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