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
Statins - Monitoring
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.
26
Statins - Patient Education
- Simvastatin is traditionally taken in the evening. | - Inform patient that the medication is to reduce risk of heart attack or stroke
27
Warfarin - Main indications
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
28
Warfarin - MOA
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.
29
Warfarin - How can it be reversed?
- Can be reversed by phytomenadione (vitamin K) or dried prothrombin complex
30
Warfarin - Side effects
- Bleeding | - Epistaxis or retroperitoneal haemorrhage
31
Warfarin - Contraindications
- Immediate risk of haemorrhage | - 1st trimester of pregnancy
32
Warfarin - Caution
- Liver disease : patients who are less able to metabolise the drug at risk - later on pregnancy due to the risk of peripartum haemorrhage
32
Warfarin - Key interactions
- 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.
34
Warfarin - Patient Education
- Advice patients it is balance between benefits (prevent clot) and risks (bleeding) - Patient receive an anticoagulant book ('Yellow Book') - ---------------------------------------------------
35
Warfarin - Prescription
- Usually taken with heparin (fast onset action). Heparin should. be stopped once INR is in target range. - Doses are guided by INR
36
Warfarin - Monitoring
- 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.
37
Heparin - Types and Examples
Types: - unfractionated heparin (UFH) - low molecular weight heparin (LMWH) Examples: LMWH: - enoxaparin - dalteparin
38
Heparin - Main indications
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
39
Heparin - MOA
- 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
40
Heparin - Side effects
- 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
41
Heparin - Contraindication
N/A
42
Heparin - Caution
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
43
Heparin - Key interactions
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
44
Heparin - Prescription
- Usually given SC | - Depends on indication and body weight
45
Heparin - Monitoring
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
46
Heparin - Patient Education
- 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.
47
Direct Oral Anticoagulants - Examples
- Apixaban - Dabigatran - Edoxaban - Rivaroxaban
48
Direct Oral Anticoagulants - Main Indications
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)
49
Direct Oral Anticoagulants - MOA
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
50
Direct Oral Anticoagulants - Adverse Effects
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
51
Direct Oral Anticoagulants - Contraindication
- Active, clinically significant bleeding - Risk factors for major bleeding : peptic ulceration, cancer, and recent surgery or trauma. - Pregnancy - Breastfeeding
52
Direct Oral Anticoagulants - Caution
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 .
53
Direct Oral Anticoagulants - Interactions
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
54
Direct Oral Anticoagulants - Prescription
- Dosage and duration depends on indication. | - Can be started without heparin treatment
55
Direct Oral Anticoagulants - Monitoring
Do not require monitoring
56
Direct Oral Anticoagulants - Patient Education
- Patient should have alert card.
57
Loop Diuretics - Examples
- Furosemide | - Bumetanide
58
Loop Diuretics - Indications
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
59
Loop Diuretics - MOA
- 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.
60
Loop Diuretics - Adverse Effects
- Dehydration - Hypotension - Low electrolyte state - Hearing loss & tinnitus
61
Loop Diuretics - Contraindication
- Hypovolaemia | - Dehydration
62
Loop Diuretics- Caution
- Hepatic encephalopathy - Hypokalaemia and/or hyponatraemia - Gout (inhibited uric acid excretion)
63
Loop Diuretics - Interactions
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
Loop Diuretics - Prescription
- oral and IV preparations
65
Loop Diuretics - Monitoring
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
Loop Diuretics - Patient Education
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
Thiazide and Thiazide- Like Diuretics - Examples
- Bendroflumethazide - Indapamide - Chlortalidone
68
Thiazide and Thiazide- Like Diuretics - Indications
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
Thiazide and Thiazide- Like Diuretics - MOA
- Inhibit the Na+/Cl- co-transporter in the distal convoluted tubule of the nephron - Prevents reabsorption of sodium and osmotically related water.
70
Thiazide and Thiazide- Like Diuretics - Adverse Effects
- Hyponatraemia - Hypokalaemia - Cardiac arrhytmias - (may increase plasma conc of glucose, LDL and triglycerides) - Impotence in men
71
Thiazide and Thiazide- Like Diuretics - Contraindications
- Hypokalaemia
72
Thiazide and Thiazide- Like Diuretics - Caution
- Hyponatraemia | - Gout
73
Thiazide and Thiazide- Like Diuretics - Interactions
- Effectiveness may reduce NSAIDs (low dose aspirin is not a concern) - Avoid loop diuretics (lower serum k+ conc)
74
Thiazide and Thiazide- Like Diuretics - Prescribing
- Oral | - higher-dose increase side effects w/o improving HTN
75
Thiazide and Thiazide- Like Diuretics - Monitoring
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
Thiazide and Thiazide- Like Diuretics - Patient Education
- 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
Beta Blockers - Examples
- Bisoprolol - Atenolol - Propanolol - Metoprolol - Carvedilol
78
Beta Blockers - Indications
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
Beta Blockers - MOA
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
Beta Blockers - Adverse Effects
Common: - Fatigue - Cold extremities - Headaches - GI disturbances ( nausea) Can cause: - sleep disturbances & nightmares - impotence in men
81
Beta Blockers - Contraindications
- Asthma | - Heart block
82
Beta Blockers - Caution
- Heart Failure - Haemodynamic instability - Hepatic Failure
83
Beta Blockers - Interactions
Should not be used: - non-dihydropyridine CCB (e.g. verapamil, diltiazem) - this combo can cause HF, bradycardia and asystole
84
Beta Blockers - Prescription
Oral regular medication | IV is available for rapid effect
85
Beta Blockers - Monitoring
Monitor patient's symptoms ( chest pain) and heart rate
86
Beta Blockers - Patient Education
- 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
α-blockers - Examples
- Doxazosin - Tamsulosin - Alfuzosin
88
α-blockers - Indications
1) Benign Prostatic Enlargement: | 2) Resistant HTN: when other medicines are insufficient
89
α-blockers - MOA
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
α-blockers - Adverse Effects
- Postural hypotension - Dizziness - Syncope
91
α-blockers - Contraindications
None
92
α-blockers - Caution
- Should not be used in existing postural hypotension
93
α-blockers - Interactions
- To avoid pronounced 1st dose hypotension, omit one or more antihypertensive tot avoid additive effect.
94
α-blockers - Prescription
- Doxazosin and tamsulosin is the most commonly prescribed
95
α-blockers - Monitoring
Efficacy: - patient's urinary symptoms and/or BP For tolerability and safety: - enquire about symptom - measure BP : lying and standing
96
α-blockers - Patient Education
Explain the treatment is for urinary symptoms or BP. - may cause dizziness on standing - take medicine at bedtime to minimise impact
97
Calcium Channel Blockers - Examples
- Amlodipine - Nifedipine - Diltiazem - Verapamil
98
Calcium Channel Blockers - Indications
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
Calcium Channel Blockers - MOA
- 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
Calcium Channel Blockers - Adverse Effects
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
Calcium Channel Blockers - Contraindications
Amlodipine & Nifedipine: - Unstable angina - Severe aortic stenosis Verapamil & Diltiazem: - AV nodal conduction delay
102
Calcium Channel Blockers - Caution
Verapamil & Diltiazem: - poor left ventricular function -
103
Calcium Channel Blockers - Interactions
- Should not be prescribed with β-blockers
104
Calcium Channel Blockers - Prescribing
....
105
Calcium Channel Blockers - Monitoring
Efficacy: - regular monitoring of BP Enquire: - chest pain for angina - pulse rate from examination or ECG
106
Calcium Channel Blockers - Patient Education
- Purpose of medication depending on indication - Discuss other measure to reduce CV risk inc smoking cessation. - Discuss common SE esp ankle oedema.
107
Calcium Channel Blockers - Classification
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
Angiotensin - converting enzyme inhibitors (ACEi) - Examples
- Ramipril - Lisinopril - Perindopril
109
ACEi - Indications
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
ACEi - MOA
- 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
ACEi - Adverse Effects
Common: - hypotension - persistent dry cough - hyperkalaemia - renal failure Rare: - angioedema - anaphylactoid reactions
112
ACEi - Contraindications
- Renal artery stenosis - AKI - Pregnancy - Breastfeeding
113
ACEi - Caution
- CKD
114
ACEi - Interactions
- 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
ACEi - Prescription
....
116
ACEi - Monitoring
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
ACEi - Patient Education
- 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
Angiotensin Receptor Blockers - Examples
- Losartan - Candesartan - Irbesartan
119
ARBs - Indication
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
ARBs - MOA
- 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
ARBs - Adverse Effects
- Hypotension (esp after 1st dose) - Hyperkalaemia - Renal failure - Unlike ACEi, less likely to cause dry cough and angioedema
122
ARBs - Contraindications
- Renal artery stenosis - AKI - Pregnant - Breastfeeding
123
ARBs - Caution
- Lower doses in CKD (renal function must be monitored closely)
124
ARBs - Interactions
- 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
ARBs - Prescription
.... - Can be taken with or without food - Best to take the 1st dose before bed to reduce symptomatic hypotension
126
ARBs - Monitoring
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
ARBs - Patient Education
- 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
Mineralocorticoid Receptor Antagonist - Examples
AKA - Aldosterone anatonists Examples: - Spironolactone - Eplerenone
129
MRA - Indications
1) Ascites & odema due to liver cirrhosis : spironolactone is the 1st line diuretic 2) Chronic HF :
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MRA - MOA
- 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.
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MRA - Adverse Effects
- 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.
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MRA - Contraindications
- Severe renal impairment - Hyperkalaemia - Addison's disease
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MRA - Caution
- Pregnancy or lactating women
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MRA - Interactions
- Combination with other potassium-elevating drugs increases the risk of hyperkalaemia. - However, this combination may be beneficial in HF. - Avoided with potassium supplements.
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MRA - Prescribing
.... - Should be taken with food - Taken several days to start having an effect
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MRA - Monitoring
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.
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MRA - Patient Education
- 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.
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Nitrates - Examples
- Glyceryl Trinitrate (GTN) | - Isosorbide mononitrate
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Nitrates - Indications
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)
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Nitrates - MOA
- 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.
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Nitrates - Adverse Effects
- Flushing - Headaches - Light- headedness - Hypotension -Prolonged use can lead to tolerance
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Nitrates - Contraindications
- Severe Aortic stenosis - Haemodynamic instability - Hypotension
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Nitrates - Interaction
Phosphodiesterase (PDE) inhibitors --> sildenafil - prolong & enhance the hypotensive effect. Used with caution for those with antihypertensive medication
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Nitrates - Prescribing
- Stable angina - sublingual tablets or spray | - ACS or HF - continuous IV infusion
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Nitrates - Monitoring
- Best indication of efficacy is patients symptoms | - Monitor BP
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Nitrates - Patient Education
- Nitrate relieve chest pain and/or breathlessness - Side effects - Due to possible postural hypotension, advise patient to sit down and rest for 5 minutes
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Digoxin - Indications
1) Atrial Fibrillation & Atrial flutter - Reduce ventricular rate 2) Severe Heart Failure - option for pt already on ACEo, BB, ARB
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Digoxin - MOA
- 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
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Digoxin - Adverse Effects
- Bradycardia - GI disturbances - Rash - Dizziness - Visual disturbance (blurred or yellow vision)
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Digoxin - Contraindications
- 2nd degree heart block - Intermittent complete heart block - Ventricular arrhythmias
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Digoxin - Caution
- Renal failure (digoxin is eliminated in kidneys) - Hypokalaemia - Hypomagnesaemia - Hypercalcaemia
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Digoxin - Interactions
Loop & thiazide diuretic -->digoxin toxicity by hypokalaemia Amiodarone, CCB, spironolactone, quinine --> increase plasma conc of digoxin thus toxicity
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Digoxin - Prescription
- Oral or IV | - taken with or without food
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Digoxin - Monitoring
- Monitor symptoms & heart rate - Check ECG - In acute setting -> regular cardiac monitoring
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Digoxin - Patient Education
- Slow heart and make heart beat more strong | - Common SE : sickness, diarrhoea, headache