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MOA + Classes Flashcards

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1
Q

Non-narcotic analgesia examples

A

Panadol

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2
Q

Panadol MOA

A

Inhibits prostaglandin synthesis in the CNS and activates descending pathways
Has an antipyretic effect

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3
Q

NSAIDS examples

A

Ibuprofen, Diclofenac, Celecoxib

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4
Q

NSAIDS MOA

A

Inhibits prostaglandin production by blocking cyclooxygenase (COX1 and 2):

* Inhibition of COX‑1 results in impaired gastric cytoprotection and antiplatelet effects 
* Inhibition of COX‑2 results in anti-inflammatory and analgesic action
* Reduction in glomerular filtration rate and renal blood flow occurs

Analgesic, anti-inflammatory, and antipyretic actions

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5
Q

Opioid examples

A

Morphine, Oxycodone (Endone/Tagin), Fentanyl

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6
Q

Opioid MOA

A

Act on opioid receptors in the CNS and GIT (mu receptors) producing analgesia by reducing the transmission of pain impulses.

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7
Q

Macrolide examples

A

Erythromycin, Azithromycin, Clarithromycin

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8
Q

Aminoglycoside examples

A

Gentamycin

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9
Q

Aminoglycoside MOA

A

Inhibit ribosome (protein) synthesis.
Bind to the 30s ribosome subunit.

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10
Q

Macrolide MOA

A

Inhibit ribosome (protein) synthesis.
Bind to the 50s ribosome subunit.

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11
Q

Beta Lactams

A

Penicillins; Cephalosporins; Carbapenems

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12
Q

Carbapenems examples

A

Ertapenem, Doripenem, Imipenem, Meropenem

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13
Q

Cephalosporins examples

A

Cefalotin, Cefazolin, Cefalexin

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14
Q

Penicillins examples

A

Ticarcillin; Piperacillin; Ampicillin

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15
Q

Beta Lactams MOA

A

Inhibit bacterial cell wall synthesis by preventing formation of polymers and peptidoglycans.

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16
Q

Glycopeptides examples

A

Vancomycin

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17
Q

Glycopeptides MOA

A

Inhibit bacterial cell wall synthesis by preventing formation of polymers and peptidoglycans

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18
Q

Ritonavir MOA

A

Inhibits HIV1 and HIV2 protease, preventing viral maturation and replication.

HIV damages CD4 T-lymphocytes, reducing immune function. Without protease, HIV cells are unable to replicate.

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19
Q

Neuraminidase Inhibitors example

A

Oseltamivir

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20
Q

Oseltamivir MOA

A

Reduce influenza virus replication by inhibiting the viral surface enzyme neuraminidase (glycoprotein), preventing release of new virus from cells.

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21
Q

Anti-fungal examples

A

Caspofungin Acetate; Nystatin

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22
Q

Caspofungin Acetate MOA

A

Inhibits the synthesis of glucan derivative (essential component of fungal cell wall)

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23
Q

Nystatin MOA

A

Binds selectively to ergosterol in the fungal cell membrane, impairing its ability to prevent leakage of intracellular components. Fungistatic and fungicidal.

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24
Q

Beta Blocker examples

A

Atenolol, Metoprolol, Bisoprolol, Sotalol

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25
Q

Beta Blocker MOA

A

Beta blockers are antagonists that competitively block beta receptors.
* Prevent catecholamines (norepinephrine and epinephrine) from binding
○ Sympathetic NS action; negative feedback
* Reduce HR, BP, and contractility
* Depress SA node rate > slows conduction through AV node

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26
Q

Digoxin MOA

A

Increases the efficiency of the heart to improve cardiac output; influences the movement of ions into and out of the myocardial fibres; alters autonomic nervous system.

Positive Ionotropic Effect:
* Increase in contractility > increased cardiac output.

AV Node Inhibition:
* Stimulates the parasympathetic nervous system > slows electrical conduction in the AV node > decreases HR.

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27
Q

Amiodarone MOA

A

Works to prolong the duration of the cardiac action potential to revert tachyarrhythmias to a normal heart rhythm.

Primary effect is to block the potassium channels, but it can also block sodium and calcium channels and the beta and alpha adrenergic receptors.

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28
Q

Calcium Channel Blocker examples

A

Dihydropyridines (amlodipine, nifedipine, nimodipine);
Verapamil

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29
Q

Dihydropyridines MOA

A

Act of vascular smooth muscle by blocking entry of calcium into the cell > decreases intracellular calcium concentration > smooth muscle relaxation > vasodilation.

Vasodilation of systemic arteries > reduced resistance > reduced BP > reduced work of LV > reduced myocardial O2 demand = reduced likelihood of ischemia.

Vasodilation of coronary arteries > restore coronary blood flow.

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30
Q

Verapamil MOA

A

Mainly inhibits calcium channels in the cardiac myocyte and pace maker cells (SAN; AVN) > decreases intracellular calcium concentration > reduced contractility of the cardiac muscle (negative inotropy).

Sino-atrial node (SAN): determines the rate of the heart. Blocking of Ca channels in pacemaker cells slows the generation of action potentials > slows HR

Atrio-ventricular node (AVN): CCB reduce the velocity at which action potentials travel.

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31
Q

St John’s Wort

A

Depression; anxiety; viruses

Works in a similar way to (SSRI) inhibiting the uptake of serotonin, dopamine, and noradrenaline.

Contraindicated with digoxin and warfarin.

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32
Q

Potassium

A

Regulates resting membrane potential of neural, muscular, cardiac cells; most abundant intracellular cation; maintains a normal charge difference between intracellular and extracellular space.

Low potassium prolongs the QT interval > risk of torsade des pointes, ventricular fibrillation and sudden cardiac death.

Affects the conduction of an action potential > ventricular tachycardia.

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33
Q

Sodium

A

Main extracellular cation in the body; fluid balance + osmolality; muscle contractility; role in controlling membrane potentials in the myocardium.

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34
Q

Magnesium

A

The second most abundant intracellular cation. Interacts with the enzyme sodium–potassium ATPase (which acts to pump potassium into cells in exchange for sodium).

Can cause prolonged PR and QT intervals >increased QRS duration and development of torsades de pointes.

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35
Q

Loop Diuretic MOA

A

Act in the lower portion of the ascending loop of Henle in the nephron.

Inhibits Na+, Cl- and H2O reabsorption in the ascending loop of Henle  increase osmotic pressure within tubules  increased excretion of K+, Mg+ and Ca+  water is drawn from peritubular caps and excreted.

Potent effect.

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36
Q

Loop Diuretic examples

A

Furosemide, Bumetanide, Torsemide

37
Q

Thiazide Diuretic MOA

A

Act on the proximal portion of the distal convoluted tubule.

Promote Na+ and Cl- excretion  inhibits H2O reabsorption  diuresis and vasodilation of peripheral arterioles.

Increase K+ and bicarbonate excretion; decrease Ca+ excretion.

Moderately potent as most Na+ is reabsorb prior to the DCT.

38
Q

Thiazide Diuretic examples

A

Hydrochlorothiazide (HCTZ), Chlorthalidone, Indapamide.

39
Q

Potassium Sparing Diuretic examples

A

Amiloride; Triamterene; Spironolactone

40
Q

Potassium Sparing Diuretic MOA

A

Act on the distal convoluted tubule.

Inhibit Na+ reabsorption by either blocking Na+ channels (amiloride; triamterene) or by antagonising aldosterone (spironolactone)  H2O follows Na+ by osmosis  diuresis.

Not very powerful.

41
Q

Renin-Angiotensin System

A
  1. Juxta-glomerular cells (mechanoreceptors detect pressure changes) in the kidney produce prorenin
  2. Hypotension stimulates conversion to renin
  3. Renin acts on angiotensin (produced in the lungs converting it to angiotensin I
  4. Angiotensin converting enzyme (ACE) from the lungs converts angiotensin I to angiotensin II
42
Q

Effects of Angiotensin II

A

Vasoconstriction = Increased BP
* Arteries = increased peripheral resistance
* Veins = increased cardiac venous return

Kidneys
* Direct effect: restricts afferent arterioles decreasing renal blood flow = decreased GFR = decreased urine output
* Indirect effect: stimulates release of aldosterone = increased sodium and water reabsorption
* Net increase in extracellular fluid volume  increased capillary and arteriole pressure  increased blood pressure

43
Q

ACE Inhibitor examples

A

Captopril; Enalapril; Perindopril; Ramipril

44
Q

ACE Inhibitor MOA

A

Block the conversion of angiotensin I to angiotensin II.

Reduce the effects of angiotensin induced vasoconstriction and aldosterone induced sodium retention = reduce BP.

Inhibit the breakdown of bradykinin (vasodilator peptide) = reduced BP.

45
Q

Nitrate: Glycerol Trinitrate (GTN) MOA

A

Vasodilator; affects arteriole smooth muscle  reduces venous return and preload to the heart  reduces myocardial oxygen requirements.

Prevention and treatment of stable angina; unstable angina; heart failure; acute pulmonary oedema.

46
Q

Statins examples

A

Atorvastatin; Rosuvastatin; Simvastatin

47
Q

Statins MOA

A

Inhibit HMG-COA reductase which is involved in hepatic cholesterol synthesis  reduced plasma concentration of LDL cholesterol + small increase in HDL.

Improve endothelial function thus stabilising atherosclerotic plaque preventing rupture.

48
Q

Warfarin MOA

A

Vitamin K antagonist  inhibits production of vit K by vit K epoxide reductase.

Normally vitamin KH2 is a cofactor used in the γ-carboxylation of coagulation factors and thrombin.

Un-carboxylated factors VII, IX, X, and thrombin are biologically inactive and therefore serve to interrupt the coagulation cascade.

49
Q

Heparin MOA

A

Binds reversibly to antithrombin III  inactivation of prothrombin and factor X  inhibits further clotting as it stops conversion of fibrin to fibrinogen and prothrombin to thrombin.

Accelerates the neutralisation of coagulation factors activated by ATIII.

50
Q

Enoxaparin MOA

A

Immediate onset of action.

Binds to antithrombin III forming a complex that irreversibly inactivates factor Xa  enoxaparin is released and binds to other anti-thrombin molecules (e.g. fibrin)  thrombin is unable to convert fibrinogen to fibrin.

Increases thrombin time (TT) and activated partial thromboplastin time (aPTT) preventing and reducing thromboembolic events.

51
Q

Factor Xa Inhibitor examples

A

Apixaban; Betrixaban

52
Q

Factor Xa Inhibitor MOA

A

Reversibly bind to factor Xa and inhibit the coagulation cascade from progressing. This prevents thrombin and fibrin activation inhibiting clot formation.

53
Q

Aspirin MOA

A

Blocks prostaglandin synthesis.

Non-selective for COX-1 and COX-2 enzymes.
* Inhibition of COX-1 = irreversible inhibition of platelet aggregation for about 7-10 days (average platelet lifespan) & prevents the production of pain-causing prostaglandins.
Stops the conversion of arachidonic acid to thromboxane A2 (TXA2), which is a potent inducer of platelet aggregation.

54
Q

Beta-2 Agonist examples

A

Salbutamol (Ventolin); Salmeterol; Formoterol

55
Q

Beta-2 Agonist MOA

A

Stimulation of Beta2 receptors  increased formation of cyclic adenosine monophosphate (cAMP)  bronchial smooth muscle relaxation  bronchodilation  increased alveolar ventilation.

Short acting (SABA)
* Onset in 5 mins, duration 3 hrs.
* Acute relievers.
* E.g. Salbutamol.

Long acting (LABA)
* Onset up to 20 mins, duration 12 hrs.
* Preventative
* Often in combination with corticosteroids.
* E.g. Salmeterol; Formoterol

56
Q

Anticholinergics (Antimuscarinics)

A

Ipratropium (Atrovent)

57
Q

Atrovent MOA

A

Antagonise the action of acetylcholine at the M3-muscarininc receptor  blocks PNS response  long acting bronchodilation.

58
Q

Corticosteroid examples

A

Inhaled (Beclomethasone; Fluticasone); Systemic (Prednisolone; Hydrocortisone)

59
Q

Inhaled Corticosteroid MOA

A

Enter the cell nucleus  increase or decrease the synthesis of specific proteins including enzymes that regular cell inflammation  prevent inflammation and the hyperresponsive of bronchial epithelial cells.

Asthma prophylaxis

60
Q

Systemic Corticosteroid MOA

A

Decrease inflammation by decreasing the production of inflammatory mediators  bronchodilation.

Suppress immune response  decrease in bronchoconstriction, mucous production.

Asthma prophylaxis.

61
Q

Epinephrine MOA

A

Acts on alpha and beta adrenergic receptors  minimises vasodilation and increased vascular permeability that occurs during anaphylaxis  relaxation of smooth muscle in the bronchi and iris.

Histamine antagonist  reduces inflammatory response.

62
Q

Lidocaine MOA

A

Provides local anaesthesia by nerve blockade at various sites in the body. Stabilises neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses.

Acts on sodium ion channels in nerve cell membranes  lidocaine molecules diffuse into the cytoplasm of the axon and bind with hydrogen ions  bind with sodium channels from the inside keeping them open and incapable of depolarising  no impulse transmission.

63
Q

Antacid (Mylanta) MOA

A

Alkaline chemicals/weak bases that neutralise hydrochloric acid released by parietal cells causing stomach pH to rise to 6-7.

64
Q

Proton Pump Inhibitors (Esomeprazole) MOA

A

Act on parietal cells. Inhibit the hydrogen/potassium ATPase enzyme system (proton pump), inhibiting both stimulated and basal acid secretion lowering hydrochloric acid in the stomach.

65
Q

Histamine-2 Receptor Antagonists (Ranitidine) MOA

A

Reversibly block histamine-2 receptors preventing the secretion of HCl in the parietal cell > reduced stomach acid.

After a meal, the hormone gastrin, produced by cells in the lining of the stomach, stimulates the release of histamine, which then binds to histamine H2 receptors, leading to the secretion of gastric acid.

66
Q

Sulfonylureas (Gliclazide) MOA

A

T2DM. Increases pancreatic insulin secretion from the beta cells of the pancreas. May decrease insulin resistance.

Gliclazide binds to the β cell sulfonyl urea receptor (SUR1) > blocks/closes the ATP sensitive potassium channels > leads to a decrease in potassium efflux > depolarization of the β cells > this opens voltage-dependent calcium channels in the β cell > calmodulin activation > exocytosis of insulin containing secretory granules.

67
Q

Biguanides (Metformin) MOA

A

T2DM. Inhibits glucose production in the liver (gluconeogenesis) and enhances peripheral cell sensitivity to insulin > lower BGL.

68
Q

Insulin

A

Nova rapid = short acting
- Onset of action 30 mins
- Peak effect 2-3 hrs
- Lasts 6-8 hrs

Lantus = long acting
- Onset of action 2 hrs
- Lasts 20 hours

Insulin binds to receptors on the cell membrane and facilitates cellular uptake of glucose from the blood. Acts on the liver and muscles to promote glycogenesis.

69
Q

Glucagon

A

Hyperglycaemic pancreatic hormone.

Glucagon binds to glucagon receptors in the liver, catabolism of glycogen, release of glucose.

Increases cyclic AMP independent of beta-receptors or calcium flux, positive chronotropic and inotropic effect.

70
Q

5HT3 Antagonists (Ondansetron) MOA

A

Block the binding of serotonin to the 5HT3 serotonin receptors in the chemoreceptor trigger zone and GIT preventing vomiting.

71
Q

Dopamine 2 Antagonists (Metoclopramide) MOA

A

Block the binding of serotonin to the dopamine 2 receptors in the chemoreceptor trigger zone preventing vomiting and in the GIT preventing gastroparesis and improving peristalsis.

Increase stomach emptying.

72
Q

Osmotic Laxative examples

A

Lactulose; Colonlytely

73
Q

Osmotic Laxative MOA

A

Sugars, salts, or alcohols that are partially or fully non-absorbable so remain in the GIT tract.

Hypertonic so have an osmotic effect drawing water into the colon, increase pressure in the intestine which stimulates peristalsis and bowel movement.

74
Q

Stimulant Laxative examples

A

Senna, Bisacodyl

75
Q

Stimulant Laxative MOA

A

Direct stimulation of nerve endings in the colonic mucosa to increase peristalsis.

76
Q

Stool Softener examples

A

Coloxyl; Docusate

77
Q

Stool Softener MOA

A

Allows water to mix with faeces and soften it for easier passage through the colon.

Surfactant: water soluble head and water insoluble tail. Sticks out into fat, disrupting the normal surface tension between water and fat, allowing water to penetrate the stool.

78
Q

Bulk Forming Laxative examples

A

Psyllium/Metamucil

79
Q

Bulk Forming Laxative MOA

A

Absorb water which increases the volume/bulk of the stool which stimulates peristalsis.

80
Q

Tamoxifen MOA

A

Compete with estrogen for receptor sites in breast tissue (anti-estrogenic effect) inhibiting tumour growth. Also have estrogen agonist activity on endometrium, bone and lipids. Suppression of other growth factors and cytokines may occur.

81
Q

Drugs that cause hyperkalaemia (Triple Whammy Effect)

A

NSAIDS:
- Inhibit prostaglandin > vasoconstriction of AFFERENT arteriole = decreased eGFR
- Inhibition of prostacyclin which increases potassium secretion at the distal tubule.

ACE inhibitors:
- Angiotensin II interacts with the hypothalamus and anterior pituitary gland to induce release of ADH = increased H2O absorption.
- Angiotensin II > aldosterone release > increased potassium secretion/decreased Na & H2O secretion.
- ACE blocks angiotensin II > vasodilation of EFFERENT arteriole = decreased glomerular pressure, decreased filtration

Potassium sparing diuretics
- NSAIDs decrease effect
- Retain potassium

Increased risk of AKI, fluid overload, exacerbation of CHF

82
Q

Drugs that cause hypokalaemia

A

Loop diuretics
Steroids
Beta-2 agonists

83
Q

Drugs that inhibit CYP450

A

Grapefruit
Protease inhibitors
Antifungals (Ritonavir)
Macrolides (Erythromycin)
Amiodarone
Verapamil
PPIs (Omeprazole)

84
Q

Beta blockers & Beta-2 agonists

A

Have opposing effects.

Beta-2 agonists increase sympathetic nervous function > bronchodilation, tachycardia, decreased potassium.

Beta blockers prevent binding of catecholamines to beta receptors decreasing sympathetic nervous function > lower HR, lower BP, bronchoconstriction (if non-specific), increased potassium.

85
Q

Digoxin & Amiodarone

A

Amiodarone increases the blood levels of digoxin (Lanoxin) when the two drugs are given together. Digoxin has a very narrow therapeutic range.

86
Q

Proton Pump Inhibitors & NSAIDs

A

NSAIDs can cause GIT bleeding - due to inhibiting prostaglandins that protect the stomach mucosa from HCl. Interfere with clotting.

PPIs competitively bind to proton pumps preventing the release of HCl

87
Q

Beta Blockers & Calcium Channel Blockers

A

Beta blockers should not be taken with Verapamil as bradycardia, asystole, severe hypotension, and heart failure can occur.

88
Q

Drugs contraindicated with Aminoglycosides

A

Vancomycin: increased risk of ototoxicity and nephrotoxicity
Loop diuretics: increased risk of hearing loss
NSAIDS: reduced renal function

Nursing and Mid Y2 (10 decks)

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