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Block 2: Pathophysiology and Pharmacology > Cardiac pharmacology > Flashcards

Cardiac pharmacology Flashcards

1
Q

What are acute coronary syndromes?

A

Cardiovascular conditions characterised by sudden occlusion of coronary arteries by thrombus blocking blood supply to cardiac muscle.

[STEMI, NSTEMI, unstable angina]

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2
Q

What are the principles of treating acute coronary syndromes?

A
  1. Increase oxygen supply to myocardium (by improving coronary blood flow and administering oxygen)
  2. Reduce oxygen demand of myocardium (by reducing heart rate/ force of contraction, reducing cardiac preload and cardiac afterload)
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3
Q

What is heart failure?

A

Inability of the heart to deliver oxygen at a sufficient rate to metabolising tissues throughout the body - caused by abnormality of cardiac structure or cardiac function

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4
Q

What is the treatment strategy for chronic heart failure?

A
  1. Improve contractibility using positive ionotropes - Sympathomimetics (e.g. Dobutamine) and sometimes a Beta Blocker
  2. Reduce oedema - loop diuretics commonly used (e.g. Furosemide)
  3. Reduce preload and afterload - ACE inhibitors (e.g. Ramipril) and Angiotensin II receptor blocker (e.g. Losartan)
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5
Q

Describe how a contraction is initiated in a vascular smooth muscle cell

A
  1. Calcium enters cell via L-type calcium channels and is also released from the sarcoplasmic reticulum (triggered by binding of Inositol Triphosphate to calcium channels on SR membrane) - IP3 release is triggered by binding of angiotensin II to angiotensin II-receptors on the cell membrane
  2. Calcium binds to Calmodulin (a calcium-binding protein)
  3. Calcium activates the enzyme Myosin Light Chain Kinase which phosporylates MLC initiating a contraction
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6
Q

What is the mechanism of action for calcium channel blockers?

A

Prevent opening of voltage-gated calcium channels (L-type) which reduces the influx of Ca2+ into muscle cells.
Has a vasodilator effect on resistance in vessels and reduced afterload
Generally act on arteries to improve blood flow (not veins)

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7
Q

What are the common calcium channel blockers?

A

Nifedipine

Amlodipine

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8
Q

What is the MoA of nitrate vasodilators?

A
  1. Metabolised to release Nitric Oxide
  2. NO stimulates Guanylate Cyclase
  3. Increased cGMP in vascular smooth muscle cells (via dephosphorylation of GTP)
  4. Drives dephosphorylation of myosin light chains via activation of MLC Phosphatase
  5. Increased intracellular cGMP inhibits influx of calcium ions into smooth muscle cells

= Vascular smooth muscle relaxation

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9
Q

What are the common nitrate vasodilators?

A 
Glyceryl Trinitrate (GTN) 
Isosorbide Mononitrate (ISMN)
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10
Q

What are the key side effects of calcium channel blockers?

A

Ankle swelling

Palpitations

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11
Q

What is the key side effect of nitrate vasodilators?

A

Headache

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12
Q

How do nitrate vasodilators effect the heart?

A

Dilate arteries and veins
Reduce cardiac preload (by promoting venodilation)
Increased blood and oxygen supply to the myocardium (by promoting coronary artery vasodilation)
Reduce cardiac afterload (by promoting moderate arteriolar dilation)

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13
Q

What is the MoA of Beta Blockers?

A 
Competitive inhibitors of adrenaline and noradrenaline at Beta-adrenoreceptor sites (thus inhibiting sympathetic stimulation of heart muscle) 
Negative inotropes (decrease HR) and negative chronotropes (decrease contractility), reducing workload of heart which relieves oxygen demand
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14
Q

What is a key example of a Beta1-antagonist selective for the heart?

A

Atenolol

Bisoprolol

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15
Q

What are the key side effects of Beta Blockers?

A

Dizziness

Constipation

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16
Q

What is the MoA of Neprilysin inhibitors?

A

Neprilysin is an enzyme involved in the breakdown and inactivation of natriuretic peptides - by inhibiting breakdown this prolongs the activity of these peptides to promote water and sodium excretion (ANPs act on principal cells in the late DCT and cortical collecting tubule to reduce NaCl reabsorption)

[Nb. new treatment for heart failure - used in combination with an ARB - Valsartan]

17
Q

How does adrenaline work as a treatment for cardiac arrest?

A

Administered IV
Binds and stimulates cardiomyocyte Beta1-adrenergic receptors - activates cAMP cascade to increase intracellular calcium and initiate cardiomyocyte contraction

[Drug class = Sympathomimetic]

18
Q

How is atropine used as a treatment for acute heart failure?

A

Administered IV to raise heart rate in patients with sinus bradycardia
Works by blocking muscarinic-type M2 acetylcholine receptors on cardiomyocytes thus inhibiting the effect of parasympathetic, cholinergic vagus nerve transmission (ACh)
Accelerates the repolarisation rate in cardiac muscles.

19
Q

Give an example for the 2 types of antiplatelet drugs used in cardiac disease prevention

A

COX inhibitor = Aspirin

ADP receptor inhibitor = Clopidogrel

[Nb. do not affect BP]

20
Q

How do ADP receptor inhibitors work in CVD prevention?

A

Blocks the function of ADP receptors on platelet surfaces thus inhibiting platelet activation and subsequent thrombus formation

21
Q

How do COX inhibitors work in CVD prevention?

A

Inhibits the action of platelet COX enzymes thus inhibiting synthesis of Thromboxane A2 - this inhibits platelet activation and subsequent thrombus formation

22
Q

How do HMG-CoA Reductase Inhibitors (statins) work in CVD prevention?

A

Reduce levels of circulating cholesterol by inhibiting the enzyme HMCCR which is essential in the cholesterol synthetic pathway (in liver).
Can also promote uptake of excess cholesterol from the bloodstream into the liver
Protection against development of atherosclerosis

[Nb. does not affect BP]

23
Q

Give 2 examples of HMGCR inhibitors

A

Simvastatin

Atorvastatin

24
Q

What pathologies does untreated hypertension put you at risk of?

A

Atherosclerosis

Left ventricular hypertrophy

25
Q

What causes relaxation of a vascular smooth muscle cell in normal circumstances (i.e. no pharmacological influence)?

A
  1. Nitric Oxide (NO) enters cell which activates enzyme Guanylate Cyclase that catalyses the dephosporylation of GTP to cGMP
  2. cGMP activates the enzyme Myosin Light Chain Phosphatase
  3. MLCP dephosphorylates MLC which causes relaxation of smooth muscle
26
Q

How are ACEi and ARBs used in the management of cardiovascular disease?

A

ACEi inhibit conversion of angiotensin I to angiotensin II
ARBs inhibit angiotensin II receptors

Both lead to decreased vasoconstriction in blood vessels which lowers blood pressure, reduces peripheral resistance and reduces cardiac afterload

Also blocks RAAS pathway, inhibiting release of Aldosterone thus decreasing water retention which lowers plasma volume and cardiac preload

27
Q

What is the key side effect of ACE inhibitors?

A

Persistent, dry cough - caused by build up of bradykinin in the lungs (metabolic waste product normally broken down by ACE)

28
Q

What enables contraction of cardiomyocytes?

A
  1. Sympathetic stimulation of beta1-adrenoreceptors triggers cAMP cascase by activating Adenylyl Cyclase that drives dephosphorylation of ATP to cAMP
  2. cAMP activates Protein Kinase A
  3. Protein Kinase A acts directly on the Sarcoplasmic Reticulum to increase intracellular calcium levels driving a contraction
  4. Protein Kinase A also opens calcium channels on cell membrane driving influx of calcium into the cell
29
Q

Name 3 beta adrenergic receptor antagonists (beta-blockers)

A

Bisoprolol (cardioselective beta1-antagonist)
Atenolol (cardioselective beta1-antagonist)
Propranolol (beta1 and beta2 antagonist)

30
Q

How are diuretics used in the management of cardiovascular disease?

A

Increase water and sodium output in urine thus reducing plasma volume (and therefore cardiac preload)
Also reduce oedema

31
Q

Name a Neprilysin inhibitor

A

Sacubritil

[Used in combination with Valsartan]

32
Q

What drugs can be used to treat acute heart failure (emergency situations)?

A

Adrenaline (increases cardiomyocyte contraction)

Atropine (increases HR)

Block 2: Pathophysiology and Pharmacology (11 decks)

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