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APPLIED PHARMACOLOGY > CARDIOLOGY > Flashcards

CARDIOLOGY Flashcards

1
Q

Antiplatelet drug

What are the common indications of Aspirin?

A
  • Acute coronary syndrome, & acute ischaemic stroke by inhibiting platelet aggregation to prevent arterial thrombosis.
  • For Secondary prevention of major cardiovascular events in Ischaemic heart disease, peripheral vascular disease, or cerebrovascular disease to prolong life.
  • High doses can be used for mild-moderate pain and fever.

Prescription recommendations:
- In ACS, a once-only loading dose of 300mg followed by a regular dose of 75mg daily.
- Initial dose 300mg daily for 2 weeks used for acute ischaemic stroke
- Long term prevention of thrombosis after an acute event low-dose aspirin 75mg daily.
- Pain: Much higher doses of 4g maximum daily
- Should be taken with food

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2
Q

Mechanism of action: Aspirin

A

Inhibits cyclooxygenase (COX) to reduce production of the pro-aggregatory factors such as thromboxane from arachidonic acid.
Reducing the risk arterial occlusion.

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3
Q

Side effects: Aspirin

A
  • GI upset
  • Peptic ulceration
  • Haemorrhage
  • Bronchospasm
  • Tinnitus

Gastroprotection (with PPI) should be considered at low-dose Aspirin for patients with peptic ulcer, or GI complications.

Aspirin overdose is life-threatening as it can cause hyperventilation, metabolic acidosis, hearing changes, cardiovascular collapse, confusion, respiratory arrest.

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4
Q

Who should avoid/ be cautions of this drug?

Contraindications: Aspirin

A
  • Children < 16yrs - risk of Reye’s syndrome (affects liver and brain)
  • Aspirin hypersensitivity - if had bronchospasm before or allergic reaction to NSAID.
  • 3rd trimester in pregnant women
  • Patients with peptic ulcers and gout as it may trigger attack
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5
Q

Drug interactions: Aspirin

A

Increased risk of bleeding if taking with other anti-platelets (clopidogrel) and anticoagulants (Heparin, Warfarin).

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6
Q

Monitoring & stopping: Aspirin

A
  • Antiplatelet therapy is indefinite, should be monitored by efficacy and side effects.
  • Dual antiplatelet therapy, should be limited to 12 months.
  • Aspirin is preferred as long-term therapy for Coronary artery disease and Peripheral Vascular Disease.

Clopidegerel is preferred following stroke or transient ischamic attack (TIA).

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7
Q

Antiplatelet

What are the common indications of Clopidogrel?

A
  • Treatment of acute coronary syndrome, used in combination with aspirin
  • Prevents coronary artery stent occlusion
  • Secondary prevention of major adverse cardiovascular events in people with ischaemic heart disease, cerebrovascular or peripheral vascular disease.
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8
Q

Mechanism of action: Clopidogrel

A
  • Adenosine Diphosphate (ADP) receptor antagonist prevent platelet aggregation, reducing risk of arterial occlusion.
  • Binds to ADP receptors on the surface of platelets.
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9
Q

Side effects: Clopidogrel

A
  • Increased risk of bleeding
  • GI upset: diarrhoea, abdominal pain, indigestion
  • Thrombocytopenia = platelet deficiency. This causes bleeding into the tissues, bruising, and slow blood clotting after injury.
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10
Q

Who should avoid/be cautious of this drug?

Contraindications: Clopidogrel

A
  • Active bleeding
  • Elective surgery (needs to be stopped 7 days before)
  • Kidney and liver impairment
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11
Q

Drug interactions: Clopidogrel

A
  • Efficacy is reduced by Cytochrome P450 (CYP - enzyme in the liver) inhibitors
    e.g. Omeprazole, Erythromycin, Ciprofloxacin, and some antifungals.
  • Dual therapy with other antiplatelet, anticoagulants, or NSAIDs increase risk of bleeding.

Clopidogrel is a pro-drug = activated after intake, metabolises in the liver by cytochrome P450 enzymes. CYP P450 activates the metabolism of drugs and xenobiotics (plant constituents, drugs, pesticides, cosmetics, flavorings, fragrances, food additives, industrial chemicals and environmental pollutants).

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12
Q

Monitoring & stopping: Clopidogrel

A
  • Monitor for adverse side effects
  • Should be long-term but limited to 12 months if dual therapy
  • Seek advice from Cardiologist before stopping dual therapy.
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13
Q

What are the common indications of Statins ?

A
  • Primary prevention of major adverse cardiovascular events like MI or stroke in people over 40yrs with a Q-risk of < 10%.
  • Secondary prevention in people with ischamic heart disease like acute stroke, peripheral vascular diease, and acute coronary syndrome.
  • Dyslipidaemia (high cholesterol regulation)
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14
Q

Mechanism of action: Statins

A
  • Slows/reverses the atherosclerotic process.
  • Inhibits 3-hydroxy-3-methyl-glutaryl coenzyme A ( HMG CoaA) reductase, the enzyme that catalyses the rate-limiting step in cholesterol synthesis.
  • Reduces cholesterol simulating the uptake of low density lipoprotein (LDL) by hepatocytes in the liver.

Lipid lowering effect helps modulate inflammatory response and improve endothelial production.

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15
Q

4 examples of Statins

A

Atorvastatin, Simvastatin, Rosuvastatin, Pravastatin

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16
Q

Side effects: Statins

A
  • Headache
  • GI upset
  • Muscle aches
  • Myopathy
  • Rhabdomyolysis
  • Rise in liver enzymes - drug induced hepatiti*s (inflammation of the liver)
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17
Q

Who should avoid/be cautious this drug?

Contraindications: Statins

A
  • Statins should be used with caution in hepatic impairment.
  • Statins are dependent on the kidneys for elimination of metabolites, so dosage should be reduced in renal impairment.
  • Pregnant women - as cholesterol is essential for normal fetal development.
  • Breastfeeding

With the exception of which Rosuvastatin does not depend on the kidneys to metabolise.

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18
Q

Drug interactions: Statins

A
  • The metabolism of statin (not rosuvastation) is impaired by cytochrome P450 inhibitors. Such as protease inhibitors (ritonavir, saquinavor) amiodarone, itraconazole, macrolides (clarithromycin), diltiazem
  • Grapefruit juice
  • Amlodipine (CCB)

Temporarily STOP statin if on short-term clarithromycin for an acute infection

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19
Q

Monitoring & Stopping: Statin

A
  • Primary prevention of CVD, check lipid profile before starting Statin and at 3 months. Aiming for 40% reduction in non-HDL cholesterol levels.
  • Secondary prevention of CVD, baseline lipid profile is helpful but not essential. Efficacy should be monitored.
  • For safety, check liver enzymes (ALT alanine tranaminase) at baseline, 3 & 12 months.
  • Check creatinine kinase before starting Statin, if experienced unexplained muscle pains.
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20
Q

What are the common indications of
Warfarin?

A
  • Treat and prevent venous thromboembolism (VTE)
  • Prevent arterial embolism from atrial fibrillation
  • Prevent arterial embolism from mechanical heart valves.
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21
Q

Mechanism of action: Warfarin

A
  • Inhibits Vitamin K epoxide reductase, which reduces production of the vitamin K-dependent clotting factors (II, VII, IX, X) to prodcuce an anticoagulant effect.

  • Vitamin K can change how warfarin works, and this changes your International Normalised Ratio/Prothrombin Time test. Vitamin K lowers your INR values.
  • The lower your INR, the less time it takes for your blood to clot. Warfarin raises your INR values. The higher your INR, the more time it takes for your blood to clot.
  • A high INR means that warfarin is working too well, so you bleed more quickly and easily. It should be balanced.
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22
Q

Side effects: Warfarin

A
  • Risk of bleeding from minor trauma
  • Severe over warfarisation can trigger spontaneous bleeding, such as epistaxis or retroperineal haemorrage.
  • Skin necrosis

The effect of warfarin can be reversed with Vitamin K - phytomenadione or dried prothrombin complex!

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23
Q

Drug interactions: Warfarin

A
  • Cytochrome P450 (CYP) inducers like rifampicin, carbamazepine, increase warfarin metabolism and risk of blood clots.
  • Antiplatelet drugs like Aspirin which also have high risk of bleeding.
  • CYP inhibtors (fluconazole, macrolides) decrease warfarin metabolism and increase bleeding risk.
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24
Q

Who should avoid/ be cautions of this drug?

Contraindications: Warfarin

A
  • Contraindicated by the risk of active bleeding.
  • Liver disease impairs the metabolisim of Warfarin and clotting factors synthesis.
  • First trimester of pregnancy due to tetragenicity (fetal cardiac/cranial abnormalities)
  • Full term pregnancy due to risk of peripartum haemorrage

  • Heparin is preferred in pregnancy!
25
Q

Monitoring and Stopping: Warfarin

A
  • The INR is a ratio expressing the intensity of anticoagulation. It is calculated using the Prothrombin time of an individual divided by normal control samples.
  • Target INR ranges depends on the indication, risk-benefit should be reviewed periodically.
  • Long-term treatment used in AF patients, or recurrent VTE
26
Q

Common indications: Heparin

A
  • Used to prevent deep vein thrombosis, and pulmonary embolisim.
  • Used alongside antiplatelet drugs, used to treat acute coronary syndrome to reduce clot progression.
27
Q

Mechanism of action: Heparin

A
  • Enhance the antiplatelet effect of antithrombonin.

  • Antithrombonin inactivates clotting factors that generates a fibrin clot.
28
Q

Side effects: Heparin

A
  • Haemorrage
  • Bruising
  • Hyperkalaemia due to the effect on adrenal aldosterone secretion
  • Heparin-induced thrombocytopenia (HIT)
29
Q

Who should avoid/ be cautions of this drug?

Contraindications: Heparin

A
  • Patients with clotting disorders
  • Severe uncontrolled hypertension
  • Patients going for invasive surgical procedures
  • Renal impairment : low molecular weight heparin (LMWH) accumulate in the kidneys, so lower dose should be used instead or unfractioned heparin (UFH).
30
Q

Drug interactions: Heparin

A
  • Combination with antithrombotic drugs - antiplatelets, like warfarin) can be a beneficial effect, especially for treating ACS - but is associated with increased risk of bleeding.

Promatine can be used as an option to reverse heparin anticoagulation.

31
Q

Monitoring and Stopping: Heparin

A
  • FBC, INR, and renal profiles should be checked before starting treatment.
  • In >4 days, platelet count and serum potassium concentration should be monitored due to risk of hyperkalaemia and thrombocytopenia.
32
Q

DOAC’s are les influenced by diet and other medications

Common indications: Direct oral anticoagulants

A
  • Treatment and prevention of VTE
  • Atrial fibrillation: prevent stroke and systemic embolism in non-vulvar AF.
33
Q

Mechanism of action: Direct oral anticoagulants

A
  • Directly inhibit activated factor X (Xa), preventing conversion of prothrombin to thrombin.
  • All DOACs inhibit fibrin formation, preventing clot formation.

They are less effective in the arterial circulation where clots are largely platelet driven - antiplatelet drugs are better prevention of this.

34
Q

Name 4 examples of Direct oral anticoagulants (DOAC)

A
  • Apixaban
  • Rivaroxaban
  • Dabigatran
  • Edoxaban
35
Q

Side effects: Direct oral anticoagulants

A
  • Bleeding - genito-urinary haemorrage, epistaxis
  • GI bleed
  • GI upset
  • Anaemia
  • Dizziness
  • Elevated liver enzymes
36
Q

Contraindications: DOACs

A
  • Active or clinically significant bleeding
  • Peptic ulceration, cancer, recent surgery, trauma
  • hepatic or renal disease as DOACs are excreted by multiple routes (faeces and urine)
  • Pregnancy and breastfeeding
37
Q

Drug interactions: DOACs

A
  • Antiplatelets like Clopidegrel and Aspirin due to bleeding risk
  • Anticoagulants - heparin and warfarin
  • NSAIDs
  • Antifungal drugs - ‘azole like flucanozole
  • Macrolides (Antibacterials) Clarithromycin, Erythromycin
38
Q

Monitoring and stopping: DOACs

A
  • Clinical monitoring for signs of bleeding
  • Stopped 24-72 hours before surgery depending on surgery bleeding risk
39
Q

Furosemide, Bumetanide, Torsemide

Common Indications: Loop diuretics

A
  • Relief of breathlessness in acute pulmonary oedema in conjunction with oxygen and nitrates.
  • Symptomatic relief of fluid overload in chronic heart failure
  • Symptomatic treatment of fluid overload in other oedematous states.

Furosemide, Bumetanide, Torsemide

40
Q

Mechanism of action: Loop Diuretics

A
  • They act on the ascending limb of the loop of Henle.
  • Inhibit the Na+/K+/2Cl- co-transporter.
  • They have a direct effect on the blood vessels, causing dilation of the capacitance veins, decreasing venous BP. In HF this reduces preload and improves contractile function of the ‘overstreched’ heart muscle.

This protein is responsible for transporting sodium, potassium, and chloride ions from the tubular lumen into the epithelial cell. Water then follows by osmosis. Inhibiting this process has a diuretic effect.

41
Q

Side effects: Loop Diuretics

A
  • Dehydration - increased urine output
  • Hypotension
  • Low electrolyte state: inhibiting Na+/K+/2Cl- co-transporter increases urinary loss of sodium, potassium, and hydrogen ions. This leads to Hyponatraemia (low sodium levels)
    -> hypokalaemia, hypomagnesaemia, metabolic alkalosis
  • Tinnitus and hearing loss
42
Q

Examples of Loop Diuretics

A

Furosemide, Bumetanide, Torsemide

43
Q

Contraindications: Loop Diuretics

A
  • Patients with severe hypovolemia (conditions where the body loses fluids like blood, water)
  • Dehydration
  • Patients at risk of hepatic encephalopathy
  • Patients with gout as LD inhibit uric acid excretion.
44
Q

Drug interactions: Loop Diuretics

A
  • Affect drugs that are excreted by the kidneys, i.e Lithium, Digoxin, broad-spectrum abx (aminoglycosides)
    Due to urinary losses
45
Q

Monitoring and Stopping: Loop diuretics

A
  • Monitor efficacy in acute management of pulmonary oedema - response to symptom relief like tachycardia, hypertension, oxygen requirement.
  • Safety: monitoring sodium, potassium, and renal function.
46
Q

B-BLOCKERS END IN -LOL

Common Indications:
B-blockers

A
  • Ischaemic heart disease: improves symptoms of angina and ACS.
  • Chronic heart failure: Bisoprolol and Carvedilol used to improve prognosis. The heart does not need to contract as hard and fast, increasing perfusion.
  • Atrial fibrillation: reduce ventricular rate, and maintain sinus rhythm in paroxsymal AF. Slows heart rate.
  • Supraventricular tachycardia (SVT): restore sinus rhythm, slows down heart rate.
  • HTN: not first line but used when CCBs, ACE, or thiazide diuretics are insufficient as is decreases renin secretion.
  • Stage fright - slows heart rate.
47
Q

Examples of b-blockers

A
  • Bisoprolol
  • Atenolol
  • Propranolol
  • Metoprolol
  • Carevdilol
48
Q

Mechanism of action:
B-Blockers

A
  • B1 adrenoreceptors - on the heart
  • B2 receptors - blood vessels/airways
  • Via B1 receptor, B-blockers reduce force of contraction, speed of conduction in the heart, renin secretion fromt he kidney as this is medicated by B1 receptors.
  • This lowers BP, decreases O2 demand, and increases myocardial prefusion
  • They slow ventricular rate in AF mainly by prolonging the refractory period of the atrioventricular (AV) node.
49
Q

Side effects: B-Blockers

A
  • Fatigue
  • Cold extremities
  • headache
  • GI upset - nausea
  • sleep disturbance
  • Impotence in men
  • Bradycardia
50
Q

Contraindications: B-Blockers

A
  • Asthma patients:
    B-blockers can cause life-threatening bronchospasms due to blockade of B2 receptors in the lung airways.
  • Start at very low dose in ACUTE HF and increased slowly due to risk of impaired cardiac function.
  • Avoided in Haemodynamic instability
  • Heart block
  • Low dosage in Hepatic failure patients

  • Safe to use in COPD patients: choose a B1-selective like bisoprolol rather than non-selective like proponalol.
51
Q

Drug interactions: B-Blockers

A
  • Must not be used with non-dyhydropyridine CCBs
  • E.g. Verapamil, diltiazem - except by a specialist as this can cause HF, bradycardia, or asytole.
52
Q

Monitoring & Stopping: B-blockers

A
  • Before initiation: check HR/BP
  • **After **initiation: HR/BP
  • In IHD aim for resting heart rate around 55-60 beats/min.
  • In HF, daily measurement of body weight as progressively increasing body suggests fluid accumulation
  • Should be stopped in titration gradually over 1-2 weeks to avoid MI.
53
Q

Common indications: Alpha blockers

A
  • Lower urinary tract symptoms in benign prostate enlargement
  • Resistant hypertension (add-on treatment if other medications don’t work)
54
Q

end in ‘sin’

Examples of alpha blockers

A
  • Tamsulosin
  • Doxazosin
  • Alfuzosin
55
Q

Mechanism of action: Alpha blockers

A
  • A1 adrenoreceptors are mainly found in the smooth muscle within the blood vessels and urinary tract (bladder neck, prostate)
  • Stimulation induces contraction, blockage induces relaxation.
  • Inhibits a-1 adrenoreceptors which blocks the action of neurotransmitters and causes vasodilation and a fall in BP and reduces resistance to urinary outflow from the bladder.
56
Q

Side effects: Alpha blockers

A
  • Dizziness
  • Syncope
  • Postural hypertension
57
Q

Drug interactions: Alpha blockers

A
  • Caution with other antihypertensive drugs due to BP lowering.
  • B-Blockers form a part of the vasodilation response. If blood pressure decreases, the heart beats faster in an attempt to raise it (reflex tachycardia) - enhanced hypotensive effect.
58
Q

Contraindications: Alpha blockers

A
  • ## Patients with extisting postural hypertension

APPLIED PHARMACOLOGY (2 decks)

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