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2015 - Year 3 Summative > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Pharmacology

Antiplatelet Classes

A

1) Cyclooxygenase inhibitors
2) ADP receptor antagonists
3) Glycoprotein IIb/IIIa receptor inhibitors
4) Phosphodiesterase III Inhibitor

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2
Q

Pharmacology

Antiplatelet Cyclooxygenase inhibitors

A

Aspirin

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3
Q

Pharmacology

ADP receptor antagonist

A

1) Clopidogrel
2) Prasugrel
3) Ticagrelor
4) Ticlopidine

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4
Q

Pharmacology

Glycoprotein IIb/IIIa receptor inhibitors

A

1) Abciximab
2) Eptifibatide
3) Tirofiban

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5
Q

Pharmacology

Phosphodiesterase III inhibitor

A
  • Cilostazol

- Dipyridamole

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6
Q

Pharmacology

Anticoagulant drug classes

A

1) Direct anticoagulant

2) Indirect anticoagulant

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7
Q

Pharmacology

Heparin effect reversing drug

A

1) Protamine sulfate

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8
Q

Pharmacology

Direct anticoagulant

A

1) Heparin (antithrombin activator)

2) LMW heparin
- enoxaparin

3) Indirect inhibitors of factor Xa
- fondaparinux

4) Direct thrombin inhibitors
- dabigatran
- hirudin
- lepirudin
- argatroban

5) Direct factor Xa inhibitor
- Rivaroxaban
- Apixaban

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9
Q

Pharmacology

Indirect anticoagulant

A

1) Warfarin

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10
Q

Pharmacology

Warfarin effect reversing drug

A

1) Vitamin K1

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11
Q

Pharmacology

Thrombolytic drugs

A

1) Streptokinase
2) Anistreplase
3) Urokinase
4) Tissue plasminogen activators (Alteplase; tPA)
5) Reteplase (rPA)
6) Tenecteplase (TNK-tPA)

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12
Q

Pharmacology

Thrombolytics effect reversing agents

A

1) tranexamic acid

2) Fresh plasma/coagulation factor

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13
Q

Pharmacology

Fibrinolytic inhibitors

A

1) tranexamic acid

2) Aminocaproic acid

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14
Q

Pharmacology

Coagulants agents

A

1) Vitamin K1 and K2

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15
Q

Pharmacology

1st generation H1 receptor blocker

A

1) Chlorpheniramine
2) Diphenhydramine
3) Dimenhydrinate
4) Promethazine (promethazine theoclate)
5) Doxylamine
6) Hydroxyzine

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16
Q

Pharmacology

2nd generation H1 receptor blocker

A

1) fexofenadine
2) Loratadine
3) Cetirizine

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17
Q

Pharmacology

Antihistamine (H1) somnifacients / sedate

A

1) Diphenhydramine
2) Doxylamine
3) Promethazine

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18
Q

Pharmacology

Antihistamine (H1) antiemetics

A

1) Dimenhydrinate
2) hydroxyzine
3) Promethazine theoclate

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19
Q

Pharmacology

Immunosuppressive drug classes

A

1) Cytokine production inhibitors
2) Immunosuppressive antimetabolites
3) immunosuppresive antibodies
4) Adrenocorticoids

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20
Q

Pharmacology

Immunosuppresive Cytokine production inhibitors

A

1) Cyclosporine
2) Sirolimus
3) Tacrolimus (FK506)

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21
Q

Pharmacology

Immunosuppressive antimetabolites

A

1) Azathioprine2) Mycophenolate mofetil3) Cyclophosphamide4) MEthotrexate

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22
Q

Pharmacology

Immunosuppressive antibodies

A

1) Basiliximab2) Rho (D) immune globulin3) Muromonab (OKT3)4) Daclizumab

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23
Q

Pharmacology

Anti-CD25 antibodies (aka IL-2 receptor antagonist)

A

1) Basiliximab2) Daclizumab

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24
Q

Pharmacology

Immunosuppressive corticosteroids

A

1) methylprednisolone2) Prednisone

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25
Q

Pharmacology

Cytokine release syndrome prophylaxis drugs

A

1) methylprednisolone2) Diphenhydramine3) paracetamol

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26
Q

Pharmacology

Chemotherapy drug classes

A

I. Cell cycle-specific 1) Antimetabolites a) Folate antagonist b) Purine antagonist c) Pyramidine antagonist 2) Mitotic Inhibitors (Microtubule) a) Vinca Alkaloids b) Taxanes 3) Topoisomerase inhibitors a) Topoisomerase I inhibitor b) Topoisomerase II Inhibitor 4) Ribonucleotide reductase inhibitors a) HydroxyureasII. Cell-cycle Non-specific drugs 5) Alkylating agents a) Phosphoramide mustard precursor b) Nitrosureas c) Heavy metal platinum complex 6) Antibiotics a) Dactinomycin b) Bleomycin c) Anthracyclines 7) Glucocorticoids

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27
Q

Pharmacology

Cell cycle-specific Chemotherapy drug classes

A

1) Antimetabolites a) Folate antagonist b) Purine antagonist c) Pyramidine antagonist2) Mitotic Inhibitors (Microtubule) a) Vinca Alkaloids b) Taxanes3) Topoisomerase inhibitors a) Topoisomerase I inhibitor b) Topoisomerase II Inhibitor4) Ribonucleotide reductase inhibitors a) Hydroxyureas

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28
Q

Pharmacology

Cell cycle non-specific Chemotherapy drug classes

A

1) Alkylating agents a) Phosphoramide mustard precursor b) Nitrosureas c) Heavy metal platinum complex2) Antibiotics a) Dactinomycin b) Bleomycin c) Anthracyclines3) Glucocorticoids

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29
Q

Pharmacology

Targeted therapy drug classes

A

1) Hormone antagonist a) SERMs2) Monoclonal antibodies 3) Enzyme inhibitors

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30
Q

Pharmacology

Folate antagonist and mechanism

A

Methotrexate (MTX)

Mechanism:
- blocking the active site of dihydrofolate reductase, thus no reduced folate produced which is a co-enzyme for methylation in various metabolic processes

  • MTX polyglutamated to be retained in the cell
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31
Q

Pharmacology

Purine antagonist

A
  • Azathioprine- 6-mercaptopurine (6-MP)- 6-thioguanine (6-TG)
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32
Q

Pharmacology

Pyramidine antagonist

A
  • 5-fluorouracil (5-FU)- Cytarabine (ara-c)
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33
Q

Pharmacology

Antimetabolites

A

a) Folate antagonist - Methotrexate (MTX)b) Purine antagonist - Azathioprine - 6-mercaptopurine (6-MP) - 6-thioguanine (6-TG)c) Pyramidine antagonist - 5-fluorouracil (5-FU) - Cytarabine (ara-c)

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34
Q

Pharmacology

Vinca Alkaloids

A
  • Vincristine (VX)- Vinblastine (VBL)- Vinorelbine (VRB)
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35
Q

Pharmacology

Taxanes

A
  • Paclitaxel- Docetaxel
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36
Q

Pharmacology

Mitotic Inhibitors

A

a) Vinca Alkaloids - Vincristine (VX) - Vinblastine (VBL) - Vinorelbine (VRB)b) Taxanes - Paclitaxel - Docetaxel

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37
Q

Pharmacology

Topoisomerase I inhibitor

A
  • Irinotecan- Topotecan
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38
Q

Pharmacology

Topoisomerase II Inhibitor

A
  • Etoposide (VP-16)- Teniposide (VM-26)
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39
Q

Pharmacology

Topoisomerase inhibitors

A

a) Topoisomerase I inhibitor - Irinotecan - Topotecanb) Topoisomerase II Inhibitor - Etoposide (VP-16) - Teniposide (VM-26)

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40
Q

Pharmacology

Ribonucleotide reductase inhibitors

A

Hydroxyureas

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41
Q

Pharmacology

Phosphoramide mustard precursor

A
  • Cyclophosphamide- Ifosfamide
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42
Q

Pharmacology

Nitrosureas

A
  • carmustin (BCNU)- Lomustin (CCNU)- Fotemustin- Semustin- Streptozocin
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43
Q

Pharmacology

Heavy metal platinum complex

A
  • Cisplatin- Carboplatin
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44
Q

Pharmacology

Alkylating agents

A

a) Phosphoramide mustard precursor - Cyclophosphamide - Ifosfamideb) Nitrosureas - carmustin (BCNU) - Lomustin (CCNU) - Fotemustin - Semustin - Streptozocinc) Heavy metal platinum complex - Cisplatin - Carboplatin

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45
Q

Pharmacology

Antitumour Antibiotics

A

a) Dactinomycinb) Bleomycinc) Anthracyclines - Doxorubicin (DOX) - Daunorubicin (DNR) - Epirubicin - Idarubicin

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46
Q

Pharmacology

Anthracyclines

A

Doxorubicin (DOX)Daunorubicin (DNR)EpirubicinIdarubicin

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47
Q

Pharmacology

Antitumour Glucocorticoids

A
  • Prednisone- Prednisolone
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48
Q

Pharmacology

SERMs

A
  • Tamoxifen- Raloxifene
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49
Q

Pharmacology

Antitumour Monoclonal antibodies

A

Rituximab (CD20)
Cetuximab (EGFR)
Trastuzumab (HER-2 Breast Cancer)
Bevacizumab (VEGF)

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50
Q

Pharmacology

Antitumour Enzyme inhibitors

A

Imatinib DasatinibBosutinib(Imma das bossu) -> all for BCR-ABL tyrosine kinase blocking in CML

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51
Q

Pharmacology

Anti-tumour Drugs Overview

A

CHEMOTHERAPYI. Cell cycle-specific 1) Antimetabolites a) Folate antagonist - Methotrexate (MTX) b) Purine antagonist - Azathioprine - 6-mercaptopurine (6-MP) - 6-thioguanine (6-TG) c) Pyramidine antagonist - 5-fluorouracil (5-FU) - Cytarabine (ara-c) 2) Mitotic Inhibitors (Microtubule inhibitors) a) Vinca Alkaloids - Vincristine (VX) - Vinblastine (VBL) - Vinorelbine (VRB) b) Taxanes - Paclitaxel - Docetaxel 3) Topoisomerase inhibitors a) Topoisomerase I inhibitor - Irinotecan - Topotecan b) Topoisomerase II Inhibitor - Etoposide (VP-16) - Teniposide (VM-26) 4) Ribonucleotide reductase inhibitors a) HydroxyureasII. Cell-cycle Non-specific drugs 5) Alkylating agents a) Phosphoramide mustard precursor - Cyclophosphamide - Ifosfamide b) Nitrosureas - carmustin (BCNU) - Lomustin (CCNU) - Fotemustin - Semustin - Streptozocin c) Heavy metal platinum complex - Cisplatin - Carboplatin 6) Antibiotics a) Dactinomycin b) Bleomycin c) Anthracyclines - Doxorubicin (DOX) - Daunorubicin (DNR) - Epirubicin - Idarubicin 7) Glucocorticoids - Prednisone - Prednisolone——————TARGETED THERAPY 8) Hormone antagonist a) SERMs - Tamoxifen - Raloxifene 9) Monoclonal antibodies - Rituximab - Bevacizumab - Cetuximab - Trastuzumab 10) Enzyme inhibitors - Imatinib - Vemurafenib

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52
Q

Pharmacology

Doxorubicin cardiotoxicity reverse therapy

A

dexrazone (iron-chelator)

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53
Q

Pharmacology

rescue therapy for MTX toxicity; its mechanism

A

Leucovorin, an active form of folic acid to perform methylation in metabolic processes

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54
Q

Pharmacology

Cyclophosphamide andIfosfamide –> Hemorrhagic cystitis rescue drug

A

Mesna

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55
Q

Pharmacology

LMW heparin

A

enoxaparin

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56
Q

Pharmacology

Indirect inhibitors of factor Xa

A

Fondaparinux

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57
Q

Pharmacology

Direct thrombin inhibitors

A
  • dabigatran - hirudin - lepirudin - argatroban
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58
Q

Pharmacology

Direct factor Xa inhibitor

A
  • Rivaroxaban - Apixaban
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59
Q

Pharmacology

Drug-induced parkinsonisim

A

Reserpine (depleting dopamine store) Haloperidol (dopaminergic blocker)

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60
Q

Pharmacology

anti-parkinsonian drugs Classes

A

Dopaminergic acting:

1) Dopamine precursors, e.g. levodopa
2) peripheral DOPA decarboxylate inhibitor
3) dopamine agonists
4) MAO-B inhibitors
5) COMT inhibitors
6) Dopamine facilitator

Cholinergic acting;

7) central anticholinergics

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61
Q

Pharmacology

Counter indicated drugs with Levodopa

A

1) Nonselective MAO inhibitors
(Resulting in excess dopamine in the periphery, which could lead to a life-threatening hypertensive crisis)

2) Pyridoxine (Vitamin B6)
(Increasing peripheral breakdown of L-dopa)

3) Antipsychotics
(Blocking dopamine receptors and causing parkinsonian-like symptoms)

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62
Q

Pharmacology

Dopamine precursors drug (anti-parkinosonism)

A

levodopa

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63
Q

Pharmacology

Peripheral DOPA decarboxylase inhibitors (antiparkinosonism)

A

carbidopa, benserazide

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64
Q

Pharmacology

MADOPAR

A

levodopa + benserazide (4:1 ratio)

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65
Q

Pharmacology

Dopaminergic agonists (antiparkinsonism)

A

Ergot-derived:

  • Bromocriptine (D2)
  • Pergolide (D1,2)

Non-ergot:
Pramipexole (D2)
ropinirole (D2)
rotigotine (D2-like)

Bro Per-Plexed into Roping-role and got rot

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66
Q

Pharmacology

Ergot-derived dopaminergic D2 receptor agonist

A

Bromocriptine

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67
Q

Pharmacology

Ergot-derived dopaminergic D1&2 receptor agonist

A

Pergolide

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68
Q

Pharmacology

Non-ergot dopaminergic D2 receptor agonist

A

Pramipexole

ropinirole

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69
Q

Pharmacology

Non-ergot dopaminergic D2-like receptor agonist

A

rotigotine

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70
Q

Pharmacology

MAO-B inhibitors (antiparkinsonism)

A

Selegiline

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71
Q

Pharmacology

COMT inhibitors (antiparkinsonism)

A

Entacapone, tolcapone

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72
Q

Pharmacology

Dopamine facilitator (antiparkinsonism)

A

Amantadine

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73
Q

Pharmacology

Anticholinergic agents (antiparkinsonism)

A

Benztropine
Biperiden
Trihexyphenidyl
Benzhexol

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74
Q

Pharmacology

Huntington’s disease drug classes

A

1) Dopamine receptor antagonists - Haloperidol2) dopamine-depleting drug - Tetrabenazine3) depression and irritability drug - Fluoxetine

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75
Q

Pharmacology

Tourette’s syndrome drugs

A

ClonidineHaloperidol

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76
Q

Pharmacology

Alzheimer’s disease drugs

A

1) Anticholinesterases - Donepezil
Rivastigmine
Galantamine
(To increase the amount of ACh available for CNS functions such as memory)

2) NMDA receptor antagonists
Memantine
( improve cognitive ability by protecting CNS neurons from the excitotoxic effects of glutamate)

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77
Q

Pharmacology

Anticholinesterases (anti Alzheimer)

A

Donepezil
Rivastigmine
Galantamine

(To increase the amount of ACh available for CNS functions such as memory)

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78
Q

Pharmacology

NMDA receptor antagonist

A

Memantine

improve cognitive ability by protecting CNS neurons from the excitotoxic effects of glutamate

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79
Q

Pharmacology

Antidepressants drug classes

A
  1. Selective serotonin reuptake inhibitor
  2. Norepinephrine reuptake inhibitor
  3. Serotonin-Norepinephrine reuptake inhibitor
  4. Tricyclic antidepressants
  5. Serotonin antagonist-reuptake inhibition (SARI)
  6. α2 adrenoceptor antagonist
  7. Monoamine oxidase (MAO) inhibitors
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80
Q

Pharmacology

Serotonin selective reuptake inhibitor (Antidepressants)

A

Fluoxetine (Prozac)/CYP2D6

Paroxetine/CYP2D6

Fluvoxamine/CYP3A4

Citalopram
Escitalopram
Sertraline

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81
Q

Pharmacology

Noradrenaline reuptake inhibitor (Antidepressants)

A

Atomoxetine
Maprotiline
Reboxetine

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82
Q

Pharmacology

Serotonin-Norepinephrine Reuptake inhibitors (Antidepressants)

A 
Venlafaxine 
Desvenlafaxine 
Duloxetine 
Bupropion 
Mirtazapine
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83
Q

Pharmacology

Tricyclic Antidepressants

A

Tertiary Amines:

  • Amitriptyline
  • Imipramine

Secondary Amines

  • Desipramine
  • Nortriptyline
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84
Q

Pharmacology

Serotonin antagonist-reuptake inhibition (SARI)(Antidepressants)

A

Trazodone

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85
Q

Pharmacology

α2 adrenoceptor antagonist (Antidepressants)

A

Mianserin

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86
Q

Pharmacology

Monoamine Oxidase Inhibitors (antidepressant)

A

Non-selective:

  • Phenelzine
  • Tranylcypromine

MAO-A selective:
- Moclobemide

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87
Q

Pharmacology

antipsychotics Classes

A

1) Typical (D2)
- Chlorpromazine
- Fluphenazine
- Haloperidol
- Thioridazine
- Trifluoperazine

2) Atypical (5-HT2)
- Aripiprazole
- Clozapine
- Olanzapine
- Quetiapine
- Risperidone
- Ziprasidone
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88
Q

Pharmacology

Typical antipsychotics

A
  • Chlorpromazine
  • Fluphenazine
  • Haloperidol
  • Thioridazine
  • Trifluoperazine
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89
Q

Pharmacology

Atypical antipsychotics

A

- Aripiprazole

  • Clozapine
  • Olanzapine
  • Quetiapine
  • Risperidone
  • Ziprasidone
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90
Q

Pharmacology

anxiolytic and hypnotic drugs classes

A

1) Benzodiazepines

2) Barbiturates
———•
Other anxiolytic drugs
– Buspirone/CYP3A4
– Hydroxyzine
– Antidepressants

• Other hypnotic agents
– Zolpidem (GABA inhibit; P450)
- Zaleplon
– Ramelteon
– Chloral hydrate
– Antihistamines (diphenhydramine, doxylamine, promethazine)
– Ethanol
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91
Q

Pharmacology

benzodiazepines by duration of acting

A

Cloned ox tempted Lora to Diarrhoea and flu

i) Short-acting (2 to 8 hr) 
Triazolam
Oxazepam
Midazolam
Clonazepam

ii) Intermediate-acting (10 to 20 hr)
Temazepam
Lorazepam
Alprazolam

iii) Long-acting (1 to 3 days)
Chlordiazepoxide
Diazepam (Valium)
Flurazepam

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92
Q

Pharmacology

Benzodiazepine antagonist (rescue drug)

A

Flumazenil (GABAA receptor competitive inhibitor)

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93
Q

Pharmacology

barbiturates (by duration of acting)

A

i) Ultra-short-acting (10-20 min)
Thiopental

ii) Short-acting (2 to 8 hr)
Pentobarbital
Amobarbital
Secobarbital

iii) Long-acting (1 to 2 days)
Phenobarbital

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94
Q

Pharmacology

Anxiolytic benzodiazepine

A 
– Alprazolam
– Chlordiazepoxide
– Clonazepam
– Diazepam
– Lorazepam
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95
Q

Pharmacology

Hypnotic benzodiazepine

A

– Triazolam
– Temazepam
– Flurazepam

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96
Q

Pharmacology

IV General anaesthetics

A

Thiopentone
Propofol
Ketamine
Etomidate

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97
Q

Pharmacology

Inhaled General Anaesthetics

A
  • Desflurane
  • Isoflurane (most potent)
  • Sevoflurane
  • nitrous oxide
  • Xeon——
  • Halothane
  • Enflurane
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98
Q

Pharmacology

Endogenous analgesics

A

EnkephalinsBeta-endorphin

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99
Q

Pharmacology

Opioid analgesics classes (by structure)

A
  • Morphine and related- Phenylpiperidine series - Methadone series- Mixed agonist-antagonist
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100
Q

Pharmacology

Morphine and related compounds (opioid analgesics)

A

Morphine (to morphine 6-beta glucuronide 6MG)CodeineHeroin

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101
Q

Pharmacology

Phenylpiperidine series (opioid analgesics)

A

Merperidine (pethidine)Fentanyl family - fentanyl - sufentanil - alfentanil - remifentanil

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102
Q

Pharmacology

Methadone family

A

Methadone (aka physeptone)Dextropropoxyphene

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103
Q

Pharmacology

Mixed agonist-antagonist

A

PentazocineBuprenorphineButorphanolTramadol

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104
Q

Pharmacology

Opioid analgesics by efficacy

A

Strong- morphine- pethidine - fentanyl familyMild- codeine- Dextropropoxyphene - mixed agonist-antagonist

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105
Q

Pharmacology

Opioid analgesics antagonist

A

Naloxone (narcan)

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106
Q

Pharmacology

Insulin preparations

A

Short acting
- regular human insulin (humulin, novolin)

Rapid onset and Ultrashort acting

  • Lispro insulin (humalog)
  • Aspart insulin (novolog)

Intermediate acting

  • protamine (NPH) insulin
  • Lente insulin

Long acting

  • ultralente insulin
  • glargine insulin
  • detemir insulin
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107
Q

Pharmacology

Anti-diabetic agent classes

A

A) enhance insulin secretion

1) insulin secretagogues
- sulfonylurea
- meglitinide analogs
2) incretin mimetics
- GLP analog
3) dipeptidyl peptidase-4 (DPP-4) inhibitor

B) increases insulin action

1) insulin sensitizer
- biguanides
- thiazolidinediones

C) inhibits glucose uptake

1) alpha-glucosidase inhibitor
2) SGLT inhibitor

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108
Q

Pharmacology

Insulin secretagogues (diabetic drugs)

A

Sulfonylureas

  • glipizide
  • glimepiride

Meglitinide analogues

  • repaglinide
  • nateglinide
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109
Q

Pharmacology

Incretin mimetics (diabetic)

A

Glucagon-like peptide (GLP) analogs- exenatide- Liraglutide

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110
Q

Pharmacology

DDP-4 inhibitors (diabetic)

A

Sitagliptin phosphate

Vidagliptin

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111
Q

Pharmacology

Insulin sensitizer (diabetic)

A

A) biguanides
- metformin

B) thiazolidinediones

  • rosiglitazone
  • pioglitazone
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112
Q

Pharmacology

alpha-glucosidase inhibitor (diabetic)

A

Acarbose

Miglitone

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113
Q

Pharmacology

Short term treatment of hypertyroidism

A

Before surgery
Thyrotoxic crisis
Initial treatment for hyperthyroidism while waiting for effect of long term drugs

1) Beta blockers
- propanolol

2) Lugol’s solution
- 5% iodine + 10% potassium iodide

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114
Q

Pharmacology

Long term treatment of hyperthyroidism

A

1) Thionamides
- methimazole
- carbimazole
- propylthiouracil

2) Radioiodine
- iodine 131

3) Thyroidectomy

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115
Q

Pharmacology

Acute hypothyroidism drugs

A

T3 - Liothyronine

Due to quicker onset of effects

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116
Q

Pharmacology

Routine replacement therapy of hypothyroidism

A

Thyroxine (T4)

Due to longer half life

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117
Q

Pharmacology

B cell lymphoma medication

A

R-CHOP

Rituximab (anti-CD20)

Cyclophosphamide

Hydroxydaunarubicin

Vincristine

Prednisone

(purine analogue for low grade)

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118
Q

Thyroid Hormone replacement ADR

A

1) Thyrotoxicosis
2) worsening ischemic symptoms (caution in patients with cardiovascular disorder) due to beta-adrenoceptor and related vasoconstriction
3) Risk of acute adrenal crisis (because thyroxine ↑ metabolic clearance of adrenocortical hormones) -> hypoglycaemia and hypotension

THEREFORE MONITOR T4 AND TSH LEVELS

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119
Q

Propanolol use in hyperthyroidism

A

Beta blocker, for symptomatic relief:

1) Blocks beta 1 in heart, relieve palpitation
2) Blocks beta 1 in brain, relieve nevousness
3) Blocks beta 2 in skeletal muscles, relieve tremor

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120
Q

Mechanism of action of Lugol’s solution

A

1) By inhibition of H2O2 generation so thyroidal peroxidase cannot oxidise iodide to iodine
2) Decrease vascularity of thyroid
3) By inhibition of T3/T4 release

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121
Q

Angel dust effect

A

i.e. PCP, behaviour mimics schizophrenia

PCP binds to and inhibits NMDA glutamate receptor (block Na Ca entry)

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122
Q

Strategy for type 1 DM

A

Diet
Exercise
Insulin

123
Q

DM type 2 treatment strategy

A

1) Diet, Exercise
2) add Anti-diabetic agents monotherapy
3) switch to combined therapy
4) add further Insulin injection

124
Q

Gestational diabetes mellitus treatment strategy

A

Diet
Insulin
Anti diabetic agents

125
Q

Criteria for basal insulin

A
  • mimics normal pancreatic basal insulin secretion
  • smooth peak less profile
  • long lasting effect: 24 hours or more
  • predictable or reproducible effects
126
Q

Bolus insulin criteria

A
  • rapid onset of action; usually given before meals
  • short duration of action to avoid hypoglycaemia
  • predictable and reproducible effects
127
Q

Source of replacement insulin

A

Produced by recombinant DNA technology with E Coli or yeast

128
Q

Regular insulin biochemistry and use

A

Self aggregate in antiparallel fashion to form dimers that stabilise around zinc ions to create hexamers –> delayed onset and prolonged time to peak actions

Useful for management of diabetic ketoacidosis (DMT1) or when insulin requirement is changing rapidly (post surgery and acute infection)

Not useful for bonus injection

129
Q

Why is humulin not good for insulin bonus injection

A

1) slow onset of action due to self aggregation (hexameric insulin does not bind to insulin receptor)

  • > inconvenient administration of 40 mins before meal
  • > hypoglycaemic risk if meal delayed
  • > mismatch with postprandial hyperglycemia peak

2) long duration of activity
- > potential for late postprandial hypoglycaemia

130
Q

Lispro and Aspart insulin

A

Rapid onset and ultrashort acting insulin

  • prevent hexameric formation so they break into monomer after SC injection
  • closely mimics endogenous postprandial insulin secretion
  • taken just before meal
  • without risk of hypoglycaemia between meals
131
Q

NPH insulin

A

Insulin mixed with protamine

  • intermediate acting
  • insulin bound to protamine -> slowly dissolve in body fluid
  • facilitate control of glycemic over an extended period
132
Q

Lente insulin

A

Mixture of 30% semilente and 70% ultralente insulin

  • intermediate acting
  • insulin bound to zinc -> slowly dissolve in body fluid
  • facilitate control of glycemic over an extended period
133
Q

Ultralente insulin

A

Long acting insulin, withdrawn from market due to unsafe

Entirely crystalline zinc -> slow onset, slow effect

134
Q

Insulin glargine

A

Long acting insulin

  • 2 arginine added to carboxyl terminal and substitution and glycine substituted for asparagine at A21 -> lower solubility and prolonged action
  • ultra long acting, maximal effect maintained for 24 hours
  • peakless activity, clear solution, no zinc in formula
  • once daily at bedtime
135
Q

Detemir insulin

A

Long acting insulin

  • > added fatty acid moiety
  • > when added to circulation, fatty acid cause it to bind to albumin -> slow release and extended circulating life
136
Q

Insulin administration

A

1) Subcutaneous or intramuscular injection
2) Insulin pump

– experimental –

3) transdermal
4) oral
5) inhalation
6) pancreatic transplant and ST therapy

137
Q

Insulin pump

A

Aka continuous subcutaneous insulin infusion device (CSII)

Major components:
1) pump

2) disposable reservoir for insulin inside the pump
3) disposable infusion set, including cannula for SC insertion, a tubing system to interface insulin reservoir to cannula

138
Q

Insulin replacement therapy complications and solutions

A

1) hypoglycaemia (nausea, confusion, weakness, coma)
+ glucose administration

2) insulin allergy and immune resistance (rarely happen now with recombinant DNA production)

3) lipodystrophy at injection site
+ use multiple site injection

4) long term risk like DMT2, and lifelong dependency on exogenous insulin

139
Q

SGLT2 inhibitors

A

Dapagliflozin

140
Q

sulphonylureas mechanism

A

Anti diabetic (type 2) e.g. Glipizide, glibencalmide

Insulin secretagogue, long duration of action

Bind extracellularly to receptor on pancreatic beta cells to close K channel, which reduce K efflux, leading to depolarisation, Ca channel opening and Ca influx, then exocytosis of insulin

(ONLY USE IN CASES WITH INTACT beta cells! Primary and secondary failure)

141
Q

Sulphonylureas ADRs

A
  • stimulate appetite and weight gain
  • hypoglycaemia (esp in hepatic or renal insufficients)
  • GI upset (must give with food) and rashes
  • cross placenta and deplete fetal pancreatic insulin
142
Q

Meglitinide analogues mechanism

A

Anti diabetic (type 2) e.g. Repaglinide, nateglinide

Insulin secretagogue, rapid onset and short duration of action -> good for postprandial glucose control

Bind extracellularly to receptor on pancreatic beta cells to close K channel, which reduce K efflux, leading to depolarisation, Ca channel opening and Ca influx, then exocytosis of insulin

(ONLY USE IN CASES WITH INTACT beta cells!)

143
Q

Meglitinide ADRs

A
  • increase appetite and weight gain (rarely compared with sulphonylureas)
  • hypoglycaemia (rarely compared with sulphonylureas)
144
Q

Biguanides mechanism

A

Insulin sensitizer; Antidiabetic (type 2) eg metformin

Activating liver’s AMP-activated protein kinase (AMPK), which will:

  • decrease glyconeogenic genes, decrease hepatic glucose production, thus reduce hyperglycemia
  • decrease fatty acid synthesis and increase fatty acid oxidation, thus reduce hyperlipidemia
145
Q

Metformin usage

A

Antidiabetic used for obese patients or patients with insulin resistance

  • reduce CVS complications
  • decrease incidence of diabetes related cancers
146
Q

Metformin ADRs

A
  • GI upset with nausea, diarrhoea and abdominal discomfort
  • lactic acidosis, esp with glucocorticoid (because glucocorticoid cause steatosis and steatohepatitis that makes liver susceptible to metformin induced lactate production)
  • Long term use -> Vit B12 deficiency

(Usage alone does not cause hypoglycaemia)

147
Q

Metformin contraindications

A

Renal disease, hepatic disease, severe infection, alcoholism, glucocorticoids (lactic acidosis)

148
Q

Thiazolidinediones mechanism

A

Insulin sensitizer: For prevention of type 2 DM

Acts on adipose tissue (liver and muscle too), by binding to the nuclear hormone receptor PPAR gamma (peroxisome proliferator-activated receptor) to decrease insulin resistance

Anti-inflammatory and improve lipid profile

149
Q

Rosiglitazone ADRs

A

1) weight gain, fluid retention

2) increased risk of heart attack

150
Q

Pioglitazone ADRs

A
  • weight gain and fluid retention

- risk of bladder cancer

151
Q

Alpha-glucosidase mechanism

A

DMT2, eg Acarbose, Miglitol

Inhibits small intestine’s alpha-glucosidase through competition with substrate, thus blocking postprandial digestion and absorption of starch and disaccharides -> lower blood glucose and insulin level after meals

WEAK antIdiabetic EFFECTS

152
Q

Alpha-glucosidase inhibitor ADRs

A

Not absorbed into blood stream, therefore little systemic ADRs (no weight gain or hypoglycaemia)

  • Flatulence
  • diarrhoea
  • abdominal pain
153
Q

Exenatide mechanism

A

incretin mimetics, NEED INJECTION

  • synthetic version of GLP-1 agonist, which acts to pancreatic cells to enhance insulin secretion and inhibit glucagon release
  • only ~50% homology with GLP, therefore greater resistance to DPP-4 and have longer half life
  • may decrease fatty liver too!
154
Q

Examples of incretins

A

Gut derived hormones:

  • glucagon like peptide 1 (GLP-1)
  • glucose-dependent insulinotropic peptide (GIP)
155
Q

Exenatide ADRs

A

1) GI disorder, acid stomach, belching, vomiting, diarrhoea
2) dizziness, headache
3) weight loss by slowing gastric emptying time

156
Q

DPP-4 inhibitors mechanism

A

DMT2

Inhibits gut’s DPP-4 mediated degradation of GLP-1, thus increasing GLP-1 level, which acts in pancreatic alpha and beta cells to enhance insulin and reduce glucagon secretion

Long term blood glucose control

157
Q

DPP-4 inhibitor ADRs

A

Upper respiratory tract infection

Sore throat

Diarrhoea

158
Q

SGLT2 inhibitor (DM)

A

Blocks SGLT2 sodium glucose cotransporter in proximal tubule, thus reducing glucose reabsorption

159
Q

SGLT2 inhibitor side effect

A

Genital infection

160
Q

HSV drug

A

Acyclovir, valaciclovir

Foscarnet, cidofovir

161
Q

CMV antiviral

A

Ganciclovir, valganciclovir

Foscarnet, Cidofovir

162
Q

VZV antiviral

A

Acyclovir, valaciclovir

Foscarnet, Cidofovir

163
Q

HIV antiviral overview

A

Entry inhibitor
1) fusion inhibitor Enfuvirtide (gp41)

2) binding inhibitor Maraviroc (CCR5 with gp120)

Reverse transcriptase inhibitor
1) Nucleoside: lamivudine, zidovudine, abacavir

2) nucleotide: tenofovir
3) non-nucleoside: nevirapine, efavirenz

Integrase inhibitor (HIV I integrase)
1) raltigravir

Protease inhibitor
1) ritonavir, atazanavir

164
Q

Influenza antiviral

A

1) Amantadine, rimantadine (Viral uncoating inhibitor; blocks pore formation by M2 protein, thus prevent H+ influx to virus, prevent acidification of viral core, thus inhibits RNA transcriptase)
2) Oseltamivir, Zanamivir (Viral release inhibitor)

165
Q

RSV antiviral

A

Ribavirin (IV for RSV in pre engraftment BM transplant)

Prophylaxis:

  • Respigam (RSV-IVIg)
  • palivizumab (anti RSV fusion protein)
166
Q

Interferon alpha mechanism

A

Blocks viral RNA transcription, protein synthesis and augment immune response

(For HBV and HCV)

Peginterferon-α2a or 2b: interferon conjugated with polyethylene glycol, prolongs persistence of drug in blood.

167
Q

Lugol’s solution ADRs

A

1) Allergy (rash, fever, angioedema, bronchitis, salivary gland pain)
2) Counterindicated for breastfeeding because will enter infant via milk; leads to hypothyroidism in baby, which will leads to feedback increase of TSH and thyroid hyperplasia (goitre)

168
Q

Use of lugol’s solution

A

1) Improve acute thyroxic symptoms (in acute hyperthyroidism)
2) pre-operatively before thyroidectomy to decrease vascularity to Reduce bleeding risk during operation
3) NOT for long term use due to desensitisation

169
Q

Thionamides mechanism

A

Anti-hyperthyroidism

Carbimazole converted to active Methimazole, which inhibits thyroidal peroxidase, thus preventing iodide conversion to iodine, and prevent organification of iodine with tyrosine and reduce formation of T3 T4

Propylthiouracil, apart from inhibiting thyroidal peroxidase, also block peripheral cell’s deiodinization of T4 to T3, thus preventing activation of thyroid hormone

170
Q

Use of thionamides

A

1) Slow onset of action of 3-4 weeks (require depletion of T3, T4 store)

  • long term therapy of 12-18 months
  • higher dose initially, reduce when euthyroid reached
  • if hypersensitive to carbimazole, then use propylthiouracil
  • seldom curative, relapse common
171
Q

Thionamides ADRs

A

1) Skin rash and pruritus (use antihistamine!)
2) Myelosuppression (thrombocytopenia, agranulolytosis)
3) Cross placenta and secreted in breast milk

  • raised liver transaminase
  • LOW risk of hypothyroidism
172
Q

Iodine-131 mechanism against hyperthyroidism

A

Taken up by NI symport, and oxidised by thyroidal peroxidase into iodine and organified with tyrosine; emits beta radiation that damages the thyroid

173
Q

Use of iodine-131

A

Oral administration as sodium iodide for:

1) Hyperthyroidism
- Preferred definitive treatment for Graves’ disease, toxic nodular goitre
- relapse of hyperthyroidism after thionamide therapy

2) Thyroid Tumour
- ablate well-differentiated thyroid cancer including papillary thyroid cancer and follicular thyroid cancer, especially after thyroidectomy

3) radioactive label for certain radiopharmaceuticals

174
Q

Iodine-131 ADRs (in usual hyperthyroidism treatment)

A
  • tolerable acute side effects (e.g. mild neck swelling, pain on swallowing -> use steroid)
  • post-radiotherapy hypothyroidism (need lifelong TH replacement)
  • Potential damage to thyroid glands of fetus and infants (via placenta and breast milk, therefore counter indicated)
  • radioactive iodine may harm others
  • Graves’ ophthalmopathy may develop or worsen after treatment

NO congenital defects or infertility

175
Q

Counterindications for I-131

A

1) pregnancy and lactation (Potential damage to thyroid glands of fetus and infants via placenta and breast milk )
2) Children and adolescent
3) severe Graves’ ophthalmopathy (may develop or worsen after treatment)

176
Q

I-125

A

nuclear imaging tracer and radioactive treatment for prostate cancer

177
Q

I-123,I-124

A

nuclear imaging tracers for thyroid diseases

178
Q

Use of thyroidectomy for hyperthyroidism

A

Usually total thyroidectomy with T4 replacement, uncommonly performed, used for:

  • for multinodular/large goitre
  • pregnant patients intolerant to antithyroid drugs
  • suspected coexistent thyroid cancer

–> need to restore to uethyroidism before surgery

179
Q

Complications of thyroidectomy

A

Hypothyroidism -> lifelong T4 replacement

Vocal cord paralysis (recurrent laryngeal nerve and external laryngeal nerves lies close)

180
Q

Precautions before and after I-131 therapy

A
  • 4 weeks of low iodine diet
  • 4 weeks avoiding anti-thyroid medication
  • Pregnancy test for patients with child-bearing potential
  • symptomatic control of hyperthyroidism (e.g. propranolol for palpitation)
  • No close contact with spouse/partner and children after for 2 weeks
  • contraception for 6 months after, avoid pregnancy and breast feeding
181
Q

Use of thyroidectomy for thyroid tumours

A
  • ablate well-differentiated thyroid cancer including papillary thyroid cancer and follicular thyroid cancer, especially after thyroidectomy against residual microscopic tumour cells
  • Destroys remaining normal thyroid tissue
  • Makes serum thyroglobulin (Tg) a more specific tumor marker
  • Facilitates future surveillance for relapse with I131- Whole Body Scan
  • Reduces loco-regional recurrences
  • Eradicates distant metastases
  • Reduces relapse and improves overall survival

** Shorter effective half-life of I-131 due to: uptake via NIS is reduced, iodine organification is markedly reduced => therefore require larger dose

182
Q

Iodine-131 ADRs (for tumours)

A

1) Sialadenitis, nausea/vomiting, epigastric discomfort, cystitis

LARGE DOSE:

  • bone marrow suppression (very rare),
  • aplastic anaemia (very rare)
  • leukaemia (very rare)
  • pulmonary fibrosis (lung metastasis)
  • neurological complication (vertebral metastasis)
183
Q

Pituitary dwarfism treatment

A

(deficiency of GH)

replacement therapy with somatropin

184
Q

somatropin ADRs

A

1) Hypothyroidism (induce conversion of T4 to T3, depletes pool)
2) Peripheral edema (induces retention of sodium, potassium and phosphate)
3) Increase Intracranial hypertension -> Papilloedema (visual change) and headache
4) Impaired glucose tolerance

185
Q

Hypopituitarism (gonadotrophin deficiency) treatment

A

Replacement therapy with

FOR FSH:

  • Follitropin (recombinant FSH)
  • HMG (Human menopausal gonadotrophin; contains both FSH and LH)

FOR LH:

  • Lutropin α (recombinant LH)
  • Choriogonadotropin α (recombinant HCG)
  • Human chorionic gonadotrophin (HCG)

NOTE: FSH (follitropin α and β, HMG) must be used with LH (lutropin α, HCG, choriogonadotropin α)

186
Q

FSH LH replacement therapy ADRs

A

FSH:

1) Ovarian hyperstimulation syndrome
- Ovarian enlargement
- Ascites
- Hydrothorax (difficult to breathe)
- Hypovolemia
2) Hemoperitoneum
3) Arterial thromboembolism (from hypovolemia)
4) Multiple birth
5) Gynaecomastia

LH:

1) Edema
2) Depression
3) Headache
4) Gynaecomastia
5) Precocious puberty

187
Q

ACTH deficiency treatment

A

(Adrenal cortisol release is reduced but adolsterone release is regulated by renin-angiotensin system)

Corticosteroids with only glucocorticoid activity e.g. Hydrocortisone

  • In replacement therapy, anti-inflammatory & immunosuppressive effects become unwanted side effects (e.g. increase chance of infection)
188
Q

Primary hypoadrenalism (e.g. Addison’s disease)

A

Both cortisol and adolsterone release is reduced

Use corticosteroids with glucocorticoid & mineralocorticoid activity, e.g.:

1) Hydrocortisone
2) Cortisone

  • In replacement therapy, anti-inflammatory & immunosuppressive effects become unwanted side effects (e.g. increase chance of infection)
189
Q

Adverse effect of cortisol replacement therapy

A

Iatrogenic Cushing’s syndrome

190
Q

hyperprolactinaemia treatment

A

Dopamine receptor agonists that acts on anterior pituitary:

1) Bromocriptine
2) cabergoline (longer t1/2 and higher selectivity for dopamine receptor)

191
Q

Adverse effects of dopamine receptor agonists

A

1) Postural Hypotension, Arrhythmias
2) Constipation
3) Nausea & vomiting

  • Bromoctiptine: Erythromelalgia i.e. swollen hand and feet
  • Pergolide: urinary tract infection
  • Pramipexole and ropinirole: dyskinesia, insomnia
  • rotigotine: skin hypersensitivity cos transdermal patch
192
Q

acromegaly and gigantism treatment

A

Somatostatin analogues:

1) Octreotide (inhibtits anterior pituitary and decrease tumour size)
2) Lanreotide (longer acting than octreotide; inhibtits anterior pituitary and decrease tumour size)
3) Pegvisomant (inhibits growth hormone’s action on liver and peripheral tissues)
4) Dopamine receptor agonists (causes a paradoxical decrease in growth hormone secretion)

193
Q

ADR of Octreotide and Lanreotide

A

1) GI disturbance (as it inhibits the secretion of gastrointestinal peptides, VIP, PP, gastrin)
- Nausea & vomiting
- Abdominal cramps
- Flatulence
- Steatorrhoea

2) Gall stones (inhibition of gall bladder motility)

3) Impaired glucose tolerance (*somatostatin inhibits the
secretion of insulin from pancreas)

194
Q

ADR of Pegvisomant

A
  • Hepatotoxicity and Hepatitis (elevated LFT enzymes)

- Nausea & diarrhea

195
Q

Cushing’s Syndrome treatment

A
  • Metyrapone (inhibits 3-β-dehydrogenase)

- Trilostane (inhibits 11-β-hydroxylase)

196
Q

Adverse effects of metyrapone and trilostane

A
  • Hypotension
  • Nausea & vomiting
  • Headache
  • Rash
197
Q

Treatment of diabetes insipidus

A

ADH Replacement therapy with:
- Synthetic vasopressin
- Desmopressin (longer acting, less vasopressor
effect because it is more V2 selective)

198
Q

ADR of ADH replacement therapy

A

1) Fluid retention
2) Dilutional Hyponatremia
3) Headache
4) Nausea
5) Allergy
- ——
6) Spasm of coronary artery => angina (unlikely in desmopressin)
7) Abdominal and uterine cramps (unlikely in desmopressin)

199
Q

Treatment of hyperparathyroidism

A

Severe hypercalcemia corrected by rehydration via saline and loop diuretics, and calcitonin injection for short term

Long term:

  • surgical removal of tumour (primary)
  • treat underlying cause (secondary)
200
Q

Hypoparathyroidism treatment

A

IV calcium infusion (for severe hypocalcemia)

Oral calcium with vit D

PTH replacement therapy

201
Q

Mechanism of opioid analgesics

A

1) Peak plasma conc instantaneously, gradually decrease because Unionized form and lipid soluble crosses the BBB to reach effector site (delayed onset cos time required for penetrating BBB)

2) blocks the following pain receptors:
- μ receptor: Most of pain relief and ADRs
- δ and κ receptors: some of the pain relief, less important
=> analgesia

202
Q

Context sensitive half life of opioid analgesic

A

The half life (1/2 conc) after a duration of steady infusion (context)

  • context-sensitive drugs’s half life increases with longer duration of infusion; fixed half life for context-insensitive drugs e.g. remifentanil
203
Q

Morphine metabolism

A

Converted to morphine 6-glucuronide, which is renal excreted

204
Q

Penthidine metabolism

A

Converted to norpethidine

205
Q

Strategy and Routes of administration for opioid analgesics

A

Patient Controlled Analgesia:

  • After initial loading dose, patient press a button to activate IV infusion of drug
  • hospital only
  • closely control dosage to prevent ADRs

1) IV (PCA)
2) Transdermal (fentanyl)
3) Indwelling subcutaneous cannula (for paediatrics)
4) Epidural (so that effect localised in CNS)
5) Transmucosal (via oral mucosa -> lollipops! paediatrics)

206
Q

Transdermal fentanyl pros and cons

A

PROS

  • convenient
  • can take home

CONS:

  • so convenient overdose is common
  • never multiple patches!
207
Q

Acute opioid usage ADR

A

1) Sedation
2) Respiratory depression
3) Euphoria
4) Miosis
5) Nausea, vomit

** ED95 and LD05 may overlap -> individual titration

NOTE: for mixed agonist-antagonist, acute ADR only miosis, nausea, vomit

208
Q

Chronic opioid usage ADR

A

1) Constipation
2) Tolerance/ dependence
3) Acute ADRs:
- Sedation
- Respiratory depression
- Euphoria -> addiction
- Miosis
- Nausea, vomit

NOTE: for mixed agonist-antagonist, chronic ADR only constipation, miosis, nausea, vomit

209
Q

Opioid euphoria ranking

A

Pethidine > morphine > methadone

210
Q

Drug Tolerance definition

A

a physiological state characterized by a decrease in the effects of a drug with chronic administration.

211
Q

Drug dependence definition

A

1) Physical dependence
- physiological adaptation of the body to the presence of an opioid
- withdrawal symptoms when dose abruptly discontinued or reduced, or when antagonist or partial agonist added
- relieved by gradual withdrawal

2) Addiction
- compulsive use of drugs for non medical reasons
- Craving for mood altering effect not pain relief
- dysfunctional behavior e.g. lying, forgery of prescription, theft, etc

212
Q

GA vs LA vs analgesics

A

GA: loss of all sensation, loss of consciousness

LA: loss of all sensation regionally

Analgesics: Loss of pain sensation

213
Q

Modern Balanced Anaesthesia

A

1) Unconsciousness (GA)
2) Analgesia (analgesics)
3) Muscle relaxation (NMJ blocker)

214
Q

Mechanism of GA action

A

1) Potentiate release of inhibitory neurotransmitter (GABA, glycine)
2) GABA binds to postsynaptic GABA receptor
3) Cl influx (and K efflux)
4) Hyperpolarization of cell -> reduced cell sensitivity and shut down brain

215
Q

all GA’s potential dangers

A

Dangerous due to overlapping of ED95 and LD05

1) Airway obstruction
- consequence of deep sleep
- low tongue muscle tone, may slip back when lying (obstructive apnoea)
- protective airway reflex impaired

2) Aspiration
- reduced protective airway reflex
- entry of gastric acidic content when vomiting

216
Q

Comparing pros cons of IV GAs (ADRs)

A

1) Thiopentone
- reduce BP and respiration (apnoea!)
- sulphur -> G6PD attacks

2) Propofol
- more reduced BP and respiration (apnoea! not for shock patient)
- Target controlled infusion needed to closely monitor

3) Ketamine
- no reduced BP, will increase BP
- may incease BP -> not used to coronary Heart disease
- CNS excitation! nightmare or move limbs

4) Etomidate
- no rise or drop in BP
- CNS excitation (less so)

217
Q

inhaled GA compared with IV GA

A
  • Inhaled has slower onset (30s) than IV (5s)
  • IV used for adult first, then continue with inhaled; use inhaled directly on children
  • inhaled not as precise and difficult to control amount
218
Q

Inhaled GA administration instrument

A

Generic temperature-compensated Variable bypass vaporiser:

  • incoming air into two streams, one bypass vaporising chamber, one mixes with vapour in vaporising chamber
  • concentration of outgoing vapour controlled by mixing of two straws in different amount
219
Q

Minimum alveolar concentration (definition, and level)

A

Indicator of GA potency -> smaller MAC means more potent

MAC lower in neonates and elderly

Definition: Minimum alveolar concentration of inhaled agent which prevents 50% subject’s response movement to standard painful stimulation

220
Q

Oil:gas partition coefficient

A

Higher oil:gas partition coefficient -> higher potency of inhaled GA

221
Q

Blood:gas partition coefficient

A

How easy a drug diffuse between blood and gas state, inverse with time of onset (lower means faster onset)

  • quantified by wash-in = alveolar conc/ vaporiser conc

Affected by:

1) Nature of drug
2) Ventilation rate (high ventilation -> higher)
3) Cardiac output (higher CO -> lower)

222
Q

Inhaled GA metabolism

A

Not important and negligible -> mainly leave through lungs

223
Q

Inhaled GA ADRs

A

CVS effects:

  • reduced systemic vascular resistance
  • reduce mean arterial pressure
  • reduce cardiac output
  • increase heart rate
224
Q

Parkinson’s disease treatment general mechanism

A

To re-establish the balance between dopamine and acetylcholine in the brain by:

1) Increasing dopamine in the nigrostriatal system
2) Reducing cholinergic inputs from striatum

225
Q

Levodopa ADRs

A

1) conversion of L-dopa to dopamine in the periphery
- nausea, vomiting
- postural hypotension, Arrhythmias
- constipation

2) overstimulation of central dopamine receptors
- Dyskinesia
- Hallucinations

226
Q

Carbidopa, Benserzide mechanism

A

does not cross BBB; peripheral DOPA decarboxylase inhibitor

Against PD by decreasing peripheral conversion of levodopa to dopamine, thus increasing availability of dopamine to CNS

227
Q

Selegiline mechanism

A

Anti-PD, inhibits MAO-B

Against PD by decreasing peripheral metabolism of dopamine, thus increasing availability of dopamine to CNS

228
Q

Selegiline ADRs

A

Hypertensive crisis if large dose

229
Q

COMT inhibitor mechanism

A

Anti-PD, inhibits COMT, thus blocking the peripheral conversion of levodopa to 3-O- methyldopa

230
Q

COMT inhibitor ADRs

A
  • Postural hypotension
  • Diarrhea
  • Dyskinesias
  • HEPATIC NECROSIS (Tolcapone only)
231
Q

Amantadine anti-PD mechanism

A
  • enhance the release of dopamine from surviving nigral neurons (with surviving neurons)
  • inhibit the reuptake of dopamine at synapses
232
Q

PD treatment regimens

A

1) Madopar (levodopa + benzerazide 4:1)
2) + Dopamine agonists (pramipexole, ropinirole)
3) + MAO-B or COMT inhibitor to reduce motor fluctuations in advanced disease
4) + Anticholinergics for tremor control
5) Apomorphine for rescue of “off episode”

233
Q

When should we use antidepressants

A

The risk of untreated depression far outweigh those of antidepressant mediations

234
Q

Better alternative to anti-depressants

A

TALK THERAPY

  • Helps by teaching new ways of thinking & behaving.
  • Changing habits that may be contributing to the depression.
235
Q

Anti-depressant general ADR

A

black box warning:

  • increases the risk of suicidality and suicidal ideas and gestures in patients under the age of 25
  • after age of 65, no associated risk with suicidal.
236
Q

Contraindicated drugs in SSRI

A

Fluoxetine, Paroxetine -> CYP2D6; cannot use with tricyclic antidepressants

Fluvoxamine ->CYP3A4; cannot use with diltiazem (Ca channel blocker), otherwise hypotension and bradycardia

237
Q

SSRI ADRs

A

(suicidal under 25)

enhance serotonergic tone:

  • nausea, GI upset, dairrhoea
  • decreased libido
  • Reducing serotonin-mediated platelet activation -> bleeding risk
  • Vasoconstriction by inhibiting nitric oxide synthase (avoid in pregnancy with hypertension otherwise prematurity)
238
Q

Selective NRI ADRs

A

(suicidal under 25)

Enhance noradrenergic tone:

  • CNS activation (anxiety, agitation)
  • Increase BP
  • Heart rate
239
Q

Serotonin-noradrenaline RI ADRs

A

(suicidal under 25)

1) enhance serotonergic tone:

  • nausea, GI upset, dairrhoea
  • decreased libido
  • Reducing serotonin-mediated platelet activation -> bleeding risk
  • Vasoconstriction by inhibiting nitric oxide synthase (avoid in pregnancy with hypertension otherwise prematurity)

2) Enhance noradrenergic tone:

  • CNS activation (anxiety, agitation)
  • Increase BP
  • Heart rate
240
Q

Tricyclic Antidepressants mechanism

A

secondary amine: predominantly NE reuptake inhibition, a bit shorter acting

Tertiary: NE and 5HT transporter for reuptake affected; strongly anticholinergic; long acting

241
Q

Tricyclic ADRs

A

SERIOUS DRUG INTERACTION

Antihistamine:

  • sedation
  • weight gain

Anticholinergic (too much Fight or Flight!)

  • Dry mouth
  • constipation
  • urinary retention
  • blurred vision

Antiadrenergic (Comfy state!)

  • Sedation
  • sexual dysfunction
  • postural hypotension
242
Q

Trazodone mechanism

A

1) Mainly 5-HT2A receptor antagonism
2) Serotinin reuptake transporter (SERT) anatagonism
3) Converted to mCPP, which activates 5-HT1A receptor, leading to anti-depression effects

243
Q

Mianserin mechanism

A

Anti-depression:

Blocks α2 presynatpic autoreceptor and enhances noradrenalin release.

244
Q

Mianserin ADRs

A

Sedation
Dry mouth
Constipation
dizziness

245
Q

MAO-A VS MAO-B

A

MAO A metabolises Dopamine, Tyramine, serotonin (5HT), Noradrenaline, adrenaline

MAO B metabolises Dopamine, Tyramine Phenylylaine

246
Q

MAO inhbitor ADR

A
  • Postural hypotension
  • Weight gain

1) fatal interactions between MAOI and tyramine (e.g. in food like bananas, pineapple, eggplants):

  • Increase blood pressure and heart rate
  • Hypertensive crisis
  • Stroke, heart attack, death

2) Serotonin syndrome when combines with serotonergic agent -> due to overstimulation of 5HT receptor

247
Q

MAO-inhibitor usage guidelines

A

Serotonergic antidepressants should be discounted for at least 2 weeks before starting an MAOI (fluoxetine for 4-5 weeks due to long action)

MAOI should be discounted for at least 2 weeks before starting Serotonergic antidepressants

248
Q

Antidepressant discontinuation solution and symptoms

A

Reduce doses gradually over at least a 4-week period

ABCDEF
Agitation, anxiety
Balance problems, bad dreams
Concentration problems
Dizziness, diarrhoea, vomiting
Electric shock like sensation
Flu like symptoms
\+ psychosis, confusion, excitement
249
Q

Anti-depressant application

A
  • depression
  • general anxiety disorder
  • PTSD
  • OCD
  • smoking cessation
  • bulimia
250
Q

Psychosis treatment

A

1) Antipsychotics - symptom relief
2) Psychological therapies – help address the underlying cause of psychosis
3) Social support
4) Family therapy
5) Self-help groups

251
Q

Side effects of typical antipsychotics

A

ADR due to blockade of D2 receptor at different sites other than mesolimbic-mesocortical pathways:

1) Extrapyramidal symptoms (nigrostrital)
- Acute dystonia
- tardive dyskinesia
- Parkinsonism
- Akathisia

2) Hyperprolactinemia (Tuberoinfundibular)
- gynaecomastia
- loss of libido
- low sperm count, infertility
- galactorrhoea
- Amenorrhoea

3) vomiting (Chemoreceptor trigger Zone)
4) Drowsiness

5**) Neuroleptic malignant syndrome - sudden fever to very high level

252
Q

typical antipsychotics mechanism

A

Block D2 receptor at mesolimbic-mesocortical pathways, which controls memory, mood and motivation

253
Q

Atypical antipsychotics mechanism

A

Blocks 5HT2 receptor

254
Q

Atypical antipsychotics ADRs

A

Similar to tricyclics!

1) Antihistamine:
- sedation
- weight gain

2) Anticholinergic (too much Fight or Flight!)
- Dry mouth
- constipation
- urinary retention
- blurred vision

3) Antiadrenergic (Comfy state!)
- Sedation
- sexual dysfunction
- postural hypotension

+4) Metabolic effect

  • hyperglycaemia
  • Diabetes
  • hyperlipidemia

5) Extrapyridmal symptoms
6) Hyperprolactinemia
7) Neuroleptic malignant syndrome

255
Q

Anti-psychotic withdrawal symptoms

A

Nausea, vomiting, anxiety, insomnia

Super-sensitivity psychosis after withdrawal (due to up regulation of dopamine receptor number and sensitivity in response to blockade)

256
Q

Chemotherapy strategies

A

1) Induction therapy - high dose to induce a complete response when initiating curative regimen
2) Adjuvant therapy - short course of high dose after radiotherapy or surgery to destroy residual tumour and prevent recurrence
3) Neoadjuvant therapy - short course before radiotherapy or surgery to reduce tumour burden
4) Maintenance - long term low dose for patient in complete remission, to prevent remission of residual tumour
5) Salvage therapy - potentially curative high‐dose when recurrent or when another regimen failed

(6? Consolidation therapy)

257
Q

Advantages of drug combinations in chemotherapy

A

1) provide maximal cell killing within the range of tolerated toxicity
2) effective against a broader range of cell lines in the heterogeneous tumor population
3) delay or prevent the development of resistant cell lines
4) agents with similar dose‐limiting toxicities, such as myelosuppression, nephrotoxicity, or cardiotoxicity can be combined safely by reducing the doses of each

258
Q

Methotrexate ADR

A
  • excreted in the urine mostly as unchanged drug
  • RENAL TOXICITY: High doses of MTX undergo hydroxylation to form 7‐ hyroxymethotrexate, which is less water soluble and may lead to crystalluria

(keep the urine alkaline and the patient well hydrated to avoid)

259
Q

Purine analogue mechanism

A

Orally taken

INHIBITS DNA synthesis by blocking formation of normal purine nucleotides

  • Azathioprine -> 6MP, converted to the nucleotide analog TIMP, then converted to 6-thioguanine
  • TIMP inhibits de novo purine ring biosynthesis and blocks the formation of AMP and xanthinuric acid from inosinic acid
  • RNA and DNA containing thioguanine monophosphate (TGMP) are not functional
260
Q

6-MP ADRs

A
  • Myelosuppression (especially in defected TPMT or ppl taking XO inhibitor e.g. allopurinol)
261
Q

6-MP Pharmacokinetics

A

First pass in liver:

1) 6-MP converted to 6-methylmercaptopurine by TPMT Thiopurine S‐methyltransferase
2) 6-MP converted to 6-thiouric acid by XO xanthine oxidase

262
Q

Pyramidine analogue mechanism

A

inhibit DNA synthesis both by blocking the formation of normal pyrimidine nucleotides via enzyme (thymidylate synthetase) inhibition and by interfering with DNA synthesis after incorporation into a growing DNA molecule:

—–DETAILS:
5-FU converted to fluorouridine monophosphate 5-FUMP

5‐FUMP is further metabolized to:

i) the triphosphate 5‐FUTP which is incorporated in
DNA/RNA

ii) 5‐fluorodeoxyuridine monophosphate = a strong inhibitor of thymidilate synthetase

263
Q

5-FU ADRs

A
  • Myelosuppression -> Anemia

- Pigmentation changes in the skin

264
Q

Vinca alkaloids mechanism

A

Mitotic inhibitor

  • GTP‐dependent binding to tubulin
  • prevent polymerization to form microtubules
  • dysfunctional spindle in metaphase, prevent chromosomal segregation and cell proliferation
265
Q

Resistance to Vinca alkaloids

A

By enhanced efflux via P-glycoprotein

266
Q

Vinca alkaloids ADRs

A

Vincristine: peripheral neuropathy, myelosuppression (milder)

Vinblastine: Myelosuppression (stronger)

Vinorelbine: granulocytopenia

267
Q

Taxane mechanism

A
  • bind reversibly to the tubulin subunit
  • promote polymerization and stabilization
  • accumulation of nonfunctional microtubules
  • chromosomes cannot segregate
268
Q

Paclitaxel ADRs

A
  • neutropenia
  • serious hypersensitivity
  • myelusuppression
  • alopecia
  • neuropathy
  • nausea, vomiting
269
Q

Docetaxel ADRs

A
  • neutropenia
  • fluid retention (contraindicted in heart disease)
  • skin (rash, desquamation of the hands and feet, palmar‐plantar erythrodysesthesia)
270
Q

Drugs for Docetaxel

A

Post-regimen Corticosteroid to treat fluid retention

271
Q

Taxane drug resistance

A
  • Enhanced efflux by amplified P-glycoprotein

- Tubulin mutation

272
Q

Drugs for Paclitaxel prophylaxis

A

To prevent serious hypersensitivity reaction, premedicate with:

1) Diphenhydramine and H1, H2 blocker
2) dexamethasone

273
Q

Topoisomerase inhibitor ADRs

A

thrombocytopenia, neutropenia

274
Q

Cyclophosphamide and Ifosfamide ADR

A
  • Myelodepression
  • hemorrhagic cystitis, which can lead to fibrosis of the bladder
  • mutagenic and carcinogenic
275
Q

Alkylating agent mechanism

A
  • stop tumour growth by alkylating DNA, i.e. crosslinking guanine nucleobases in DNA double‐helix strands through covalent bonds
  • makes the strands unable to uncoil and separate
  • cells can no longer divide.
276
Q

Cyclophosphamide and Ifosfamide activation

A

cytotoxic only after hydroxylation by cytochrome P450, to form phosphor amide mustard (Majorly in liver)

277
Q

heavy metal platinum complex ADRs

A

nephrotoxicity and ototoxicity

  • severe nausea and vomiting
278
Q

Anthracyclin mechanism

A

1) Intercalating between base pairs of DNA/RNA
2) Inhibiting topoisomerase II enzyme and preventing the relaxation of supercoiled DNA
3) Interacting with oxygen, producing superoxide ions and hydrogen peroxide, which cause single‐strand breaks in DNA

279
Q

Doxorubicin ADRs

A

cardiotoxicity (result of the generation of free radicals and lipid peroxidation)

280
Q

Tamoxifen ADRs

A
  • endometrial cancer
  • thromboembolic events (stroke and pulmonary embolism),
  • cataract formation.
281
Q

Tamoxifen mechanism

A

SERM - for ER positive breast cancer

  • binding to the estrogen receptors in the target cells, making the estrogen unavailable to the tumor
  • producing estrogenic effects at various sites
282
Q

Raloxifene use

A

Not for curing breast cancer; currently prescribed to prevent osteoporosis and breast cancer

exerts pro‐estrogen effects in the bone and heart. As a consequence lowered cholesterol and stronger bones appear to be common benefits of taking this drug.

283
Q

Trastuzumab ADR

A

congestive heart failure

284
Q

Trastuzumab mechanism

A

Monoclonal antibody (for HER2 positive breast cancer)

binds to extracellular domain of the HER‐2 growth receptor, and inhibits the proliferation of cells that overexpress the HER2 protein.

285
Q

Topoisomerase I mechanism

A

(S‐phase specific.)

  • bind to and stabilize topoisomerse I-DNA complex
  • Prevent the religation of the single‐strand breaks created by the enzyme, which are converted to double‐strand breaks
  • inhibiting DNA synthesis so that cells do not enter mitosis and prophase
286
Q

Topoisomerase II mechanism

A

(premitotic, G2, and S phases)

  • Bind to and stabilize topoisomerase II‐DNA complex
  • Prevent the religation of the double‐strand breaks created by the enzyme
  • inhibiting DNA synthesis so that cells do not enter mitosis and prophase
287
Q

Potential sites of antiviral action and drugs example and disease

A

1) Attachment - Maraviroc - HIV
2) Penetration/fusion - Enfuvirtide - HIV
3) Uncoating - Amantadine - Influenza A
4) Protein synthesis - Ribavirin (HCV, RSV); Interferon (HBV, HCV)
5) Nucleuc acid synthesis - Acyclovir (HSV)
6) Virus assembly (i.e. protease) - Atazanavir
7) Virus release - oseltamivir (influenza)

288
Q

acyclovir mechanism

A

e.g. HSV and VZV
viral thymidine kinase convert it to monophosphate form, where cell enzymes convert it to triphosphate form

Triphosphate form inhibits viral DNA polymerase

289
Q

Resistance to acyclovir

A

Mutation of viral thymidine kinase to not add phosphate to acyclovir

Mutation of viral DNA polymerase to not be inhibited by acyclovir triphosphate

290
Q

Valaciclovir mechanism

A

Increase bio-availability than acyclovir

Broken down to valine and acyclovir instantaneously in the blood

e.g. HSV and VZV
viral thymidine kinase convert it to monophosphate form, where cell enzymes convert it to triphosphate form

Triphosphate form inhibits viral DNA polymerase

291
Q

Ganciclovir mechanism

A

In CMG

Phosphorylated by CMV enzyme UL97
Triphosphate form inhibits viral DNA polymerase

292
Q

Ganciclovir resistance

A

UL97 or viral DNA polymerase mutation

293
Q

zidovudine mechanism

A

Converted by cell enzyme into monophosphate and triphosphate, then selectively inhibit HIV RTase

(Some non-specific inhibition of cell polymerase)

294
Q

Palivizumab mechanism

A

humanised anti-RSV fusion protein monoclonal antibody

295
Q

Interferon α use

A

HBV HCV

296
Q

aspirin adverse effects

A

Prolonged bleeding

GI irritation -> never use with peptic ulcer

297
Q

Heparin usage and counterindicator, ADR

A

1) use for immediate anticoagulation

Counter indicated in haemophilia or bleedin

ADR: HIT

heparin induced thrombocytopenia -> use protamine sulphate and switch to direct thrombin inhibitor

298
Q

Thrombolytic mechanism

A

Conversion of plasminogen to plasmin, which will break down fibrin and lyse the thrombus

299
Q

Fibrinolytic inhibitor mechanism usage and ADRs

A

Competitive inhibitor of plasminogen activation

  • > use for adjunctive therapy with clotting factor in haemophilia
  • > uncontrolled bleeding eg fibronolytic overdose

ADRs: intravascular thrombosis

300
Q

Haemophilia treatment

A

Clotting factor concentrate and Fibrinolytic inhibitor eg tranexemic acid

301
Q

Benzodiazepines VS barbiturates

A

Benz is safer (drowsiness, anterograde annesia, respiratory depression with ethanol VS drowsiness, induction of P450, respiratory depression and coma)

Benz does not induce hepatic drug metabolising enzymes

Less marked dependence and withdrawal symptoms

Benzodiazepine antagonist available (Flumazenil)

302
Q

Benzodiazepine mechanism

A

Increase affinity of GABA for its receptor

Selectively activates GABA-A receptor to increase chloride influx

-> decrease neuronal activity

303
Q

Barbiturate action

A

Bonds to GABAa receptor, prolong chloride channel opening

Block excitatory glutamate receptors

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