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Phase 3 > Drugs > Flashcards

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
Q

Ticagrelol

A

Prevents ADP mediated P2Y12 dependent platelet activation and aggregation by P2Y12 inhibition

26
Q

Cardioselective Beta-Blockers

A

Cardioselective beta-1 adrenoreceptor antagonist, inhibiting sympathetic stimulation
e.g. bisoprolol

27
Q

Non-Cardioselective Beta-Blockers

A

Inhibits sympathetic stimulation in heart

e.g. propranolol

28
Q

Thiazide Diuretic

A

E.g. bendroflumethiazide

MOA: Inhibits Na/CL transporter at the DCT and CD, increasing NA, CL and H20 excretion

29
Q

Loop Diuretic

A

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
Q

ACE Inhibitors

A

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
Q

Non-rate limiting Calcium Channel Blockers

A

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
Q

Sacubitril/Valsartan (entresto)

A

MOA: Inhibits neprilysin, increasing natuiretic peptides and inhibition of angiotensin receptor

Uses: Heart failure

33
Q

SABA

A

Short Acting Beta Agonist
e.g. salbutamol
Relaxes bronchial smooth muscle, inducing bronchodilation

34
Q

SAMA

A

Short Acting Muscarinic Receptor Antagonist
e.g. ipratropium
Bonchodilitation

35
Q

LABA

A

Long Acting Beta Agonist

e.g. salmeterol

36
Q

LAMA

A

Long Acting Muscarinic Antagonist

e.g. tiotropium

37
Q

Corticosteroids

A

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
Q

Beta 2 Agonists

A

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
Q

Anti-Muscarinics

A

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
Q

Methylxanthines

A

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
Q

Combination Inhalers

A

LABA and LAMA - anoro, duaklir

LABA and ICS - Relvar ellipta, seretide, symbicort

42
Q

Leukotriene Receptor Antagonists

A

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
Q

Azoles

A

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
Q

Biguanide

A

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
Q

Sulphonylureas

A

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
Q

DPP4 Inhibitors ‘gliptins’

A

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
Q

SGLT2 Inhibitors ‘flozins’

A

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
Q

Thiazolidinediones ‘glitazones’

A

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
Q

GLP1 Receptor Agonists

A

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
Q

Insulin (in T2DM)

A

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
Q

Levothryoxine

A

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
Q

Thionamide (anti-thyroids)

A

e.g. carbimazole
MOA: Reduces activity of peroxidase enzyme
Uses: Hyperthyroidism

53
Q

Radioactive Iodine

A

Used in hyperthyroidism if antithyroid drugs are unsuccessful.

54
Q

Acne Medication

A

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
Q

Oral isotretinoin (roaccutane)

A

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
Q

Management of Eczema

A 
Emollients
Topical steroids
Bandages
Anti Histamines
Antibiotics
Avoidance of exacerbating factors
Systemic drugs e.g. methotrexate, cyclosporin
57
Q

Treatment of Psoriasis (increasing effectiveness and toxicity)

A

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

Phase 3 (1 decks)

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