16/10/2024 Flashcards
Antibiotic choice for bacterial meningitis?
IV cefotaxime
If <3 months or >50 then amoxillicin should be given too
Antibiotic choice for managing bacterial meningitis contacts?
Oral ciprofloxacin
(Or rifampicin)
Interpretation of AAA screening?
<3.0 Cm is normal
3-4.4 = rescan every 12 months
4.5-5.4 = rescan every 3 months
>=5.5cm OR expanding >1cm a year = 2 week referral to vascular surgery for EVAR or open repair
pathophysiology of acoustic neuroma
Benign, slow growing tumours that form along the branches of the vestibulocichlear nerve
Features of acoustic neuroma and relate them to the cranial nerve?
CN 5 - absent corneal reflex
CN 7 - facial palsy (palsy of forehead too as LMN lesion)
CN 8 - vertigo, U/L sensorineural hearing loss, U/L tinnitus
Investigations for acoustic neuroma?
Audiometry to show sensorineural hearing loss
MRI with gadolinium contrast
Features of neurofibromatoiss type 2?
B/L acoustic neuromas
Multiple intracranial schwannomas, meningiomas and ependymomas
Management of eclampsia?
Once a decision to deliver baby has been made give IV bolus of 4g magnesium sulphate over 5-10 minutes followed by an infusion of 1g/hour
Continue Tx for 24 hours after last seizure or after delivery
Remember if considering delivery <34/40 give corticosteroids
Causes of gingival hyperplasia
Drugs - phenytoin, Ciclosporin, CCB
AML
When should you consider medical/surgical management of miscarriage rather than expectatnt management?
- If increased risk of haemorrhage e.g. late first trimester or coagulopathy
- Previous adverse/traumatic experience associated with pregnancy
- Infection
Management of missed miscarriage?
Oral mifepristone -> 48 hours give misoprostol (oral, vaginal, sublingual)
If bleeding has not started within 48 hours of misoprostol advise pt to contact HCP
Offer antiemetics and analgesia
Tx of incomplete miscarriage?
Single dose of misoprostol (vaginal, oral, sublingual)
When should a pregnancy test be performed after medical miscarriage?
3 weeks
Tx of thyrotoxicosis?
Propanolol to control Sx
Carbimazole - high doses for 6 weeks until pt is euthyroid and then reduced
Radioiodine Tx
Why is Carbimazole used first line for thyrotoxicosis ahead of propothyluracil?
Due to its risk of liver damage
MOA of Carbimazole?
blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin → reducing thyroid hormone production
Rules for breastfeeding with HIV?
Never advised
Which antibodies should you test for in suspected T1DM?
Anti-glutamic acid decarboxylase (anti-GAD)
Insulin autoantibodies (IAA)
Islet cell antibodies (ICA)
Note they are present in up to 70% of people at time of diagnosis but titre declines with time!
When should you test c-peptide and autoantibodies in suspected diabetes?
Not routinely to confirm T1DM but if some atypical features e.g. high GMI, >=50
Basically when you are unsure between T1 and T2
Why can mitral stenosis cause haemoptysis?
Mitral valve will become thicker, obstructing blood flow across the mitral valve from the left atrium to the left ventricle, leading to an increase in pressure within the left atrium, pulmonary vasculature and right side of the heart.
This might cause increased pressure in the pulmonary circulation causing rupture of pulmonary vessels, leading to haemoptysis.
Outline acute asthma Tx?
Stepwise progression:
Oxygen 15L NRB
Inhaled salbutamol
Nebulised Salbutamol (if severe or life threatening)
40-50mg prednisolone orally (at least 5 days)
Add nebulised ipratropium bromide 0.5mg 4-6 hourly
Consider IV magnesium sulphate 1.2-2g over 20 minutes
Consult with senior medical start -> consider IV aminophylline
Treat in ITU/HDU - consider intubation & ventilation or ECMO
When should you give further Tx after metformin monotherapy in T2DM?
If already on 1 drug and HbA1c has risen to 58mmol/mol\
(Note SGLT2 inhibitors may be added on at any point if any risk of or established CVD/heart failure)
HbA1c target if T2DM treated with metformin?
48
HbA1c target if T2DM treated with any diabetic drug which can cause hypoglycaemia?
53
HbA1c target if T2DM is already being treated with 1 drug but HbA1c previously rose to 58?
53
What are typical carboxyhaemoglobin levels in smokers and non-smokers?
Non-smoker = <3%
Smoker = <10%
What should you think if a pt has cabroxyhaemoglobin levels of >10%?
CO poisoning
Features of carbon monoxide toxicity?
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
How long do cephalohaematomas take to resolve?
Up to 3 months
What type of murmur does tricuspid regurgitation produce?
Pan-systolic
Which antibiotics are used as prophylaxis in oesophageal variceal haemorrhage?
Quinolones
What should you do if you have an uncontrolled varicella haemorrhage?
Insert a Sengstaken-Blakemore tube
If this fails then consider TIPSS
Prophylaxis of variceal haemorrhage?
Propanolol
Endoscopic variceal band ligation at 2-weekly intervals until all varices have been eradicated. Use PPI cover
If not successful in preventing further episodes consider TIPSS
What is Pseudocholinesterase deficiency?
Autosomal dominant condition
Causes a defective form of the enzyme which is unable to metabolize succinylcholine leading to prolonged neuromuscular paralysis
Peripheral blood smear findings in AML?
Myeloblast cells
Auer rods
Peripheral blood smear findings in ALL?
Lymphoblast cells
Peripheral blood smear findings in CML?
Immature granulocytes
Eosinophilia and basophilia
Usually few blast cells
Peripheral blood smear findings in CLL?
Small lymphocytes with scant cytoplasm
Smudge cells
Management of a breast abscess as a complication of mastitis?
Incision and drainage
What are precipitating factors for hyperosmolar hyperglycaemic states?
Inter current illnes
Dementia
Sedative drugs
BG level in HHS?
> 30mmol/L
Management of HHS?
IV 0.9% sodium chloride 0.5-1L
(Monitor K+ levels!!)
Insulin should only be given if BG stops falling whilst giving IV fluids
VTE prophylaxis
Catheter to monitor urine output
Tx underlying cause
Complications of HHS?
Usually hyperviscocity -> MI or stroke
What are metabolic consequences of refeeding syndrome?
Low phosphate - hallmark feature!
Low K+
Low magnesium
Abnormal fluid balance
Pathophysiology of low phosphate in refeeding syndrome?
Reintroduction of carbs causes a shift from fat to carbohydrate metabolism which activates insulin secretion = increases cellular uptake of glucose
This also stimulates intracellular movement of phosphate as its used in synthesis of ATP and 2,3-diphosphoglycerate levels in erythrocytes = reduces serum phosphate levels
So chronic malnutrition = depleted phosphate stores and when refeeding starts the sudden demands for phosphate in anabolic processes exceeds supplies = hypophosphataemia
Clinical consequences of hypophosphataemia seen in refeeding syndrome?
Cardiac Dysfunction: Hypophosphatemia can impair myocardial contractility, leading to heart failure. It may also cause arrhythmias due to its role in maintaining normal cellular electrophysiology.
Respiratory Failure: Phosphate is essential for ATP production, necessary for respiratory muscle function. Severe hypophosphatemia can lead to muscle weakness, including the diaphragm and intercostal muscles, potentially resulting in acute respiratory failure.
Neurological Complications: These can range from confusion and seizures to coma, attributable to disturbed ATP metabolism in the central nervous system.
Haematological Effects: Reduced 2,3-diphosphoglycerate levels in erythrocytes affect oxygen release from haemoglobin, leading to tissue hypoxia. Hypophosphatemia can also result in hemolysis.
Rhabdomyolysis: Phosphate depletion impairs ATP production in muscles, which can lead to muscle breakdown and rhabdomyolysis.
How to prevent refeeding syndrome?
Try to correct electrolytes before starting nutrition support
if a patient hasn’t eaten for > 5 days or is at risk, aim to re-feed at no more than 50% of requirements for the first 2 days.
Investigation for phaeochromocytoma?
24 hour urinary collection of metanphrines
Tumour localisation with MRI or CT abdo
Management of phaeochromocytoma?
Surgery is definitive
But pt must be stabilised with medical Tx first. Give alpha blockers before beta blockers
Sx of trichomonas vaginalis?
vaginal discharge: offensive, yellow/green, frothy
vulvovaginitis
strawberry cervix
pH > 4.5
in men is usually asymptomatic but may cause urethritis
Investigation of trichomonas vaginalis?
microscopy of a wet mount shows motile trophozoites
Tx of trichomonas?
oral metronidazole for 5-7 days, although the BNF also supports the use of a one-off dose of 2g metronidazole
Differences between BV and trochomonas?
BV has thin white discharge. Trichomonas has frothy, yellow-green
Trichomonas causes vulvovaginitis and strawberr crevices
BV on microscopy: clue cells
Trochomonas wet mount: motile trophozoites
Both cause pH >4.5 and you treat both with metronidazole
Tx of hypercalcaemia?
Rehydration with normal saline - usually 3-4L a day
Following rehydration - bisphosphanates
Most common type of breast cancer?
Invasive ductal carcinoma
What scoring tool is used to estimate prognosis in breast cancer?
Nottingham prognostic index
Breast cancer referral guidelines
2WW:
>=30 and any new breast lump
>=50 and any symptoms in 1 nipple e.g. discharge or retraction
Consider
If any skin Sx suggestive of breast cancer
If >=30 and unexplained lump in axilla
Non-urgent referral for unexplained breast lump in women <30
Pathophysiology of haemochromatoiss?
Autosomal recessive - inheritance of both mutations on copies of HFE gene on chromosome 6
Causes a disorder or iron absorption and metabolism = iron accumulation
Symptoms of haemochromatoiss?
Early = fatigue, ED and arthralgia often in hands
Later = bronzing of skin, hypogonadism e.g. amenorrhoea, diabetes, chronic liver disease, cardiac failure and arthritis
Investigations for haemochromatoiss?
Liver studies - transferrin saturation >55% in men and >50% in women, raised ferritin, raised iron, low TIBC
LFTs for liver accumulation (can consider a liver biopsy for cirrhosis)
MRI to quantify liver and cardiac iron
Test family members using genetic testing for HFE mutation
Investigations for haemochromatoiss?
Liver studies - transferrin saturation >55% in men and >50% in women, raised ferritin, raised iron, low TIBC
LFTs for liver accumulation (can consider a liver biopsy for cirrhosis)
MRI to quantify liver and cardiac iron
Test family members using genetic testing for HFE mutation
Tx of haemochromatoiss?
Venesections - aim to keep transferrin saturation <50% and ferritin concentration <50
Second line - desferioxamine (iron chelation)
Complications of haemochromatoiss?
Diabetes
Liver disease or cirrhosis or hepatocellular carcinoma
Sexual and endocrine dysfunction
Seconday cardiomyopathy
Hypothyroidism - iron can cause oxidative damage to the thyroid
Pseudogout due to chondrocalcinosis
Interpretations ABPI?
> 1.4 suggests calcification e.g, in diabetes
1-1.4 normal
0.6-0.9 - claudication
Anything <0.5 suggests chronic limb-threatening ischaemia (used to be called critical limb ischaemia)
0.3-0.6 indicates rest pain
<0.3 is impending
Statin and antiplatelet for peripheral arterial disease?
Atorvastatin 80mg ON
Clopidogrel 75mg OD
What drug can sometimes be used for PAD when pts are not responding to exercise therapy and lifestyle modifications?
naftidrofuryl oxalate: vasodilator, sometimes used for patients with a poor quality of life
What classification is used to grade chronic limb ischaemia?
Rutherford classification
First line investigations for peripheral arterial disease?
Duplex USS
CT angiogram can guide revascularisation treatment
Management of intermittent claudication?
offer a supervised exercise programme (~2 hours a week for 3 months - should be exercising to the point of maximal pain) if not available consider suggesting unsupervised exercise.
Offer referral for consideration of angioplasty or bypass surgery if this has not lef to Sx improvement alongside modifying RF
Consider offering naftidrofuryl oxalate only when exercise hasn’t helped and pt does not want referral. Review at 3-6 months. This is a vasodilator!
Offer information of cause, risk of limb loss and CVD risk, key modifiable risk factors, how to manage pain. Offer advice on foot care e.g. daily checking of feet, good shoes, not walking bare feet etc.
Management of acute limb ischaemia?
emergency assessment by vascular specialist -> endovascular therapies or surgical interventions e.g. bypass surgery, amputation, percutaneous mechanical thrombus extraction etc
Pts are usually given IV opioids and IV UFH to prevent thrombus propagation.
All these pts need follow up with managing CVD risk… smoking cessation, diet, weight management, exercise, statin therapy with 80mg atorvastatin, prevention/Tx of diabetes, Tx of hypertension and clopidogrel 75mg daily.
Management of chronic limb-threatening ischaemia?
refer urgently to a vascular MDT. Anage pain with paracetamol or opioids (+/- laxative)
All these pts need follow up with managing CVD risk… smoking cessation, diet, weight management, exercise, statin therapy with 80mg atorvastatin, prevention/Tx of diabetes, Tx of hypertension and clopidogrel 75mg daily.
Counsel them on risk of limb loss or cardiovascular events associated with PAD
Chronic limb-threatening ischaemia vs acute limb ischaemia?
Chronic limb-threatening ischaemia — characterised by chronic, inadequate tissue perfusion in combination with ischaemic rest pain, with or without tissue loss (for example ulcers, gangrene) or infection. It represents the end stage of peripheral arterial disease
cute limb ischaemia is a sudden decrease in limb perfusion that threatens limb viability — decreased perfusion and symptoms and signs develop over less than 2 weeks. It is a medical emergency.
Most common cause of death in diffuse cutaneous systemic sclerosis?
the most common cause of death is now respiratory involvement, which is seen in around 80%: interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH)
