Pharmacology Flashcards

Question

# Pharmacology Cytokine release syndrome prophylaxis drugs

Answer 1

1) methylprednisolone2) Diphenhydramine3) paracetamol

Answer 2

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

Answer 3

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

Answer 4

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

Answer 5

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

Answer 6

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

Answer 7

- Azathioprine- 6-mercaptopurine (6-MP)- 6-thioguanine (6-TG)

Answer 8

- 5-fluorouracil (5-FU)- Cytarabine (ara-c)

Answer 9

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)

Answer 10

- Vincristine (VX)- Vinblastine (VBL)- Vinorelbine (VRB)

Answer 11

- Paclitaxel- Docetaxel

Answer 12

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

Answer 13

- Irinotecan- Topotecan

Answer 14

- Etoposide (VP-16)- Teniposide (VM-26)

Answer 15

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

Answer 16

Hydroxyureas

Answer 17

- Cyclophosphamide- Ifosfamide

Answer 18

- carmustin (BCNU)- Lomustin (CCNU)- Fotemustin- Semustin- Streptozocin

Answer 19

- Cisplatin- Carboplatin

Answer 20

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

Answer 21

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

Answer 22

Doxorubicin (DOX)Daunorubicin (DNR)EpirubicinIdarubicin

Answer 23

- Prednisone- Prednisolone

Answer 24

- Tamoxifen- Raloxifene

Answer 25

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

Answer 26

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

Answer 27

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

Answer 28

dexrazone (iron-chelator)

Answer 29

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

Answer 30

enoxaparin

Answer 31

Fondaparinux

Answer 32

- dabigatran - hirudin - lepirudin - argatroban

Answer 33

- Rivaroxaban - Apixaban

Answer 34

Reserpine (depleting dopamine store) Haloperidol (dopaminergic blocker)

Answer 35

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

Answer 36

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)

Answer 37

carbidopa, benserazide

Answer 38

levodopa + benserazide (4:1 ratio)

Answer 39

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

Answer 40

Bromocriptine

Answer 41

Pramipexole | ropinirole

Answer 42

rotigotine

Answer 43

Selegiline

Answer 44

Entacapone, tolcapone

Answer 45

Amantadine

Answer 46

Benztropine Biperiden Trihexyphenidyl Benzhexol

Answer 47

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

Answer 48

ClonidineHaloperidol

Answer 49

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)

Answer 50

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

Answer 51

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

Answer 52

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

Answer 53

Fluoxetine (Prozac)/CYP2D6 Paroxetine/CYP2D6 Fluvoxamine/CYP3A4 Citalopram Escitalopram Sertraline

Answer 54

Atomoxetine Maprotiline Reboxetine

Answer 55

``` Venlafaxine Desvenlafaxine Duloxetine Bupropion Mirtazapine ```

Answer 56

Tertiary Amines: - Amitriptyline - Imipramine Secondary Amines - Desipramine - Nortriptyline

Answer 57

Non-selective: - Phenelzine - Tranylcypromine MAO-A selective: - Moclobemide

Answer 58

1) Typical (D2) - Chlorpromazine - Fluphenazine - Haloperidol - Thioridazine - Trifluoperazine ``` 2) Atypical (5-HT2) - Aripiprazole - Clozapine - Olanzapine - Quetiapine - Risperidone - Ziprasidone ```

Answer 59

- Chlorpromazine - Fluphenazine - Haloperidol - Thioridazine - Trifluoperazine

Answer 60

- Aripiprazole - Clozapine - Olanzapine - Quetiapine - Risperidone - Ziprasidone

Answer 61

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 ```

Answer 62

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

Answer 63

Flumazenil (GABAA receptor competitive inhibitor)

Answer 64

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

Answer 65

``` – Alprazolam – Chlordiazepoxide – Clonazepam – Diazepam – Lorazepam ```

Answer 66

– Triazolam – Temazepam – Flurazepam

Answer 67

Thiopentone Propofol Ketamine Etomidate

Answer 68

- Desflurane - Isoflurane (most potent) - Sevoflurane - nitrous oxide - Xeon------ - Halothane - Enflurane

Answer 69

EnkephalinsBeta-endorphin

Answer 70

- Morphine and related- Phenylpiperidine series - Methadone series- Mixed agonist-antagonist

Answer 71

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

Answer 72

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

Answer 73

Methadone (aka physeptone)Dextropropoxyphene

Answer 74

PentazocineBuprenorphineButorphanolTramadol

Answer 75

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

Answer 76

Naloxone (narcan)

Answer 77

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

Answer 78

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

Answer 79

Sulfonylureas - glipizide - glimepiride Meglitinide analogues - repaglinide - nateglinide

Answer 80

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

Answer 81

Sitagliptin phosphate | Vidagliptin

Answer 82

A) biguanides - metformin B) thiazolidinediones - rosiglitazone - pioglitazone

Answer 83

Acarbose Miglitone

Answer 84

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

Answer 85

1) Thionamides - methimazole - carbimazole - propylthiouracil 2) Radioiodine - iodine 131 3) Thyroidectomy

Answer 86

T3 - Liothyronine Due to quicker onset of effects

Answer 87

Thyroxine (T4) Due to longer half life

Answer 88

R-CHOP Rituximab (anti-CD20) Cyclophosphamide Hydroxydaunarubicin Vincristine Prednisone (purine analogue for low grade)

Answer 89

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

Answer 90

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

Answer 91

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

Answer 92

i.e. PCP, behaviour mimics schizophrenia PCP binds to and inhibits NMDA glutamate receptor (block Na Ca entry)

Answer 93

Diet Exercise Insulin

Answer 94

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

Answer 95

Diet Insulin Anti diabetic agents

Answer 96

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

Answer 97

- rapid onset of action; usually given before meals - short duration of action to avoid hypoglycaemia - predictable and reproducible effects

Answer 98

Produced by recombinant DNA technology with E Coli or yeast

Answer 99

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

Answer 100

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

Answer 101

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

Answer 102

Insulin mixed with protamine - intermediate acting - insulin bound to protamine -> slowly dissolve in body fluid - facilitate control of glycemic over an extended period

Answer 103

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

Answer 104

Long acting insulin, withdrawn from market due to unsafe Entirely crystalline zinc -> slow onset, slow effect

Answer 105

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

Answer 106

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

Answer 107

1) Subcutaneous or intramuscular injection 2) Insulin pump -- experimental -- 3) transdermal 4) oral 5) inhalation 6) pancreatic transplant and ST therapy

Answer 108

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

Answer 109

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

Answer 110

Dapagliflozin

Answer 111

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)

Answer 112

- 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

Answer 113

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!)

Answer 114

- increase appetite and weight gain (rarely compared with sulphonylureas) - hypoglycaemia (rarely compared with sulphonylureas)

Answer 115

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

Answer 116

Antidiabetic used for obese patients or patients with insulin resistance - reduce CVS complications - decrease incidence of diabetes related cancers

Answer 117

- 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)

Answer 118

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

Answer 119

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

Answer 120

1) weight gain, fluid retention | 2) increased risk of heart attack

Answer 121

- weight gain and fluid retention | - risk of bladder cancer

Answer 122

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

Answer 123

Not absorbed into blood stream, therefore little systemic ADRs (no weight gain or hypoglycaemia) - Flatulence - diarrhoea - abdominal pain

Answer 124

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!

Answer 125

Gut derived hormones: - glucagon like peptide 1 (GLP-1) - glucose-dependent insulinotropic peptide (GIP)

Answer 126

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

Answer 127

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

Answer 128

Upper respiratory tract infection Sore throat Diarrhoea

Answer 129

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

Answer 130

Genital infection

Answer 131

Acyclovir, valaciclovir Foscarnet, cidofovir

Answer 132

Ganciclovir, valganciclovir Foscarnet, Cidofovir

Answer 133

Acyclovir, valaciclovir Foscarnet, Cidofovir

Answer 134

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

Answer 135

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)

Answer 136

Ribavirin (IV for RSV in pre engraftment BM transplant) Prophylaxis: - Respigam (RSV-IVIg) - palivizumab (anti RSV fusion protein)

Answer 137

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.

Answer 138

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)

Answer 139

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

Answer 140

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

Answer 141

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

Answer 142

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

Answer 143

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

Answer 144

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

Answer 145

- 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

Answer 146

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)

Answer 147

nuclear imaging tracer and radioactive treatment for prostate cancer

Answer 148

nuclear imaging tracers for thyroid diseases

Answer 149

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

Answer 150

Hypothyroidism -> lifelong T4 replacement Vocal cord paralysis (recurrent laryngeal nerve and external laryngeal nerves lies close)

Answer 151

- 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

Answer 152

- 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

Answer 153

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)

Answer 154

(deficiency of GH) | replacement therapy with somatropin

Answer 155

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

Answer 156

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)

Answer 157

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

Answer 158

(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)

Answer 159

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)

Answer 160

Iatrogenic Cushing's syndrome

Answer 161

Dopamine receptor agonists that acts on anterior pituitary: 1) Bromocriptine 2) cabergoline (longer t1/2 and higher selectivity for dopamine receptor)

Answer 162

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

Answer 163

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)

Answer 164

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)

Answer 165

- Hepatotoxicity and Hepatitis (elevated LFT enzymes) | - Nausea & diarrhea

Answer 166

- Metyrapone (inhibits 3-β-dehydrogenase) | - Trilostane (inhibits 11-β-hydroxylase)

Answer 167

- Hypotension - Nausea & vomiting - Headache - Rash

Answer 168

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

Answer 169

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)

Answer 170

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)

Answer 171

IV calcium infusion (for severe hypocalcemia) Oral calcium with vit D PTH replacement therapy

Answer 172

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

Answer 173

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

Answer 174

Converted to morphine 6-glucuronide, which is renal excreted

Answer 175

Converted to norpethidine

Answer 176

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)

Answer 177

PROS - convenient - can take home CONS: - so convenient overdose is common - never multiple patches!

Answer 178

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

Answer 179

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

Answer 180

Pethidine > morphine > methadone

Answer 181

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

Answer 182

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

Answer 183

GA: loss of all sensation, loss of consciousness LA: loss of all sensation regionally Analgesics: Loss of pain sensation

Answer 184

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

Answer 185

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

Answer 186

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

Answer 187

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)

Answer 188

- 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

Answer 189

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

Answer 190

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

Answer 191

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

Answer 192

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)

Answer 193

Not important and negligible -> mainly leave through lungs

Answer 194

CVS effects: - reduced systemic vascular resistance - reduce mean arterial pressure - reduce cardiac output - increase heart rate

Answer 195

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

Answer 196

1) conversion of L-dopa to dopamine in the periphery - nausea, vomiting - postural hypotension, Arrhythmias - constipation 2) overstimulation of central dopamine receptors - Dyskinesia - Hallucinations

Answer 197

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

Answer 198

Anti-PD, inhibits MAO-B Against PD by decreasing peripheral metabolism of dopamine, thus increasing availability of dopamine to CNS

Answer 199

Hypertensive crisis if large dose

Answer 200

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

Answer 201

- Postural hypotension - Diarrhea - Dyskinesias - HEPATIC NECROSIS (Tolcapone only)

Answer 202

- enhance the release of dopamine from surviving nigral neurons (with surviving neurons) - inhibit the reuptake of dopamine at synapses

Answer 203

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"

Answer 204

The risk of untreated depression far outweigh those of antidepressant mediations

Answer 205

TALK THERAPY - Helps by teaching new ways of thinking & behaving. - Changing habits that may be contributing to the depression.

Answer 206

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.

Answer 207

Fluoxetine, Paroxetine -> CYP2D6; cannot use with tricyclic antidepressants Fluvoxamine ->CYP3A4; cannot use with diltiazem (Ca channel blocker), otherwise hypotension and bradycardia

Answer 208

(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)

Answer 209

(suicidal under 25) Enhance noradrenergic tone: - CNS activation (anxiety, agitation) - Increase BP - Heart rate

Answer 210

(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

Answer 211

secondary amine: predominantly NE reuptake inhibition, a bit shorter acting Tertiary: NE and 5HT transporter for reuptake affected; strongly anticholinergic; long acting

Answer 212

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

Answer 213

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

Answer 214

Anti-depression: | Blocks α2 presynatpic autoreceptor and enhances noradrenalin release.

Answer 215

Sedation Dry mouth Constipation dizziness

Answer 216

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

Answer 217

- 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

Answer 218

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

Answer 219

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 ```

Answer 220

- depression - general anxiety disorder - PTSD - OCD - smoking cessation - bulimia

Answer 221

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

Answer 222

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

Answer 223

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

Answer 224

Blocks 5HT2 receptor

Answer 225

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

Answer 226

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

Answer 227

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)

Answer 228

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

Answer 229

- 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)

Answer 230

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

Answer 231

- Myelosuppression (especially in defected TPMT or ppl taking XO inhibitor e.g. allopurinol)

Answer 232

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

Answer 233

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

Answer 234

- Myelosuppression -> Anemia | - Pigmentation changes in the skin

Answer 235

Mitotic inhibitor - GTP‐dependent binding to tubulin - prevent polymerization to form microtubules - dysfunctional spindle in metaphase, prevent chromosomal segregation and cell proliferation

Answer 236

By enhanced efflux via P-glycoprotein

Answer 237

Vincristine: peripheral neuropathy, myelosuppression (milder) Vinblastine: Myelosuppression (stronger) Vinorelbine: granulocytopenia

Answer 238

- bind reversibly to the tubulin subunit - promote polymerization and stabilization - accumulation of nonfunctional microtubules - chromosomes cannot segregate

Answer 239

- neutropenia - serious hypersensitivity - myelusuppression - alopecia - neuropathy - nausea, vomiting

Answer 240

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

Answer 241

Post-regimen Corticosteroid to treat fluid retention

Answer 242

- Enhanced efflux by amplified P-glycoprotein | - Tubulin mutation

Answer 243

To prevent serious hypersensitivity reaction, premedicate with: 1) Diphenhydramine and H1, H2 blocker 2) dexamethasone

Answer 244

thrombocytopenia, neutropenia

Answer 245

- Myelodepression - hemorrhagic cystitis, which can lead to fibrosis of the bladder - mutagenic and carcinogenic

Answer 246

- 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.

Answer 247

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

Answer 248

nephrotoxicity and ototoxicity - severe nausea and vomiting

Answer 249

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

Answer 250

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

Answer 251

- endometrial cancer - thromboembolic events (stroke and pulmonary embolism), - cataract formation.

Answer 252

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

Answer 253

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.

Answer 254

congestive heart failure

Answer 255

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.

Answer 256

(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

Answer 257

(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

Answer 258

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)

Answer 259

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

Answer 260

Mutation of viral thymidine kinase to not add phosphate to acyclovir Mutation of viral DNA polymerase to not be inhibited by acyclovir triphosphate

Answer 261

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

Answer 262

In CMG Phosphorylated by CMV enzyme UL97 Triphosphate form inhibits viral DNA polymerase

Answer 263

UL97 or viral DNA polymerase mutation

Answer 264

Converted by cell enzyme into monophosphate and triphosphate, then selectively inhibit HIV RTase (Some non-specific inhibition of cell polymerase)

Answer 265

humanised anti-RSV fusion protein monoclonal antibody

Answer 266

Prolonged bleeding GI irritation -> never use with peptic ulcer

Answer 267

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

Answer 268

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

Answer 269

Competitive inhibitor of plasminogen activation - > use for adjunctive therapy with clotting factor in haemophilia - > uncontrolled bleeding eg fibronolytic overdose ADRs: intravascular thrombosis

Answer 270

Clotting factor concentrate and Fibrinolytic inhibitor eg tranexemic acid

Answer 271

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)

Answer 272

Increase affinity of GABA for its receptor Selectively activates GABA-A receptor to increase chloride influx -> decrease neuronal activity

Answer 273

Bonds to GABAa receptor, prolong chloride channel opening Block excitatory glutamate receptors