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pharm Flashcards

1
Q

which drugs can precipitate an attack of acute intermittent porphyria?

A

barbiturates
benzodiazepines

halothane
alcohol

oral contraceptive pill
sulphonamides

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2
Q

how much adrenaline is used in different situations?

A

anaphylaxis: 0.5ml 1:1,000 IM

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

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3
Q

how is accidental adrenaline injection managed?

A

local infiltration of phentolamine

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4
Q

which drugs act as alpha 1/beta 1/2 agonists/ antagonists?

A

Alpha-1 agonists
phenylephrine

Alpha-2 agonists
clonidine

Beta-1 agonists
dobutamine

Beta-2 agonists
salbutamol

Alpha antagonists
alpha-1: doxazosin
alpha 1a:  tamsulosin - 
alpha-2: yohimbine
non-selective: phenoxybenzamine (previously used in peripheral arterial disease)

Beta antagonists
beta-1: atenolol
non-selective: propranolol

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5
Q

what do the different alpha adrenoreceptors do?

A 
Alpha-1
vasoconstriction
relaxation of GI smooth muscle
salivary secretion
hepatic glycogenolysis

Alpha-2
mainly presynaptic: inhibition of transmitter release (inc NA, Ach from autonomic nerves)
inhibits insulin
platelet aggregation

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6
Q

what do the different B adrenoreceptors do?

A

Beta-1
mainly located in the heart
increase heart rate + force

Beta-2
vasodilation
bronchodilation
relaxation of GI smooth muscle

Beta-3
lipolysis

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7
Q

what drugs can be used for alcohol addiction?

A

disulfram: promotes abstinence - alcohol intake causes severe reaction due to inhibition of acetaldehyde dehydrogenase. Patients should be aware that even small amounts of alcohol (e.g. In perfumes, foods, mouthwashes) can produce severe symptoms. Contraindications include ischaemic heart disease and psychosis
acamprosate: reduces craving, known to be a weak antagonist of NMDA receptors, improves abstinence

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8
Q

how does allopurinol work?

A

inhibiting xanthine oxidase.

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9
Q

when should allopurinol be initiated?

A

2 weeks after an attack .. thought to precipitate an attack.

after 1st attack

colchicine should be considered when using allopurinol

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10
Q

what is the dose of allopurinol?

A

initial dose of 100 mg od, with the dose titrated every few weeks to aim for a serum uric acid of < 300 µmol/l. Lower initial doses should be given if the patient has a reduced eGFR

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11
Q

what are the serious adverse effects of allopurinol?

whos at risk of this?

A

dermatological..
advised to stop immediately if they develop a rash…

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

Chinese, Korean and Thai people
HLA-B *5801 allele.

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12
Q

how does allopurinol interact with azothioprine?

A

increases effects of azothioprine

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13
Q

how does allopurinol interact with cyclophosphamide?

A

reduces renal clearance and thus increases risk of marrow toxicity of cyclophosphamide

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14
Q

how does allopurinol interact with theophylline?

A

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

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15
Q

why does amiodarone lead to hypothyroid?

A

thought to be due to the high iodine content of amiodarone causing a Wolff-Chaikoff effect

This is an autoregulatory phenomenon where thyroxine formation is inhibited due to high levels of circulating iodide

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16
Q

what are the different types of amiodarone induced thyrotoxicosis?

A

type 1

  • excess iodine induced thyroid hormone synthesis.
  • goitre
  • treat with carbimazole

type 2

  • amiodarone related destructive thyroiditis
  • treat with steroids.
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17
Q

should amiodarone be stopped if it causes thyroid dysfunction?

A

hypo - can continue if needed

hyper - should be stopped

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18
Q

how does propofol work?

A

GABA receptor agonist
Rapid onset of anaesthesia
Pain on IV injection

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19
Q

does sodium thiopentone have a slow or rapid onset of action?

A

very rapid.

often used for rapid sequence induction.

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20
Q

how does ketamine work?

A

NMDA receptor antagonist
May be used for induction of anaesthesia
Has moderate to strong analgesic properties
Produces little myocardial depression making it a suitable agent for anaesthesia in those who are haemodynamically unstable

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21
Q

which anaesthetic agents have little cardiovascular effects?

A

etomidate

ketamine

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22
Q 
What is the mechanism of class 1a antiarrhythmics? 
give examples of drugs in this class
A

Procainamid, quinidine, Disopyramide

blocks Na channels and increases AP duration

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23
Q

what is a side effect of:
quinidine
procainamide?

A

quinidine - headache, tinnititus, thrombocytopenia

procainamide - drug induced lupus

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24
Q 
What is the mechanism of class 1b antiarrhythmics? 
give examples of drugs in this class
A

blocks Na channels and decreases AP duration
Lidocaine
Mexiletine
Tocainide

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25
Q 
What is the mechanism of class 1c antiarrhythmics? 
give examples of drugs in this class
A

blocks Na channel , no effect on AP duration
Flecainide
Encainide
Propafenone

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26
Q

What is the mechanism of class II antiarrhythmics?

A

B blockers

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27
Q 
What is the mechanism of class III antiarrhythmics? 
give examples.
A 
K+ channel blockers
miodarone
Sotalol
Ibutilide
Bretylium
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28
Q 
What is the mechanism of class IV antiarrhythmics? 
give examples.
A

Ca CB
Verapamil
Diltiazem

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29
Q

which antibiotics effect cell wall synthesis?

A

peptidoglycan cross linking: carbopenems, penicillin, cephalosporins

peptidoglycan synthesis: glycopeptides e.g vancomycin

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30
Q

which antibiotics affect protein synthesis?

A

30S subunit: aminoglycosides, tetracyclines

50S: macrolides, chloramphenicol, clindamycin, linezolid, streptogrammins

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31
Q

what anitbiotics affect DNA?

A

DNA topoisomerase - Quinolones

damages DNA - metronidazole

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32
Q

which antibiotic effects RNA polymerase?

A

rifampicin

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33
Q

which antibiotics affect folate synthesis?

A

dihydrofolate reductase: trimethroprim

dihydroptorate synthase : sulphonamides

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34
Q

how does aspirin work?

A

blocking the action of both cyclooxygenase-1 and 2.

Cyclooxygenase is responsible for prostaglandin, prostacyclin and thromboxane synthesis.

The blocking of thromboxane A2 formation in platelets reduces the ability of platelets to aggregate

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35
Q

which drugs potentiate aspirin?

A

warfarin
steroids
oral hypoglycaemics

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36
Q

what age is aspirin contraindicated?

A

Aspirin should not be used in children under 16 due to the risk of Reye’s syndrome. An exception is Kawasaki disease, where the benefits are thought to outweigh the risks.

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37
Q

what are the features of a B blocker overdose?

A

bradycardia
hypotension
heart failure
syncope

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38
Q

how is B blocker overdose managed?

A

atropine for bradycardia

if resistant - glucagon

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39
Q

what are the two groups of CaCB?

A

mainly affects on myocardium - diltiazam and verapamil

mainly affects on peripheral blood - Nifedipine, amlodipine, felodipine

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40
Q

what are the indications/use of verapamil?

A

Angina, hypertension, arrhythmias

Highly negatively inotropic

Should not be given with beta-blockers as may cause heart block

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41
Q

what are the indications/use of diltiazam?

A

Angina, hypertension

Less negatively inotropic than verapamil but caution should still be exercised when patients have heart failure or are taking beta-blockers

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42
Q

what are indications/ use of Nifedipine, amlodipine, felodipine

A

HTN, raynauds, angina

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43
Q

what are the side effects of CaCB?

A

verapamil: Heart failure, constipation, hypotension, bradycardia, flushing
diltiazam: Hypotension, bradycardia, heart failure, ankle swelling

amlodipine etc: Flushing, headache, ankle swelling

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44
Q

what is the pathogenesis behind carbon monoxide poisoning?

A

has high affinity for Hb and myoglobin therefore left shift in dissociation curve - tissue hypoxia

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45
Q

what are the features of carbon monoxide toxicity?

A 
headache: 90% of cases
nausea and vomiting: 
vertigo: 
confusion: 
subjective weakness
severe toxicity: 'pink' skin and mucosae, hyperpyrexia, arrhythmias, extrapyramidal features, coma, death
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46
Q

what Ix is useful / not useful for CO poisoning?

A

pulse oximetry - unreliable, will be high as carboxyHb gives same as oxyHb

blood gas - reliable.

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47
Q

how is carbon monoxide poisoning managed?

A

high flow O2
target sats 100%
for atleast 6 hours
until symptoms have resolved

hyperbaric chamber

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48
Q

what are the indications of using a hyperbaric O2 chamber?

A

CO poisoning AND…. loss of consciousness at any point, neurological signs other than headache, myocardial ischaemia or arrhythmia and pregnancy as indications for hyperbaric oxygen

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49
Q

what is the mechanism of cyclosporin?

A

immunosuppressant which 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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50
Q

what are the ADRs of cyclosporin?

A

nephrotoxicity
hepatotoxicity

fluid retention
hypertension
hyperkalaemia

hypertrichosis - hair growth
gingival hyperplasia
tremor

impaired glucose tolerance
hyperlipidaemia
increased susceptibility to severe infection

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51
Q

when might ciclosporin be indicated?

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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52
Q

how does cocaine work?

A

cocaine blocks the uptake of dopamine, noradrenaline and serotonin

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53
Q

what are the cardiovascular effects of cocaine?

A

coronary artery spasm → myocardial ischaemia/infarction
both tachycardia and bradycardia may occur
hypertension
QRS widening and QT prolongation
aortic dissection

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54
Q

what are the neuro effects of cocaine?

A

seizures
mydriasis
hypertonia
hyperreflexia

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55
Q

other than neuro/ CVS effects, what are the other S.E of cocaine?

A

ischaemic colitis
hyperthermia
metabolic acidosis
rhabdomyolysis

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56
Q

how is cocaine toxicity managed?

A

benzodiazepines are generally first-line for most cocaine-related problems

chest pain: benzodiazepines + glyceryl trinitrate.

hypertension: benzodiazepines + sodium nitroprusside
the use of beta-blockers in cocaine-induced cardiovascular problems is a controversial issue.

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57
Q

what are the contrainidication of COCPs?

A

relative - probably not worth the risk if…
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

absolute:
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

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58
Q

what risk should women taking COCP be warned of?

A

only effective if taken correctly,
risk of blood clots
risk of cervical and breast ca
small risk of heart attack and stroke

may not be effective if on rifampicin or suffering from diarrhoea/vomitting.

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59
Q

what is the mechanism of cyanide poisoning?

A

Cyanide may be used in insecticides, photograph development and the production of certain metals.

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

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60
Q

what are the symptoms of cyanide poisoning?

A

classical’ features: brick-red skin, smell of bitter almonds

acute: hypoxia, hypotension, headache, confusion
chronic: ataxia, peripheral neuropathy, dermatitis

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61
Q

how is cyanide poisoning managed?

A

100% O2
definitive: hydroxocobalamin (intravenously), also combination of amyl nitrite (inhaled), sodium nitrite (intravenously), and sodium thiosulfate (intravenously)

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62
Q

how does digoxin work?

A

decreases conduction through the atrioventricular node which slows the ventricular rate in atrial fibrillation and flutter
increases the force of cardiac muscle contraction due to inhibition of the Na+/K+ ATPase pump. Also stimulates vagus nerve
digoxin has a narrow therapeutic index

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63
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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64
Q

what are the precipitating factors for digoxin toxicity?

A

classically: hypokalaemia
digoxin normally binds to the ATPase pump on the same site as potassium. Hypokalaemia → digoxin more easily bind to the ATPase pump → increased inhibitory effects

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

drugs: amiodarone, quinidine, verapamil, diltiazem, spironolactone (competes for secretion in distal convoluted tubule therefore reduce excretion), ciclosporin. Also drugs which cause hypokalaemia e.g. thiazides and loop diuretics

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65
Q

how is digoxin toxicity managed?

A

Digibind
correct arrhythmias
monitor potassium

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66
Q

what is DRESS syndrome?

A

DRESS is an unexpected, severe reaction to medication. Several organs are affected including the skin, liver, kidneys, lungs and heart.

Patients develop a morbilliform skin rash in 80% cases which often leads to an exfoliative dermatitis, high fever, and inflammation of one or more organs.
Vesicles and bullae may be seen. Erythroderma can occur, mucosal involvement and facial swelling. The reaction usually occurs 2-8 weeks after commencing the offending drug.

May develop systematic symptoms

  • haematological abnormalities (raised and low white count, eosinophilia, thrombocytopaenia, anaemia,
  • enlarged lymph nodes
  • kidney disease
  • myocarditis, pericarditis,
  • liver enlargement, hepatitis and rarely hepatic necrosis with liver failure
  • lung disease (pneumonitis, pleuritis, pneumonia),
  • neurological involvement which may lead to meningitis and encephalitis
  • gastrointestinal symptoms, in severe cases, acute colitis and pancreatitis can occur
  • endocrine abnormalities may include thyroiditis and diabetes.
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67
Q

what drugs can commonly cause DRESS syndrome?

A

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

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68
Q

what is RegiSCAR diagnostic criteria for DRESS?

A

Patients require at least 3 of the following:
Hospitalisation
Reaction suspected to be drug related
Acute skin rash
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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69
Q

how can DRESS syndrome be diagnosed?

A

Skin biopsy can help to confirm the diagnosis.
This may show inflammatory infiltrate in particularly eosinophils, extravasated erythrocytes and oedema.

Regular blood tests
Investigations looking for complications should be undertaken including ECG, CXR, echocardiogram, and urinalysis.

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70
Q

how is DRESS syndrome managed?

A

Antihistamines, topical steroids and emollients can be used to help control the rash.

Careful fluid balance

Systemic steroids may be started in severe cases where exfoliative dermatitis / pneumonitis / hepatitis is present.

Occasionally immunosuppressants, intravenous immunoglobulin and plasmapheresis may be started. Potential culprit drugs should not be restarted again.

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71
Q

when are dopamine receptor agonists indicated?

A

Parkinson’s disease
prolactinoma/galactorrhoea
cyclical breast disease
acromegaly

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72
Q

give examples of dopamine receptor agonists…

A

e.g. bromocriptine, ropinirole, cabergoline, apomorphine

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73
Q

what are the side effects of dopamine receptor agonists?

A

ergot-derived dopamine receptor agonists (bromocriptine, cabergoline) have been associated with pulmonary, retroperitoneal and cardiac fibrosis.
ESR, creatinine and chest x-ray should be obtained prior to treatment and patients should be closely monitored

nausea/vomiting
postural hypotension
hallucinations
daytime somnolence

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74
Q

which drugs cause agranulocytosis?

A

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

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75
Q

what are the most common drugs that can cause urticaria?

A

aspirin
penicillins
NSAIDs
opiates

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76
Q

For the following drugs what is the monitoring regimes..

a) statins
b) ACEi
c) amiodarone

A

statins LFTs - at baseline, 3 months, 12 months

ACIi - U&Es - prior to treatment, after increasing dose, atleast annually after that.

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

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77
Q

For the following drugs what is the monitoring regimes..

a) methotrexate
b) azothioprine

A

methotrexate: FBC, UEs, LFTs before starting treatment and repeated weekly until therapy stabilised, thereafter patients should be monitored every 2-3 months

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

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78
Q

For the following drugs what is the monitoring regimes..

a) lithium
b) sodium valproate
c) glitazones

A

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

sodium valproate: LFT, FBC before treatment
LFT ‘periodically’ during first 6 months

glitazones: LFT before treatment
LFT ‘regularly’ during treatment

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79
Q

which drugs can impair glucose tolerance?

A 
thiazides
steroids
tacrolimus, ciclosporin
interferon-alpha
nicotinic acid
antipsychotics

B blockers too slightly

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80
Q

which drugs can induce thrombocytopenia?

A

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

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81
Q

which drugs can induce urinary retention?

A 
tricyclic antidepressants e.g. amitriptyline
anticholinergics
opioids
NSAIDs
disopyramide
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82
Q

which drugs cause lung fibrosis?

A

amiodarone
cytotoxic agents: busulphan, bleomycin
anti-rheumatoid drugs: methotrexate, sulfasalazine
nitrofurantoin
ergot-derived dopamine receptor agonists (bromocriptine, cabergoline, pergolide)

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83
Q

which drugs can cause optic neuritis?

A

ethambutol
amiodarone
metronidazole

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84
Q

what can steroids do to the eyes?

A

cataractss

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85
Q

which drugs can induce photosensitivity?

A 
thiazides
amiodarone
tetracyclines, sulphonamides, ciprofloxacin
NSAIDs e.g. piroxicam
psoralens
sulphonylureas
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86
Q

which drugs act on serotonin receptors?

A

sumatriptan is a 5-HT1D receptor agonist

ergotamine is a partial agonist of 5-HT1 receptors

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

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87
Q

what are the features of ecstasy toxicity?

A

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

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88
Q

how is ecstacy toxicity managed?

A

supportive

dantrolene can be used for hyperthermia

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89
Q

where is ethylene glycol found?

A

anti-freeze

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90
Q

what are the stages of ethylene glycol toxicity?

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

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91
Q

how is ethylene glycol toxicity managed?

A

used to be ethanol which competes with ethylene glycol for the enzyme alcohol dehydrogenase
this limits the formation of toxic metabolites

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

haemodialysis also has a role in refractory cases

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92
Q

what is the action of finesteride?

A

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

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93
Q

what are the indications for fenasteride?

A

male pattern baldness

BPH

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94
Q

what does finesteride do to PSA?

A

decreases levels

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95
Q

what are the indications of finasteride?

A

impotence
decrease libido
ejaculation disorders
gynaecomastia and breast tenderness

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96
Q

what class drug does flecainide belong to?

A

class 1c antiarrhythmics

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97
Q

when is flecanide contraindicated?

A

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

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98
Q

when is flecanide indicated?

A

atrial fibrillation

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

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99
Q

what are the adverse effects of flecainide?

A 
negatively inotropic
bradycardia
proarrhythmic
oral paraesthesia
visual disturbances
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100
Q

what are the adverse effects of gentamicin?

A

ototoxic - vestibular nerve damage, irreversible.

nephrotoxic - acute tubular necrosis. use with furosemide increases risk.

dosing required due to this

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101
Q

what are the contraindications of gentamicin use?

A

myasthenia gravis

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102
Q

which drugs can be cleared by haemodialysis?

A 
BLAST: 
barbiturates. 
lithium 
alcohol
salicyclates
theophyllines
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103
Q

which drugs cant be cleared by haemodialysis?

A 
tricyclics
benzodiazepines
dextropropoxyphene (Co-proxamol)
digoxin
beta-blockers
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104
Q

how does heparin work?

A

by activating antithrombin III

e.g. lmwh increases action of ATIII on factor Xa.

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105
Q

what are the adverse effects of heparin?

A

bleeding
thromocytopenia (lower risk in LMWH)
osteoporosis (lower risk in LMWH)
hyperK

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106
Q

how is heparin given compared to LMWH?

A

LMWH sub cut

heparain - IV

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107
Q

what is the mechanism behind heparin induced thrombocytopenia?

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

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108
Q

how does heparin induced thrombocytopenia present?

A

despite being associated with low platelets HIT is actually a prothrombotic condition
features include reduction in platelets, thrombosis and skin allergy

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109
Q

how is heparin overdose reversed?

A

protamine sulphate, although this only partially reverses the effect of LMWH.

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110
Q

what is the mechanism of action of

a) statin
b) ezetimibe
c) nicotinic acid
d) fibrates
e) cholestyramine

A

a) HMG coA reductase inhibitor
b) decreases cholesterol absorption in the small intestine
c) decreases hepatic VLDL
d) agonist of PPAR-a and so increases lipoprotein lipase expression
e) Decreases bile acid reabsorption in the small intestine, upregulating the amount of cholesterol that is converted to bile acid

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111
Q

what are the side effects of

a) statin
b) ezetimibe
c) nicotinic acid
d) fibrates
e) cholestyramine

A

a) myositis, deranged LFTs
b) headache
c) flushing, myositis
d) myositis, pruritis, cholestasis
e) GI side effects

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112
Q

what are the causes of low Mg

A 
PPI, diuretics, 
TPN
diarrhoea 
hypoK
hyperCa
alcohol
gitleman/bartters
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113
Q

what are the features of hypocalcaemia?

A

paraesthesia
tetany
seizures
arrhythmias

ECG features similar to those of hypokalaemia
exacerbates digoxin toxicity

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114
Q

how is low Mg managed?

A

if <0.4 or arrhyhmias, seizures, tetany - IV MG SO4

otherwise oral

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115
Q

what can lithium toxicity be precipitated by?

A

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

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116
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
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117
Q

how is lithium toxicity managed?

A

mild-moderate toxicity may respond to volume resuscitation with normal saline
haemodialysis may be needed in severe toxicity
sodium bicarbonate is sometimes used

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118
Q

what effect does adrenaline have on anaesthetic drugs?

A

drenaline may be added to local anaesthetic drugs. It prolongs the duration of action at the site of injection and permits usage of higher doses

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119
Q

where is a photosensitive rash likely to present?

A

forehead and arms

120
Q

what are the side effects of metformin?

A

GI symptoms

lactic acidosis

121
Q

what are the side effects of sulphonylureas?

A

weight gain
hypoglycaemia
SiADH
liver dysfunction.

122
Q

what is chlorpropamide?

A

sulphonlyurea

123
Q

what are the side effects of glitazones?

A

weight gain
liver dysfunction
fluid retention
fracture

124
Q

what are the side effects of gliptins?

A

pancreatitis.

125
Q

when is lithium monitored?

A

12 hours post dose

126
Q

when is phenytoin monitored?

A

Phenytoin levels do not need to be monitored routinely but trough levels, immediately before dose should be checked if:
adjustment of phenytoin dose
suspected toxicity
detection of non-adherence to the prescribed medication

127
Q

when is ciclosporin monitored?

A

immediately before

128
Q

when should digoxin be monitored?

A

6 hours post dose

129
Q

after causative substance ingestion what time frame should ogd be avoided?

A

5-15 dys due to oesophageal strength being at its weakess

130
Q

what does st johns wort do?

A

treats mild depression. similar action to ssri

131
Q

what are the adverse effects of st johns wort?

A

induces cytochorme p450
therefore reduces efficacy of e.g. warfarin, cyclosporin, COCP
similar adverse effects to placebo
may cause serotonin syndrome

132
Q

what is Trastuzumab

A

herceptin - monoclonal antibody that acts on the HER2/neu receptor

133
Q

what are the side effects of trastuzumab (herceptin)?

A

flu-like symptoms and diarrhoea are common

cardiotoxicity: echo before treatemt.

134
Q

what is the main limitation of monoclonal antibodies? how is it overcome?

A

Mouse antibodies are immunogenic leading to the formation of human anti-mouse antibodies (HAMAs). This problem is overcome by combining the variable region from the mouse body with the constant region from an human antibody.

135
Q

what are the following monoclonal Ab used in?

Infliximab
rituximab
cetuximab
trastuzumab

A

Infliximab (anti-TNF): used in rheumatoid arthritis and Crohn’s

rituximab (anti-CD20): used in non-Hodgkin’s lymphoma and rheumatoid arthritis

cetuximab (epidermal growth factor receptor antagonist): used in metastatic colorectal cancer and head and neck cancer

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

136
Q

where are the following monoclonal Ab used?

Alemtuzumab
abciximab
OKT3

A

alemtuzumab (anti-CD52): used in chronic lymphocytic leukaemia

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

OKT3 (anti-CD3): used to prevent organ rejection

137
Q

how is tremor related to lithium?

A

fine tremor at therapeutic levels

course tremor at toxicity

138
Q

which drugs reduce the efficacy of COCP?

A 
rifampicin
rifaxicin
phenytoin, 
phenobarbital, 
carbamazepine or
 St John's Wort
all enzyme indcing drugs
139
Q

which two cholesterol drugs when used together give a bigger risk of muscle toxicity?

A

fibrates and statins - myostitis

140
Q

what is a common side effect of verapamil?

A

constipation

141
Q

which drugs should be avoided in G6PD deficiency?

A

sulphonylureas
ciprofloxacin
nitrofurantoin,
chloramphenicol

142
Q

give examples of quinolones

A

ciprofloxacin

levofloxacin

143
Q

how do quinolones work?

A

topoisomerase inhibitors

144
Q

what are the mechanisms of quinolone resistance?

A

topoisomerase mutation

efflux pump to reduce conc of drug

145
Q

what are the adverse effects of quinolones?

A

lower seizure threshold
long QT
tendon damage
cardiac damage

146
Q

when should quinolones be avoided?

A

G6PD deficiency

pregnancy/ breast feeding

147
Q

what types of reactions are involved in phase 1 drug metabolism

A

oxidation
reduction
hydrolysis

mainly carried out by p450 enzymes

148
Q

what types of reactions are involved in phase 2 drug metabolism

A

conjugation to inactive products for excretion

149
Q

what is first pass metabolism?

A

Phenomenon where the concentration of a drug is greatly reduced before it reaches the systemic circulation due to hepatic metabolism. As a consequence much larger doses are need orally than if given by other routes.

150
Q

what is zero order kinetics?

A

Zero-order kinetics describes metabolism which is independent of the concentration of the reactant. This is due to metabolic pathways becoming saturated resulting in a constant amount of drug being eliminated per unit time.

151
Q

which drugs exhibit zero order kinetics?

A

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

152
Q

which drugs are affected by the acetylator status?

A

50% of population is deficient in hepatic N-acetyltransferase and this is known as your acetylator status.

isoniazid
procainamide
hydralazine
dapsone
sulfasalazine
153
Q

which drugs are inducers of p450?

A

antiepileptics: phenytoin, carbamazepine
barbiturates: phenobarbitone
rifampicin
St John’s Wort
chronic alcohol intake
griseofulvin
smoking - smokers require more aminophylline

154
Q

which drugs inhibit p450?

A 
antibiotics: ciprofloxacin, erythromycin
isoniazid
cimetidine,omeprazole
amiodarone
allopurinol
imidazoles: ketoconazole, fluconazole
SSRIs: fluoxetine, sertraline
ritonavir
sodium valproate
acute alcohol intake
quinupristin
155
Q

how does pilocarpine work?

A

Pilocarpine is a muscarinic agonist that is sometimes used in the treatment of glaucoma.
It is thought to reduce intraocular pressure by widening the trabecular spaces and allowing for increased aqueous flow.
Muscarinic receptors are found in the ciliary muscles and iris sphincter, therefore it also causes pupillary constriction.
Miosis usually persists for 4-8 hours following administration.

156
Q

how does timolol work?

A

beta-blocker which inhibits the production of aqueous humour.

157
Q

what is oculogyric crisis?

A

dystonic reaction to certain meds e.g. metaclopramide, antipsycotics

features include restlessness, agitation
involuntary upward deviation of the eyes

158
Q

how is oculogyric crisis managed?

A

Intravenous antimuscarinic: benztropine or procyclidine

159
Q

what are the effects of methanol poisoning?

A

same as alcohol intoxication + visual problems

160
Q

what is the mechanism of methanol poisoning?

A

formic acid

161
Q

how is methanol poisoning managed?

A

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

162
Q

what is HLA-B *5801 allele screening done for?

A

Screen for HLA-B *5801 allele in a patient at high risk for allopurinol induced severe cutaneous adverse reaction

163
Q

what are risk factors for developing allopurinol sensivity?

A

Certain ethnic groups such as the Chinese, Korean and Thai people
CKD
diuretic use

allopurinol should be avoided in those with mild-moderate kidney diseaee

164
Q

what is octreotide?

A

ong-acting analogue of somatostatin

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

165
Q

when is octreotide used?

A 
acute treatment of variceal haemorrhage
acromegaly
carcinoid syndrome
prevent complications following pancreatic surgery
VIPomas
refractory diarrhoea
166
Q

what are the side effects of octreotide?

A

gallstones

167
Q

what are the side effects of sildenafil?

A

visual disturbances e.g. blue discolouration, non-arteritic anterior ischaemic neuropathy

nasal congestion
flushing
gastrointestinal side-effects
headache

168
Q

what are phosphodiesterase type 5 inhibitors?

A

DE5 inhibitors cause vasodilation through an increase in cGMP leading to smooth muscle relaxation in blood vessels supplying the corpus cavernosum.

used for erectile dysfunction and pulmonary HTN

e.g. sildenafil (Viagra)
tadalafil (Cialis)
vardenafil

169
Q

what are the contraindications of phosphodiesterase type 5 inhibitors?

A

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

170
Q

which enzyme does smoking affect and what does this mean?

A 
CYP1A2 enzyme (of p450 system) 
smokers usually require more aminophylline.
171
Q

what drug is MCAT similar to?

A

similar to MDMA, amphetamines and cocaine, resulting in increased levels of serotonin, dopamine and noradrenaline, resulting in a ‘high’ and feeling of euphoria
similar risk of causing serotonijn syndrome

172
Q

what drug group is mexxy similar too?

A

new illegal high - hallucinogen

173
Q

what drug is GHB?

what is the major side effect

A

similar to liquid ectasy

can cause resp depression esp when taken with alcohol

174
Q

what should be done if a patient is having unbearable GI effects from metformin?

A

switch to modified release

if still no good try a sitagliptin/gliclazide

175
Q

how does metformin work?

A

acts by activation of the AMP-activated protein kinase (AMPK)
increases insulin sensitivity
decreases hepatic gluconeogenesis
may also reduce gastrointestinal absorption of carbohydrates

176
Q

what are the adverse effects of metformin?

A

GI - nausea, anorexia, diarrhoea
reduced b12 absorption - rarely an issue
lactic acidosis with severe liver disease or renal failure

177
Q

what are the contraindications of using metformin?

A

CKD - dose should be reviewed if the creatinine is > 130 µmol/l (or eGFR < 45 ml/min) and stopped if the creatinine is > 150 µmol/l (or eGFR < 30 ml/min)

metformin may cause lactic acidosis if taken during a period where there is tissue hypoxia. Examples include a recent myocardial infarction, sepsis, acute kidney injury and severe dehydration

iodine-containing x-ray contrast media: increasing risk of provoking renal impairment due to contrast nephropathy; metformin should be discontinued on the day of the procedure and for 48 hours thereafter

alcohol abuse - relative contraindication

178
Q

how does rifampicin work? what are the side effects?

A

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

hepatitis, orange secretions
flu-like symptoms

179
Q

how does isoniazid work? what are the side effects?

A

inhibits mycolic acid synthesis

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

180
Q

how does Pyrazinamide work? what are the side effects?

A

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

hyperuricaemia causing gout
arthralgia, myalgia
hepatitis

181
Q

how does ethambutol work? what are the side effects?

A

inhibits the enzyme arabinosyl transferase which polymerizes arabinose into arabinan

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

182
Q

what are the features of Organophosphate insecticide poisoning?

A 
Ach build up .. presents as SLUD..
salivation
lacrimaton
urinary incontinence
diarrhoea
others - bradycardia and hypotension, small pupils and muscle fasciculations.
183
Q

how is Organophosphate insecticide poisoning managed?

A

atropine

184
Q

what is the mechanism of aspirin?

A

Aspirin is a non reversible COX 1 and 2 inhibitor

185
Q

what are the features of salicylate overdose?

A

mixed respiratory alkalosis and metabolic acidosis
early stimulation of resp system leads to resp alkalosis
later acid effects of salicylates + renal fialure leads to metabolic acidosis

hyperventilation (centrally stimulates respiration)
tinnitus
lethargy
sweating, pyrexia
nausea/vomiting
hyperglycaemia and hypoglycaemia
seizures
coma
186
Q

how is salicylate poisoning managed?

A

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

187
Q

what are the indications for haemodyalysis in salicylate poisoning?

A 
serum concentration > 700mg/L
metabolic acidosis resistant to treatment
acute renal failure
pulmonary oedema
seizures
coma
188
Q

what are the features of tricyclic overdose?

A

anticholinergic effects early on - dry mouth, dilated pupils, agitation, sinus tachycardia, blurred vision.

features of severe poisoning:
arrhythmias
seizures
metabolic acidosis
coma
189
Q

what are the ECG changes in tricyclic overdose?

A

sinus tachycardia
widening of QRS
prolongation of QT interval

190
Q

in tricyclic OD what is the QRS changes associated with?

A

Widening of QRS > 100ms is associated with an increased risk of seizures whilst QRS > 160ms is associated with ventricular arrhythmias

191
Q

How is tricyclic OD managed?

A

IV bicarbonate
- first-line therapy for hypotension or arrhythmias

can also use other drugs for arrhythmias

Intravenous lipid emulsion is increasingly used to bind free drug and reduce toxicity

dialysis is ineffective in removing tricyclics

192
Q

what are the indications for IV bicarbonate in tricyclic OD?

A

widening of the QRS interval >100 msec or a ventricular arrhythmia

193
Q

which drugs are contraindicated in tricyclic OD?

A

+ class 1a (e.g. Quinidine) and class Ic antiarrhythmics (e.g. Flecainide) are contraindicated as they prolong depolarisation

class III drugs such as amiodarone should also be avoided as they prolong the QT interval

194
Q

what are the causes of raised anion gap?

A 
lactic acidosis
ketoacidosis
renal failure (high urate)
toxins such as methanol, ethylene glycol, salicylates
195
Q

what type of drug is tamoxifen?

A

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

196
Q

what are the ADRs of tamoxifen?

A

hot flushes
menstural disturbances
VTE
endometrial Ca

197
Q

how long is tamoxifen used?

A

5 years after removal of tumour

198
Q

what is raloxifene?

A

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

199
Q

which antibiotic lowers seizure threshold?

A

ciprofloxacin

200
Q

which antibiotic can increase QT?

A

erythromycin

201
Q

which Abx can interact with alcohol?

A

metronidazole

202
Q

what is a complication of methanol poisoning?

A

visual disturbance

metabolite of methanol, formic acid, accumulates in the optic nerve causing visual disturbance and eventually blindness.

203
Q

what is meant by efficacy and potency of a drug?

A

‘Efficacy’ is the measure of how able an agonist is to produce a response once it has bound to the receptor.

‘Potency’ is related to the concentration at which a drug is effective.

204
Q

which method of VTE prophylaxis should be used in renal failure?

A

unfractionated heparin.
LMWH should not be used

Current NICE guidelines state that unfractionated heparin (UFH) is the anticoagulant of choice in patients with severe chronic kidney disease.

205
Q

does diazepam undergo first pass metabolism?

A

no

206
Q

what factors are associated with increased hepatotoxicity with paracetamol OD?

A

chronic alcohol intake
carbemazepine
malnutrition- due to depletion of glutathione
st johns wart

(acute alcohol intake IS NOT associated with increased toxicity - may actually be protective)

207
Q

which drugs are seemed to be harmful in pregnancy?

A

Antibiotics
tetracyclines
aminoglycosides
sulphonamides and trimethoprim
quinolones: the BNF advises to avoid due to arthropathy in some animal studies
some reports of co-amox causing necrotising entercolitis

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

The majority of antiepileptics including valproate, carbamazepine and phenytoin are known to be potentially harmful. however risk of seizure is also harmful.

208
Q

which antibiotic allergy is associated with penicillin allergy?

A

cephalosporins e.g. cefalexin
Penicillins, cephalosporins, and carbapenems are all members of the beta-lactam group of antibiotics and share a common beta-lactam ring.

cefixime, cefotaxime, ceftazidime, ceftriaxone, or cefuroxime - have less risk

cefalexin - should be avoided in pen allergy

209
Q

what is timentin?

A

ticarcillin with clavulanic acid

contains penicillin

210
Q

which Abx is contraindiciated in G6PD deficinecy?

A

quinolones e.g. ciprofloxacin

211
Q

which drug can precipitate lithium toxicity?

A

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

212
Q

how is paracetamol normally metabolised? what happens in overdose

A

conjugation with glucuronic acid/sulphate.
in overdose this becomes saturated and instead there is oxidation by p450 leading to toxic metabolites
glutathione can conjugate this metabolite into non-toxic form.
if glutathione stores also become saturated it can lead to damage - hepatocytes and renal cells

213
Q

what chemical can help with paracetamol OD. how does this work?

A

N-acetyl cysteine is used in the management of paracetamol overdose as it is a precursor of glutathione and hence can increase hepatic glutathione production

214
Q

why is there a lower threshold for treating paracetamol OD in patients on phenytoin/rifampicin?

A

these are p450 inducing agents.

thus paracetamol is oxidised into toxic metabolites quicker.

215
Q

which drug can give green vision?

A

digoxin

216
Q

what is the action of pilocarpine?

A

muscarinic agonist
pupillary constriction and contraction of the ciliary muscles, which opens up the trabecular meshwork allowing greater drainage of aqueous humour and reduces intraocular pressure.

217
Q

what is sarin gas? what affect does poisoning with this have?

A

Sarin gas is a highly toxic synthetic organophosphorus compound which causes inhibition of the enzyme acetylcholinesterase
excess ACh levels

218
Q

what are the effects of excess ACh?

A 
he effects of excessive ACh can be remembered by the mnemonic DUMBELLS:
Diarrhoea
Urination
Miosis/muscle weakness
Bronchorrhea/Bradycardia
Emesis
Lacrimation
Salivation/sweating
219
Q

name 3 macrolides

A

erythromycin
azithromycin
clarithromycin

220
Q

how do macrolides work?

A

inhibit translocation

221
Q

what is the mechanism of macrolide resistance?

A

post-transcriptional methylation of the 23S bacterial ribosomal RNA

222
Q

what are the ADRs of macrolides?

A

prolongation of the QT interval

gastrointestinal side-effects are common. Nausea is less common with clarithromycin than erythromycin
cholestatic jaundice

P450 inhibitor

azithromycin is associated with hearing loss and tinnitus

223
Q

what are the DDIs of macrolides

A

statins should be stopped whilst taking a course of macrolides.
Macrolides inhibit the cytochrome P450 that metabolises statins.
increases the risk of myopathy and rhabdomyolysis.

224
Q

what are the features of mercury poisoning?

A 
paraesthesia
visual field defects
hearing loss
irritability
renal tubular acidosis
225
Q

how can motion sickness be managed?

A

hyoscine (e.g. transdermal patch) - most effective treatment.
non-sedating antihistamines such as cyclizine or cinnarizine are recommended in preference to sedating preparation such as promethazine

226
Q

what does digoxin do to QT interval?

A

shorten it

227
Q

how do aminoglycosides cause AKI?

A

e.g. gentamicin

acute tubular necrosis

228
Q

which meds can cause renal injury via Acute interstitial nephritis ?

A

penicillins, quinolones and diuretics

229
Q

which drugs can cause crystal nephropathy?

A

methotrexate and ganciclovir

230
Q

how should amiodarone induced hypothyroid be managed?

A

cont amiodarone, start thyroxine

231
Q

how should metformin be initiated?

A

start slow and titrate - 500mg OD for 2 weeks then BD, then review.

232
Q

which two tumours are known to over express HER2?

A

breast

gastric adenocarcinoma

233
Q

How is HER2 positive gastric adenocarcinoma treated?

A

NICE state trastuzumab in combination with cisplatin and capecitabine or 5-fluorouracil is a recommended option for HER2 positive metastatic adenocarcinoma of the stomach.

234
Q

which cancers over express HER1? which monoclonal can be used here?

A

squamous and colorectal

Cetuximab

235
Q

what is muddy brown casts on urinalysis indicative of?

A

acute tubular necrosis

236
Q

when can charcoal be used in paracetamol OD?

A

within 1 hour

237
Q

when should N-acetylcysteine be given in paracetamol OD?

A

if there is a staggered overdose or there is doubt over the time of paracetamol ingestion, regardless of the plasma paracetamol concentration;
OR
the plasma paracetamol concentration is on or above a single treatment line joining points of 100 mg/L at 4 hours and 15 mg/L at 15 hours, regardless of risk factors of hepatotoxicity

238
Q

how quickly is Nacetylcysteine transfused?

A

over 1 hour

239
Q

what is one allergic complication of N-acetylcysteine?

A

can cause anaphalactoid reaction.

should be stopped and restarted at slower rate

240
Q

what is the kings college criteria for liver transplant after 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

241
Q

what is a good prognostic marker in paracetamol OD?

A

elevated PT - signifies poor prognosis and liver failure

242
Q 
how do the following work...
suxamethonium
atracurium
Vecuronium
Pancuronium
A

suxamethonium:
Depolarising neuromuscular blocker
Inhibits action of acetylcholine at the neuromuscular junction
Degraded by plasma cholinesterase and acetylcholinesterase

atracurium, vecuronium and pancuronium:
Non depolarising neuromuscular blocking drug

243
Q

out of the muscle relaxants which is the quickest acting and shortest duration?

A

suxamethonium

244
Q

what are the ADRs of suxamethonium?

A

hyperkalaemia,
malignant hyperthermia
and lack of acetylcholinesterase

245
Q

how is atracurium metabolised?

A

not by kidney/.liver

hydrolysed by tissues

246
Q

what are the ADRs of atracurium?

A

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

247
Q

how is atracurium reversed?

A

neostigmine

also reverses pancuronium and vecuronium

248
Q

how is salicylate overdose managed?

A

urinary alkalinization with IV bicarbonate

haemodialysis

249
Q

what is the antidote for..
opioids
benzos
heparin

A

a) naloxone
b) flumazenil
c) protamine sulphate

250
Q

how is lithium toxicity managed?

A

mild-moderate toxicity may respond to volume resuscitation with normal saline
haemodialysis may be needed in severe toxicity

251
Q

how is bblocker toxicity treated?

A

atropine if bradycardic

glucagon if resistant

252
Q

how is lead poisoning managed?

A

dimercaprol

253
Q

how is cyanide poisoning managed?

A

Hydroxocobalamin

254
Q

which groups of patients are more at risk of developing hepatotoxicity from paracetamol OD?

A 
patients taking liver enzyme-inducing drugs (rifampicin, phenytoin, carbamazepine, chronic alcohol excess, St John's Wort)
malnourished patients (e.g. anorexia nervosa) or patients who have not eaten for a few days

Acute alcohol intake is actually maybe protective

255
Q

what are the following symptoms suggestive of: headache, confusion, pink mucosa, low grade fever.

A

CO poisoning

256
Q

when is haemodyalysis for lithium indicated?

A

severe toxicity e.g.. >2 or when renal/neuro involvement

257
Q

what affect do the following teratogens have?

ACEi
alcohol
aminoglycosides

A

ACEi - craniofacial abnorm , renal dysgenesis

alcohol: craniofacial abnorm

aminog - ototoxic

258
Q

what affect do the following teratogens have?

chloramphenicol
carbemazapines
cocaine

A

chloramphenicol: grey baby syndrome
‘
carbemazapines: neural tube defects, craniofacial

cocaine: IUGR, preterm labour

259
Q

what affect do the following teratogens have?
warfarin
valproate
tetracyclines

A

warfarin: craniofacial
valproate: neural tube defects, craniofacial
tetracyclines: discoloured teeth

260
Q

what affect do the following teratogens have?
smoking
lithium
Diethylstilbesterol

A

smoking: IUGR, preterm labour
lithium: ebstein anomoly
Diethylstilbesterol: vaginal clear cell adenocarcinoma

261
Q

how does tacrolimus work?

A

decreases clonal proliferation of T cells by reducing IL-2 release
calcinurin inhibitor

262
Q

what is more potent tacrolimus or ciclosporin?

A

tacrolimus

also more likely to cause renal toxocity and glucose intolerance

263
Q

what is the function of amiloride?

A

blocks the epithelial sodium channel in the distal convoluted tubule
also leads to high K

264
Q

what is the function of spironolactone?

A

Aldosterone antagonist

in colecting duct

265
Q

which medications exacerbate heart failure?

A

pioglitazone is contraindicated as it causes fluid retention
verapamil - negative inotropic effect
NSAIDs/glucocorticoids - should be used with caution as they cause fluid retention
class I antiarrhythmics - flecainide (negative inotropic and proarrhythmic effect

266
Q

which drugs should be avoided in renal failure?

A

antibiotics: tetracycline, nitrofurantoin
NSAIDs
lithium
metformin

267
Q

which drugs need adjusting in renal failure due to accumulation?

A 
most antibiotics including penicillins, cephalosporins, vancomycin, gentamicin, streptomycin
digoxin, atenolol
methotrexate
sulphonylureas
furosemide
opioids
268
Q

can progesterone only pill be used while breast feeding?

A

yes

269
Q

what affect may progesterone have on ovarian cysts?

A

increase of functional ovarian cysts.

270
Q

what is cinchonism?

A

Quinine toxicity
it can be fatal, usually by cardiac arrhythmia or flash pulmonary oedema in the short term, although incipient renal failure may be fatal more long-term.

cardiac arrhythmias - long QT due to blockage of na and k channels. can lead to VT/VF
hypoglycaemia - quinine stimulates pancreatic insulin release

classical hallmarks of cinchonism are tinnitus, visual blurring, flushed and dry skin and abdominal pain.

271
Q

why is measuring salicylate levels important in quinine toxicity?

A

Clinically, quinine toxicity is difficult to distinguish from aspirin poisoning
however the effects are usually reversible with aspirin and irreversible for quinine e.g. tinnitus and visual blurring

272
Q

what drugs can cause serotonin syndrome?

A

MAOi
SSRIs
ecstasy
amphetamines

273
Q

what are the features of serotonin syndrome?

A 
neuromuscular excitation (e.g. hyperreflexia, myoclonus, rigidity)
autonomic nervous system excitation (e.g. hyperthermia)
altered mental state
274
Q

how is serotonin syndrome managed?

A

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

275
Q

how does serotonin syndrome and neuroleptic malignant syndrome compare?

A

both have tachycardia, increased BP and fever and rigidity

serotonin syndrome has much faster onset and increased reflexes
wheereas neuroleptic malignant syndrome is slower in onset and reduced reflexes
dilated pupils in serotonin but not in neuroleptic MS

276
Q

how is neuroleptic malignancy syndrome managed?

A

benzos and fluids

severe cases - dantrolene.

277
Q

what are the side effects of Ca blockers?

A

Headache
• Flushing
• Ankle oedema

Verapamil also commonly causes constipation

278
Q

what are the side effects of nitrates

A

Headache
• Postural hypotension
• Tachycardia

279
Q

what are the side effects of nicorandil

A

• Headache
• Flushing
• Anal ulceration

280
Q

what are the side effects of sulphonylureas?

A

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

281
Q

what are the side effects of glitazones?

A

Weight gain
Fluid retention
Liver dysfunction
Fractures

282
Q

What is the kings college criteria for liver transplant?

A

pH <7.3
Creatinine > 300
PT > 100 s
Hepatic encephalopathy 3 or 4

283
Q

What is the mechanism of rifampicin , isoniazid and pyrazinamide?

A

Rifampicin - inhibits DNA dep RNA pol

Isoniazid - reduces mycolic synthesis

Pyrazinamide - inhibits fatty acids

284
Q

What are the ADRs of rifampicin

A

Orange secretions
Hepatitis
Flu like symptoms
Liver enzyme inducer

285
Q

What are the side effects of isoniazid ?

A

Peripheral neuropathy - give pyroxidine
Hepatitis
Agranulocytosis

286
Q

What are the side effects of pyrazinamide?

A

Gout
Arhralgia, myalgia
Hepatitis

287
Q

What is side effects of ethambutol

A

Optic neuritis

288
Q

What drugs should not be taken with statins ?

A

Macrolides - erythromycin / clarithromycin

These inhibit p450 so statin levels rise to toxic

289
Q

Which electrolyte can promote digoxin toxicity

A

HypoK

Because digoxin competes for pottasium binding site on Na/ K ATPase

290
Q

What are the complications of transtuzumab?

A

Transtuzumab = herceptin
Cardiomyopathy
Do ECHO before starting
Don’t take with antracyclines e.g doxorubicin as these also cause cardiomyopathy

291
Q

What are the side effects of dopamine agonists

A 
Fibrosis - pulmonary , retrroperitoneal 
Sleepiness
Hallucination 
Nausea 
Postural hypotension
292
Q

What should be given in tricyclic OD and when ?

A

IV bicarb if pH <7.1, QRS >160, arrhythmia

293
Q

When can gastric lovage and charcoal be used

A

Both only within 1 hour

294
Q

What is the dose of adrenaline in adults for cardiac arrest and anaphylaxis

A

Anaphylaxis - 500microG 1 in 1000 (0.5ml)

Cardiac arrest - 1mg (1ml 1 in 1000)

295
Q

How does methanol poisoning present and how is it treated ?

A

Like alcohol toxicity but with visual changes/ effects

Fomepizole

296
Q

Which drugs have 0 order kinetics

A

Salicyclates
Heparin
Phenytoin
Ethanol

MRCP (7 decks)

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