q

Thiazide and Thiazide- Like Diuretics - Prescribing

A
  • Oral

- higher-dose increase side effects w/o improving HTN

75
Q

Thiazide and Thiazide- Like Diuretics - Monitoring

A

Efficacy:

  • patient’s BP
  • severity of oedema
  • Measure patient’s serum electrolyte conc before drug, 2-4 weeks into therapy and after any change in therapy
76
Q

Thiazide and Thiazide- Like Diuretics - Patient Education

A
  • Explain treatment with a ‘water tablet’ for their high BP.
  • If they have leg swelling - tablet helps.
  • Will make them pass urine more
  • anti-inflammatory drugs like ibuprofen may reduce effectiveness of diuretics
  • at review, ask male patients about impotence
77
Q

Beta Blockers - Examples

A
  • Bisoprolol
  • Atenolol
  • Propanolol
  • Metoprolol
  • Carvedilol
78
Q

Beta Blockers - Indications

A

1) Ischaemic heart disease : improve symptoms and prognosis associated with - angina and ACS
2) Chronic HF: Bisoprolol and carvedilol used to improve prognosis
3) AF : reduce ventricular rate in paroxysmal AF - maintain sinus rhythm
4) Supraventricular tachycardia: In patients w/o circulatory compromise to restore sinus rhythm
5) HTN : used when other medications are insufficient or inappropriate

79
Q

Beta Blockers - MOA

A

β1-adrenoreceptors are located mainly in the heart.
β2-adrenoreceptors are found mostly in smooth muscle of blood vessels and airways.

  • β-blockers reduce force of contraction and speed of conduction in the heart.
  • relieves myocardial ischaemia by reducing cardiac work and oxygen demand increasing myocardial perfusion

Improve prognosis in HF:
- ‘protecting’ the heart from chronic sympathetic stimulation

Slow the ventricular rate in AF:

  • by prolonging the refractory period of AV node.
  • through the same effect, they terminate SVT

In HTN :
- β-blockers lower BP by reducing renin secretion from the kidney, since this is mediated by β1-receptors

80
Q

Beta Blockers - Adverse Effects

A

Common:

  • Fatigue
  • Cold extremities
  • Headaches
  • GI disturbances ( nausea)

Can cause:

  • sleep disturbances & nightmares
  • impotence in men
81
Q

Beta Blockers - Contraindications

A
  • Asthma

- Heart block

82
Q

Beta Blockers - Caution

A
  • Heart Failure
  • Haemodynamic instability
  • Hepatic Failure
83
Q

Beta Blockers - Interactions

A

Should not be used:

  • non-dihydropyridine CCB (e.g. verapamil, diltiazem)
  • this combo can cause HF, bradycardia and asystole
84
Q

Beta Blockers - Prescription

A

Oral regular medication

IV is available for rapid effect

85
Q

Beta Blockers - Monitoring

A

Monitor patient’s symptoms ( chest pain) and heart rate

86
Q

Beta Blockers - Patient Education

A
  • Explain the rationale for treatment
  • Discuss common SE inc impotence
  • In HF : warn risk of initial deterioration in their symptoms and advise to seek medical attention if this occurs.
  • Obstructive airway disease: stop treatment if there is any breathing difficulty
87
Q

α-blockers - Examples

A
  • Doxazosin
  • Tamsulosin
  • Alfuzosin
88
Q

α-blockers - Indications

A

1) Benign Prostatic Enlargement:

2) Resistant HTN: when other medicines are insufficient

89
Q

α-blockers - MOA

A

Drugs are highly selective for α1-adrenoceptor.

  • α1-adrenoceptors are found mainly in smooth muscle, including in blood vessels and the urinary tract.
  • stimulation induces contraction; blockade induces relaxation

Therefore, α1-blockers causes: - vasodilatation

  • a fall in blood pressure (BP)
  • reduced resistance to bladder outflow
90
Q

α-blockers - Adverse Effects

A
  • Postural hypotension
  • Dizziness
  • Syncope
91
Q

α-blockers - Contraindications

92
Q

α-blockers - Caution

A
  • Should not be used in existing postural hypotension
93
Q

α-blockers - Interactions

A
  • To avoid pronounced 1st dose hypotension, omit one or more antihypertensive tot avoid additive effect.
94
Q

α-blockers - Prescription

A
  • Doxazosin and tamsulosin is the most commonly prescribed
95
Q

α-blockers - Monitoring

A

Efficacy:
- patient’s urinary symptoms and/or BP

For tolerability and safety:

  • enquire about symptom
  • measure BP : lying and standing
96
Q

α-blockers - Patient Education

A

Explain the treatment is for urinary symptoms or BP.

  • may cause dizziness on standing
  • take medicine at bedtime to minimise impact
97
Q

Calcium Channel Blockers - Examples

A
  • Amlodipine
  • Nifedipine
  • Diltiazem
  • Verapamil
98
Q

Calcium Channel Blockers - Indications

A

1) HTN: Amlodipine & Nifedipine used for 1st and 2nd line.
- Reduce risk of stroke, MI and death from CVD

2) Stable Angina : control symptoms
3) Supraventricular arrhythmias (SVT, Atrial flutter, AF): Diltiazem and Verapamil are used to control cardiac rate

99
Q

Calcium Channel Blockers - MOA

A
  • Decrease Ca2+ entry into vascular and cardiac cells
  • Reducing intracellular calcium concentration.
  • This causes relaxation and vasodilation in arterial smooth muscle, lowering arterial pressure.
  • In the heart, calcium channel blockers reduce myocardial contractility.
  • They suppress cardiac conduction, particularly across the atrioventricular (AV) node, slowing ventricular rate.
  • Reduced cardiac rate, contractility and afterload reduce myocardial oxygen demand, preventing angina.
100
Q

Calcium Channel Blockers - Adverse Effects

A

Amlodipine & Nifedipine - Common:

  • Ankle swelling
  • Flushing
  • Headache
  • Palpitations
Verapamil - 
Common:
- Constipation
Less common:
- Bradycardia
- Heart Block
- Cardiac Failure

Diltiazem:
mixed vascular and cardiac actions.

101
Q

Calcium Channel Blockers - Contraindications

A

Amlodipine & Nifedipine:

  • Unstable angina
  • Severe aortic stenosis

Verapamil & Diltiazem:
- AV nodal conduction delay

102
Q

Calcium Channel Blockers - Caution

A

Verapamil & Diltiazem:
- poor left ventricular function
-

103
Q

Calcium Channel Blockers - Interactions

A
  • Should not be prescribed with β-blockers
104
Q

Calcium Channel Blockers - Prescribing

105
Q

Calcium Channel Blockers - Monitoring

A

Efficacy:
- regular monitoring of BP

Enquire:

  • chest pain for angina
  • pulse rate from examination or ECG
106
Q

Calcium Channel Blockers - Patient Education

A
  • Purpose of medication depending on indication
  • Discuss other measure to reduce CV risk inc smoking cessation.
  • Discuss common SE esp ankle oedema.
107
Q

Calcium Channel Blockers - Classification

A

Two classes:
Dihydropyridines:
- E.g.: Amlodipine & Nifedipine,
- Relatively selective for the vasculature

Non-dihydropyridines:

  • More selective for the heart.
  • Verapamil is the most cardioselective
  • Diltiazem has some effects on blood vessels also.
108
Q

Angiotensin - converting enzyme inhibitors (ACEi) - Examples

A
  • Ramipril
  • Lisinopril
  • Perindopril
109
Q

ACEi - Indications

A

1) HTN : 1st or 2nd line. Reduce risk of stroke, MI & death from CVD
2) Chronic HF: 1st line, to improve symptoms & prognosis
3) Ischaemic heart disease: reduce CV events e.g. MI & stroke
4) Daibetic nephropathy & CKD with proteinuria: reduce proteinuria & progression of nephropathy

110
Q

ACEi - MOA

A
  • ACEi block the action of ACE, to prevent the conversion of angiotensin I to angiotensin II.
  • Angiotensin II is a vasoconstrictor and stimulates aldosterone secretion.
  • Blocking its action reduces peripheral vascular resistance (afterload), which lowers BP.
  • Dilates the efferent glomerular arteriole, which reduces intraglomerular pressure and slows the progression of CKD.
  • Reducing the aldosterone level promotes sodium and water excretion.
  • This can help to reduce venous return (preload), which is beneficial in HF.
111
Q

ACEi - Adverse Effects

A

Common:

  • hypotension
  • persistent dry cough
  • hyperkalaemia
  • renal failure

Rare:

  • angioedema
  • anaphylactoid reactions
112
Q

ACEi - Contraindications

A
  • Renal artery stenosis
  • AKI
  • Pregnancy
  • Breastfeeding
113
Q

ACEi - Caution

114
Q

ACEi - Interactions

A
  • Avoid with other potassium -elevating drugs icluding potassium supplement and potassium-sparing diuretics due to risk of hyperkalaemia.
  • Combination with NSAID increases the risk of nephrotoxicity
115
Q

ACEi - Prescription

116
Q

ACEi - Monitoring

A

Efficacy:

  • Monitor clinically : reduced symptoms of breathlessness in heart failure or improved BP control in HTN.
  • Check BP in 4 weeks

Safety:

  • Check electrolytes and renal function before starting treatment.
  • Check U & E 1-2 weeks after initiation and after each dose change
  • ACE should be stopped if the serum creatinine concentration rises more than 30% or the estimated GFR falls more than 25%.
  • If serum potassium rises above 5.0 mmol/L, stop other potassium-elevating and nephrotoxic drugs (see Important interactions).
  • If, despite this, it remains above 5.0 mmol/L, reduce the dose of ACE inhibitor.
  • If it exceeds 6.0 mmol/L, stop the ACE inhibitor and seek expert advice.
117
Q

ACEi - Patient Education

A
  • Explain medication is to improve blood pressure and reduce strain on their heart.
  • Advise on common SE: dry cough, dizziness.
  • Mention that, very rarely, this medicine can cause effects similar to severe allergic reactions; they should stop taking it and seek urgent medical advice if they develop facial swelling or stomach pains.
  • Explain need for blood test monitoring.
  • Explain that ACE inhibitors can interfere with their kidney function and upset potassium balance.
  • Advise them to avoid taking over-the-counter antiinflammatories (e.g. ibuprofen) due to the risk of kidney damage.
118
Q

Angiotensin Receptor Blockers - Examples

A
  • Losartan
  • Candesartan
  • Irbesartan
119
Q

ARBs - Indication

A

Usually used when ACEi are not tolerated due to cough.

1) HTN : 1st or 2nd line. Reduce risk of stroke, MI & death from CVD
2) Chronic HF: 1st line, to improve symptoms & prognosis
3) Ischaemic heart disease: reduce CV events e.g. MI & stroke
4) Daibetic nephropathy & CKD with proteinuria: reduce proteinuria & progression of nephropathy

120
Q

ARBs - MOA

A
  • ARBs have similar effects to ACE inhibitors.
  • ARBs block the action of angiotensin II on the angiotensin type 1 (AT1) receptor.
  • Angiotensin II is a vasoconstrictor and stimulates aldosterone secretion.
  • Blocking its action reduces peripheral vascular resistance (afterload), which lowers blood pressure.
  • It particularly dilates the efferent glomerular arteriole, which reduces intraglomerular pressure and slows the progression of CKD.
  • Reducing the aldosterone level promotes sodium and water excretion.
  • This can help to reduce venous return (preload), which has a beneficial effect in heart failure.
121
Q

ARBs - Adverse Effects

A
  • Hypotension (esp after 1st dose)
  • Hyperkalaemia
  • Renal failure
  • Unlike ACEi, less likely to cause dry cough and angioedema
122
Q

ARBs - Contraindications

A
  • Renal artery stenosis
  • AKI
  • Pregnant
  • Breastfeeding
123
Q

ARBs - Caution

A
  • Lower doses in CKD (renal function must be monitored closely)
124
Q

ARBs - Interactions

A
  • Avoid with other potassium -elevating drugs icluding potassium supplement and potassium-sparing diuretics due to risk of hyperkalaemia.
  • Combination with NSAID increases the risk of nephrotoxicity
125
Q

ARBs - Prescription

A

….

  • Can be taken with or without food
  • Best to take the 1st dose before bed to reduce symptomatic hypotension
126
Q

ARBs - Monitoring

A

Efficacy:
- Monitor clinically : reduced symptoms of breathlessness in heart failure or improved BP control in HTN.

Safety:

  • Check electrolytes and renal function before starting treatment.
  • ACE should be stopped if the serum creatinine concentration rises more than 30% or the estimated GFR falls more than 25%.
  • If serum potassium rises above 5.0 mmol/L, stop other potassium-elevating and nephrotoxic drugs (see Important interactions).
  • If, despite this, it remains above 5.0 mmol/L, reduce the dose of ACE inhibitor.
  • If it exceeds 6.0 mmol/L, stop the ACE inhibitor and seek expert advice.
127
Q

ARBs - Patient Education

A
  • Explain medication is to improve blood pressure and reduce strain on their heart.
  • Advise on common SE: dry cough, dizziness.
  • Explain if the previously had cough, ARBs does not cause cough.
  • Explain need for blood test monitoring.
  • Explain that ARBs can interfere with their kidney function and upset potassium balance.
  • Advise them to avoid taking over-the-counter antiinflammatories (e.g. ibuprofen) due to the risk of kidney damage.
128
Q

Mineralocorticoid Receptor Antagonist - Examples

A

AKA - Aldosterone anatonists

Examples:

  • Spironolactone
  • Eplerenone
129
Q

MRA - Indications

A

1) Ascites & odema due to liver cirrhosis : spironolactone is the 1st line diuretic
2) Chronic HF :

130
Q

MRA - MOA

A
  • Aldosterone is a mineralocorticoid that is produced in the adrenal cortex.
  • It acts on mineralocorticoid receptors in the distal tubules of the kidney to increase the activity of luminal epithelial sodium (Na+) channels (ENaC).
  • This increases the reabsorption of sodium and water, elevating blood pressure, with a corresponding increase in potassium excretion.
  • Aldosterone antagonists inhibit the effect of aldosterone by competitively binding to the aldosterone receptor.
  • This increases sodium and water excretion and potassium retention.
  • Their effect is greatest when circulating aldosterone is increased, e.g. in primary hyperaldosteronism or cirrhosis.
131
Q

MRA - Adverse Effects

A
  • Hyperkalaemia : can lead to muscle weakness , arrhythmias & even cardiac arrest
  • Gynaecomastia
  • Can cause liver impairment and jaundice
  • Can cause Stevens–Johnson syndrome (a T-cell-mediated hypersensitivity reaction) that causes a bullous skin eruption.
132
Q

MRA - Contraindications

A
  • Severe renal impairment
  • Hyperkalaemia
  • Addison’s disease
133
Q

MRA - Caution

A
  • Pregnancy or lactating women
134
Q

MRA - Interactions

A
  • Combination with other potassium-elevating drugs increases the risk of hyperkalaemia.
  • However, this combination may be beneficial in HF.
  • Avoided with potassium supplements.
135
Q

MRA - Prescribing

A

….

  • Should be taken with food
  • Taken several days to start having an effect
136
Q

MRA - Monitoring

A

Efficacy:

  • Monitored by patient report of symptoms and clinical findings.
  • E.g. reduction in ascites, oedema and/or blood pressure.

Safety:

  • Monitored by checking renal function and serum potassium concentration.
  • Due to the risk of renal impairment and hyperkalaemia.
137
Q

MRA - Patient Education

A
  • Warn men about the possibility of growth and tenderness of tissue under the nipples and impotence.
  • Reassure them that such effects are benign and reversible, but acknowledge that they may be uncomfortable and embarrassing.
  • Ask patients to return if they have troublesome side effects, as these may respond to dose reduction.
  • Advise all patients that aldosterone antagonists can cause their potassium level to rise and reinforce the importance of attending for blood tests.
138
Q

Nitrates - Examples

A
  • Glyceryl Trinitrate (GTN)

- Isosorbide mononitrate

139
Q

Nitrates - Indications

A

1) Short acting (GTN)
- Acute angina
- Chest pain associated with ACS

2) Long acting (ISO)
- Prophylaxis of angina ( when beta-blocker & CCB is not tolerated)

3) IV Nitrate
- Pulmonary oedema (with furosemide & oxygen)

140
Q

Nitrates - MOA

A
  • Nitrates are converted to NO.
  • NO increases cGMP synthesis & reduces intracellular Ca2+ in vascular smooth muscle cells causing them to relax.
  • Results in venous & artial vasodilation.
  • Which reduced cardiac preload & ventricular filling.
  • Essentially reducing cardiac work & myocardial oxygen demand - relieving angina & cardiac failure.
  • Nitrates can relieve coronary vasospasm & dilate collateral vessels –> improving coronary perfusion.
141
Q

Nitrates - Adverse Effects

A
  • Flushing
  • Headaches
  • Light- headedness
  • Hypotension

-Prolonged use can lead to tolerance

142
Q

Nitrates - Contraindications

A
  • Severe Aortic stenosis
  • Haemodynamic instability
  • Hypotension
143
Q

Nitrates - Interaction

A

Phosphodiesterase (PDE) inhibitors –> sildenafil
- prolong & enhance the hypotensive effect.

Used with caution for those with antihypertensive medication

144
Q

Nitrates - Prescribing

A
  • Stable angina - sublingual tablets or spray

- ACS or HF - continuous IV infusion

145
Q

Nitrates - Monitoring

A
  • Best indication of efficacy is patients symptoms

- Monitor BP

146
Q

Nitrates - Patient Education

A
  • Nitrate relieve chest pain and/or breathlessness
  • Side effects
  • Due to possible postural hypotension, advise patient to sit down and rest for 5 minutes
147
Q

Digoxin - Indications

A

1) Atrial Fibrillation & Atrial flutter
- Reduce ventricular rate

2) Severe Heart Failure
- option for pt already on ACEo, BB, ARB

148
Q

Digoxin - MOA

A
  • Negatively Chronotropic –> reduces heart rate
  • Positively Inotropic –> increases force of contraction

In AF = increased vagal (parasympathetic) tone
- reduces conduction at AV node –> prevents some impulses from being transmitted to the ventricle –> thus reducing ventricular rate

In Heart Failure = direct effect on myocytes through inhibition of Na+/K+ enzyme pump causing Na+ to accumulate in the cell.

  • Cellular extrusion of Ca2+ requires low intracellular Na+ conc
  • Elevation of intracellular Na+ causes Ca2+ to accumulate in the cell –> thus increasing contractile force
149
Q

Digoxin - Adverse Effects

A
  • Bradycardia
  • GI disturbances
  • Rash
  • Dizziness
  • Visual disturbance (blurred or yellow vision)
150
Q

Digoxin - Contraindications

A
  • 2nd degree heart block
  • Intermittent complete heart block
  • Ventricular arrhythmias
151
Q

Digoxin - Caution

A
  • Renal failure (digoxin is eliminated in kidneys)
  • Hypokalaemia
  • Hypomagnesaemia
  • Hypercalcaemia
152
Q

Digoxin - Interactions

A

Loop & thiazide diuretic
–>digoxin toxicity by hypokalaemia

Amiodarone, CCB, spironolactone, quinine
–> increase plasma conc of digoxin thus toxicity

153
Q

Digoxin - Prescription

A
  • Oral or IV

- taken with or without food

154
Q

Digoxin - Monitoring

A
  • Monitor symptoms & heart rate
  • Check ECG
  • In acute setting -> regular cardiac monitoring
155
Q

Digoxin - Patient Education

A
  • Slow heart and make heart beat more strong

- Common SE : sickness, diarrhoea, headache

Applied Pharmacology (11 decks)

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