General deck Flashcards
what are the types of trigeminal autonomic cephalgia?
- cluster headache
- paroxysmal hemicrania
- hemicrania continua
- short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT syndrome)
- short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms (SUNA)
What is the initial tx for acute flare of UC?
1.) Intravenous fluid and electrolyte replacement
2.) Blood transfusion if required to maintain a haemoglobin >10g/dL
3.) Intravenous antibiotics ONLY if infection is considered or prior to surgery
4.) Subcutaneous heparin to reduce the risk of thromboembolism
5.) Intravenous corticosteroids (either hydrocortisone 100mg four times a day or methylprednisolone 60mg/day)
6.) Flexible sigmoidoscopy and biopsy within 72 hours to confirm diagnosis and exclude cytomegalovirus infection
7.) Daily monitoring with physical examination, recording of vital signs, stool chart, bloods (full blood count, c-reactive protein, serum electrolytes, serum albumin, liver function tests and glucose) and consider the need for daily abdominal X-ray.
What is the predictor for need of surgery in UC?
At day three a c-reactive protein >45 mg/l or a stool frequency of >8/day predicts the need for surgery in 85% of cases.
what is the tx of acute UC flare which has not responded to 72 hrs of IV steroids?
The National Institute for Clinical Excellence (NICE) recommends that if no improvement is seen after 72 hours of intravenous steroid treatment or if the patient deteriorates at any time despite corticosteroid treatment then an urgent surgical review is required ciclosporin (2mg/kg/day) should be added. NICE recommends that in this acute setting infliximab reserved for patients in whom ciclosporin is contraindicated or clinically inappropriate
How are patients within 24 hours of onset of TIA or minor ischaemic stroke and with a low risk of bleeding managed?
clopidogrel (initial dose 300 mg followed by 75 mg od) + aspirin (initial dose 300 mg followed by 75 mg od for 21 days) followed by monotherapy with clopidogrel 75 mg od
what are the causes of pulmonary eosinophilia?
Churg-Strauss syndrome
allergic bronchopulmonary aspergillosis (ABPA)
Loffler’s syndrome
eosinophilic pneumonia
hypereosinophilic syndrome
tropical pulmonary eosinophilia
drugs: nitrofurantoin, sulphonamides
less common: Wegener’s granulomatosis
what are special findings on pleural fluid and its associated diagnosis?
low glucose: rheumatoid arthritis, tuberculosis
raised amylase: pancreatitis, oesophageal perforation
heavy blood staining: mesothelioma, pulmonary embolism, tuberculosis
In T2Dm, what do you aim for Hba1c with just metformin and when do you add a second drug?
you can titrate up metformin and encourage lifestyle changes to aim for a HbA1c of 48 mmol/mol (6.5%), but should only add a second drug if the HbA1c rises to 58 mmol/mol (7.5%)
how do you convert percentage Hba1c to mmol?
11(HbA1c %)-24 = (HbA1c mmol/mol)
what are the CYP450 inducers and inhibitors?
CRAP GPS induce
Carbemazepines
Rifampicin
Alcohol (chronic)
Phenytoin
Griseofulvin
Phenobarbitone
Sulphonylureas
SICKFACES.COM inhibit
Sodium valproate
Isoniazid
Cimetidine
Ketoconazole
Fluconazole
Alcohol
Chloramphenicol
Erythromycin
Sulfonamides
Ciprofloxacin
Omeprazole
Metronidazole
Grapefruit juice
how is cocaine toxicity managed?
benzodiazepines are generally first-line
what drugs should be avoided in cocaine toxocity?
Beta-blockers should be avoided in cocaine-induced chest pain. The rationale is that beta-antagonism may result in unopposed alpha-mediated coronary vasospasm.
what are the rare causes of pappiloedema
Rare causes include
hypoparathyroidism and hypocalcaemia
vitamin A toxicity
what are factors that increase the risk of haemoptysis in goodpastures disease?
smoking
lower respiratory tract infection
pulmonary oedema
inhalation of hydrocarbons
young males
what lung nodules spotted on CT scans do not need any further follow up?
Solitary, solid and non-calcified lung nodules of less than 5mm in size do not warrant further investigations or monitoring
which lung nodules need follow up? and how do you follow up??
Nodule <5mm –> discharge
Nodule 5-6mm –> CT at 1 year
Nodule >6mm –> CT at 3 months
Nodule >8mm and/or high risk features (as per Brock model) –> Urgent CT PET +/- biopsy (if PET shows high uptake)
what medication is used for executive and visuospatial dysfunction on a background of PD?
rivastigmine
what are some acquired causes of Methaemoglobinaemia?
drugs: sulphonamides, nitrates (including recreational nitrates e.g. amyl nitrite ‘poppers’), dapsone, sodium nitroprusside, primaquine
chemicals: aniline dyes
How do you differentiate barter syndrome to gitelman’s syndrome?
Bartter’s syndrome presents early in life, with classical features of triangular facies, polyuria, polydipsia and renal failure. Serum renin and aldosterone levels are high despite a low or normal blood pressure. Urine calcium may be raised, and renal stones are a common feature.
In Gitelman’s syndrome patients may present later on in adulthood, but have a milder disease course or may be asymptomatic compared to patients with Bartter’s syndrome. Hypomagnesaemia and hypocalciuria differentiates Gitelman’s syndrome from Bartter’s syndrome.
what are the causes of Hypokalaemia with acidosis
diarrhoea
renal tubular acidosis
acetazolamide
partially treated diabetic ketoacidosis
what are the causes of Hypokalaemia with alkalosis
vomiting
thiazide and loop diuretics
Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)
what do you see on biopsy in polymyositis vs dermatomyosistis vs inclusion body myosistis?
- Endomysial CD8 positive T-cell mediated lymphocytic infiltrates that invade nonnecrotic muscle fibres = polymyositis
- Perimysial inflammation by CD4 positive T-lymphocytes and parafascicular atrophy = dermatomyositis
- Inflammatory infiltrates and inclusions within muscle fibres = inclusion body myositis
what is the kings college criteria for liver transplant?
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
What is macrophage activation syndrome?
Macrophage activation syndrome is a rare disorder that is associated with rheumatological conditions such as juvenile idiopathic arthritis, rheumatoid arthritis or systemic lupus erythematosus. It commonly presents with a pancytopenia and intercurrent infection - particularly EBV - and is usually initially treated as neutropaenic sepsis.
Left untreated, the disease is often fatal after two months.
Diagnosis: bone marrow aspiration can reveal haemophagocytosis as the key feature.
Other features: excessive hyperferritinemia, elevated triglycerides, deranged LFTs, and hypofibrinogenemia.
Treatment: immunosuppression.