MRCP2 Flashcards
Nutritional support in alcohol misuse?
Thiamine
How to promote alcohol withdrawal?
BZD
Disulfram mechanism of action?
inhibition of acetaldehyde dehydrogenase
Contraindications of disulfram?
Ischaemia
Heart disease
Psychosis
Mechanism of acamprost?
NMDA antagonist
Action of acamprost?
Reduce cravings
Mechanism of amiodarone induced hypothyroidism?
High iodine content of amiodarone causing a Wolff-Chaikoff effect*
Pathophysiology of type 1 amiodarone induced thyrotoxicosis?
Excess iodine-induced thyroid hormone synthesis
Pathophysiology of type 2 amiodarone induced thyrotoxicosis ?
Amiodarone-related destructive thyroiditis
Differentiate between type 1 and type 2 amiodarone induced thyrotoxicosis?
Goitre –> type 1
No goitre –> type 2
Management of type 1 AIT?
Carbimazole or potassium perchlorate
Management of type 2 AIT?
Corticosteroids
Should amiodarone be stopped in amiodarone induced hypothyroidism?
No.
Should Amiodarone be stopped in amiodarone induced hyperthyroidism
Yes.
Side effects of amiodarone?
thyroid dysfunction: both hypothyroidism and hyper-thyroidism
corneal deposits
pulmonary fibrosis/pneumonitis
liver fibrosis/hepatitis
peripheral neuropathy, myopathy
photosensitivity
‘slate-grey’ appearance
thrombophlebitis and injection site reactions
bradycardia
lengths QT interval
Amiodarone + warfarin
Decreases metabolism of warfarin
Elevates INR
Amiodarone + digoxin
Increased digoxin level
Problems with anabolic steroid use ?
Cardiac morbidity and mortality
hepatocellular carcinoma and hepatic adenoma.
Psychiatric illness
Coming off anabolic steroids, how do you wean?
Do not need to wean - Just stop
WHat is the effect of verapmil?
Highly negatively inotropic
Side effects of verapamil
Heart failure
constipation
hypotension
bradycardia
flushing
What is the effect of diltiazem?
Highly inotropic
Side effect of diltiazem?
Hypotension
Bradycardia
Heart failure
Ankle swelling
Sides effect of dihydropyridine calcium channel blockers?
Flushing
Headache
Ankle swelling
Features of canabinoid overdose?
CNS: agitation, tremor, anxiety, confusion, somnolence, syncope, hallucinations, changes in perception, acute psychosis, nystagmus, convulsions and coma.
Cardiac: tachycardia, hypertension, chest pain, palpitations, ECG changes.
Renal: acute kidney injury.
Muscular: hypertonia, myoclonus, muscle jerking and myalgia.
Other: cold extremities, dry mouth, dyspnoea, mydriasis, vomiting and hypokalaemia
Features of carbon monoxide poisoning?
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
Typical caroxyhaemoglobin for non-smokers?
< 3% non-smokers
Typical caroxyhaemoglobin for smokers?
<10%
Caroxyhaemoglobin for
10 - 30% symptomatic: headache, vomiting
> 30% severe toxicity
Management of carbon monoxide poisoning?
100% high-flow oxygen via a non-rebreather mask
from a physiological perspective, this decreases the half-life of carboxyhemoglobin (COHb)
What is cathinone ?
NRG-1 is a synthetic cathinone drug
derivative of phenylpropanone which is a naturally occurring psychotrope in khat (Catha edulis).
Mechanism of cathinone?
increasing synaptic concentrations of noradrenaline, dopamine and serotonin
sensation of euphoria, detachment and wellbeing as well as upregulation of the sympathetic system.
What is seen in cathinone toxicity?
Hyponatraemia
Serotonin syndrome
Management of cathinone toxicity: Hyponatraemic + neurological compromise?
Infusion of 3% saline solution at a maximum rate of 1ml/kg/hour
Feautres of serotonin syndrome?
Liberated serotonin and causes agitation, confusion, muscle hyperactivity with fasciculations, hypertonia and clonus.
Creatine kinase and white cell counts are often raised and body temperature may be extremely high.
Mechanism of ciclosporin?
Decreases clonal proliferation of T cells by reducing IL-2 release
Adverse effects of ciclosporin?
nephrotoxicity
hepatotoxicity
fluid retention
hypertension
hyperkalaemia
hypertrichosis
gingival hyperplasia
tremor
impaired glucose tolerance
hyperlipidaemia
increased susceptibility to severe infection
What immunosuppression is not myelid toxic?
Ciclosporin
Mechanism of cocaine?
cocaine blocks the uptake of dopamine, noradrenaline and serotonin
Cardiovascular effects of cocaine?
coronary artery spasm → myocardial ischaemia/infarction
both tachycardia and bradycardia may occur
hypertension
QRS widening and QT prolongation
aortic dissection
Neurological effects of cocaine?
seizures
mydriasis
hypertonia
hyperreflexia
Psychiatric effects of cocaine?
agitation
psychosis
hallucinations
Other features of cocaine overdose?
ischaemic colitis is recognised in patients following cocaine ingestion. This should be considered if patients complain of abdominal pain or rectal bleeding
hyperthermia
metabolic acidosis
rhabdomyolysis
Management of cocaine over?
benzodiazepines are generally first-line for most cocaine-related problems
Features of cyanide posioning?
‘classical’ features: brick-red skin, smell of bitter almonds
acute: hypoxia, hypotension, headache, confusion
chronic: ataxia, peripheral neuropathy, dermatitis
Management of cyanide poisoning?
supportive measures: 100% oxygen
definitive: hydroxocobalamin (intravenously)
+
combination of amyl nitrite (inhaled), sodium nitrite (intravenously), and sodium thiosulfate (intravenously)
dicobalt edetate
Mechanism of action of digoxin?
decreases conduction through the atrioventricular node
slows the ventricular rate in atrial fibrillation and flutter
increases the force of cardiac muscle contraction due to inhibition of the Na+/K+ ATPase
stimulates vagus nerve
When does digoxin toxicity occur?
Toxicty can occur even if within therapeutic range
BNF advises that the likelihood of toxicity increases progressively from 1.5 to 3 mcg/l.
Features of digoxin toxicity?
generally unwell, lethargy, nausea & vomiting, anorexia, confusion, yellow-green vision
arrhythmias (e.g. AV block, bradycardia)
gynaecomastia
Precipitating factors of digoxin toxocity?
classically: hypokalaemia
increasing age
renal failure
myocardial ischaemia
hypomagnesaemia, hypercalcaemia, hypernatraemia, acidosis
hypoalbuminaemia
hypothermia
hypothyroidism
Why does hypokalaemia cause toxicity?
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
Management of digoxin toxicity?
Digibind
correct arrhythmias
monitor potassium
Indications for dopamine receptor antaongists?
Parkinson’s disease
prolactinoma/galactorrhoea
cyclical breast disease
acromegaly
Side effects of dopamine receptor antagonists?
nausea/vomiting
postural hypotension
hallucinations
daytime somnolence
DRESS syndrome typically affects?
Skin, liver, kidneys, lungs and heart.
Rash associated with DRESS?
morbilliform skin rash
exfoliative dermatitis, high fever, and inflammation of one or more organs
Features of dress syndrome?
Can develop any of:
raised and low white count, eosinophilia , thrombocytopaenia, anaemia, atypical lymphocytes
develop kidney disease which is usually mild (interstitial nephritis is common, renal failure is rare),
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
severe cases, acute colitis and pancreatitis can occur, and endocrine abnormalities may include thyroiditis and diabetes.
Diagnostic criteria for DRESS?
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.
Drugs that impair glucose tolerance?
thiazides, furosemide (less common)
steroids
tacrolimus, ciclosporin
interferon-alpha
nicotinic acid
antipsychotics
Beta-blockers cause a slight impairment of glucose tolerance
Drugs that induce urinary rentetion?
tricyclic antidepressants e.g. amitriptyline
anticholinergics e.g. antipsychotics, antihistamines
opioids
NSAIDs
disopyramide
Alpha agonists?
Alpha-1: Decongestants (e.g. phenylephrine/oxymetazoline)
Alpha-2: Glaucoma (e.g. topical brimonidine)
Alpha antagonist?
Benign prostatic hyperplasia (e.g. tamsulosin)
Hypertension (e.g. doxazosin)
Beta 1 agonist?
Inotropes (e.g. dobutamine)
Beta 1 antagonist?
Non-selective & selective beta-blockers (e.g. atenolol, bisoprolol
Beta 2 agonist?
Bronchodilators (e.g. salbutamol)
Beta 2 antagonist?
Non-selective beta-blockers (e.g. propranolol, labetalol)
Dopamine agonist?
Parkinson’s disease (e.g. ropinirole)
Prolactinoma
Dopamine antagonist?
Schizophrenia (antipsychotics e.g. haloperidol)
Anti-emetics (e.g. metoclopramide/domperidone)
GABA agonists?
Benzodiazepines
Baclofen
GABA antagonist?
Flumazenil
Muscarinic agonist?
Glaucoma (e.g. pilocarpine)
Muscarinic antagonist?
Atropine (e.g. for bradycardia)
Bronchodilator (e.g. ipratropium bromide, tiotropium)
Urge incontinence (e.g. oxybutynin)
Nicotinic agonist?
Nicotine
Varenicline (used for smoking cessation)
Depolarising muscle relaxant (e.g. suxamethonium)
Nicotinic antagonist?
Non-depolarising muscle relaxants (e.g. atracurium)
Serotonin agonists?
Triptans (for acute migraine, e.g. zolmitriptan)
Serotonin antagonists?
Anti-emetics (e.g. ondansetron)
Drugs that cause lung fibrosis?
amiodarone
cytotoxic agents: busulphan, bleomycin
anti-rheumatoid drugs: methotrexate, sulfasalazine
nitrofurantoin
ergot-derived dopamine receptor agonists (bromocriptine, cabergoline, pergolide)
What is the actual name of ectasy?
Ecstasy (MDMA, 3,4-Methylenedioxymethamphetamine
Features of ectasy pisoning?
neurological: agitation, anxiety, confusion, ataxia
cardiovascular: tachycardia, hypertension
hyponatraemia
hyperthermia
rhabdomyolysis