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Block 2 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What 4 corticosteroids are used in the treatment of asthma?

A

Oral - prednisolone
IV - hydrocortisone
Inhaled - beclomethasone
- fluticasone

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2
Q

What are the cellular targets of glucocorticoids?

A

Immune cells of the lung - Macrophages
T-lymphocytes
Eosinophils

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3
Q

What are the molecular targets of glucocorticoids?

A

Intracellular glucocorticoid receptor (GR).

Activated GR interacts with selected nuclear DNA sequences and influences the expression of genes:
-suppression of pro-inflammatory mediators (TH2 cytokines e.g. IL3 and IL5)

  • expression of anti-inflammatory products (secreted leukocyte peptidase inhibitor)
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4
Q

What are the side effects of glucocorticoids?

A

Moon face, weight gain, osteoporosis, hyperglycaemia

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5
Q

Name 2 short acting and 2 long action B2 adrenoreceptor agonists

A

Short term
Salbutamol
Terbutaline

Long acting
Salmeterol
Formoterol

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6
Q

Describe the mechanism of action of B2 adrenoreceptor agonists

A

B2 adrenoreceptor agonist stimulate B2 adrenergic receptors on bronchiolar smooth muscle cells. This activation increases the action of the enzyme adenylate cyclase, increasing cAMP production from ATP. cAMP activates protein kinase A which drives Ca2+ into storage vesicles away from the cytoplasm, reducing smooth muscle contractility. PKA inactivates MLCK and drives dephosphorylation on myosin light chain

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7
Q

Name 2 methylxanthines

A

Theophylline

Aminophylline

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8
Q

Describe the mechanism of action of methylxanthines

A

Methylxanthines block the enzyme phosphodiesterase in the bronchiolar smooth muscle cells. This increases the levels of cAMP levels, promoting uptake of calcium into vesicles and promoting bronchodilation.

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9
Q

What are the side effects of beta 2 agonists?

A

Tremor
Tachycardia
Cardiac arrhythmia

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10
Q

What is the cellular target of Beta -2 adrenoreceptor agonist

A

Bronchiolar smooth muscle cells

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11
Q

What are the molecular targets of beta2 agonists

A

Stimulation of B2 adrenergic receptors

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12
Q

What are the cellular targets of anti-cholinergics in asthma treatment?

A

Bronchiolar smooth muscle cells

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13
Q

What are the molecular targets of anti-cholinergics?

A

Blockade of M3 muscarinic acetylcholine receptors

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14
Q

What are the side effects of anti-cholinergics?

A

Dry mouth, constipation, urinary retention

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15
Q

Describe the mechanism of action of anti-cholinergics

A

The blockade of the M3 muscarinic acetylcholine receptors reduces the action of phospholipase C enzyme (PLC), reducing the release of Ca2+ into the cytoplasm.
This reduces smooth muscle contraction, resulting in bronchodilation and resolution of asthma symptoms

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16
Q

Name 2 anti-cholinergic drugs

A

Ipratropium (short acting)

Tiotropium (long acting)

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17
Q

Name 2 leukotriene receptor antagonists

A

Montelukast

Zafirlukast

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18
Q

What are the cellular targets of leukotriene receptor antagonists?

A

Eosinophils in the lungs

Bronchiolar smooth muscle cells

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19
Q

What are the molecular targets of leukotriene receptor antagonists?

A

Blockade of CysLT1 leukotriene receptors

20
Q

Describe the mechanism of action of leukotriene receptor antagonists

A

Blockade of intracellular signals on smooth muscle cells –> inactivation of PLC –> bronchodilation

Blockade of receptors on eosinophils - less chemotaxis to site of inflammation

21
Q

What are the side effects of leukotriene receptor antagonists?

A

Abdominal pain

Headache

22
Q

What releases leukotrienes?

A

Mast cell IgE complex

TH2 releases IL-4, IL-13, this activates B cells to secrete IgE which then binds to mast cells

23
Q

Describe the mechanism of action of ACE inhibitors

A

Block conversion of Angiotensin I to Angiotensin II by angiotensin converting enzyme.
Decreased vasoconstriction in peripheral blood vessels because of reduction of release of Ca2+ into the cytoplasms –> reduced cardiac afterload –>reduction in BP
Aldosterone secretion reduced –> less water retention –> lower plasma volume –> reduced preload

24
Q

Describe the mechanism of action of angiotensin receptor blockers

A

Directly blocks the activation of the angiotensin receptors.
Decreased vasoconstriction in peripheral blood vessels because of reduction in IP3 which reduces release of Ca2+ into cytoplasm –> reduced cardiac afterload –>reduction in BP
Aldosterone secretion reduced –> less water retention –> lower plasma volume –> reduced preload

25
Q

What are the common side effects of ACEi

A

Persistent cough

26
Q

What are the main treatment strategies for chronic heart failure?

A

Improve contractility using ionotropes - sympathomimetics (Dobutamine, adrenergic stimulants)

Reduce oedema with diuretics - furosemide

Reduce preload and afterload - ACEi and ARBs

27
Q

Give an example of an ACEi

A

Ramipril

28
Q

Give 2 examples of ARBs

A

Losartan

Valsartan

29
Q

Describe the mechanism of action of calcium channel blockers

A

Prevent opening of voltage-gated calcium channels on vascular smooth muscle
Reduce Ca2+ influx
Vasodilator effect on resistance in vessels –> reduces afterload (easier for heart to pump)
Coronary artery dilation

30
Q

What are the side effects of CCBs?

A

Ankle swelling, palpitations

31
Q

Give 2 examples of CCBs

A

Nifedipine

Amlodipine

32
Q

Give 2 examples of nitrate vasodilators

A 
Glyceryl Trinitrate (GTN)
Isosorbide Mononitrate (ISMN)
33
Q

Describe the mechanism of action of nitrate vasodilators

A

Metabolised to release nitric oxide (NO)
NO stimulates soluble guanylate cyclase
This causes an increase in cGMP in vascular smooth muscle cells
Drives dephosphorylation of MLC via activation of MLC phosphatase
Inhibits influx of Ca2+ into smooth muscle cells
Drives vascular smooth muscle relaxation
Promotes venodilation –> reduces preload
Promote coronary artery vasodilation –> increased blood supply to myocardium

34
Q

Give an example of a beta blocker

A

Atenolol

35
Q

What are the side effects of beta blockers

A

Dizziness

Constipation

36
Q

Describe the mechanism of action of beta blockers

A

Beta blockers competitively inhibit adrenaline and noradrenaline at B1-adrenoceptor sites on cardiac smooth muscle cells, thereby inhibiting sympathetic stimulation of the heart muscle.

Reduce heart rate and cardiomyocyte contractility

Reduce the workload of the heart and relieve oxygen demand

37
Q

How does activation of a beta receptor give a different response in cardiomyocytes and smooth muscle?

A

The bronchiolar smooth muscles contain beta 2 adrenergic receptors. This activates the cAMP cascade, which in bronchiolar cells drives Ca2+ into storage vesicles in the cells, reducing contractility.

In cardiomyocytes, activation of the B1 adrenoreceptors drives muscle contractility by activation of cAMP, increasing PKA levels and stimulating release of Ca2+ from intracellular stores and increasing uptake of Ca2+ from extracellular sites

38
Q

What diuretic is used to treat HF?

A

Spironolactone (potassium sparing)

Increase water and sodium output in urine
Reduce plasma volume and reduce cardiac preload

Review block 1 drugs

39
Q

Give an example of a neprilysin inhibitor

A

Sacubitril

40
Q

Describe the mechanism of action of neprilysin inhibitors

A

Inhibits the action of neprilysin - therefore inhibits the inactivation of natriuretic peptides.

Inhibition of neprilysin prolongs the presence & activity of NPs, which promote water & sodium excretion

41
Q

What drug is used in the treatment of sinus bradycardia?

A

Atropine

42
Q

Describe the mechanism of action of atropine

A

Blocks muscarinic-type M2 acetylcholine receptors on cardiomyocytes.
This inhibits the parasympathetic cholinergic vagus nerve transmission, which normally decreases heart rate
Atropine also accelerates the repolarisation rate in cardiac muscle, leading to an increased heart rate

43
Q

Name 2 antiplatelet drugs

A

Aspirin (COX inhibitor)

Clopidogrel (ADP receptor blocker)

44
Q

Describe the mechanism of clopidogrel (ADP receptor blocker)

A

Binds to and blocks the function of ADP receptors on platelet surfaces. This inhibits platelet activation and subsequent thrombus formation

45
Q

Describe the mechanism of action of aspirin (COX inhibitor)

A

Blocks the enzyme action of platelet COX enzyme

This leads to a reduction in TXAs synthesis which inhibits platelet activation and thrombus formation

46
Q

Give 2 examples of HMG-CoA Reductase Inhibitors

A

Atorvastatin (Any time)

Simvastatin (night time)

47
Q

Describe the mechanism of action of HMG-CoA Reductase Inhibitors

A

Cholesterol is produced in the liver.
The enzyme HMG-CoA Reductase rate limits cholesterol.
HMG-CoA Reductase inhibitors reduce circulating cholesterol levels and can promote uptake of excess cholesterol into the liver

Block 2 (10 decks)

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