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MRCP part 1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Inheritance of acute intermittent porphyria

A

Autosomal dominant (defect in porphobilinogen deamine - enzyme involved in biosynthesis of haem)

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2
Q

Presentation of acute intermittent porphyria

A

Neuropsychiatric/abdominal symptoms in 20-40 year olds

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3
Q

Sedation in someone with acute intermittent porphyria

A

Chlorpromazine - NOT diazepam

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4
Q

Drugs that could precipitate acute intermittent porphyria

A

Barbiturates, benzos, alcohol, OCP, sulphonamides

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5
Q

Management of accidental adrenaline injection

A

Phentolamine (short acting alpha blocker)

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6
Q

Effects of adrenaline

A

Very similar to DKA - hyperglycaemia (mostly alpha adrenergic response), inhibits insulin secretion, increased lactate by adipose tissue

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7
Q

What is used for alcohol abstinence?

A

Disulfuram (inhibition acetaldehyde)

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8
Q

Contraindication to disulfuram use

A

Psychosis, IHD

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9
Q

What can be used to reduce alcohol cravings

A

Acamprostate - weak antagonist of NMDA

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10
Q

MOA allopurinol

A

Inhibits xanthine oxidase

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11
Q

What drugs used in acute gout attack

A

Clochicine/NSAIDs/steroids

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12
Q

Who is at increased risk of gout?

A

Ethnic minotirites

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13
Q

What allele should be screened for in gout in ethnic minorities?

A

HLA B 5801

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14
Q

Key drug interactions allopurinol

A

Azathioprine (25% dose reduction - allopurinol increases active compound due to 6-mercaptopurine), cyclophosphamide (decreased renal clearance), theophylline (inhibits breakdown)

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15
Q

Adrenoreceptor agonists acting on alpha-1

A

Phenylephrine eg eyedrops, hypotension

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16
Q

Adrenoreceptor agonists acting on alpha-2

A

Clonidine (menopause, HTN)

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17
Q

Adrenoreceptor agonists acting on beta-1

A

Dobutamine eg inotrope

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18
Q

Adrenoreceptor agonists acting on beta-2

A

Salbutamol

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19
Q

Adrenoreceptor agonists acting on beta-3

A

Being developed, role in obesity

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20
Q

Key roles alpha 1 adrenoreceptors

A

Vasoconstriction, salivary secretion, hepatic gluconeogenesis

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21
Q

Key roles alpha 2 adrenoreceptors

A

Mainly pre-synaptic inhibition, inhibits insulin, platelet aggregation

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22
Q

Key role beta adrenoreceptors

A

Mainly located in heart - increase HR and force, vasodilation, lipolysis

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23
Q

Adrenoreceptor antagonists acting on alpha

A

Alpha 1 - doxazosin, 1a tamsulosin, 2 yohimbine, non selective - phenoxybenzamine, carvedilol, labetalol

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24
Q

Adrenoreceptor antagonists acting on beta

A

B1 Atenolol, non selective propranolol

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25
Q

Cellular pathway of all adrenoreceptors

A

G coupled

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26
Q

What adrenoreceptors activate phospholipase C

A

Alpha 1

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27
Q

What adrenoreceptors inhibit phospholipase C

A

Alpha 2

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28
Q

What adrenoreceptors stimulate phospholipase C

A

Beta 1,2,3

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29
Q

What class of anti-arrhythmic is amiodarone

A

III

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30
Q

How does amiodarone work

A

Blocks potassium channels, which inhibits repolarisation therefore prolonging action potential. Also blocks Na.

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31
Q

Half life amiodarone

A

20-100 days

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32
Q

Monitoring of amiodarone

A

TFT, LFT, Us+Es, CXR prior to tx
TFT, LFT, every 6 months

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33
Q

Adverse effects amiodarone

A

(Amiodarone is a Bitch)
Bradycardia/Blue man (slate grey)
Interstitial Lung Disease
Thyroid (hyper and hypo)
Corneal (ocular)/photosensitivity
Hepatic(liver fibrosis, hepatitis)/Hypotension when IV (due to solvents)

Lengthens QT, peripheral neuropathy

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34
Q

What is Wolff-Chaikoff effect

A

An autoregulatory phenomenon, whereby a large amount of ingested iodine acutely inhibits thyroid hormone synthesis (leading to hypothyroidism)

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35
Q

What is type 1 amiodarone induced thyrotoxicosis

A

Increased iodine induces thyroid hormone synthesis, goitre present, managed with carbimazole or potassium perchlorate

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36
Q

What is type 2 amiodarone induced thyrotoxicosis

A

Destructive thyroiditis, goitre absent, managed with corticosteroids

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37
Q

Draw chemotox man

A

https://www.google.co.uk/search?q=+chemotox+man&tbm=isch&ved=2ahUKEwih8-DXi8j9AhUtpCcCHWx7AgMQ2-cCegQIABAA&oq=+chemotox+man&gs_lcp=CgNpbWcQAzIECAAQQ1DgCVjgCWDLC2gAcAB4AIABQ4gBeJIBATKYAQCgAQGqAQtnd3Mtd2l6LWltZ8ABAQ&sclient=img&ei=FkYGZKGQLK3InsEP7PaJGA&bih=969&biw=1920#imgrc=okRVfISvxNK2RM

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38
Q

MOA propofol

A

GABA receptor agonist

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39
Q

What is propofol used for

A

Rapid onset anaesthesia, pain, antiemetic

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40
Q

Risk of propofol

A

Moderate myocardial depression

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41
Q

What is sodium thiopentone used for

A

Extremely rapid onset anaesthetic agent (rapid sequence induction), little analgesic effects

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42
Q

Risk of sodium thiopentone

A

Marked myocardial depression

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43
Q

MOA Ketamine

A

NMDA receptor antagonist

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44
Q

What is ketamine used for

A

Anaesthetic induction, strong analgesic. Used in those who are haemodynamically unstable - little myocardial depression

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45
Q

What is etomidate used for

A

Anaesthetic induction - not used in maintenance due to adrenal suppression, good cardiac profile, post op vom common

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46
Q

List antiarrhythmic drug classifications

A

Son of a Bitch is Potentially Correct
I - Blocks Na
II - Beta-blocker
III - Blocks K
IV - Calcium channel blockers

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47
Q

List class I antiarrhythmics

A

Double Quarter Pounder, Lettuce Mayo, Fries Please:

  1. Class IA = Disopyramide, Quinidine, and Procainamide
  2. Class IB = Lidocaine and Mexiletine
  3. Class IC = Flecainide and Propafenone
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48
Q

List class 2 antiarrhythmics

A

MANBABE:
Metoprolol
Acebutolol
Nebivolol
Betaxolol
Atenolol
Bisoprolol
Esmolol

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49
Q

List class 4 antiarrhythmics

A

Verapamil, diltiazem

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50
Q

List class 3 antiarrhythmics

A

AIDS:
A = amiodarone
I = ibutilide
D = dofetilide
S = Sotalol

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51
Q

What antibiotics inhibit cell wall formation (petidoglycan cross linking)

A

Penicillins, cephalosporins, carbopenems

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52
Q

What antibiotics inhibit cell wall formation (peptidoglycan synthesis)

A

Glycopeptides (vanc)

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53
Q

What antibiotics inhibit protein synthesis (50S subunit) (ribosomal)

A

Macrolides, chloramphenicol, streptogrammins, clindamycin, linezolid

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54
Q

What antibiotics inhibit protein synthesis (30S subunit) (ribosomal)

A

Aminoglycosides, tetracyclines

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55
Q

What antibiotics inhibit DNA synthesis

A

Quinolones (ciprofloxacin)

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56
Q

What antibiotics damage DNA

A

Metronidazole

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57
Q

What antibiotics inhibit folic acid formation

A

Sulphonamides, trimethoprim

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58
Q

What antibiotics inhibit RNA synthesis

A

Rifampicin

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59
Q

How does aspirin work

A

Blocks cox 1+2 (responsible for prostaglandin, prostacycline and thromboxane synthesis).
Blocking of thromboxane A2 decreases ability of platelets to aggregate

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60
Q

What does aspirin potentiate?

A

Oral hypoglycaemics, warfarin, steroids

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61
Q

What is the exception to U16 use of aspirin

A

Kawasaki

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62
Q

How does clopidogrel work?

A

inhibits P2Y12

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63
Q

Features of beta blocker overdose

A

Bradycardia. hypotension, heart failrue, syncope

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64
Q

Treatment of beta blocker overdose

A

If bradycardia - atropine, in resistant cases glucagon. HAEMODIALYSIS IS NOT EFFECTIVE

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65
Q

How does botox work

A

Blocks release of acetylchloride

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66
Q

Indications botox

A

Blepharospasm, hemifacial spasm, focal spasticity, spasmodic torticollis, severe hyperhidrosis, achalasia

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67
Q

Classes of calcium channel blocker

A

Centrally acting - focus on heart rhythm (non-dihydropyridines), eg verapamil, diltiazem.
Members of the other class (dihydropyridines) all end in -dipine (e.g., nicardipine, amlodipine).

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68
Q

Side effects verapamil

A

HF, constipation, hypotension, brady

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69
Q

Side effects diltiazem

A

Hypotension, brady, HF, ankle swelling

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70
Q

Side effects dihydropyridines

A

Flushing, headache, ankle swelling

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71
Q

Features of CO poisoning

A

Headache, confusion, N+V. subjective weakness, vertigo
Severe - pink skin, hyperpyrexia, extrapyramidal features

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72
Q

Investigations CO poisoning

A

Pulse oximetry may be high, carboxyhaem levels <3% in non smokers, <10% in smokers

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73
Q

Management CO poisoning

A

100% O2 for minimum 6 hours, treat until symptoms resolve

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74
Q

Indications for hyperbaric oxygen CO poisoning

A

LOC, neurology, MI/arrhythmia

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75
Q

Management of corrosive substance ingestion

A

Gen surg if perf, IV PPI, if symptomatic needs endoscopy
If asymptomatic - fluids and observation

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76
Q

MOA ciclosporin

A

DMARD - ecreases clonal proliferation of T cells by decreasing IL2 release

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77
Q

Side effects of ciclosporin

A

Increases everything (fluid, BP, hair, gums, glucose). Increased susceptibility to severe infection.

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78
Q

Indications cuclosporin

A

Following organ transplant, RA, psoriasis, UC, red cell aplasia

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79
Q

Risks COCP

A

VTE, breast and cervical cal, stroke and IHD, temproary SE

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80
Q

Contraindications COCOP

A

UKMEC 4 -
BMI >35, smoking > 15/day
Migraine with aura
VTE
Stroke
Breast feeding <6 weeks postpartum
Uncontrolled htn
BReast ca
Major surgery
SLE

UKMEC 3-
Gallbladder disease, controlled HTN, BMI >35

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81
Q

What decreases COCP efficacy

A

Vomit within 2 hours, liver enzyme inducing drugs eg rifampicin

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82
Q

MOA cocaine

A

Blocks uptake of dopamine, noradrelaine, serotonin

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83
Q

Rare SE cocaine

A

Ichaemic colitis, hyperthermia, metabolic acidosis, rhabdomylosis

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84
Q

Management of cocaine toxicity

A

Benzos

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85
Q

Management of HTN in context of cocaine

A

Benzos and sodium nitroprusside

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86
Q

Physiology of cyanide poisoning

A

Inhibits enzyme cytochrome C, resulting in cessation of mitochondrial electron transfer chain

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87
Q

Presentation of cyanide poisoning

A

Brick red skin, smell of bitter almonds:
- Acute: hypoxia, hypotension, headache
- Chronic: ataxia, peripheral neuropathy, dermatitis
(metabolic acidosis due to increased lactate)

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88
Q

Management of cyanide posioning

A

100% Oxygen, IV hydroxycoblamain, inhaled amynitrate, sodium nitrate, sodium thiosulphate

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89
Q

MOA digoxin

A

Decreases conduction through AV node, increased force of cardiac muscle contraction due to inhibition of Na/K/ATPase pump

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90
Q

When is digoxin level taken

A

Within 8-12 hours of last dose

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91
Q

Features of digoxin toxicity

A

Lethargy, nausea, green/yellow vision, gynaecomastia

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92
Q

Precipitating factors of digoxin toxicity

A

Hypokalaemia, hypomagnesmia, hypercalcaemia, hypernatraemia, acidosis, hypothyroidism

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93
Q

What drugs can precipitate digoxin toxicity

A

Amiodarone, CCB, spironolactone, ciclosporin, any drugs causing decrease in K eg loop diuretics

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94
Q

Management of digoxin toxicity

A

Digibind, correct arrhythmias, monitor K

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95
Q

Indications dopamine receptor agonists

A

Parkinsons, cyclical breast disease, acromegaly, prolactinoma

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96
Q

What must be checked before starting bromocriptine

A

Associated with pulmonary, retronperoneal and cardiac fibrosis so ESR, CXR and Cr obtained prior to treatment

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97
Q

Adverse effects dopamine agonists

A

N+V, daytime solomence, postural hypotension, hallucinations

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98
Q

Triad dress syndrome

A

Dermatitis, high fever, inflammation in 1 or more organs
+ eosinophilia, abnormal LFT

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99
Q

When does rash normally commence DRESS syndrome

A

2-8 weeks following commencement of drug

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100
Q

Drug precipitants of dress

A

Allopurinol, anti epileptics, Abu, immunosuppressants

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101
Q

Management of dress syndrome

A

Stop cause, antihistamines, topical steroids, emollients. Occasionally immunosupressants, IVIG, plasma

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102
Q

Drug monitoring statins

A

LFTs 3 months, 12 months

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103
Q

Drug monitoring ACEi

A

Prior, after dose change, annually

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104
Q

Drug monitoring amiodarone

A

TFTs, LFTs, Us+Es, xray prior to Tx
TFT and LFTs 6 monthly

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105
Q

Drug monitoring methotrexate

A

FBC, LFTs, Us+Es before, weekly until stabilised, 2-3 monthly

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106
Q

Drug monitoring azathioprine

A

FBC, LFTs, before treatment, weekly first 4 weeks, every 3 months

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107
Q

Drug monitoring lithium

A

TFTs, Us+ES prior to, weekly until stabilised then 6 monthly

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108
Q

Drug monitoring sodium valproate

A

LFT, FBC before treatment. LFTs periodically during first 6 months

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109
Q

Drug monitoring glitazones

A

Before treatment and regularly

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110
Q

Drug causes agranulocytosis (WBC most commonly neutrophils)

A

Drugs can cause pretty major collapse to granulocytes:

Dapsone
Clozapine
Carbamazepine
Propylthiouracil, penicillin
Mirtazapine, methotrexate
Colchicine, chloramphenicaol
Co-Trim
Ganciclovir

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111
Q

Drug causes urticaria

A

Penicillins, aspirin, NSAIDs, opiates

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112
Q

Drug causes impaired glucose tolerance

A

Thiazides, furosemide, steroids, tacrolimus, cilosporin, interferon alpha, nicotinic acid, antipsychotics.
BB used in caution in diabetics

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113
Q

Drugs causing thrombocytopenia

A

ABCDE - HI

anti- Arrhythmics: quinidine, beta-blockers
antiBiotics: Penicillins, cephalosporins, sulphonamides, rifampicin
anti- Coagulants: Heparin, abciximab
Diuretics - furosemide
anti- Epileptics: Valproic acid, carbamazepine
-
anti- Histamines: cimetidine
anti- Inflammatory: Aspirin, Indomethacin, NSAIDs

Quinine

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114
Q

Drugs causing urinary retention

A

Tricyclic antidepressants, anticholinergics, opioids, NSAIDs, Disopyramide (class 1A anti-arrhythmic)

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115
Q

Drugs causing lung fibrosis

A

amiodarone, cytotoxic, anti-rheumatoid, nitrofurantoin, dopamine receptor agonists

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116
Q

Drugs causing ocular problems

A

Sildenafil can cause both blue discolouration and non-arteritic anterior ischaemic neuropathy

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117
Q

Drugs causing cataracts

A

Steroids (ster-eye-ds)

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118
Q

Drugs causing corneal opacities

A

Amiodarone, indomethacin

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119
Q

Drugs causing optic neuritis

A

Ethambutol, amiodarone, metronidazole

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120
Q

Drugs causing retinopathy

A

Chloroquine, quinine

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121
Q

What causes blue discolouration and non aretritic anterior ischaemic neuropathy?

A

Sildenafil

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122
Q

Can hydroxychloroquinine cause eye problems

A

Yes lol

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123
Q

Drugs causing photosensitivity

A

Thiazides, tetracyclines, sulphonamides, ciprofloxacin, amiodarone, NSAIDs, sulphonylureas

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124
Q

Name agonists of 5-HT system (migraine mx)

A

Sumatriptan, ergomatine (partial)

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125
Q

Name antagonists of 5-HT system (prophylaxis migraine)

A

Pizotifen (migraine), cyproheptadine (diarrhoea in carcinoid), ondansetron (5HT3)

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126
Q

Features of ecstasy poisoning

A

Tachy, hypertension, agitation, hyperthermia, rnhabdomylosis

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127
Q

Management ecstacy poisoning

A

Supportive, dantrolene for hyperthermia if simple measures fail

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128
Q

Stages of ethylene glycol toxicity (coolant, anti-freeze)

A
  1. Confusion, slurred speech, dizziness
  2. Metabolic acidosis with high anion gap + high osmolar gap
  3. AKI
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129
Q

Management of ethylene glycol toxicity

A

Fomepizole (alcohol dehydrogenase inhibitor)

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130
Q

How does ethanol work in management of ethylene glycol toxicity

A

Competes with ethylene glycol for alcohol dehydrogenase enzyme therefore limiting formation of toxic metabolites (glycoaldehyde and glycolic acid)

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131
Q

Is haemodialysis used in ethylene glycol toxicity?

A

Only in refractory cases

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132
Q

MOA finasteride

A

Inhibitor of 5 alpha reductase - enzyme testosterone

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133
Q

Indications finasteride

A

BPH, male pattern baldness

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134
Q

Adverse effects finasteride

A

Decreased libido, gynaecomastia, impotence, can decrease PSA

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135
Q

MOA flecanide

A

Na channel blocker - slows conduction of action potential widening of QRS, prolongs PR

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136
Q

Indications flecanide

A

AF, SVT with accessory

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137
Q

Contraindications flecanide

A

Post MI, structural heart disease, sinus mode dysfunction, atrial flutter

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138
Q

Adverse effects flecainide

A

Neg inotrop, bradycardia, oral parasthesia, visual disturbance

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139
Q

What type of antibiotic is gentamicin?

A

Aminoglycoside

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140
Q

Nephrotoxicity in gentamicin toxicity is caused by

A

Renal tubular necrosis

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141
Q

Contraindication to gentamicin use

A

Myasthenia gravis

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142
Q

Drugs that can be cleared with haemodialysis

A

Barbiturate, lithium, alcohol, salictyes, theophyllines

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143
Q

Is heparin allowed in pregnancy?

A

Yes, but no DOACs

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144
Q

How does heparin work?

A

Activates antithrombin 3

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145
Q

Adverse effects heparin

A

Bleeding, thrombocytopenia, osteoporosis, increased K

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146
Q

Standard heparin - MOA

A

Activates antithrombin 3, forms a complex that inhibits thrombin, factors Xa, IXa, XIa, and XIIa

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147
Q

Standard heparin - monitoring

A

APTT

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148
Q

LMWH - MOA

A

Activates antithrombin 3 - forms a complex that in habits factor Xa (monitor this)

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149
Q

When is standard heparin used

A

Renal failure, contexts where may need reversed rapidly

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150
Q

Mechanism in heparin induced thrombocytopenia

A

Antibodies form against complexes of platelet factor 4 (PF4) and heparin. These antibodies bind to the PF4-heparin complexes on the platelet surface and induce platelet activation by cross-linking FcγIIA receptors

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151
Q

Reversal of heparin overdose

A

Protamine sulphate, although this only partially reverses the effect of LMWH

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152
Q

When does heparin induced thrombocytopenia occur?

A

5-10 days after treatment. Also remember it is a prothrombotic state despite the low platelets

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153
Q

Statins MOA and adverse effects

A

HMG CoA reductase inhibitors,
Myositis, deranged LFTs

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154
Q

Ezetimibe MOA and adverse effects

A

Decreases cholesterol absorption in the small intestine,
Headache

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155
Q

Nicotinic acid MOA and adverse effects

A

Decreases hepatic VLDL secretion,
Flushing and myositis

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156
Q

Fibrates MOA and adverse effects

A

Agonist of PPAR-alpha therefore increases lipoprotein lipase expression,
Myositis, pruritus, cholestasis

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157
Q

Cholestyramine MOA and adverse effects

A

Decreases bile acid reabsorption in the small intestine, upregulating the amount of cholesterol that is converted to bile acid
GI side-effects

158
Q

Causes of low Mg

A

Diuretics, PPI, TPN, low K, high Ca (2ndary to hyperparathyroidism), metabolic disorders - bartters, gitelmans

159
Q

Features low Mg

A

Parasthesia, tetany, decreased PTH secretion so decreased Ca, also exacerbates digoxin toxicity, seizures

160
Q

What is the half life of immunoglobulins (IgG)?

A

3 weeks

161
Q

What is the therapeutic range of lithium?

A

0.4-1 (toxicity >1.5)

162
Q

Precipitants of lithium toxicity

A

Dehydration, renal failure, drugs = DAMN: diuretics, ACEi, metronidazole, NSAIDs
Or remember it as less water, kidneys, met

163
Q

Features of lithium toxicity

A

Coarse tremor (fine in therapeutic levels), hyperreflexia, polyuria, seizure, coma

164
Q

Management lithium toxicity

A

Mild - fluid resuscitation, severe - haemodialysis. Limited evidence for NaHCO3 (supposed to increased alkalinity of urine)

165
Q

What type of drug is lidocaine?

A

An amdie

166
Q

Management of lidocaine toxicity

A

IV 20% lipid emulsion

167
Q

Key drug interactions of lidocaine

A

Beta blockers, ciprofloxacin, phenytoin

168
Q

Features of lidocaine toxicity

A

Initial CNS over activity then depression as lidocaine initially blocks inhibitory pathways then blocks both inhibitory and activating pathways. Cardiac arrhythmias.

169
Q

When is cocaine mostly used?

A

As a paste in ENT surgery (great vasoconstriction)

170
Q

MOA bupivicaine

A

Binds to the intracellular portion of sodium channels and blocks sodium influx into nerve cells, which prevents depolarization - long duration of action

171
Q

Why is bupivocaine not used in regional blockage?

A

Cardiotoxic and is therefore contra indicated in regional blockage in case the tourniquet fails

172
Q

What local anaesthetic can be used as regional blockage?

A

Prilocaine - because far less cardiotoxic

173
Q

How would an abscess affect efficacy of local anaesthetic?

A

All local anaesthetic agents dissociate in tissues and this contributes to their therapeutic effect. The dissociation constant shifts in tissues that are acidic e.g. where an abscess is present, and this reduces the efficacy.

174
Q

Max doses lignocaine

A

Lignocaine 1% plain - 3mg/ Kg - 200mg (20ml)
Lignocaine 1% with 1 in 200,000 adrenaline - 7mg/Kg - 500mg (50ml)

175
Q

Max doses bupivicaine

A

Bupivicaine 0.5% - 2mg/kg- 150mg (30ml) (adrenaline does not allow increased dose)

176
Q

Contraindication to adrenaline use with local anaesthetic

A

MAOI’s or tricyclic antidepressants

177
Q

Name macrolides

A

Erythromycin, clarithromycin, azithromycin

178
Q

MOA macrolides

A

Inhibit bacterial protein synthesis by blocking translocation. Bacteriostatic

179
Q

Mechanism of resistance macrolides

A

Post-transcriptional methylation of the 23S bacterial ribosomal RNA

180
Q

SE macrolides

A

prolongs QT interval
GI SE - nausea is less common with clarithromycin than erythromycin. Also promotes gastric emptying!
Cholestatic jaundice
P450 inhibitor
Azithromycin is associated with hearing loss and tinnitus

181
Q

What drug should be stopped if starting macrolide?

A

Statin - increased risk of myopathy and rhabdomylosis

182
Q

Features of mercury poisoning

A

paraesthesia
visual field defects
hearing loss
irritability
renal tubular acidosis

183
Q

Treatment of motion sickness

A

Hyoscine > cyclising > promethazine

184
Q

MOA metformin

A

Biguanide. Activation of AMP-activated protein kinase:
Increases insulin sensitivity
Decreases hepatic gluconeogenesis
Decreases gastrointestinal absorption of carbs

185
Q

Adverse effects metforin

A

Diarrhoea, lactic acidosis in severe liver disease/renal failure. Can cause decrease vit B12

186
Q

CI to metformin use

A

CKD - dose review if eGFR <45, stop if <30
Alcohol abuse relative contraindication

187
Q

When should you withhold metformin?

A

Recent MI, sepsis, AKI, severe dehydration

188
Q

If someone cant tolerate metformin due to GI upset what’s the next step?

A

Try reduced dose and MR before switching to second line

189
Q

Over what time period is metformin titrated

A

1 week

190
Q

What are monoclonal antibodies?

A

Manmade proteins that bind to antigens

191
Q

How are monoclonal antibodies made?

A

Somatic cell hybridisation - fusion of myeloma and spleen cells from a mouse that has been immunised with the desired antigen –> hybridoma –> can produce myoconal antibodies

192
Q

What is humanising (monoclonal antibodies)?

A

A process that decreases immunogenicity of non human derived monoclonal antibodies

193
Q

What is infliximab used for?

A

Anti-TNF - Rheumatoid arthritis and Crohn’s

194
Q

What is rituximab used for?

A

Anti-CD20 - used in non-Hodgkin’s lymphoma and rheumatoid arthritis

195
Q

What is cetuximab used for?

A

Epidermal growth factor receptor antagonist - used in metastatic colorectal cancer and head and neck cancer

196
Q

What is trastuzumab used for?

A

(HER2/neu receptor antagonist): used in metastatic breast cancer

197
Q

What is alemtuzumab used for?

A

(anti-CD52): used in chronic lymphocytic leukaemia

198
Q

What is abciximab used for?

A

(glycoprotein IIb/IIIa receptor antagonist): prevention of ischaemic events in patients undergoing percutaneous coronary interventions

199
Q

What is OKT3 used for?

A

(anti-CD3): used to prevent organ rejection

200
Q

Other uses monoclonal antibodies? In terms of diagnosis

A

medical imaging when combined with a radioisotope
identification of cell surface markers in biopsied tissue
diagnosis of viral infections

201
Q

Features of methanol poisoning?

A

Intoxication, nausea, blindness

202
Q

Mechanism of blindness methanol poisoning?

A

Thought to be caused by a form of optic neuropathy, formed by accumulation of formic acid

203
Q

Management methanol poisoning

A

Fomepizole (competitive inhibitor of alcohol dehydrogenase) or ethanol
Haemodialysis
Cofactor therapy with folinic acid to reduce ophthalmological complications

204
Q

MOA suxamethonium

A

Depolarising neuromuscular blocker (only depolarising of muscle relaxants!)
Inhibits action of acetylcholine at the neuromuscular junction

205
Q

Adverse effects suxamethonium

A

Hyperkalaemia, malignant hyperthermia and lack of acetylcholinesterase
Fastest onset and shortest duration of all muscle relaxants

206
Q

MOA atracurium

A

Non depolarising neuromuscular blocking drug

207
Q

Adverse effects atracurium

A

Generalised histamine release on administration may produce facial flushing, tachycardia and hypotension

208
Q

MOA vecuronium

A

Non depolarising neuromuscular blocking drug

209
Q

MOA pancuronium

A

Non depolarising neuromuscular blocker

210
Q

What is used to reverse non depolarising muscle relaxants?

A

Neostigmine (pancuronium only partially)

211
Q

What are novel psychoactive susbtances (legal highs) chemically similar to?

A

MDMA and cannabis (so side effect profile similar - serotonin syndrome)

212
Q

What are hallucinogenics similar to?

A

Ketamine

213
Q

When taken with alcohol Gamma-hydroxybutyric acid (GHB) can cause what?

A

Life threatening respiratory depression

214
Q

What is octreotide?

A

Long-acting analogue of somatostatin
somatostatin is released from D cells of pancreas and inhibits the release of growth hormone, glucagon and insulin

215
Q

Uses of octreotide

A

Acute treatment of variceal haemorrhage
Acromegaly
Carcinoid syndrome
Prevent complications following pancreatic surgery
VIPomas
Refractory diarrhoea

216
Q

Adverse effect ocreotide

A

gallstones (secondary to biliary stasis)

217
Q

What is oculogyric crisis?

A

Dystonic reaction to certain drugs

218
Q

Features of oculogyric crisis

A

Restlesness, involuntary upward deviation of eyes

219
Q

Causes oculogyric crisis

A

Antipsychotics, metaclopramide, postencephalitic Parkinson’s disease

220
Q

Management of oculogyric crisis

A

Intravenous antimuscarinic: benztropine or procyclidine

221
Q

Those with a penicillin allergy might also be allergic to

A

cephalosporins.
Also remember - co-amox, co-fluampicil, tazocin, timentin

222
Q

Can POP be used when breastfeeding

A

Yes, also used in smoking and increased BMI

223
Q

Adverse effect POP

A

Increased incidence of functional ovarian cysts

224
Q

Describe physiology of paracetamol overdose

A

Liver normally conjugates paracetamol to glnucaronic acid. Saturation -> oxidation by p450 -> toxic metabolite (NAPQI).
Non toxic normal production forms mercaptopuric. If glutathione runs out toxins form covalent bonds with cell proteins leading to cell death.

Note low threshold for treating those taking P450 meds)

225
Q

Whats N-acetyle cystine

A

Precursor of glutathione so can increase hepatic glutathione production

226
Q

Criteria for liver transplant paracetamol OD

A

Arterial pH < 7.3, 24 hours after ingestion

or all of the following:
prothrombin time > 100 seconds
creatinine > 300 µmol/l
grade III or IV encephalopathy

227
Q

Who may benefit from activated charcoal in paracetamol OD?

A

Those who present within 1 hour

228
Q

Increased risk of hepatotoxicity in paracetamol OD

A

Liver enzyme inducing drugs
Malnourished

Note acute alcohol may be protective!

229
Q

Management of paracetamol OD

A

<1 hour activated charcoal
NAC if staggered regardless of plasma conc (Staggered is taking >1 hour)
Or if above line at 4 hours

patients who present 8-24 hours after ingestion of an acute overdose of more than 150 mg/kg of paracetamol even if the plasma-paracetamol concentration is not yet available

patients who present > 24 hours if they are clearly jaundiced or have hepatic tenderness, their ALT is above the upper limit of normal acetylcysteine should be continued if the paracetamol concentration or ALT remains elevated whilst seeking specialist advice

230
Q

Adverse reaction of NAC

A

Acetylcysteine commonly causes an anaphylactoid reaction (non-IgE mediated mast cell release). Anaphylactoid reactions to IV acetylcysteine are generally treated by stopping the infusion, then restarting at a slower rate.

Watch for delayed nephrotoxicity

231
Q

MOA rifampicin

A

inhibits bacterial DNA dependent RNA polymerase preventing transcription of DNA into mRNA

232
Q

SEs rifampicin

A

potent liver enzyme inducer
hepatitis, orange secretions
flu-like symptoms

233
Q

MOA isoniazid

A

inhibits mycolic acid synthesis

234
Q

SE isoniazid

A

peripheral neuropathy: prevent with pyridoxine (Vitamin B6)
hepatitis, agranulocytosis
liver enzyme inhibitor

235
Q

MOA pyrazinamide

A

converted by pyrazinamidase into pyrazinoic acid which in turn inhibits fatty acid synthase (FAS) I

236
Q

SE pyrazinamide

A

hyperuricaemia causing gout
arthralgia, myalgia
hepatitis

237
Q

MOA ethambutol

A

inhibits the enzyme arabinosyl transferase which polymerizes arabinose into arabinan

238
Q

SE ethambutol

A

optic neuritis: check visual acuity before and during treatment
dose needs adjusting in patients with renal impairment

239
Q

What are phosphodiesterase type V inhibitors used for?

A

Erectile dysfunction, pulmonary hypertension

240
Q

MOA phosphodiesterase type V inhib

A

Vasodilation through increased cGMP leading to smooth muscle relaxation in blood vessels supplying corpus callous

241
Q

Contraindication to phosphodiesterase type V inhib

A

Those taking nitrates and related drugs
Recent stroke/MI - need to wait 6 months

242
Q

SE phosphodiesterase type V inhib

A

Blue discolouration of vision
Non arteric anterior ischaemic nephropathy
Nasal congestion
Flushing
Headache
Priapism

243
Q

Risks of fluid overload post pic (acidosis)

A

Hyperchloraemic acidosis
Note if oedematous treat hypovolaemia first

244
Q

What are the groups for potassium sparing diuretics?

A

Epithelial Na channel blockers - amiloride, triamterene
Aldosterone antagonist - spironolactone, eplerenone

245
Q

How is amiloride normally given?

A

With a thiazide as an alternative to K supplementation

246
Q

Where do aldosterone antagonists work?

A

Cortical collecting duct

247
Q

Indication aldosterone antagonists

A

Ascites - patients with cirrhosis develop 2ndary hyperaldosteronism
HF
Nephrotic syndrome
Conns

248
Q

What abx should not be given in pregnancy

A

Tetracyclines, aminoglycosides, sulphonamides and trimethoprim, quinolone

249
Q

Can ACEi/ARBs be used in pregnancy

A

No
Neither can warfarin, sulphonylureas or statins

250
Q

What medications can exacerbate HF?

A

thiazolidinediones - pioglitazone is contraindicated as it causes fluid retention

verapamil - negative inotropic effect

NSAIDs/glucocorticoids - should be used with caution as they cause fluid retention. Low-dose aspirin is an exception - many patients will have coexistent cardiovascular disease and the benefits of taking aspirin easily outweigh the risks

Class I antiarrhythmics
flecainide (negative inotropic and proarrhythmic effect)

251
Q

Key drugs to avoid in renal failure

A

antibiotics: tetracycline, nitrofurantoin
NSAIDs
lithium
metformin

252
Q

Drugs needing dose adjustment in CKD

A

most antibiotics including penicillins, cephalosporins, vancomycin, gentamicin, streptomycin
digoxin, atenolol
methotrexate
sulphonylureas
furosemide
opioids

253
Q

Mechanism of st johns wort

A

Shown to be as effective as tricyclic antidepressants in the treatment of mild-moderate depression

mechanism: thought to be similar to SSRIs (although noradrenaline uptake inhibition has also been demonstrated)

254
Q

Adverse effects st johns wort

A

Profile in trials similar to placebo
Can cause serotonin syndrome
Inducer of P450 system, therefore decreased levels of drugs such as warfarin, ciclosporin. The effectiveness of the combined oral contraceptive pill may also be reduced

255
Q

Tamoxifen MOA

A

Tamoxifen is a Selective oEstrogen Receptor Modulator (SERM) which acts as an oestrogen receptor antagonist and partial agonist. It is used in the management of oestrogen receptor positive breast cancer

256
Q

Adverse effects tamoxifen

A

menstrual disturbance: vaginal bleeding, amenorrhoea
hot flushes - 3% of patients stop taking tamoxifen due to climacteric side-effects
venous thromboembolism
endometrial cancer

257
Q

How long is tamoxifen typically used for?

A

5 years following removal of the tumour.

Note - Raloxifene is a pure oestrogen receptor antagonist, and carries a lower risk of endometrial cancer

258
Q

MOA tacrolimus

A

decreases clonal proliferation of T cells by reducing IL-2 release
binds to FKBP forming a complex which inhibits calcineurin, a phosphotase that activates various transcription factors in T cells

259
Q

MOA ciclosporin

A

Same as tacrolimus but binds to cyclophilin rather than FKBP

260
Q

What type of drug is tacrolimus

A

Calcineurin inhibitor

261
Q

Adverse effects tacrolimus

A

Nephrotoxicity and impaired glucose tolerance (more common than cyclosporin because more potent and risk of organ rejection is therefore less)

262
Q

Monitoring of lithium

A

range = 0.4 - 1.0 mmol/l
take 12 hrs post-dose

263
Q

Montioring ciclosporin

A

trough levels immediately before dose

264
Q

Monitoring digoxin

A

at least 6 hrs post-dose

265
Q

When should phenytoin levels be checked

A

Trough level immediately before dose if:
adjustment of phenytoin dose
suspected toxicity
detection of non-adherence to the prescribed medication

266
Q

Whats the other name for trastuzumab and what’s its MOA

A

Herceptin - monoclonal antibody directed against the HER2/neu receptor

267
Q

Adverse effects trastuzumab

A

flu-like symptoms and diarrhoea are common
cardiotoxicity - more common when anthracyclines have also been used, an echo is usually performed before starting treatment

268
Q

MOA organophosphate insecticide poisoning

A

Inhibits acetylcholinesterase - leads to up regulation of nicotinic and muscarinic cholinergic neurotransmission
(Sarin gas) (accumulat acetylechloride)

269
Q

Features organophosphate insecticide poisoning

A

SLUD
Salivation
Lacrimation
Urination
Defication/diarrhoea

Bradycardia, hypoT, small pupils, muscle fasciculations

270
Q

Management organophosphate insecticide poisoning

A

Atropine

271
Q

Management of salicyte overdose

A

Urinary alkalinization with IV bicarbonate
haemodialysis

272
Q

Management opiod overdose

A

Naloxone

273
Q

Management of benzodiazepine overdose

A

Flumazenil
The majority of overdoses are managed with supportive care only due to the risk of seizures with flumazenil. It is generally only used with severe or iatrogenic overdoses.

274
Q

Management tricyclic antidepressant OD

A

IV bicarbonate may reduce the risk of seizures and arrhythmias in severe toxicity - priority is to correct the acidosis over direct correction of arrhythmias (class 1a and 1c contraindicated)
Dialysis ineffective

275
Q

Management of lithium toxicity

A

Mild-moderate toxicity may respond to volume resuscitation with normal saline
haemodialysis may be needed in severe toxicity
sodium bicarbonate is sometimes used but there is limited evidence to support this. By increasing the alkalinity of the urine it promotes lithium excretion

276
Q

Management warfarin OD

A

Vitamin K, prothrombin complex

277
Q

Management heparin OD

A

Protamine sulphate

278
Q

Management beta blocker OD

A

if bradycardic then atropine
in resistant cases glucagon may be used

279
Q

Management of ethylene glycol OD

A

Ethanol has been used for many years
works by competing with ethylene glycol for the enzyme alcohol dehydrogenase

this limits the formation of toxic metabolites (e.g. Glycoaldehyde and glycolic acid) which are responsible for the haemodynamic/metabolic features of poisoning

fomepizole, an inhibitor of alcohol dehydrogenase, is now used first-line in preference to ethanol
haemodialysis also has a role in refractory cases

280
Q

Management methanol OD

A

fomepizole or ethanol
haemodialysis

281
Q

Management of organophosphate insecticide OD

A

atropine

282
Q

Management digoxin OD

A

Digoxin-specific antibody fragments

283
Q

Management iron OD

A

Desferrioxamine, a chelating agent

284
Q

Management lead OD

A

Dimercaprol, calcium edetate

285
Q

Management OD poisoning

A

100% oxygen
hyperbaric oxygen

286
Q

Management cyanide poisoning

A

Hydroxocobalamin; also combination of amyl nitrite, sodium nitrite, and sodium thiosulfate

287
Q

What is P450 enzyme?

A

Haem protein that plays a role in drug metabolism. Mainly found in liver and gut. Main effect is to catalyse oxidation, making the substrate more water soluble so can be excreted by kidneys

288
Q

p450 inducers

A

CRAPGPs:
Carbemazepines
Rifampicin
Alcohol (chronic)
Phenytoin
Griseofulvin
Phenobarbitone
Sulphonylureas, St Johns Wort, Smoking (affects CYPIA2)

289
Q

p450 inhibitors

A

SICKFACES.COM:
Sodium valproate, SSRI
Isoniazid
Cimetidine
Ketoconazole
Fluconazole
Acute alcohol & Grapefruit juice, amiodarone , allopurinol
Chloramphenicol
Erythromycin
Sulfonamides
Ciprofloxacin
Omeprazole
Metronidazole

290
Q

Features tricyclic overdose

A

Early - dry mouth, dilated pupils, agitation, sinus tachy, blurred vision
Severe - acidosis, arrhythmia, seizures, coma

291
Q

ECG changes tricyclic overdose

A

Sinus tachy, widening QRS (>100 risk of seizures, >160 risk of ventricular arrhythmias), prolong QT

292
Q

Why might IV lipid emulsion be used in tricyclic overdose?

A

Bind free drug and reduce toxicity
Remember dialysis ineffective in tricyclic

293
Q

Effect on fetus of ACEi

A

Renal dysgenesis
Craniofacial abnormalities

294
Q

Effect on fetus aclohol

A

Craniofacial abnormalities

295
Q

Effect on fetus aminoglycosides

A

Ototoxicity

296
Q

Effect on fetus carbamazepine

A

Neural tube defects
Craniofacial abnormalities

297
Q

Effect on fetus chloramphenicol

A

Grey baby syndrome

298
Q

Effect on fetus cocain

A

IUGR, preterm labour

299
Q

Effect on fetus diethylstilbestrol

A

Vaginal clear cell adenocarcinoma

300
Q

Effect on fetus lithium

A

Ebstein anomaly (atrialized right ventricle)

301
Q

Effect on fetus maternal diabetes

A

Macrosomia
Neural tube defects
Polyhydramnios
Preterm labour
Caudal regression syndrome

302
Q

Effect on fetus smoking

A

Preterm labour, IUGR

303
Q

Effect on fetus tetracyclines

A

Discoloured teeth

304
Q

Effect on fetus thalidomide

A

Limb reduction defects

305
Q

Effect on fetus valproate

A

Neural tube defects, craniofacial abnormalities

306
Q

Effect on fetus warfarin

A

Craniofacial abnormalities

307
Q

Other name for quinine toxicity

A

Cinchonism

308
Q

Signs/symptoms cinchonism

A

Tinnitus, visual blurring, flushed dry skin, abdo pain. Similar to salivate.
Hypoglycaemia - stimulates pancreas insulin secretion

309
Q

Cardiac arrhythmias associated with cinchonism

A

Prolonged QT due to blockade of Na and K channels –> v fib/v tach

310
Q

Management cinchonism

A

Fluid, inotropes, bicarbonates, PPV - pulmonary oedema

311
Q

SE metformin

A

Gastrointestinal side-effects
Lactic acidosis

312
Q

SE sulphonylureas

A

Hypoglycaemic episodes
Increased appetite and weight gain
Syndrome of inappropriate ADH secretion
Liver dysfunction (cholestatic)

313
Q

SE glitazones

A

Weight gain
Fluid retention
Liver dysfunction
Fractures

314
Q

SE gliptins

A

Pancreatitis

315
Q

SE CCB

A

Headache
Flushing
Ankle oedema

316
Q

SE verapamil

A

Constipation

317
Q

SE Beta blocker

A

Bronchospasm (especially in asthmatics)
Fatigue
Cold peripheries
Sleep disturbance

318
Q

SE Nitrates

A

Headache
Postural hypotension
Tachycardia

319
Q

SE Nicorandil

A

Headache
Flushing
Anal ulceration

320
Q

Causes of serotonin syndrome

A

Monoamine oxidase inhibitors
SSRIs (St John’s Wort can interact with SSRIs to cause serotonin syndrome)
Tramadol may also interact with SSRIs
Ecstasy
Amphetamines

321
Q

Features of serotonin syndrome

A

Neuromuscular excitation - hyperreflexia, myoclonus, rigidity
Autonomic nervous system excitation - hyperthermia, sweating
Altered mental state
confusion

322
Q

Management of serotonin syndrome

A

Supportive including IV fluids
Benzodiazepines
More severe cases are managed using serotonin antagonists eg cyproheptadine and chlorpromazine

323
Q

Difference between serotonin syndrome and neuroepileptic syndrome

A

Neuroepileptic tends to be slower onset, decreased reflexes not increased, no dilated pupils. Also more associated with a raised CK (though both might)

324
Q

Management of severe neuroepileptic syndrome

A

Dantrolene

325
Q

MOA quinolones

A

Inhibiting DNA synthesis and are bactericidal in nature. inhibit topoisomerase II (DNA gyrase) and topoisomerase IV

326
Q

Mechanism of resistance quinolones

A

mutations to DNA gyrase, efflux pumps which reduce intracellular quinolone concentration

327
Q

Adverse effects quinolones

A

Lower seizure threshold in patients with epilepsy

Tendon damage (including rupture) - the risk is increased in patients also taking steroids

Cartilage damage has been demonstrated in animal models and for this reason quinolones are generally avoided (but not necessarily contraindicated) in children

Lengthens QT interval

328
Q

Contraindications quinolones

A

Pregnancy
G6PD

329
Q

Salicyte overdose acidosis or alkalosis?

A

Mixed respiratory alkalosis and metabolic acidosis.

Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst later the direct acid effects of salicylates (combined with acute renal failure) may lead to an acidosis.

In children metabolic acidosis tends to predominate.

330
Q

Features salivate overdose

A

hyperventilation (centrally stimulates respiration)
tinnitus
lethargy
sweating, pyrexia (increased O2 consumption and increased CO2 and heat production)
nausea/vomiting
hyperglycaemia and hypoglycaemia
seizures
coma

331
Q

Management salicyte overdose

A

gGneral (ABC, charcoal)

Urinary alkalinization with intravenous sodium bicarbonate - enhances elimination of aspirin in the urine

Haemodialysis

332
Q

Indications for haemodialysis

A

Serum concentration > 700mg/L
Metabolic acidosis resistant to treatment
Acute renal failure
Pulmonary oedema
Seizures
Coma

333
Q

Drug receptor decongestants (e.g. phenylephrine/oxymetazoline)

A

Alpha 1 agonist

334
Q

Drug receptor glaucoma (e.g. topical brimonidine)

A

Alpha 2 agonist

335
Q

Drug receptor benign prostatic hyperplasia (e.g. tamsulosin)

A

Alpha antagonist

336
Q

Drug receptor hypertension (e.g. doxazosin)

A

Alpha antagonist

337
Q

Drug receptor inotropes (e.g. dobutamine)

A

Beta 1 agonist

338
Q

Drug receptor non-selective & selective beta-blockers (e.g. atenolol, bisoprolol)

A

Beta 1 antagonist

339
Q

Drug receptor bronchodilators (e.g. salbutamol)

A

Beta 2 agonist

340
Q

Drug receptor non-selective beta-blockers (e.g. propranolol, labetalol)

A

Beta 2 antagonist

341
Q

Drug receptor parkinson’s disease (e.g. ropinirole)
Prolactinoma

A

Dopamine agonist

342
Q

Drug receptor schizophrenia (antipsychotics e.g. haloperidol), anti-emetics (e.g. metoclopramide/domperidone)

A

Dopamine antagonist

343
Q

Drug receptor benzodiazepines eg baclofen

A

GABA agonist

344
Q

Drug receptor Flumazenil

A

GABA antagonist

345
Q

Drug receptor antihistamines (e.g. loratadine)

A

Histamine 1 antagonist

346
Q

Drug receptor antacids (e.g. ranitidine)

A

Histamine antagonist

347
Q

Drug receptor glaucoma (e.g. pilocarpine)

A

Muscarinic agonist

348
Q

Drug receptor:
Atropine (e.g. for bradycardia)
Bronchodilator (e.g. ipratropium bromide, tiotropium)
Urge incontinence (e.g. oxybutynin)

A

Muscarinic antagonist

349
Q

Drug receptor:
Nicotine
Varenicline (used for smoking cessation)
Depolarising muscle relaxant (e.g. suxamethonium)

A

Nictonic agonist

350
Q

Drug receptor: Non-depolarising muscle relaxants (e.g. atracurium)

A

Nictonic antagonist

351
Q

Drug receptor Inducing labour (e.g. Syntocinon)

A

Oxytocin agonist

352
Q

Drug receptor Tocolysis (e.g. atosiban)

A

Oxytocin antagonist

353
Q

Drug receptor Triptans (for acute migraine, e.g. zolmitriptan)

A

Serotonin agonist

354
Q

Drug receptor anti-emetics (e.g. ondansetron)

A

Serotonin antagonist

355
Q

Adrenaline dose anaphylaxis

A

anaphylaxis: 0.5ml 1:1,000 IM

356
Q

Adrenaline dose cardiac arrest

A

cardiac arrest: 10ml 1:10,000 IV or 1ml of 1:1000 IV

357
Q

Management of accidental injection e.g. resulting in digital ischaemia

A

local infiltration of phentolamine

358
Q

Where is adrenaline released from

A

adrenal glands

359
Q

Effects of adrenaline in CO, pulse pressure and total peripheral resistance

A

Increases cardiac output and total peripheral resistance
causes vasoconstriction in the skin and kidneys causing a narrow pulse pressure

360
Q

Actions of adrenaline on alpha adrenergic receptors

A

Inhibits insulin secretion by the pancreas
Stimulates glycogenolysis in the liver and muscle
Stimulates glycolysis in muscle

361
Q

Actions of adrenaline on beta adrenergic receptors

A

Stimulates glucagon secretion in the pancreas
Stimulates ACTH
Stimulates lipolysis by adipose tissue

362
Q

What receptors does adrenaline act on

A

acts on α 1 and 2, β 1 and 2 receptors
acts on β 2 receptors in skeletal muscle vessels-causing vasodilation

363
Q

What is pharmacodynamics?

A

What drugs do to the body

364
Q

What is pharmacokinetcis?

A

What the body does to the drugs

365
Q

What is an ion channel? (pharmacodynamics)

A

Simplest form of receptor. Channel either opened or closed (agonist or antagonist). Eg most local anaesthetics work on voltage gated Na channels

366
Q

Give an example of a drug that works via ion channel

A

Zolpidem

367
Q

What are G-protein coupled (pharmacodynamics)

A

When drugs bind to a target it causes a sequence of events with G protein subunits - production of secondary messengers eg cyclic AMP or protein phospholyration cascade

368
Q

Give an examaple of a drug that works via G protein coupled

A

Adrenaline

369
Q

What are tyrosine kinase receptors (pharmacodynamics)

A

Series of steps. Phosphorylation causing effects eg cell growth and differentiation

370
Q

Example of a drug that works via tyrosine kinase receptors

A

Insulin like growth factor, cytokines like IL-2

371
Q

What are nuclear receptors (pharmacodynamics)

A

Increased or decreased gene transcription. Lipid soluble because penetrate cell membrane. Then forms a complex with receptor protein before exhibiting effect

372
Q

Give and example of a drug that works via nuclear receptors

A

Steroids, levothyroxine

373
Q

What are agonists

A

drugs which activates the receptor.

374
Q

What are antagonists

A

Those which block a receptor preventing activation, it is important to note they do not deactivate a receptor

375
Q

What are competitive antagonists

A

Binds at same site as agonist

376
Q

What are non competitive antagonists

A

Binds at another site causing change at site where agonist would otherwise bind

377
Q

What is binding affinity

A

How readily the drug will bind to a specific receptor

378
Q

What is efficacy

A

How able an agonist is to produce a response once bound

379
Q

What is potency

A

Concentration at which drug is effective

380
Q

What is therapeutic index

A

Ratio of the dose of a drug resulting in an undesired effect compared to desired effect

381
Q

What is first order kinetics

A

The rate of drug elimination is proportional to drug concentration

382
Q

What is zero order kinetics

A

Rate of excretion is constant despite changes in plasma) conc (saturation of metabolic process)

383
Q

Example of drugs exhibiting zero order kinetics

A

Phenytoin and salicylates

384
Q

What are phase 1 reactions?

A

Oxidation, reduction, hydrolysis. Mainly p450 enzymes.
Other enzymes eg alcohol dehydrogenase and xanthine oxidase

385
Q

What are phase 2 reactions?

A

Conjugation eg Glucuronyl, acetyl, methyl, sulphate

386
Q

What is first pass metabolism

A

Conc of drug greatly reduced before it reaches the systemic circulation due to hepatic metabolism (so higher dose have to be given orally)

387
Q

Example of drugs undergoing first pass

A

aspirin
isosorbide dinitrate
glyceryl trinitrate
lignocaine
propranolol
verapamil
isoprenaline
testosterone
hydrocortisone

(its important you know these!!)

388
Q

Whats zero order kinetics?

A

Describes metabolism which is independent of concentration of metabolism. Because metabolic pathway saturated so constant amount eliminated eg failing a breathalyser test the morning after!

389
Q

Examples of drugs exhibiting zero order kinetics

A

phenytoin
salicylates (e.g. high-dose aspirin)
heparin
ethanol

390
Q

Drugs affected by acetylator status

A

isoniazid
procainamide
hydralazine
dapsone
sulfasalazine

(DHIPS)

MRCP part 1 (3 decks)

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