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Drugs Flashcards

1
Q

Cardiac Glycosides

A

Example(s): Digoxin
MOA: Increases vagal parasympathetic activity and inhibits the Na/K pump, causing Na build up - in effort to remove Na, more Ca is brought in. build up of Ca is responsible for the increased force of contraction and reduced rate of conduction through the AV node - slowing down heart rate and allowing heart to fill regularly

Indication(s): Heart Failure, Atrial Fibrillation rate control

Side Effects(s): Nausea, Vomiting, Diarrhoea, Confusion

Important Pharamcokinetics/Dynamics:
Narrow therapeutic index
Risk of toxicity
Long half life - maintenance dose once daily

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2
Q

Mesalazine

A

Indications: Ulcerative Colitis
MOA:reduces inflammation
Side Effects:headache, nausea, feve, abdo pain
Can be used topically or orally or both

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3
Q

Azathioprine

A

Class: Immunisuppressant
MOA: Blocks purine synthesis in lymphocytes
Indication: ulcerative colitis with sever relapse or frequently relapsing disease or frequent steroid courses needed

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4
Q

Infliximab

A

Monoclonal Antibody
MOA: monoclonal antibody to TNF alpha
Reduces inflammation

Indications: RA, severe ulcerative colitis, sever active crohns
Side effects: flu like symptoms, immune deficiency

Given parenterally by subcut injection

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5
Q

Alkylating Agents

A

MOA:form covalents bonds with DNA interferes with transcription and replication
Examples: melphalon, cisplatin
Use: Cancer Chemotherapy

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6
Q

Antimetabolites

A

MOA:interfere with nucleotide synthesis or DNA synthesis
Examples: methotrexate, cytarabine
Use: Cancer Chemotherapy

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7
Q

Cytotoxic Antibiotics

A

MOA: act mainly by direct action on dna as intercalators
Examples: dactinomycin, doxorubicin
Use: Cancer chemotherapy

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8
Q

Steroid Hormones

A

MOA: tumour may be responsive to a specific hormone which makes it regress
Exmaples: prednisone, prednisolone
Use: cancer chemotherapy

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9
Q

Hormone Antagonists

A

MOA: An antagonist of the hormone will suppress the growth
Exmaples: tamoxifen, biclutamide
Use: Cancer Chemotherapy

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10
Q

Microtubule Inhibitors

A

MOA: Binds to microtubular proteins to disrupt cell division
Examples: vincristine
Use: cancer chemotherapy

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11
Q

Anti-Platelet

A

Aspirin
MOA: Irreversible inactivation of COX enzyme, reduces platelet thromboxane (TXA2) production and endothelial prostaglandin (PGI2) production
-therefore reducing platelet aggregation and thrombus formation
-reduced prostaglandin synthesis decreases nociceptive sensitisation and inflammation (painkilling properties)

Indication: Secondary prevention of thrombotic events, pain relief

Side Effects: bleeding, peptic ulceration, bronchospasm

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12
Q

Hydroxycarbamide

A

Chemotherapy Drug

use: essential thrombocytosis, polycythaemia, cml

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13
Q

Imatinib

A

MOA: A BCR-ABL tyrosine kinase inhibitor
Uses: Chronic Myeloid Leukaemia

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14
Q

Heparin

A

MOA: Anticoagulant: Enhances activity of antithrombin which inhibits thrombin and also inhibit other factors of the coagulation cascade

Uses: Treatment and prophylaxis of thromboembolic disease

Side Effect: Bleeding, thrombocytopenia

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15
Q

Warfarin

A

MOA: Vitamin K Antagonist - Inhibits vitamin K reductase, prevents recycling of vitamin k prevents thrombus formation

Uses: Venous thromboembolism, thombroprophylaxis in AF,metallic heart valves

Side Effects: bleeding

Important: numerous food and drug interactions, and alcohol interactions, needs INR monitoring

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16
Q

Direct Oral Anti-Coagulants (DOACS)

A

MOA: Directly inhibit factors in the coagulation cascade by binding to active site e.g. Factor Xa
e.g. apixaban

Uses: Prophylaxis in thromboembolism, AF

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17
Q

Fibronlytics

A

MOA: Enhancement of fibrinolysis - breakdown of fibrin thrombosis
Two major classes:
Kinase
Tissue Plasminogen Activators (TPA)

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18
Q

Kinases

A

bind to plasminogen, releasing plasmin and the enhanced breakdown of fibrin into FDPs

  • Activity on both clot bound and free systemic plasminogen - significant bleeding risk
    e. g. streptokinase, urokinase
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19
Q

TPA Derivatives

A

Tissue Plasminogen Activators
e.g.alteplase, tenecteplase
MOA: Activate plasminogen to relase plasmin and breakdown fibrin into FDPs
-Relatively selective of only clot pound plasminogen

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20
Q

Anti-Platelet Drugs

A

Inhibit platelet activation or aggregation by platelet receptor inhibition or platelet signalling pathway inhibition

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21
Q

Clopidogrel

A

MOA: Irreversible blockage of ADP receptor which effects signalling in platelet and therefore reduced binding of fibrinogen

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22
Q

Abciximab

A

GPIIb/IIIa antagonists
Monoclonal antibodies which antagonise GPIIB/IIIa receptors reducing platelet aggregation and reduced binding of fibrinogen

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23
Q

Aspirin

A

Irreversible inhibition of cyclooxygenase which blocks the conversion of arachidonic acid into thromboxane A2 - decreased platelet activation and therefore thrombus formation

24
Q

Dipyridamole

A

Increases concentration cAMP in platelets, which decreases platelets responsiveness to ADP - reduced platelet aggregation

25
Ticagrelol
Prevents ADP mediated P2Y12 dependent platelet activation and aggregation by P2Y12 inhibition
26
Cardioselective Beta-Blockers
Cardioselective beta-1 adrenoreceptor antagonist, inhibiting sympathetic stimulation e.g. bisoprolol
27
Non-Cardioselective Beta-Blockers
Inhibits sympathetic stimulation in heart | e.g. propranolol
28
Thiazide Diuretic
E.g. bendroflumethiazide | MOA: Inhibits Na/CL transporter at the DCT and CD, increasing NA, CL and H20 excretion
29
Loop Diuretic
e.g. furosemide | MOA: Na/CL/K symporter antagonist, acts on thick ascending loop of henle, increasing secretion of Na, K , CL and water
30
ACE Inhibitors
e.g. ramipril, lisinopril MOA: Inhibits conversion of angiotensin 1 to angiotensin 2, inhibiting aldosterone release, depressing renal sodium and fluid retention and decreasing blood volume Uses: Hypertension, HF
31
Non-rate limiting Calcium Channel Blockers
e.g. amlodipine, nifedipine MOA: Prevents cellular entry of Ca by blocking L-type Calcium channels, myocardial contractility depressed, dilates coronary blood vessels and reduces afterload do not lower heart rate Uses: Hypertension, Angina
32
Sacubitril/Valsartan (entresto)
MOA: Inhibits neprilysin, increasing natuiretic peptides and inhibition of angiotensin receptor Uses: Heart failure
33
SABA
Short Acting Beta Agonist e.g. salbutamol Relaxes bronchial smooth muscle, inducing bronchodilation
34
SAMA
Short Acting Muscarinic Receptor Antagonist e.g. ipratropium Bonchodilitation
35
LABA
Long Acting Beta Agonist | e.g. salmeterol
36
LAMA
Long Acting Muscarinic Antagonist | e.g. tiotropium
37
Corticosteroids
MOA: Bind to activated glucocorticoid receptors to suppress pro-inflammatory genes that are activated in asthmatic airways Indications: Asthma, COPD, Adrenal Insufficiency, Addisons e.g. prednisolone, hydrocortisone
38
Beta 2 Agonists
MOA: Higher specificity for pulmonary b2 receptors vs cardiac b1 receptors. Stimulates adenyl cyclase to increase intracellular cAMP - relaxation of smooth muscle in bronchi Indications: Asthma, COPD Side Effects: Tremor, Hypokalaemia e.g. SABA - salbutamol, LABA - salmeterol
39
Anti-Muscarinics
MOA: Antagonist of cholinergic M1 and M3 musarinic receptors in the lung counteracting the direct musarinic bronchoconstriction Uses: Asthma, COPD Side Effects: Blurred vision, dry mouth, urinary retenetion e.g. SAMA - ipratropium, LAMA - tiotropium
40
Methylxanthines
MOA: Non-selective inhibition of phosphiodiesterases - increased intracellular cAMP causing bronchial smooth muscle relaxation Immunomodulatory effect - Improved mucocilliary clearance and anti-inflammatory effect Indications: Adjunct to inhaled therapy in asthma, IV infusion in severe exacerbations of asthma Side Effects: GI upset, palpitation, arrhythmia e.g. aminophylline, theophylinne
41
Combination Inhalers
LABA and LAMA - anoro, duaklir | LABA and ICS - Relvar ellipta, seretide, symbicort
42
Leukotriene Receptor Antagonists
MOA: Antagonist of leukotriene receptor inhibiting action of LTD4 in smooth muscle cells of the airway reducing airway oedema and smooth muscle contraction Use: Asthma Maintenance therapy
43
Azoles
Anti-Fungal MOA: Inhibitors of 14-methylsterol alpha-demethylase which produces ergosterol (an essential component of the fungal plasma membrane) Use: Anti-fungal E.g. - ketoconazole, miconazole, clotrimazole
44
Biguanide
e.g. Metformin MOA: Suppresses hepatic gluconeogenesis - reducing glucose output from the liver Increases peripheral insulin sensitivity and increases glucose uptake and utilisation Pros: weight loss, low hypo risk, CV benefit Cons: GI side effects, not if eGFR<30, risk of lactic acidosis (stop immediately in sepsis etc)
45
Sulphonylureas
e.g. gliclazide MOA: Close potassium channels on beta cells, stimulating release of stored insulin, Increasing cellular glucose uptake and glycogenesis, reduces gluconeogenesis Pros: high efficacy Cons: no CV benefit, weight gain, high hypo risk caution in CKD
46
DPP4 Inhibitors 'gliptins'
e.g. sitagliptin, alogliptin MOA: Inhibit DPP 4 and enhances the effects of endogenous incretins (i.e. GLP1) Increase glucose mediated insulin secretion and suppress glucagon production Pros: low hypo risk, few adverse events Cons: weight neutral, no CV benefit, reduce dose in CKD
47
SGLT2 Inhibitors 'flozins'
e.g. dapagliflozin, empagliflozin MOA: Inhibit SGLT2 in the PCT of kidney decreasing renal absorption of glucose Pros: CV benefit, renal benefit, weight loss, low hypo risk, decreased CV events Cons: Risk of GU infection, small risk of DKA, do not start if eGFR<60
48
Thiazolidinediones 'glitazones'
MOA: PPAR gamma receptor antagonists - increase sensitivity of fat, muscles and liver to endogenous and exogenous insulin Pros: CV protection, low hypo risk Cons: Weight gain, fluid retention, fractures
49
GLP1 Receptor Agonists
e.g liraglutide MOA: Increased glucose mediated insulin secretion - suppresses glucagon secretion Increases satiety and reduces appetite Pros: Cv benefit, low hypo risk, weight loss Cons: Injected, Gi side effects
50
Insulin (in T2DM)
MOA: Increase glucose uptake and utilisation in skeletal muscle. Reduced hepatic glucose output, increased glycogenesis, decreased lipolysis, decreased gluconeogenesis Pros: High efficacy Cons: Injected, weight gain, no CV benefit, highest hypoglycaemic risk
51
Levothryoxine
MOA: Synthetic throid hormone, acts like T4 and gets converted into T3 in the liver and kidney Uses: Hypothryroidism Note: Take 30-60 mins before breakfast
52
Thionamide (anti-thyroids)
e.g. carbimazole MOA: Reduces activity of peroxidase enzyme Uses: Hyperthyroidism
53
Radioactive Iodine
Used in hyperthyroidism if antithyroid drugs are unsuccessful.
54
Acne Medication
Reduce plugging - topical retinoid, topical benzyl peroxide Side effects: burning, irritant, peeling Reduce bacteria - topical antibiotics (erythromycin - zineryt), oral antibiotics (tetracyclines e.g. lymecycline) Side Effects: GI upset Reduced sebum production - Hormones e.g. OCP Side Effects: increased DVT risk
55
Oral isotretinoin (roaccutane)
An oral retinoid licensed for acne vulgaris concentrated form of vitamin A reduces sebum, plugging and bacteria Side effects: Dry lips, nose bleeds, dry skin, deranged liver function, increased lipids, mood disturbance, teratogenicity
56
Management of Eczema
``` Emollients Topical steroids Bandages Anti Histamines Antibiotics Avoidance of exacerbating factors Systemic drugs e.g. methotrexate, cyclosporin ```
57
Treatment of Psoriasis (increasing effectiveness and toxicity)
Topical Therapies - Moisturisers - Steroids - Salicyclic Acid (dissolves dead skin) - Vitamin D Analogues, Coal Tar (slows down keratinocyte proliferation) Ultraviolet Phototherapy - Non specific immunosuppressant therapy - can reduce T cell proliferation - Encourages vitamin D and reduces skin turnover Systemic Therapy -Immunosuppressants e.g. methotrexate, cyclosporin Aciterin (oral retinoid) Biologics - adalinumba, ustekinumab

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