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MRCP: Pharmacology > General > Flashcards

General Flashcards

1
Q

What is acute porphyria?

A

Autosomal dominant
defect in porphobilinogen deaminase, an enzyme involved in the biosynthesis of haem

Abdominal pain + neuropsychiatric

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2
Q

What drugs precipitate a porphyria attack?

A

Alcohol
Barbiturate
BZD
Contraceptive pill
Halothane
Sulphonadmies

If you go to a BAR on a BENZ,say HALO to a guy,take a SULFi,have some ALCOHOL n dont forget the OCP.

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3
Q

What is the dose for adrenaline in anaphylaxis?

A

anaphylaxis: 0.5ml 1:1,000 IM

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4
Q

What is the dose of adrenaline for cardiac arrest?

A

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

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5
Q

What is the action of adrenaline?

A

responsible for the fight or flight
vessels-causing vasodilation
increases cardiac output and total peripheral resistance
causes vasoconstriction in the skin and kidneys causing a narrow pulse pressure

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6
Q

What receptors dose adrenaline work on ?

A

α 1, α 2, β 1, β 2 receptors

acts on β 2 receptors in skeletal muscle vessels-causing vasodilation

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7
Q

Action of adrenaline on alpha adrenergic receptors?

A

inhibits insulin secretion by the pancreas
stimulates glycogenolysis in the liver and muscle
stimulates glycolysis in muscle

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8
Q

What type of receptor is alpha adrenergic receptors?

A

G protein coupled receptor

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9
Q

Action of adrenaline on beta adrenergic receptors?

A

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

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10
Q

What is an agonist of alpha 1 adrenoceptors?

A

Phenylephrine

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11
Q

What is an agonist of alpha 2 adrenoceptors?

A

Clonidine

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12
Q

What is an agonist of beta 1 adrenoceptors?

A

Dobutamine

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13
Q

What is an agonist of beta 2 adrenoceptors?

A

Salbutamol

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14
Q

What is an antagonist of alpha 1 adrenoceptors?

A

alpha-1: doxazosin

alpha-1a: tamsulosin - acts mainly on urogenital tract

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15
Q

What is a non-selective alpha 1 adrenceptor antagonist?

A

phenoxybenzamine (previously used in peripheral arterial disease)

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16
Q

What is a non-selective beta adrenoceptor antagonist?

A

Carvedilol and labetalol are mixed alpha and beta antagonists

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17
Q

What is a beta 1 adrenoceptor antagonist?

A

Atenolol

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18
Q

What is activation of alpha 1 adrenoceptor cause?

A

vasoconstriction
relaxation of GI smooth muscle
salivary secretion
hepatic glycogenolysis

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19
Q

What is activation of alpha 2 adrenoceptor cause?

A

mainly presynaptic: inhibition of transmitter release (inc NA, Ach from autonomic nerves)
inhibits insulin
platelet aggregation

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20
Q

What does activation of Beta 1 adrenoceptors cause?

A

increase heart rate + force

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21
Q

What does activation of beta 2 adrenoceptors cause?

A

vasodilation
bronchodilation
relaxation of GI smooth muscle

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22
Q

What does activation of beta 3 receptors cause?

A

Lipolysis

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23
Q

What is the secondary messenger system of alpha 1 receptors?

A

Phospholipase C

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24
Q

What is the secondary messenger system of alpha 2 receptors?

A

Inhibit adenylate cyclase A
→ IP3 → DAG

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25
Q

What is the secondary messenger system of beta receptors?

A

Activation of adenolyte cyclase

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26
Q

What is management of acute alcohol withdrawal?

A

BZD

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27
Q

What drug can be used to promote abstinence?

A

Disulfram

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28
Q

What is the mechanism of action of disulfram?

A

acetaldehyde dehydrogenase.

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29
Q

What drug has been shown to promote abstinence?

A

Acamprost

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30
Q

What is the mechanism of action of acampost?

A

Weak NMDA antagonist

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31
Q

What is the mechanism of allopurinol?

A

Inhibits xanthine oxidase

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32
Q

How should gout be managed?

A

100 mg allopurinol
Reduce if renal function a problem
Start colchicine
If cannot tolerate colchicine consider ibuprofen

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33
Q

What are the indications for starting allopurinol?

A

Start in first flare of gout. Particularly if:
>= 2 attacks in 12 months
tophi
renal disease
uric acid renal stones
prophylaxis if on cytotoxics or diuretics

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34
Q

What sever adverse affects are seen in allopurinol?
Who is at increased risk of these reactions?

A

severe cutaneous adverse reaction (SCAR)
drug reaction with eosinophilia and systemic symptoms (DRESS)
Stevens-Johnson syndrome

Asian populations increased risk

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35
Q

If severe skin reaction occurs with allopurinol, what additional test should be completed?

A

HLA B 5801 panel

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36
Q

What drugs interact with allopurinol?
What are the drug interaction mechanisms?

A

Azathioprine
- metabolised to active compound 6-mercaptopurine
- xanthine oxidase is responsible for the oxidation of 6-mercaptopurine to 6-thiouric acid
- High levels of active metabolite - required dose reduction

Cyclophosphamide
- allopurinol reduces renal clearance, therefore may cause marrow toxicity

Theophylline
-allopurinol causes an increase in plasma concentration of theophylline by inhibiting its breakdown

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37
Q

What can amiodarone do to the thyroid?

A

Hypothyroidism
Hyperthyroidism

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38
Q

What is the mechanism of amiodarone hypothyroidism?

A

Wolff-Chaikoff effect
an autoregulatory phenomenon where thyroxine formation is inhibited due to high levels of circulating iodide

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39
Q

What are the types of hyperthyroidism caused by amiodarone?

A

Autoimmune thyroid type 1:
- Excess iodine-induced thyroid hormone synthesis
- Goitre
- Mnx: Carbimazole / potassium percholate

Autoimmune thyroid type 2:
- Amiodarone related destruction
- No goitre
- Mnx: corticosteroids

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40
Q

Mechanism of propofol?

A

GABA receptor agonist

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41
Q

Side effect of propofol

A

Moderate cardiovascular depressant
Rapid onset anaesthesia
Painful IV injection
Metabolites with few accumulations / toxicity

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42
Q

What is the most appropriate anaesthetic for rapid sequence induction?

A

Sodium thiopentate

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43
Q

Side effects of sodium thiopentate?

A

Marked myocardial depression may occur
Metabolites build up quickly
Unsuitable for maintenance infusion
Little analgesic effects

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44
Q

Mechanism of ketamine is anaesthesia?

A

NMDA receptor antagonist

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45
Q

Side effects of ketamine?

A
  • Has moderate to strong analgesic properties
  • Produces little myocardial depression making it a suitable agent for anaesthesia in those who are haemodynamically unstable
  • May induce state of dissociative anaesthesia resulting in nightmares
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46
Q

Features of etomdiate as anaesthetic?

A

Has favorable cardiac safety profile with very little haemodynamic instability
No analgesic properties
Unsuitable for maintaining sedation as prolonged (and even brief) use may result in adrenal suppression
Post operative vomiting is common

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47
Q

Actions of class 1a anti-arrhythmic? Examples?

A

Block sodium channels - Increases AP duration

Quinidine
Procainamide
Disopyramide

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48
Q

Actions of class 1b anti-arrhythmic? Examples?

A

Block sodium channel blockers - Decrease AP duration

Lidocaine
Mexiletine
Tocainide

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49
Q

Actions of class 1c anti-arrhythmic?Examples?

A

Block sodium channels No effect on AP duration

Flecainide
Encainide
Propafenone

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50
Q

Actions of class II anti-arrhythmic? Examples?

A

Beta-adrenoceptor antagonists

Propranolol
Atenolol
Bisoprolol
Metoprolol

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51
Q

Actions of class III anti-arrhythmic? Examples?

A

Block potassium channels

Amiodarone
Sotalol
Ibutilide
Bretylium

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52
Q

Actions of class IV anti-arrhythmic? Examples?

A

Verapamil
Diltiazem

Calcium channel blockers

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53
Q

What antibiotics work by inhibiting cell wall synthesis by preventing peptidoglycan cross-linking?

A

Penicillin
Cephalosporins
Carbopenems

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54
Q

What antibiotics work by inhibiting cell wall synthesis by preventing peptidoglycan synthesis?

A

Glycopeptides (e.g. vancomycin)

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55
Q

What antibiotics inhibits ribosomes, by disrupting the 50 S subunit?

A

Macrolides
chloramphenicol
clindamycin
linezolid,

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56
Q

What antibiotics inhibits ribosomes, by disrupting the 30 S subunit?

A

Aminoglycosides (Gentamicin)
Tetracyclines

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57
Q

What antibiotics inhibits DNA synthesis?

A

Quinolones

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58
Q

What antibiotics damages DNA?

A

Metronidazole

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59
Q

What antibiotics inhibits folic acid formation?

A

sulphonamides
trimethoprim

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60
Q

What antibiotics inhibits RNA synthesis?

A

Rifampicin

R = RNA

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61
Q

What is the mechanism of aspirin ?

A

Cyclooxygenase-1 and 2 inhibit
Prevents prostaglandin, prostacyclin and thromboxane synthesis

By blocking thromboxane A2 prevents platelet aggregation

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62
Q

Features of beta blocker overdose?

A

bradycardia
hypotension
heart failure
syncope

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63
Q

Mnx of beta blocker overdose?

A

Bradycardia –> Atropine

If resistant –> Glucagon

Haemodialysis does not work in beta blocker overdose

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64
Q

Mechanism of botulism toxin ?

A

Blocks presynaptic neurone from releasing in the synaptic cleft -
Neuromuscular blockade

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65
Q

What is the effect of verapamil?

A

Calcium channel blocker
Heavily inotropic

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66
Q

What is the effect of Diltiazem ?

A

Less inotropic than verapamil, but still inotropic

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67
Q

What is the effect and mechanism of dihydroperidine calcium channel blocker?

A

Peripheral vascular smooth muscle relaxation greater than myocardial. No inotropic effect

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68
Q

What is the order of antihypertensives?

A
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69
Q

What is the mechanism of carbon monoxide poisoning?

A

Carbon monoxide has a greater affinity for haemoglobin than O2
Left shift of the o2 dissociation curve

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70
Q

Features of carbon monoxide poisoning?

A

headache: 90% of cases
nausea and vomiting: 50%
vertigo: 50%
confusion: 30%
subjective weakness: 20%

severe toxicity: ‘pink’ skin and mucosae, hyperpyrexia, arrhythmias, extrapyramidal features, coma, death

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71
Q

What are the levels of severity of carboxyhaemoglobin ?

A

May give a high reading on O2 due to similarity of carboxyhemoglobin and oxyhemoglobin

< 3% non-smokers
< 10% smokers
10 - 30% symptomatic: headache, vomiting
> 30% severe toxicity

an ECG is a useful supplementary investgation to look for cardiac ischaemia

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72
Q

How should carbon monoxide be managed?

A

100% high-flow oxygen via a non-rebreather mask
from a physiological perspective, this decreases the half-life of carboxyhemoglobin (COHb)
should be administered as soon as possible, with treatment continuing for a minimum of six hours
target oxygen saturations are 100%
treatment is generally continued until all symptoms have resolved, rather than monitoring CO levels

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73
Q

What caustic substance is found in bleach? What type of agent is it?

A

Oxidising agent

Hydrogen peroxide
Sodium hypocholite

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74
Q

What caustic substance is found in cleaning substances

A

Strong alkali

sodium hydroxide
potassium hydroxide

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75
Q

What type of damage does a strong alkali cause?

A

liquefactive necrosis, more commonly resulting in oesophageal injury

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76
Q

What type of damage does a strong acid cause?

A

coagulative necrosis, more commonly resulting in gastric injury

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77
Q

What is the mechanism of action of cyclosporin?

A

Decreases clonal proliferation of T cells by reducing IL-2 release. It acts by binding to cyclophilin forming a complex which inhibits calcineurin, a phosphatase that activates various transcription factors in T cells

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78
Q

What are the adverse affects of cyclosporin?

A

Everything is increases: K+, Hair, Lipid, Glucose, BP

nephrotoxicity
hepatotoxicity
fluid retention
hypertension
hyperkalaemia
hypertrichosis
gingival hyperplasia
tremor
impaired glucose tolerance
hyperlipidaemia
increased susceptibility to severe infection

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79
Q

What are the indications of ciclosporin?

A

following organ transplantation
rheumatoid arthritis
psoriasis (has a direct effect on keratinocytes as well as modulating T cell function)
ulcerative colitis
pure red cell aplasia

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80
Q

What is the mechanism of cocaine?

A

blocks the uptake of dopamine, noradrenaline and serotonin

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81
Q

Effects of cocaine toxicity?

A

Cardiovascular effects include:
coronary artery spasm → myocardial ischaemia/infarction (including ischaemic colitis)
both tachycardia and bradycardia may occur
hypertension
QRS widening and QT prolongation
aortic dissection

Neurological effects
- seizures
- mydriasis (dilation)
- hypertonia
- hyperreflexia

Psychiatric effects
- agitation
- psychosis
- hallucinations

Hyperthermia
rhabdomyolysis
Metabolic acidosis

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82
Q

What is a recognised complication post ischaemic colitis?

A

ischaemic colitis is recognised in patients following cocaine ingestion. This should be considered if patients complain of abdominal pain or rectal bleeding

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83
Q

Management of cocaine toxicity?

A

BZD!!

If chest pain:
BZD + GTN infusion
If primary MI:
PCI
If Hypertension :
BZD + Sodium nitropusside

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84
Q

What are disadvantages of taking the OCP?

A

Increased risk of venous thromboembolic disease
Increased risk of breast and cervical cancer
Increased risk of stroke and ischaemic heart disease (especially in smokers)
temporary side-effects such as headache, nausea, breast tenderness may be seen

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85
Q

What are advantages of taking the pill?

A

usually makes periods regular, lighter and less painful
reduced risk of ovarian, endometrial - this effect may last for several decades after cessation
reduced risk of colorectal cancer
may protect against pelvic inflammatory disease
may reduce ovarian cysts, benign breast disease, acne vulgaris

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86
Q

What are the levels of contraindication for OCP?

A

UKMEC 1: a condition for which there is no restriction for the use of the contraceptive method
UKMEC 2: advantages generally outweigh the disadvantages
UKMEC 3: disadvantages generally outweigh the advantages
UKMEC 4: represents an unacceptable health risk

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87
Q

What are UKMEC 3 for OCP?

A

More than 35 years old and smoking less than 15 cigarettes/day
BMI > 35 kg/m^2*
Family history of thromboembolic disease in first degree relatives < 45 years
Controlled hypertension
Immobility e.g. wheel chair use
Carrier of known gene mutations Associated with breast cancer (e.g. BRCA1/BRCA2)
Current gallbladder disease
Diabetes (depends on severity)

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88
Q

What are UKMEC 4?

A

More than 35 years old and smoking More than 15 cigarettes/day
Migraine with aura
History of thromboembolic disease or Thrombogenic mutation
History of stroke or ischaemic heart disease
Breast feeding < 6 weeks post-partum
Uncontrolled hypertension
Current breast cancer
Major surgery with prolonged immobilisation
Positive antiphospholipid antibodies (e.g. in SLE)
Diabetes - depends on severity

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89
Q

How should you start the pill?

A

If within 5 days of cycle do not need any additional protection

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90
Q

Do you need a pill free break?

A

No - can take pill back to back

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91
Q

Occasions efficacy of pill reduced?

A
  • If vomiting within 2 hours of taking COC pill
  • Medication that induce diarrhoea or vomiting may reduce effectiveness of oral contraception (for example orlistat)
  • If taking liver enzyme-inducing drugs

Generally concurrent Abx do not have an effect. Unless liver enzyme inducing

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92
Q

What is the mechanism of cyanide?

A

Cyanide inhibits the enzyme cytochrome c oxidase, resulting in cessation of the mitochondrial electron transfer chain.

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93
Q

Features of cyanide poisoning?

A
  • Classical’ features: brick-red skin, smell of bitter almonds
  • Acute: hypoxia, hypotension, headache, confusion
  • Chronic: ataxia, peripheral neuropathy, dermatitis

Think of it with burning plastics

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94
Q

Management of cyanide poisoning?

A
  1. supportive measures: 100% oxygen
  2. definitive: hydroxocobalamin (intravenously), also combination of amyl nitrite (inhaled), sodium nitrite (intravenously), and sodium thiosulfate (intravenously)
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95
Q

What type of drug is digoxin and what does it do?

A

Cardiac glycoside
Used for rate control in AF
Positive inotropic effect

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96
Q

Mechanism of action of digoxin?

A
  1. Decreases conduction through the atrioventricular node which slows the ventricular rate in atrial fibrillation and flutter
  2. Increases the force of cardiac muscle contraction due to inhibition of the Na+/K+ ATPase pump. Also stimulates vagus nerve
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97
Q

What are the features of digoxin toxicity?

A

generally unwell, lethargy, nausea & vomiting, anorexia, confusion, yellow-green vision
arrhythmias (e.g. AV block, bradycardia)
gynaecomastia

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98
Q

How does hypokalaemia precipitate digoxin toxicity?

A
  1. Digoxin normally binds to the ATPase pump on the same site as potassium.
    2.Hypokalaemia → digoxin more easily bind to the ATPase pump → increased inhibitory effects
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99
Q

Factors that cause digoxin toxicity?

A

HYPOKALAEMIA
increasing age
renal failure
myocardial ischaemia
hypomagnesaemia, hypercalcaemia, hypernatraemia, acidosis
hypoalbuminaemia
hypothermia
hypothyroidism

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100
Q

What drugs can cause digoxin toxicity? Why?

A

Compete for excretion in DCT
amiodarone, quinidine, verapamil, diltiazem, spironolactone ciclosporin.

Also drugs which cause hypokalaemia e.g. thiazides and loop diuretics

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101
Q

Management of digoxin toxicity?

A

Digibind
correct arrhythmias
monitor potassium

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102
Q

What are indications for dopamine agonist therapy?

A

Parkinson’s disease
prolactinoma/galactorrhoea
cyclical breast disease
acromegaly

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103
Q

Side effects of dopamine receptor agonists?

A

pulmonary, retroperitoneal and cardiac fibrosis

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104
Q

Side effects of dopamine receptor agonists?

A

nausea/vomiting
postural hypotension
hallucinations
daytime somnolence

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105
Q

What are features of DRESS syndrome?

A

Hospitalisation
Reaction suspected to be drug related
Acute skin rash (Morbilliform –> erythroderma / something else)
Fever about 38ºC
Enlarged lymph nodes at two sites
Involvement of at least one internal organ
Blood count abnormalities such as low platelets, raised eosinophils or abnormal lymphocyte count.

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106
Q

What are common drug causes of DRESS?

A

Allopurinol anti-epileptics, antibiotics, immunosuppresants, HIV treatment and NSAIDS.

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107
Q

What are drug causes of agranulocytosis?

A

Antithyroid drugs - carbimazole, propylthiouracil
Antipsychotics - atypical antipsychotics (CLOZAPINE)
Antiepileptics - carbamazepine
Antibiotics - penicillin, chloramphenicol, co-trimoxazole
Antidepressant - mirtazapine
Cytotoxic drugs - methotrexate

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108
Q

Drug causes of urticaria?

A

aspirin
penicillins
NSAIDs
opiates

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109
Q

How often should statins be monitored?

A

LFTs at baseline, 3 months and 12 months

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110
Q

How should amiodarone be monitored?

A

TFT, LFT, U&E, CXR prior to treatment
TFT, LFT every 6 months

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111
Q

How should methotrexate be monitored?

A

‘FBC and renal and LFTs before starting treatment and repeated weekly until therapy stabilised, thereafter patients should be monitored every 2-3 months’

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112
Q

How should azathioprine be monitored?

A

FBC, LFT before treatment
FBC weekly for the first 4 weeks
FBC, LFT every 3 months

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113
Q

How often should lithium levels be monitored?

A

TFT, U&E prior to treatment
Lithium levels weekly until stabilised then every 3 months
TFT, U&E every 6 months

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114
Q

Drugs that impair glucose tolerance?

A

thiazides, furosemide (less common)
steroids
tacrolimus, ciclosporin
interferon-alpha
nicotinic acid
antipsychotics

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115
Q

Drugs that cause thrombocytopenia?

A

quinine
abciximab
NSAIDs
diuretics: furosemide
antibiotics: penicillins, sulphonamides, rifampicin
anticonvulsants: carbamazepine, valproate
heparin

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116
Q

Drugs that cause urinary retention ?

A

tricyclic antidepressants e.g. amitriptyline
anticholinergics e.g. antipsychotics, antihistamines
opioids
NSAIDs
disopyramide

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117
Q

What drug is an agonist of Alpha receptors?

A

Alpha-1: Decongestants (e.g. phenylephrine/oxymetazoline)
Alpha-2: Glaucoma (e.g. topical brimonidine)

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118
Q

What drug is an antagonist of Alpha receptors?

A

Benign prostatic hyperplasia (e.g. tamsulosin)
Hypertension (e.g. doxazosin)

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119
Q

What drug is an agonist of Beta 1 receptors?

A

Dobutamine

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120
Q

What drug is a antagonist of Beta 1 receptors?

A

Non-selective & selective beta-blockers (e.g. atenolol, bisoprolol)

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121
Q

What drug is agonist of Beta 2 receptors?

A

Bronchodilators (e.g. salbutamol)

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122
Q

What drug is an antagonist of Beta 2?

A

Non-selective beta-blockers (e.g. propranolol, labetalol)

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123
Q

What drug is an agonist of dopamine receptor?

A

Parkinson’s disease (e.g. ropinirole)
Prolactinoma

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124
Q

What drug is a dopamine antagonist?

A

Schizophrenia (antipsychotics e.g. haloperidol)
Anti-emetics (e.g. metoclopramide/domperidone)

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125
Q

GABA agonist?

A

BZD
Baclofen

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126
Q

GABA antagonist?

A

Flumazenil

127
Q

Muscaranic agonist?

A

Pilocarpine (Glaucoma)

128
Q

Muscarinic antagonist?

A

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

129
Q

Nicotinic agonist?

A

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

130
Q

Nicotinic antagonist?

A

Non-depolarising muscle relaxants (e.g. atracurium)

131
Q

Serotonin agonist?

A

Triptans

132
Q

Serotonin antagonist?

A

pizotifen is a 5-HT2 receptor antagonist used in the prophylaxis of migraine attacks. Methysergide is another antagonist of the 5-HT2 receptor but is rarely used due to the risk of retroperitoneal fibrosis
cyproheptadine is a 5-HT2 receptor antagonist which is used to control diarrhoea in patients with carcinoid syndrome
ondansetron is a 5-HT3 receptor antagonist and is used as an antiemetic

133
Q

Drugs that cause lung fibrosis?

A

Amiodarone
Cytotoxic agents: busulphan, bleomycin
Anti-rheumatoid drugs: methotrexate, Sulfasalazine
Nitrofurantoin
Ergot-derived dopamine receptor Agonists (bromocriptine, cabergoline, pergolide)

134
Q

Drugs that cause cataracts?

A

Steroids

135
Q

Drugs that cause corneal opacity?

A

amiodarone
indomethacin

136
Q

Drugs that cause optic neuritis?

A

ethambutol
amiodarone
metronidazole

137
Q

Drugs that cause retinopathy?

A

chloroquine, quinine

138
Q

What is ecstasy?

A

MDMA, 3,4-Methylenedioxymethamphetamine)

139
Q

What is the mechanism of MDMA?

A

MDMA is a potent releaser and/or reuptake inhibitor of presynaptic serotonin (5-HT), dopamine (DA), and norepinephrine (NE)

140
Q

What are the clinical features of MDMA?

A

neurological: agitation, anxiety, confusion, ataxia
cardiovascular: tachycardia, hypertension
hyponatraemia
hyperthermia
rhabdomyolysis

141
Q

Features of ethylene glycol poisoning?

A

Stage 1: symptoms similar to alcohol intoxication: confusion, slurred speech, dizziness
Stage 2: metabolic acidosis with high anion gap and high osmolar gap. Also tachycardia, hypertension
Stage 3: acute kidney injury

142
Q

Treatment ethylene glycol?

A

fomepizole, an inhibitor of alcohol dehydrogenase, is now used first-line in preference to ethanol

Haemodialysis in refractory cases

143
Q

What is the mechanism of finasteride?

A

inhibitor of 5 alpha-reductase, an enzyme which metabolises testosterone into dihydrotestosterone.

144
Q

Side effects of finasteride?

A

Adverse effects
impotence
decrease libido
ejaculation disorders
gynaecomastia and breast tenderness

145
Q

What is the mechanism of flecanide?

A

class 1c antiarrhythmic
sodium channel blocker (specifically the Nav1.5 sodium channels)

146
Q

Indications for flecanide?

A

atrial fibrillation
SVT associated with accessory pathway e.g. Wolf-Parkinson-White syndrome

147
Q

Contraindications of flecanide?

A

post myocardial infarction
structural heart disease: e.g. heart failure
sinus node dysfunction; second-degree or greater AV block
atrial flutter

148
Q

Adverse effects of flecanide?

A

negatively inotropic
bradycardia
proarrhythmic
oral paraesthesia
visual disturbances

149
Q

What is a contraindication for gentamicin?

A

MYASTHENIA GRAVIS

150
Q

What drugs can be cleared through haemodialysis?

A

Barbiturate
Lithium
Alcohol (inc methanol, ethylene glycol)
Salicylates
Theophyllines (charcoal haemoperfusion is preferable)

151
Q

What drugs cannot be cleared by haemodialysis?

A

tricyclics
benzodiazepines
dextropropoxyphene (Co-proxamol)
digoxin
beta-blockers

152
Q

Mechanism of unfractionated heparin?

A

Forms a complex which inhibits thrombin, factors Xa, IXa, XIa and XIIa

153
Q

Mechanism of LMWH?

A

increases the action of antithrombin III on factor Xa

154
Q

Side effects of unfractionated heparin?

A

Osteoporosis
Bleeding
Heparin-induced thrombocytopaenia (HIT)

155
Q

How should unfractionated heparin be monitored?

A

APTT

156
Q

Side effects of LMWH heparin?

A

Lower risk of HIT and osteoporosis with LMWH

157
Q

How is LMWH monitored?

A

Anti-Xa level
Not routinely measured

158
Q

When should unfractionated heparin be considered?

A

Useful in situations where there is a high risk of bleeding as anticoagulation can be terminated rapidly. Also useful in renal failure

159
Q

What mediated heparin induced thrombocytopenia?

A

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

Features:
DESPITE LOW PLATELETS IS PROTHROMBOTIC
- 50% reduction in platelets, thrombosis and skin allergy

160
Q

How should patient be anti coagulated in HIT ?

A

direct thrombin inhibitor e.g. argatroban
danaparoid

161
Q

How should heparin and LMWH be reversed?

A

Protamine

162
Q

Mechanism of statins?

A

HMG CoA reductase inhibitors

163
Q

Mechanism of ezetimibe?

A

Cholesterol absorption inhibitor

Decreases cholesterol absorption in the small intestine

164
Q

Mechanism of nicotinic acid?

A

Decreases hepatic VLDL secretion

165
Q

Mechanism of fibrates?

A

Agonist of PPAR-alpha therefore increases lipoprotein lipase expression

166
Q

Mechanism of cholestryamine?

A

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

167
Q

Causes of hypomagnesaemia?

A

drugs
- diuretics
- proton pump inhibitors
-total parenteral nutrition
diarrhoea
alcohol
hypokalaemia
hypercalcaemia
- calcium and magnesium functionally compete for transport in the thick ascending limb of the loop of Henle
metabolic disorders
Gitleman’s and Bartter’s

168
Q

What are features of hypomagnesaemia?

A

paraesthesia
tetany
seizures
arrhythmias
decreased PTH secretion → hypocalcaemia
ECG features similar to those of hypokalaemia
exacerbates digoxin toxicity

169
Q

Management of magnesium < 0.4?

A

intravenous magnesium replacement is commonly given.
an example regime would be 40 mmol of magnesium sulphate over 24 hours

170
Q

Indications to use immunoglobulin?

A

primary and secondary immunodeficiency
idiopathic thrombocytopenic purpura
myasthenia gravis
Guillain-Barre syndrome
Kawasaki disease
toxic epidermal necrolysis
pneumonitis induced by CMV following transplantation
low serum IgG levels following haematopoietic stem cell transplant for malignancy
dermatomyositis
chronic inflammatory demyelinating polyradiculopathy

171
Q

What are the features of an IVIG infusion?

A

formed from large pool of donors (e.g. 5,000)
IgG molecules with a subclass distribution similar to that of normal blood
half-life of 3 weeks

172
Q

What precipitates lithium toxicity?

A

dehydration
renal failure
drugs: diuretics (especially thiazides), ACE inhibitors/angiotensin II receptor blockers, NSAIDs and metronidazole.

173
Q

What are the features of lithium toxicity?

A

coarse tremor (a fine tremor is seen in therapeutic levels)
hyperreflexia
acute confusion
polyuria
seizure
coma

174
Q

Mnx of lithium toxicity?

A

mild-moderate toxicity: Saline
Severe toxicity: Haemodialysis

175
Q

How is lidocaine metabolised?

A

Hepatic

176
Q

Mechanism of action of lidocaine?

A

Sodium channel blocker

177
Q

How is local anaesthetic toxicity treated?

A

20% lipid emulsion

178
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.

179
Q

What is the maximum dose of lignocaine ?

A

3mg/Kg plain
With adrenaline 7mg/Kg

180
Q

Side effects of macrolides?

A

Prolongation of the QT interval

Gastrointestinal side-effects are common. Nausea is less common with clarithromycin than erythromycin

Cholestatic jaundice: risk may be reduced if erythromycin stearate is used

P450 inhibitor (see below)
azithromycin is associated with hearing loss and tinnitus

181
Q

What are common interactions with macrolides?

A

statins should be stopped whilst taking a course of macrolides. Macrolides inhibit the cytochrome P450 isoenzyme CYP3A4 that metabolises statins.

increases the risk of myopathy and rhabdomyolysis.

182
Q

What are the features of mercury poisoning?

A

visual field defects
hearing loss
irritability
renal tubular acidosis

183
Q

What is the mechanism of inflixmab? What is it used in?

A

Anti-TNF

Rheumatoid
Crohn’s disease

184
Q

What is the mechanism of rituximab? What is it used in?

A

CD20

Non-hodgkin lymphoma
Rheumatoid arthritis

185
Q

What is the mechanism of cetuximab?
What is it used in?

A

EGFR

Metastatic colorectal cancer
Head and neck cancer

186
Q

What is the mechanism of trastuzumab?
What is it used in?

A

HER2

Metastatic breast cancer

187
Q

What is the mechanism of almetuzumab?
What is it used in?

A

CD52

CLL

188
Q

What is the mechanism of abciximab?

A

glycoprotein IIb/IIIa receptor antagonist

prevention of ischaemic events in patients undergoing percutaneous coronary interventions

189
Q

what is the mechanism of OKT3

A

(anti-CD3)

used to prevent organ rejection

190
Q

What type of drug is metformin?
Mechanism of action?

A

Biguanide

Acts by activation of the AMP-activated Protein kinase (AMPK)
Increases insulin sensitivity
Decreases hepatic gluconeogenesis
may also reduce gastrointestinal absorption of carbohydrates

191
Q

Side effects of metformin?

A

Gastrointestinal upsets are common (nausea, anorexia, diarrhoea),
Reduced vitamin B12 absorption - rarely a clinical problem
Lactic acidosis with severe liver disease or renal failure

192
Q

Contraindications to metformin?

A

Chronic kidney disease
- stopped if the creatinine is > 150 µmol/l (or eGFR < 30 ml/min)

Recent MI, AKI, Sepsis - increased lactic acidosis

iodine-containing x-ray contrast media

alcohol abuse is a relative contraindication

192
Q

Contraindications to metformin?

A

Chronic kidney disease
- stopped if the creatinine is > 150 µmol/l (or eGFR < 30 ml/min)

Recent MI, AKI, Sepsis - increased lactic acidosis

iodine-containing x-ray contrast media

alcohol abuse is a relative contraindication

193
Q

Features of methanol poisoning?
Mnx?

A

Alcohol intox
Blindness
High anion gap

Mnx:
fomepizole (competitive inhibitor of alcohol dehydrogenase) or ethanol
haemodialysis
cofactor therapy with folinic acid to reduce ophthalmological complications

194
Q

What is an example of a depolarising neuromuscular blocker?

A

Suxamethonium

195
Q

Examples of depolarising neuromuscular blockers?

A

Atracurium
Vecuronium
Pancuronium

196
Q

What are the adverse effects of suxamethonium?

A

hyperkalaemia, malignant hyperthermia and lack of acetylcholinesterase

197
Q

What can reuse some non-depolarising neuromuscular blockers?

A

Neostigamine

Atracurium - full reversal
Vecuronium - full reversal
Pancuronium - partial reversal

198
Q

What is the mechanism of ocreotide?

A

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

199
Q

What is ocreotide used for?

A

acute treatment of variceal haemorrhage
acromegaly
carcinoid syndrome
prevent complications following pancreatic surgery
VIPomas
refractory diarrhoea

200
Q

What is a side effect of ocreotide?

A

gallstones (secondary to biliary stasis)

201
Q

What is an oculogyric crisis?

A

restlessness, agitation
involuntary upward deviation of the eyes

202
Q

Causes of oculogyric crisis?

A

antipsychotics
metoclopramide
postencephalitic Parkinson’s disease

203
Q

What is the management of oculogyric crisis?

A

intravenous antimuscarinic: benztropine or procyclidine

204
Q

What is the mechanism of organophosphate poisoning?

A

Organophosphate poisoning is inhibition of acetylcholinesterase leading to upregulation of nicotinic and muscarinic cholinergic neurotransmission

205
Q

What are the features of organophosphate poisoning?

A

Accumulation of acetylcholine

SLUD

Salivation
Lacrimation
Urination
Defecation/diarrhoea

cardiovascular:
hypotension bradycardia
also: small pupils, muscle fasciculation

206
Q

Management of organophosphate poisoning?

A

Atropine

207
Q

Management of paracetamol overdose?

A

activated charcoal if ingested < 1 hour ago
N-acetylcysteine (NAC)
liver transplantation

208
Q

Management of salicylate poisoning?

A

Within in 1 hour - activated charcoal
urinary alkalinization with IV bicarbonate
haemodialysis

209
Q

BZD overdose reversal?

A

Flumazenil

210
Q

Management of tricyclic antidepressant overdose?

A

IV bicarbonate may reduce seizure and arrhythmias
Priority to treat acidosis

Can consider lignocaine - other arrhythmias not used, due to QT prolongation

211
Q

Heparin overdose reversal?

A

Protamine

212
Q

Iron overdose mnx?

A

Desferrioxamine, a chelating agent

213
Q

Lead poisoning mnx?

A

Dimercaprol, calcium edetate

214
Q

Cyanide poisoning mnx?

A

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

215
Q

Inducers of P450?

A

antiepileptics: phenytoin, carbamazepine
barbiturates: phenobarbitone
rifampicin
St John’s Wort
chronic alcohol intake
griseofulvin
smoking (affects CYP1A2, reason why smokers require more aminophylline)

216
Q

Inhibitors of P450?

A

antibiotics: ciprofloxacin, erythromycin
isoniazid
cimetidine,omeprazole
amiodarone
allopurinol
imidazoles: ketoconazole, fluconazole
SSRIs: fluoxetine, sertraline
ritonavir
sodium valproate
acute alcohol intake
quinupristin

p450 Inhibitor Mnemonic: CCOAAATS

217
Q

When should N-acetylcystine for paracetamol overdose?

A
  • Paracetamol level of 100mg at 4 hours
  • Staggered overdose (taken over more than one hour)
  • After 8-24 hours if > 150 mg
  • > 24 hours if they are clearly jaundiced or have hepatic tenderness, their ALT is above the upper limit of norma
218
Q

Criteria for liver transplant in paracetamol?

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

219
Q

What is the normal metabolism of paracetamol?

A

conjugates paracetamol with glucuronic acid/sulphate
conjugation system becomes saturated leading to oxidation by P450 mixed function oxidases
Produces toxic metabolite N-acetyl-B-benzoquinone imine
glutathione acts as a defence mechanism by conjugating with the toxin forming the non-toxic mercapturic acid
Glutathione used up - toxin forms covalent bonds with cell proteins,
Affects kidney tubules and liver

220
Q

What is n-acetylcycstine?

A

A precursor of glutathione

221
Q

What percentage of people of penicillin allergic patients are cephalosporin allergic?

A

0.5% - 6.5%

222
Q

What is first order kinetics?

A

the rate of drug elimination is proportional to drug concentration

223
Q

What is zero orders kinetics?

A

rate of excretion is constant despite changes in plasma concentration, this is due to saturation of the metabolic process

e.g. salicylates, phenytoin

224
Q

What are phases of metabolism?

A

phase I reactions: oxidation, reduction, hydrolysis.
Phase II conjugation

225
Q

What is first pass metabolism? What drugs go through first pass metabolism?

A

phenomenon where the concentration of a drug is greatly reduced before it reaches the systemic circulation due to hepatic metabolism.
Consequences need larger doses orally

226
Q

Mechanism of phosphodiesterase inhibitor?

A

PDE5 inhibitors cause vasodilation through an increase in cGMP leading to smooth muscle relaxation in blood vessels supplying the corpus cavernosum.

227
Q

Side effect of sildenafil ?

A

The blue pill, Viagra (sildenafil), causes blue discolouration of vision

228
Q

Contraindication to sildenafil?

A

patients taking nitrates and related drugs such as nicorandil
hypotension
recent stroke or myocardial infarction (NICE recommend waiting 6 months)

229
Q

Side effects of sildenafil?

A

visual disturbances
blue discolouration
non-arteritic anterior ischaemic neuropathy
nasal congestion
flushing
gastrointestinal side-effects
headache
priapism

230
Q

Types of potassium sparing diuretics?

A

Epithelial sodium channel blockers
- amiloride and triamterene

Aldosterone antagonists

231
Q

What is the mechanism of amiloride?

A

blocks the epithelial sodium channel in the distal convoluted tubule

232
Q

What drugs should be prescribed with caution in heart failure?

A

Thiazolidinediones - fluid retention
Verapamil - negative inotropic
NSAID / steroids - fluid
Class 1 antiarrhythmics - proarrythmic

233
Q

Advantages of progesterone pill?

A

can be used whilst breast-feeding
can be used in situations where the combined oral contraceptive pill is contraindicated e.g. in smokers > 35 years of age and women with a history of venous thromboembolic disease

234
Q

Disadvantages of progesterone pill?

A

irregular periods: some users may not have periods whilst others may have irregular or light periods. This is the most common adverse effect
increased incidence of functional ovarian cysts
common side-effects include breast tenderness, weight gain, acne and headaches. These symptoms generally subside after the first few months

235
Q

What is cinchonism?

A

Quinine toxicity

Cardiac arrhythmia
Hypoglycaemia
Tinnitus
visual blurring, flushed and dry skin and abdominal pain.

236
Q

What are features of salicylate overdose?

A

hyperventilation (centrally stimulates respiration)
tinnitus
lethargy
sweating, pyrexia*
nausea/vomiting
hyperglycaemia and hypoglycaemia
seizures
coma

237
Q

Treatment of salicylate overdose?

A

general (ABC, charcoal)
urinary alkalinization with intravenous sodium bicarbonate - enhances elimination of aspirin in the urine
haemodialysis

238
Q

what are indications for haemodilaysis in salicylate overdose?

A

serum concentration > 700mg/L
metabolic acidosis resistant to treatment
acute renal failure
pulmonary oedema
seizures
coma

239
Q

Mechanism of quinolones?

A

inhibit topoisomerase II (DNA gyrase) and topoisomerase IV

240
Q

What are adverse effects of 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

241
Q

Causes of serotonin syndrome?

A

monoamine oxidase inhibitors
SSRIs
St John’s Wort, often taken over the counter for depression, can interact with SSRIs to cause serotonin syndrome
tramadol may also interact with SSRIs
ecstasy
amphetamines

242
Q

Features of serotonin syndrome?

A

neuromuscular excitation
hyperreflexia
myoclonus
rigidity
autonomic nervous system excitation
hyperthermia
sweating
altered mental state
confusion

243
Q

Mnx of serotonin syndrome?

A

supportive including IV fluids
benzodiazepines
more severe cases are managed using serotonin antagonists such as cyproheptadine and chlorpromazine

244
Q

Difference between serotonin syndrome and neuroleptic malignant syndrome?

A
245
Q

Side effects of CCB?

A

• Headache
• Flushing
• Ankle oedema

Verapamil also commonly causes constipation

246
Q

Side effect of beta blockers?

A

• Bronchospasm (especially in asthmatics)
• Fatigue
• Cold peripheries
• Sleep disturbances

247
Q

Side effect of nitrates?

A

Headache
• Postural hypotension
• Tachycardia

248
Q

Side effect of nicorandil?

A

• Headache
• Flushing
• Anal ulceration

249
Q

Side effects of metformin?

A

Gastrointestinal side-effects
Lactic acidosis

250
Q

Side effects of sulphurylurea?

A

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

251
Q

Side effect of glitazones?

A

Weight gain
Fluid retention
Liver dysfunction
Fractures

252
Q

Side effect of gliptans?

A

Pancreatitis

253
Q

Mechanism of 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
this contrasts with ciclosporin, which binds to cyclophilin rather than FKBP

254
Q

Side effect tacrolimus

A

nephrotoxicity and impaired glucose tolerance

Tacrolimus more potent than cyclosporin

255
Q

How long should tamoxifen be used post tumour removal?

Side effects?

A

5 years

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

256
Q

Mechanism of tamoxifen?

A

Selective oEstrogen Receptor Modulator (SERM) which acts as an oestrogen receptor antagonist and partial agonist.

257
Q

teratogenic effect of ACEI?

A

Renal dysgenesis
Craniofacial abnormalities

258
Q

teratogenic effect of alcohol?

A

Craniofacial abnormalities

259
Q

teratogenic effect of ahminoglycosides?

A

Ototoxicity

260
Q

teratogenic effect of a carbamazepine?

A

Neural tube defects
Craniofacial abnormalities

261
Q

teratogenic effect chloramphenicol?

A

grey baby syndrome

262
Q

teratogenic effect o f cocaine?

A

Intrauterine growth retardation
Preterm labour

263
Q

teratogenic effect of lithium

A

Ebstein’s anomaly (atrialized right ventricle)

264
Q

effect of maternal diabetes on baby?

A

Macrosomia
Neural tube defects
Polyhydramnios
Preterm labour
Caudal regression syndrome

265
Q

teratogenic effect of tetracyclines?

A

discoloured teeth

266
Q

teratogenic effect of thalidomide?

A

Limb reduction defects

267
Q

teratogenic effect of valproate?

A

Neural tube defects
Craniofacial abnormalities

268
Q

teratogenic effect of warfarin?

A

craniofacial abnormalities

269
Q

Mechanism of action of rifampicin?

A

mechanism of action: inhibits bacterial DNA dependent RNA polymerase preventing transcription of DNA into mRNA

270
Q

Side effects of rifampicin?

A

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

271
Q

Side effects of isoniazid?

A

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

272
Q

Side effects of pyrazinamide?

A

hyperuricaemia causing gout
arthralgia, myalgia
hepatitis

273
Q

Side effects of ethambutol?

A

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

274
Q

What type of receptor does thyroxine work on?

A

Nuclear receptor

275
Q

what type of antibiotic is teicoplanin?

A

Glycopeptide

276
Q

What drugs need to be avoided in G6PD?

A

anti-malarials: primaquine
ciprofloxacin
sulph- group drugs: sulphonamides, sulphasalazine, sulfonylureas

277
Q

What is the mechanism of nephrotoxicity in gentamicin?

A

Tubule necrosis

278
Q

Choice of antiemetics in motion sickness?

A

hyoscine > cyclizine > promethazine

279
Q

How are monoclonal antibodies made?

A
  1. Somatic hybridisation
  2. Fusion of mouse spleen with myeloma
  3. Forms hybridoma
  4. Mouse cells are antigenic - requires humanising
    -involves combining the variable region from the mouse body with the constant region from a human antibody.
280
Q

What drugs affect acetylator status?

A

isoniazid
procainamide
hydralazine
dapsone
sulfasalazine

interacts with hepatic N-acetyltransferase
Important for Phase II of drug metabolism - conjugation

281
Q

Timing of lithium dose level?

A

12 hour post dose

282
Q

Timing of ciclosporin dose level?

A

Trough level immediately before dose?

283
Q

Timing of digoxin post dose?

A

6 hour post dose

284
Q

What is the most useful prognostic marker for paracetamol overdose?

A

Prothrombin time

285
Q

What are the outcomes of phase I and phase II metabolism?

A

Products of phase I reactions are typically more active and potentially toxic
Products are typically inactive and excreted in urine or bile.

286
Q

If patient cannot tolerate metformin, what should you do?

A

Try modified release metformin

287
Q

What should be completed prior to starting trastuzumab?

A

Echo

288
Q

How high can carboxyhaemglobin be in smokers?

A

Up to 15%

289
Q

What diabetic drugs can cause SIADH?

A

Sulphonylureas (particularly long-acting ones such as chlorpropamide) are well-established causes of the syndrome of inappropriate ADH1.

290
Q

What is the mechanism in HIT?

A

immune mediated - 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
usually does not develop until after 5-10 days of treatment

291
Q

What drugs undergo first pass metabolism?

A

aspirin
isosorbide dinitrate
glyceryl trinitrate
lignocaine
propranolol
verapamil
isoprenaline
testosterone
hydrocortisone

292
Q

Antibiotics not safe in pregnancy?

A

tetracyclines
aminoglycosides
sulphonamides and trimethoprim
quinolones: the BNF advises to avoid due to arthropathy in some animal studies

293
Q

Drugs not safe in pregnancy?

A

ACE inhibitors, angiotensin II receptor antagonists
statins
warfarin
sulfonylureas
retinoids (including topical)
cytotoxic agents

294
Q

Features of tricyclic overdose?

A

Block alpha 1

dilated pupils, dry skin, confusion, urinary retention and tachycardia. Divergent pupils are a common finding in tricyclic overdose. TCAs are also cardiotoxic by inactivating sodium channels in the heart leading to, as seen here, a potential prolongation of the QTc interval and a widened QRS complex.
Seizures
Metabolic acidosis

295
Q

What are side effects of 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

296
Q

Max of bleach ingestion?

A

NBM
IV PPI
Oesophageal dudenoscopy

297
Q

What is the effect of digoxin on QT?

A

shortens QT

298
Q

What are the features of hypomagnesaemia on ECG?

A

QT prolongation

299
Q

Why can adrenaline cause increased lactate?

A

increase in hepatic glycogenolysis and an increase in gluconeogenesis.

300
Q

Abnormally pink mucosa?

A

Carbon monoxide poisoning ?

301
Q

Mechanism of action of nivolumab?

A

PD-1
Lung cancer

side effect: hypothyroidism

302
Q

Drugs that cause photosensitivity ?

A

thiazides
tetracyclines, sulphonamides, ciprofloxacin
amiodarone
NSAIDs e.g. piroxicam
psoralens
sulphonylureas

303
Q

What should be monitored with hydroxychloquine?

A

Retinopathy

304
Q

What side effects of cyclosporin?

A

Adverse effects of ciclosporin (note how everything is increased - fluid, BP, K+, hair, gums, glucose)
nephrotoxicity
hepatotoxicity
fluid retention
hypertension
hyperkalaemia
hypertrichosis
gingival hyperplasia
tremor
impaired glucose tolerance
hyperlipidaemia
increased susceptibility to severe infection

305
Q

Features of excess Ach?

A

Diarrhoea
Urination
Miosis/muscle weakness
Bronchorrhea/Bradycardia
Emesis
Lacrimation
Salivation/sweating

306
Q

Features of quinine toxicity?

A

ECG changes, hypotension, metabolic acidosis, hypoglycaemia and classically tinnitus, flushing and visual disturbances. Flash pulmonary oedema may occur

307
Q

When is flecanide contraindicated?

A

structural heart disease or ischaemic heart disease

308
Q

What can paracetamol overdose do to the kidneys?

A

Delayed nephrotoxicity

309
Q

Effect of alcohol of hypothalamus?

A

Inhibits ADH secretion

310
Q

phosphodiesterase inhibitor side effects?

A

visual disturbances
blue discolouration
non-arteritic anterior ischaemic neuropathy
nasal congestion
flushing
gastrointestinal side-effects
headache
priapism

311
Q

Why marcolides in gastroparesis?

A

Promotes gastric emptying

312
Q

Adrenaline induced ischaemia treatment ?

A

phentolamine

313
Q

Side effect of doselupin?

A

Cause of pulmonary fibrosis

MRCP: Pharmacology (2 decks)

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