Past papers Flashcards
Differential diagnoses of a solid liver mass
Pyogenic liver abscess Amoebic liver abscess Hyatid disease Benign liver tumours - Haemangioma, liver cell adenoma, focal nodular hyperplasia Malignant liver tumour - HCC, mets
Approach to a liver mass
Radiological imaging is the cornerstone of diagnosis for focal liver lesions. Various algorithmic approaches have been described, all starting with an ultrasound scan. The initial questions to determine are whether lesion(s) are single or multiple, or solid or cystic. Cystic lesions of the liver are considered later in this chapter. The solitary or potentially resectable liver ‘tumour’ is best evaluated by CT and, when appropriate, MRI scanning. Each of the benign and malignant tumour types has typical but seldom diagnostic appearances. The CT evaluation of the tumour appearance and behaviour during the various phases of contrast injection may be helpful. It should be possible to distinguish most cavernous haemangiomas from other tumours by this means, though some vascular tumours may create difficulty. It is important to remember that chest radiographs (and possibly CT scans of the lungs) may avoid unnecessary investigations by demonstrating that the patient has metastatic disease, rendering further investigation and surgery futile.
The objectives in assessing a liver mass are:
· to establish a diagnosis · to determine whether surgery is indicated · to judge whether resection is possible (i.e. the extent of the lesion and relation to vascular and biliary anatomy)
Two scoring systems used to assess liver function prior to surgery
Child’s grading system modified by Pugh Model for end stage liver disease (MELD) [INR, bili, creatinine]
Treatment options for primary liver malignancy
Large tumour - Transarterial embolisation. Iodised oil and cytotoxic drugs injected into hep artery -> cleared by normal cells not malignant ones Ressection
Which HCC occurs in non-cirrhotic livers without HepB/C
Fibrolammelar carcinoma [favourable prognosis]
How to classify renal artery stenosis
Anatomical (ostial, parostial, truncal, accessory, segmental, mixed, renal artery occlusion)) Pathological (Atherosclerotic vs non-atherosclerotic [fibromuscular dysplasia, takayasus, dissection, developmental, aneurysm, trauma, radiation, anastomotic]) Severity (mild, moderate, severe)
Diagnostic appraisal of severe, medically refractory HPT
Endocrine screen (cortisol, Aldosterone, renin assay, metanepharines/catecholamines[urine and plasma], TFTs, PTH, serum calcium and phosphate) Imaging (CT abdo, chest, brain. US thyroid. Radioisotope scan adrenal, MIBG[pheo]) MAG3 renogram for single GFRs Duplex US kidneys Captopril renogram Vascular imaging
Why not togive ACEi in RAS
Angiotensin ll vasoconstricts the efferent arteriole maintaining glomerular pressure. ACEi prevent this and decrease GF pressure.
Treatment modalities for RAS
Medical Percutaneous transluminal renal angioplasty Percutaneous transluminal renal angioplasty and stenting Surgical revascularisation Nephrectomy
Atherosclerotic RAS manifests clinically in which two ways
Severe HPT Ischaemic nephropathy
Causes of secondary HPT
- Endocrine disorders · Cushing’s syndrome · Conn’s syndrome · Phaeochromocytoma · Hyperthyroidism · Hyperparathyroidism · Adreno-genital syndrome 2. Renal parenchymal disorders · Nephroblastoma (Wilm’s tumor) 3. Renovascular disorders · Renal artery stenosis (RAS) · Coarctation of the aorta · The middle aortic syndrome
Differential diagnosis for rectal bleeding
· Diverticulosis · Angiodysplasia · Colitis · Neoplasia · Haemorrhoids and other anorectal disorders · Drug related (anti-coags, NSAIDS)
Investigations for LGIB
Bloods Radiology (AXR, CT [w mesenteric angiography], technetium labelled RBC scan, selective mesenteric angiography) Endoscopy/ colonoscopy
Breast lump differentials
Physiological lumpiness Fibroadenoma Cyst Infection Fat necrosis Cancer
Major risk factors for breast Ca
Female, age, contralateral disease, fam hx, Irradiation, BRCA1/2
Minor risk factors for breast Ca
Wide estrogen window, few/late/no children, HRT, OCP, smoking
Treatment options for oesophageal varices
- Pharmacological (Vasopressin, terlipressin, somatostatin, octreotide) 2. Endoscopic (banding, injection sclerotherapy) 3. Balloon tamponade 4. TIPS (transjugular intrahepatic portosystemic shunt) 5. Surgery (shunt, oesophageal transection)
Classify causes of portal HPT
- Increased resistance to flow A. Prehepatic (portal/splenic thrombosis, exrinsic compression) B. Hepatic (cirrhosis, ALD, schistosomiasis, portal fibrosis etc. C. Post hepatic (Budd-chiari, veno-occlusive disease, constrictive pericarditis) 2. Increased portal blood flow A. A-P-V fistula B. Increased splenic flow
Long term management of variceal bleeding
- Endoscopic Therapy - Injection Sclerotherapy - Variceal band ligation 2. Pharmacotherapy - b-blockers 3. Surgery a. Shunt i) DSRS ii) Portacaval b. Non-Shunt i) Oesophageal transection and gastric devascularisation ii) Splenectomy for gastric varices due to splenic vein thrombosis 4. Liver Transplantation
What to test in ascites if TB suspected
Adenosine deaminase
Pathogenesis of DVT
Virchows triad Coagulation (antithrombotics vs prothrombotic state)
Diagnostic work up for DVT
Risk factors D-dimer Duplex ultrasound (compressability) Wells score
Prophylaxis for DVT
General (hydration, analgesia, ambulate, elevate) Mechanical (compression) Pharmacologic (Unfractionated heparin, LMWH, vitK antagonists) - INR 2-3 If knee/hip give warfarin
Broad management principles in DVT
Prevent extension, recurrance and death. 1. Early immobilisation/ elevation 2. Anticoagulation (UFH,LMWH) 3. Prevention
Post thrombotic syndrome
pain, edema, heaviness, hyperpigmentation or ulceration. Post-thrombotic syndrome are a consequence of ambulatory venous hypertension, which is determined by a combination of factors, including valvular reflux, persistent venous obstruction, and the anatomic distribution of these abnormalities.
Types of anal fistulas
Intersphincteric Trans sphincteric Suprasphincteric Extrasphincteric (Crohns, Tb, Ca and trauma)
What is an anal fissure
Painful linear tear of the distal anal canal
What clinical features of an anal fissure make you supect pathology other than trauma (eg Crohn’s)
If the fissure is not in the midline If there’s ulceration If other pathology is present
Pathogenesis of anal fissure
Anal fissures are caused by trauma to the anus and anal canal. The cause of the trauma usually is a bowel movement.
Rx for anal fissures
Many resolve spontaneously Medical (Stool bulkers and softeners, nitroglycerin cream) Surgical (Lateral internal sphincterotomy, sphincter dilatation)
Evaluate and investigate feacal incontinance
Bloods (infection etc) US Anal manometry Electromyelography Defecography
Criteria for urgent referral for soft tissue mass
>5cm Painful Increasing in size Deep to muscle fascia Recurrence after previous excision
From where do sarcomas originate
Mesoderm (Muscle, fascia, fat, synovium)
Histological grading of sarcomas
Low - few mitoses, No tumour necrosis, mild atypia Intermediate - numerous mitoses, no tumour necrosis, atypia High - tumour necrosis + mitoses + atypia
Management principles of soft tissue sarcomas
Referral Diagnosis and staging (Aspiration cytology, core biopsy, CT, MRI) Surgery (curative/palliative) Radiation Chemo
Common sarcoma subtypes
Undifferentiated soft tissue sarcoma Liposarcoma Leiomyosarcoma Synovial sarcoma Malignant peripheral nerve sheath sarcoma
Indications for emergency upper gi bleed surgery
· Exsanguinating haemorrhage · Associated perforation · Failed endoscopic therapy of active bleeding in shocked patients · Recurrent bleeding after endoscopic therapy · Patients at risk for rebleeding where endoscopic therapy is not available
Causes of small bowel obstruction
Extrinsic Adhesions (common) Hernia (common) · External eg. inguinal, umbilical · Internal eg. diaphragmatic Neoplastic Intra-abdominal sepsis/abscess · Ruptured appendix/diverticulum Wall Congenital · Malrotation · Cystic fibrosis · Meckel’s diverticulum Inflammatory · Crohn’s disease Infectious · Tuberculosis · Actinomycosis Traumatic · Haematoma · Ischaemic stricture Neoplastic · Primary · Metastatic Other · Intussusception · Endometriosis · Radiation stricture Lumen Gallstone Bezoar Foreign body Enterolith
Investigations for bowel obstruction
Bloods - electrolyte levels, acidosis[necrosis] AXR erect - air fuild level CT - extrinsic obstruction
Causes of large bowel obstruction
Colorectal cancer Volvulus Diverictular stricture Feacal impaction Foreign body Hernia
Small vs large bowel obstruction on AXR
Vulvulae coniventae vs haustra Central vs peripheral
Surgical options for left sided colonic obstruction
3 stage procedure - proximal stoma - remove obstruction - close stoma 2 stage - resect lesion and make stoma - close stoma 1 stage - subtotal colectomy + primary ileorectal anastamosis/ segmental colectomy + waskout + anatamosis
What is crohn’s disease
a chronic inflammatory disease of the intestines, especially the colon and ileum, associated with ulcers and fistulae.
Rx of high output stoma
Dietician + adjust diet Isotonic fluid resus Omeprazole High dose loperamide Antibiotic trial for bacterial overgrowth Monitor electrolytes (hypoNaMg, hyperK)
What is not absorbed if ileum is removed?
Vit B12 Bile salts _ leading to fat soluble vit deficiency Glucagon like peptide leading to poor intestinal repair
Causes of gastric outlet obstruction
Gastric Ca PUD Pancreatic pathology (Ca or pseudocyst) Corrosive stricture Rare (adenopathy, volvulus, bezoars)
What metabolic abnormailties occur in gastric outlet obstruction
Hypochloric, hypokalaemic metabolic acidosis. HCl lost due to vomit. Renal compensation secreting K. Give normal saline until not dehydrated then correct K.
Diagnostic investigations for gastric outlet obstruction
Endoscopy (+biopsy) Metastatic screen (CXR, LFT, US, CT) Barium meal
