Mocks Flashcards
How to differentiate between cholecystitis and cholangitis in the stem of the question?
Cholangitis - bilirubin has to be raised. Triad is jaundice, fever and RUQ pain. The RUQ pain is diffuse unlike cholecystitis where the pain is Murphy positive.
Cholecystiits - Patients typically present with pain and localised tenderness, with or without guarding, in the upper right quadrant. Doesn’t have to be fever + systemic upset.
Types of lung cancer and their features
Small Cell and Non-Small Cell
Small Cell - aka oat cell - is though to have derived from neuroendocrine cells in the bronchus (fetyrer cells) and so produce ectopic hormones e.g. ADH (causing SIADH and hyponatraemia), ACTH (causing Cushing’s). It rapidly divides and produces mets earlier so even though it is chemosensitive it carries a poor prognosis.
NSCC - SCC, adenoc, Large C,
SCC- smokers, male, radon gas associations, centrally located, keratinisation on histo, produces PTH which causes hypercalcaemia of malignancy
Adeno - associated with non smokers, female, far east, peripherally located, mucin production and glandular cells on histo, extra thoracic mets present early (80%)
Large Cell - Poorly differentiated large cells and poor diagnosis
PTHrp
Parathyroid hormone-related protein (or PTHrP) is a protein member of the parathyroid hormone family secreted by mesenchymal stem cells. It is occasionally secreted by cancer cells (breast cancer, certain types of lung cancer including squamous-cell lung carcinoma).
How to prescribe morphine SC
Dose of morphine sulfate SC in 24 hours = 0.5 x
Total Morphine sulfate oral dose in 24 hours
Red flags of back pain
If red flags present get XR spine, then if negative get MRI
Cancer, Cauda Equina, Fracture & Infection
Ca - >50, PMHx ca (breast, lung, gastrointestinal, prostate, renal, and thyroid cancers), pain that remains when the person is supine, aching night pain that prevents or disturbs sleep, pain aggravated by straining, Localised tenderness, refractory to back pain therapy, wt loss.
Infection - fever, recent TB/UTI, IVDU, HIV
# - Sudden onset of severe central spinal pain which is relieved by lying down, trauma hx
Cauda - bilateral neurological deficit of the legs,
Recent urinary retention (caused by bladder distension because the sensation of fullness is lost) and/or urinary incontinence (caused by loss of sensation when passing urine); faecal incontinence (due to loss of sensation of rectal fullness); Perianal or perineal sensory loss (saddle anaesthesia or paraesthesia); Unexpected laxity of the anal sphincter.
How do you manage neutropenic sepsis?
SUSPECTED:
Treat suspected neutropenic sepsis as an acute medical emergency and offer empiric antibiotic therapy immediately usually PIP-TAZ
Order FBC, kidney and LFT (including albumin), CRP, lactate and blood culture
To diagnose: pts having anticancer treatment whose neutrophil count is 0.5×109 per litre or lower and who have: > 38oC or other signs or symptoms consistent with clinically significant sepsis.
CONFIRMED:
Do a risk assessment, if low -> outpt IV if high -> admit for obs
Switch from IV to oral after 48 hours if risk is low when re-assessed
Mesenteric Ischaemia presentation
Has a widely ranging, vague presentation, and different types i.e. acute, chronic and colonic
75% have a leukocytosis and ~ 50% have metabolic acidaemia
PMHx of vascular pathology would make you suspicious
Elderly
PE different types of mx
UNSTABLE:
Thrombolysis IV alteplase < 4.5 hours + IV UFH
If CI use IV hep (need weight and gfr)
If IV hep and thrombolysis CI, use NA
STABLE:
1st line Apixaban /riva
2nd line LMWH for 5d then dabig OR LMWH + Warfarin for 5d
IVC filter – to prevent DVT becoming PE when you can’t anticoagulate the pt
Pericarditis investigation findings
Pleuritic pain
ECG: Saddle ST elevation, T wave inversion, J wave
Troponin mildly elevated
CHADVASc scoring and meaning
NB, >75 -> anticoag, >65F -> anticoag, ONLY 2 points needed
CHF history HTN Age >65 if >75 thats 2 points DM Vascular disease
2 = moderate-high and should consider anticoagulation
Also gives annual stroke risk as a percentage. Multiply this by estimate of years left to work out life time risk of stroke
Anticoagulate with DOAC (Xa e.g. apix) or Warfarin (new nice guidelines)
ACE inhibitors monitoring and how to deal with abnormal results
Side effects / interactions are often due to excessive hypotension: antihypretensives, diuretics, tetracyclines, alcohol etc
Anti-diabetics- be careful of increased blood glucose lowering
Don’t use concurrently with NSAIDs
If the serum creatinine level increases by more than 20% or the eGFR falls more than 15%, re-measure renal function within 2 weeks.
An increase of the serum creatinine level of less than 30% does not require further action.
An increase of the serum creatinine level of 30–50% (or to over 200micromol/L) or eGFR less than 30 mL/min/1.73 m2 should prompt clinical review of volume status and temporary dose reduction, or withdrawal of the diuretic or ACE-inhibitor.
Gout management
Acute Gout
1st line NSAIDs,
2nd line Colchicine (causes diarrhoea, can be very toxic OD), or Oral pred
± IA steroids
± Paracetamol (not first line)
Choice of first-line agent depends on patient preference, renal function and co-morbidities.
Ongoing (2-3 weeks post acute episode)
1st line Allopurinol
Febuxostat
Hypoglycaemia mx inside hospital
INSIDE:
If safe swallow: Give oral glucose and re-assess in 15min, repeat this 3x if necessary, if still <4 give either IM glucagon
If non safe swallow: A-E; IV access available, give 75-100ml of 20% glucose over 15 minutes, (e.g. 300-400ml/hr)
Diabetic medications MoA
Sulphonylureas - Stimulate pancreas to make more insulin
DPP4 inhibitors - Potentiate endogenous GLP-1 and GIP which stimulate insulin sec.
SGT-2 inhibitors- Sodium glucose cotransporter inhibitors
GLP-1 agonists - Lowers blood glucose post meal by increasing insulin secretion, suppress glucagon and slow gastric emptying
Thiazolidinediones - Alter transcription of genes in carb/lipid metabolism
Diabetic Medications cautions/ci
Sulphonylureas - Can cause hypoglycaemia
Modest wt gain
DPP4 inhibitors - Don’t cause hypos or weight gain
CI Pancreatitis; Can cause HF, Pancreatitis
SGT-2 inhibitors- Associated with risk of DKA, UTI,
Can’t use if impaired renal function
GLP-1 agonists - N&V, diarrhoea; Acute pancrea; Hypos
Thiazolidinediones - Several long term risks (Bone #, wt gain, visual impairment) CI HF, bladder ca
How do we manage diabetes
C: DIABETES PREVENTION PROGRAMME REFERRAL Weight loss, increase exs, reduce alcohol and smoking, refer to structured education programme
M: If HbA1c >53 commence treatment but should be an individualised goal (~48)
1) Metformin 500mg OD (can increase to 1000mg twice daily)
2) If above goal, add sulphonylurea, pioglitazone, SGLT-2 inhibitor or DPP4 inhibitor
3) Basal insulin added or triple therapy
What do you need for a diagnosis of diabetes?
Symptomatic + 1 value or A/S + 2 values on different occaisions
Fasting ≥ = 7.0 diabetes, 6.1-6.9 IFG
Random plasma glucose ≥ 11.1
75mg OGTT ≥ 11.1 Diabetes, 7.8-11 IGTT
HbA1c of ≥ 48 met, 39 to 46 HbA1c is prediabetic
Different in presentation of Ischaemic Colitis vs Sigmoid diverticulitis vs Meckel’s diverticulitis
Ischaemic - evidence of generalised atherosclerosis, and presents with abdominal pain and rectal bleeding
Acute diverticulitis - tenderness, rebound, and guarding may be present in the LLQ of abdomen, pelvic tenderness on DRE
MD - most are asymptomatic, periumbilical pain that radiates to the right lower quadrant, can present with bleeding or obstruction, clinically indistinguishable from appendicitis
Bleeding occurs in 30% to 40% of symptomatic patients in both paediatric and adult patient groups
Ischaemic Colitis Pathophysiology
Ischaemia occurs secondary to hypoperfusion of an intestinal segment. When hypoperfusion is acute, collateral blood flow may develop, precluding or minimising ischaemia; however, the regions of the intestine with a solitary arterial supply, and the watershed areas, are both at increased risk of developing ischaemia. (Watershed areas - splenic and duodenal flexure)
The degree of intestinal injury is dependent on the duration and severity of ischaemia. Acute or subacute mucosal sloughing and ulcerations occur as a result of ischaemia. The loss of the mucosal barrier allows for bacterial translocation and toxin or cytokine absorption. Re-perfusion injury can also occur if blood supply is re-established after a prolonged interruption. Segments of ischaemic bowel that do not suffer acute necrosis or perforation can heal with stenosis or stricture as the long-term sequelae of bowel ischaemia.
Types of hearing loss
Conductive hearing loss occurs usually in the external and middle ear by interfering with the ability of sound to be transmitted to the inner ear. Many causes can be treated successfully with surgery.
Sensorineural hearing losses occur in the inner ear (sensory) or auditory nerve/auditory pathway (neural). Many sensorineural hearing losses are permanent because the human inner ear and hair cells have only limited ability to repair themselves, unlike avian hair cells, which can re-generate after trauma or injury
Webers = If the sound is louder in one hear it either means conductive loss on same side or sensorineural on the opposite side (SOCS)
Rinnes = If Bone is louder than air its a conductors affair (Air should be louder than bone)
NB - rinne positive is normal, rinne negative is conductive loss
Sensorineural hearing loss managment
Lesions of the vestibularcochlear nerve (CNVIII), such as vestibular schwannoma (acoustic neuroma), usually present with unilateral hearing loss.
Can also have tinnitus, and imbalance.
It is recommended that all patients with unilateral aural symptoms, such as unilateral tinnitus and/or unilateral sudden sensorineural hearing loss, undergo magnetic resonance imaging to assess for retrocochlear pathology.
“If on one side they need the volume high, don’t forget to do an MRI” - to rule out a vestibula schwannoma
Mx Watch and wait, gamma radiation, ENT/neurosurgery:
Optic chiasm tumour will cause which visual defect
If no visual symptoms and normal visual acuity, the earliest visual field deficit will be red desaturation in the bitemporal lower visual fields and subsequent bitemporal hemianopia. The blind spots are normal in chiasmal
compression unless there is associated papilloedema from raised intracranial pressure (Foster Kennedy syndrome).
Lesion on the optic nerve will give rise to which visual defect
Monocular vision loss
if the lesion is in the retina of the eye -> Central scotoma
Lesion on the optic tract will give rise to which visual defect
Homonymous hemianopia (Right) = the brackets is the side you CAN see
Lesion on the optic radiations will give rise to which visual defect
Quadrantopia
A 33 year old man has recurrent episodes of collapse over 7 months. When angry, his muscles feel limp and he falls to the floor, but he remains conscious.
Cataplexy is loss of skeletal muscle tone with strong emotions
macula sparing lesions occur with what pathology
occipital lobe defect due to stroke because the area of the occipital lobe that corresponds to the macula has dual supply so even if you get a stroke that knocks the blood supply you will not have vision loss in retina
Causes of hypoalbuminaemia
Low - Negative acute phase reactant, Liver failure, 3rd space losses, increased GI losses, Nephrotic proteinuria
De Quervain’s tendinopathy
A stenosing tenosynovial inflammation of the 1st dorsal compartment which includes abductor pollicis longus (APL) & extensor pollicis brevis (EPB)
O/E: Special test: pain at the radial styloid with
active or passive stretch the thumb tendons over the radial styloid in thumb flexion (Finkelstein test)
PC: radial sided wrist pain, pain exacerbated by gripping and raising objects with wrist in neutral
Ix: Radiographs not needed for diagnosis
C: thumb splint
M: NSAIDs, steroid injections
S: Surgical release of 1st dorsal compartment
Rf: can be traumatic, but overuse GOLFERS SQUASHERS (Racquet balls)
Intersection syndrome
Due to inflammation at crossing point of 1st dorsal compartment (APL and EPB ) and 2nd dorsal compartment (ECRL, ECRB)
PC: Pain over dorsal forearm and wrist; tenderness on dorsoradial forearm ~ 5cm proximal to the wrist joint
Rf: ROWERS and weights LIFTERS
Scaphoid fracture
Scaphoid is most frequently fractured carpal bone, often occurring after FOOSH (high/low energy) (waist 65%; proximal 1/3 25%; distal 1/3 10%)
O/E:
anatomic snuffbox tenderness dorsally
scaphoid tubercle tenderness volarly
scaphoid compression test
positive test when pain reproduced with axial load applied through thumb metacarpal
Mx:
Proximal pole or displacement >1mm = unstable = surgical management
Adhesive capsulitis
Associations + management
Association: diabetes t1 + t2, thyroid disease
CMS Surgery: MUA or arthroscopic release controversial if done during freezing/inflammatory phase diabetics- 50% failure rate following rotator cuff or labral repair
Osteoporosis Mx
1st line - Bisphosphonate e.g. Alendronic acid
+ Calcium Vit D Supplements
2nd line- Denosumab (can be 1st line in severe osteoporosis at risk of # in post menopausal F)
3rd line - PTH receptor agonist e.g. teriparitide
If none of those are tolerated can use Raloxifene (SERM)
A 56 year old woman presents to the GP with 7 weeks of intermittent dizziness that she describes as ‘the room tilting’. The episodes start suddenly, are usually triggered by turning her head quickly, and last less than a minute before resolving completely. She reports nausea during these episodes. She is otherwise well. Otoscopic and neurological examinations are normal.
BPPV
Meniere disease vs BPPV vs Acoustic neuroma vs Vestibular neuritis vs Cerbellar pathology vs Viral labrynthitis vs Vetebrobasillar ischaemi
Meniere disease - low frequency,
sensorineuronal hearing loss, tinnitus, and aural fullness that is often exacerbated during an episode of vertigo, Recurrent episodes of vertigo last for mins- hrs + NOT provoked by positional changes
BPPV - sudden, short-lived episodes of vertigo elicited by specific head movements. Dix Hallpike maneouvre for diagnosis. Epley for treatment.
Acoustic neuroma/Vestibular Schwannoma- A benign slow-growing tumour, which, following detection, usually remains stable. Unilateral sensorineural hearing loss is the most common symptom, followed by intermittent dizziness and facial numbness
Vestibular neuritis
Often a single episode of persistent vertigo lasting for days. The vertigo can be exacerbated by any positional change, unlike the specific head movements that induce BPPV attacks. Hallpike manoeuvre doesn’t cause nystagmus/vertigo. May be preceded by a non-specific viral infection. NO HEARING LOSS. ‘Neuronitis No hearing loss”
Cerbellar pathology - nystagmus, ocular dysmetria, abnormalities of pursuit, saccadic oscillations, and an ataxic gait. If stroke, triad of NV, headache and ataxia.
Labrynthitis - short onset again (hours) of sudden vertigo and hearing loss, HPC of viral infection, vomiting, nystagmus
Vetebrobasillar ischaemia - Elderly patient
Dizziness on extension of neck
Other causes of vertigo include posterior circulation stroke trauma multiple sclerosis ototoxicity e.g. gentamicin
A 73 year old woman has abdominal pain 4 days after a laparoscopic bowel
resection with primary anastomosis for bowel cancer. Her temperature is 36.9°C,
pulse rate 105 bpm, BP 120/72 mmHg and oxygen saturation 96% breathing oxygen
6 L/min via face mask. She has reduced breath sounds in both bases. She has
abdominal tenderness with guarding and reduced bowel sounds
What is the most apporpirate investigation?
a CT with contrast (not an AXR) as this is hinting at an anastomotic leak which usually presents ~4/5days post op. CT would be required after AXR anyway in this case.
When do you activate a major haemorrhage call?
A pragmatic clinically based definition is bleeding which leads to a systolic blood pressure of less than 90 mm Hg or a heart rate of more than 110 beats per minute
Major haemorrhage is variously defined as:
- Loss of more than one blood volume within 24 hours (around 70 mL/kg, >5 litres in a 70 kg adult)
- 50% of total blood volume lost in less than 3 hours
- Bleeding in excess of 150 mL/minute.
What is the single most appropriate therapeutic change to the meds?
A 59 year old man is reviewed in clinic. He has type 1 diabetes mellitus, hypertension, ischaemic heart disease and CKD stage 4 [recent eGFR 25 mL(> 60). He is taking insulin, lisinopril, metoprolol tartrate and aspirin.
His BP is 156/96 mmHg. He has pitting oedema to the knee.
Ix:
Na 136 mmol/L (135–146)
K 5.6 mmol/L (3.5–5.3)
Urea 17.4 mmol/L (2.5–7.8)
Creatinine 237 μmol/L (60–120)
eGFR 26 mL/min/1.73 m2 (>60)
Urinalysis: protein 2+
ADD IN FUROSEMIDE
don’t get distracted by potassium, offloading fluid is priority here
When do you oxygenate in A-E of a STEMI?
Oxygen will increase mortality for STEMI with sats of >94%. (BMJ Nov 2018).
Adrenal crisis presentation + mx
Adrenal crisis is acute presentation of addison’s
Nearly all patients have a history of lethargy and weight loss
Bloods: Hyponatraemia + hyperkalaemia
1. Hydrocortisone should be given to patients with a suspected but unconfirmed diagnosis of adrenal insufficiency
2. Saline should be administered to correct hypotension and dehydration. It is usually necessary to administer 1 L rapidly and a further 2 to 4 L over the first 24 hours,
3. Glucose should be administered when necessary to correct hypoglycaemia
The underlying cause that precipitated the crisis should be sought and treated, and once the patient is stable
Cord compression imaging and management
Imaging of choice: MRI of spine
Management depends on whether its acute, traumatic infective, chronic, malignant.
ACUTE (traumatic) - Immobilise with cervical collar and then surgery (decompression/stabilisation surgery)
ACUTE (atraumatic, cauda equina) - decompressive laminectomy within 48hrs (medical intervention has shown no benefit). LMWH within 72 hrs. PPI for 4 weeks after SCC.
Infective - Abx (vanc and metro and cef) (staph)
MALIGNANT - Treatment of spinal mets is largely palliative. Historically, treatment has consisted of corticosteroids (dexamethasone) to reduce oedema and help with pain. Consider surgery (decompressive laminectomy/vertebrectomy) and radiation.
A 62 year old woman attends her GP surgery with shortness of breath on exertion and a cough productive of white sputum on most mornings. She has never had haemoptysis and has maintained a steady weight. She describes four chest infections in the past year treated with a short course of steroids and antibiotics. She has a 10 pack-year smoking history.
Her BP is 132/85 mmHg. Chest X-ray is normal.
What is the diagnosis and test needed to confirm?
COPD over HF
- BP/Smoking history doesn’t point either way
- Symptoms (breathless on exertion) could be present in either
- PMHx of repeat chest infections and chronic cough is more COPD than HF
- Spirometry
Post op oliguria differentials
Pre-renal:
- Pre-renal Hypovolaemia
- Intra-abdominal HTN
- Renal artery occlusion (rare, cause loin pain, systemically unwell)
Renal:
- ATN (nephrotoxic substances used? abx/dye?)
- embolic events (esp are releasing an aortic clamp)
- Ureteric injury (to cause AKI would need to be bilateral injury)
Post-renal:
- Catheter obstruction - anuria
- Ureteric obstruction - anuria
A 20 year old man is brought to the Emergency Department having been struck on the side of the head with a cricket ball.
He has a minor scalp abrasion. His GCS is 15/15 and there are no focal neurological signs.
Four hours later he collapses, at which point his GCS is 6/15. A CT scan of brain reveals a biconvex haemorrhage in the right parietal region.
Hit side of the head with a ball -> likely to be pterion and underneath the pterion is the MMA
A bleed in the MMA leads to an EDH
This is supported by the ‘biconvex’ which basically means LENS shaped i.e. EDH
This matches the history: clear trauma + lucid interval
What does lung malignancy look like on CXR?
Depends on type of malignancy:
Mesthelioma - 90% of these arise from the pleura and so pleural opacity which may extend around and encase the lung is common. You can get ispilateral mediastinal shift
Mets - peripheral, rounded nodules of variable size, scattered throughout both lungs
Lung cancers - often difficult to visualise as they are small (needs to be ~1cm to be seen). Its more obvious if it occurs in the bronchus and causes a lobe collapse (Golden S sign in RUL collapse due to SCC) or if it causes cavitation (SCC most common). Adenocarcinoma and large cell are most commonly peripheral lesions. Small Cell is central and often presents with hilar/perihilar mass and LN involvement (widened mediastinum) on CXR.
Plaque psoriasis vs eczema
Eczema makes your skin red and inflamed. It may be scaly, oozing, or crusty. You may see rough, leathery patches that are sometimes dark. It can also cause swelling.
Psoriasis can also cause red patches. They may be silvery and scaly – and raised. But if you look closely, the skin is thicker and more inflamed than with eczema.
Migraine prophylaxis and acute termination
Migraine prophylaxis: Topiromate, valproate, amitryptilline, propranolol, candesartan, amitryptlline
Migraine rescue therapy: 1st line ED IV antiemetic (e.g., metoclopramide or prochlorperazine) combined with diphenhydramine (or sc sumatriptan)
Myasthenia Gravis
Myasthenia gravis (MG) is a chronic autoimmune disorder of the post-synaptic membrane at the neuromuscular junction (NMJ) in skeletal muscle. Circulating antibodies against the nicotinic acetylcholine receptor (AChR) and associated proteins impair neuromuscular transmission. Patients present with muscle weakness, which typically worsens with continued activity (fatigue) and improves on rest. Severity varies from isolated eye muscle weakness to generalised muscle weakness and respiratory failure requiring mechanical ventilation Double vision, ptosis, difficulty chewing and swallowing, and slurring of speech that worsen throughout the day are characteristic symptoms
