Abdomen Flashcards
Causes of ascites
Infection (esp TB)
Malignancy
Increased hydrostatic pressure: CCF, pericarditis
Decreased oncotic pressure: cirrhosis, nephrotic syndrome
Myxoedema (severe hypothyroidism)
With portal HTN: cirrhosis, portal nodes, Budd-Chiari syndrome, IVC or portal vein thrombosis
Causes of splenomegaly
Infective: septicaemia, malaria, IE, hepatitis, EBV, TB, CMV, HIV, rheumatic fever
Haematological: sickle cell, thalassaemia, pernicious anaemia, paraproteinaemia, hypereosinophilia, myelofibrosis
AI: vasculitis (Behcet’s), Sjogren’s syndrome, RA, SLE
Malignancy: leukaemias, lymphoma, secondaries (rare)
Irreducible hernia
Cannot be pushed back into abdomen (does not necessarily mean they are obstructed or strangulated)
Incarcerated hernia
Contents of hernial sac are stuck inside by adhesions
Obstructed hernia
Bowel contents cannot pass through the hernia
Strangulated hernia
Ischaemic occurs
Types of abdominal herniae and RFs
Inguinal: men, chronic cough, constipation, urinary obstruction, heavy lifting, ascites Femoral: women Umbilical: obesity, ascites Epigastric Incisional: post-surgery, obesity Spigelian Lumbar Obturator: pain along medial thigh in thin woman Sciatic (rare)
Appearance of femoral hernia vs inguinal hernia
Femoral: inferolateral to pubic tubercle
Inguinal: superomedial to pubic tubercle
DDx of medial thigh mass
Femoral hernia Inguinal hernia Saphena varix Enlarged Cloquet's node (suggests superficial or deep inguinal involvement) Lipoma Femoral aneurysm Psoas abscess
Indirect vs direct inguinal hernia
Indirect: more common, hernia passes trough internal inguinal ring and, if large, out through external ring
Direct: push directly through the posterior wall of inguinal canal into defect in adominal wall
Relations of inguinal canal
Floor: inguinal ligament and lacunar ligamenta
Roof: fibres of transversalis and IO
Anterior: EO aponeurosis + IO for lateral 1/3
Posterior: laterally transversalis fascia, medially conjoint tendon
Identifying internal ring
Mid-point of inguinal ligament (1.5cm above femoral pulse)
Identifying external ring
Split in EO aponeurosis just superior and medial to pubic tubercle
Mid-inguinal point vs mid-point of inguinal ligament
Mid-inguinal point: halfway between ASIS and public symphisis (femoral artery crosses here)
Mid-point of inguinal ligament: halfway between ASIS and public tubercles (location of deep internal ring)
Contents of inguinal canal in male
External spermatic fascia (from EO), cremasteric fascia (from IO and transversus abdominus) and internal spermatic fascia (from transversalis fascia) covering the cord Spermatic cord (round ligament of uterus in female): vas deferans, obliterated processus vaginalis, lymphatics, arteries to vas/cremaster/testes, venous plexus, genital branch of genitofemoral nerve, sympathic nerves Ilioinguinal nerve
Mx of inguinal hernia
Diet
Surgical: mesh techniques
FU: 4/52 rest, return to manual work and driving after less than 2 weeks if all is well and the pt is comfortable
Achalasia
Lower oesophageal sphincter fails to relax due to degeneration of myenteric plexus
Mx of achalasia
Endoscopic balloon dilatation or Heller’s cardiomyotomy with fundoplication (+ PPI)
Non-invasive options: botox injection, CCBs, nitrates
Ix for achalasia
CXR: fluid level in dilated oesophagus
Barium swallow: dilated tapering oesophagus
Mx of dyspepsia
If less than 55: “test and treat” (test for H. pylori, give PPI)
If >55 (and new dyspepsia not from NSAID use and persisting for >4-6/52) or ALARM Sx: refer for urgent endoscopy
What is more common: GU or DU?
DU (4x)
Rx for dyspepsia
Lifestyle: decrease alcohol and tobacco, reduce stress, avoid aggravating foods
H. pylori eradication: triple therapy (PAC: PPI, amoxicillin, clarithromycin)
Drugs to reduce acid: PPI, H2 blockers
If drug-induced ulcer, cease drug if possible and give PPI
Testing for H. pylori
Urea breath test (best; PPI will give a false negative so stop 2/52 before) Stool Ag (PPI will give a false negative so stop 2/52 before) Serology
Mx of Barrett’s oesophagus
Pre-malignant/high grade dysplasia: oesophageal resection or eradicative mucosectomy (partial thickness resection of bowel wall) if young and fit (less invasive options e.g. targeted mucosectomy, laser ablation, used in others)
Low grade dysplasia: annual endoscopy
No pre-malignant changes: surveillance endoscopy + biopsy every 1-3 years and anti-reflux measures in interim
NB Those with long-standing GORD (e.g. >5 years, esp if over 50) should have one-off screening endoscopy
Most common site for gastric cancer
Gastro-oesophageal junction
Acute mesenteric ischaemic
Almost always involves small bowel
May follow SMA thrombosis or embolism, mesenteric vein thrombosis or non-occlusive disease (trauma, vasculitis, radiotherapy, strangulation e.g. hernia)
Presentation of acute mesenteric ischaemia
Acute severe abdominal pain (constant, central or around RIF)
No abdominal signs
Rapid hypovolaemia leading to shock
Ix for acute mesenteric ischaemia
Increased WCC
Persistent metabolic acidosis
AXR: “gasless” abdomen
Angiography (probably wouldn’t if high clinical suspicion, just progress to laparotomy)
Complications of acute mesenteric ischaemia
Septic peritonitis
Progression of systemic inflammatory response syndrome (SIRS) into multi-organ dysfunction syndrome (MODS; mediated by bacterial translocation across dying gut wall)
Rome criteria for constipation
Fewer than 3 BMs per week
For >25% of BMs:
Straining
Lumpy or hard stools
Tenesmus
Sensation of anorectal obstruction or blockage
Manual manoeuvres to facilitate (e.g. digital evacuation, support of pelvic floor)
Mx of constipation
Bulking agents: increase faecal mass and stimulate movement e.g. bran
Stimulant laxatives: increase intestinal motility (do not use in obstruction or acute colitis) e.g. bisacodyl (Dulcolax), senna
Stool softeners: e.g. liquid paraffin, particularly useful for painful anal conditions
Osmotic laxatives: retain fluid in bowel e.g. lactulose, macrogol AKA Movicol (disaccharides), Mg2+ salts, phosphate enemas (useful for rapid bowel evacuation pre-op)
Diverticulosis
Presence of diverticula (outpouchings of gut wall, usually at sites of entry of perforating arteries)
Diverticular disease
Diverticulosis which is symptomatic
Diverticulitis
Inflammation of diverticulum
Pathogenesis of diverticulosis
Most occur in sigmoid colon
Lack of dietary fibre is thought to lead to high intraluminal pressures which force the mucosa to herniate through the muscle layers of the gut at weak points adjacent to penetrating vessels
Ix for diverticulitis
Pyrexia
Raised WCC
Raised CRP/ESR
Erect CXR, AXR: can detect perforation, free fluid, collections (CT with contrast enema is more accurate)
Mx of diverticulitis
Analgesia
NBM
IVFs
IV Abx (e.g. cefuroxime + metronidazole)
Complications of diverticulitis
Perforation Haemorrhage Fistulae: enterocolic, colovaginal, colovesical Abscesses Post-infective strictures: in sigmoid
Hartmann’s procedure
Temporary colostomy + partial colectomy
Mx of perforation secondary to diverticulitis
Hartmann’s procedure
Mx of fistulae (esp colicovesical) secondary to diverticulitis
Surgical (e.g. colonic resection)
Angiodysplasia
Submucosal AVMs that typically present as fresh PR bleeding in elderly (underlying cause unknown)
Mx of angiodysplasia
Embolisation
Endoscopic laser electrocoagulation
Resection
Ix of angiodysplasia
Mesenteric angiography: also allows therapeutic embolisation (CT angiography is a non-invasive option)
Tc radionuclide-labelled red-cell imaging during active bleeding
Meckel’s diverticulum
Distal ileum contains embryonic remnants of gastric and pancreatic tissue; TRUE diverticulum (all layers of wall)
May be gastric acid secretion, causing GI pain and occult bleeding or malaena
Rule of 2s for Meckel’s diverticulum
2% (of the population)
2 feet (proximal to the ileocecal valve)
2 inches (in length)
2 types of common ectopic tissue (gastric and pancreatic)
2 years is the most common age at clinical presentation
2:1 male:female ratio
Red-currant jelly stool
Intussusception (mucus and malaena)
Rectal prolapse
Mucosa (partial/type 1) or all layers (complete/type 2), may protrude through anus
Causes incontinence
Causes of rectal prolapse
Lax sphincter, prolonged straining
Related to chronic neurological or psychological disorders
Mx of rectal prolapse
Rectopexy (to fix rectum to sacrum) +/- mesh insertion +/0 rectosigmoidectomy
Types of anal cancers
Squamous cell (85%) Rarely basaloid, melanoma or adenocarcinoma
Anal margin vs anal canal tumours
Margin: usually well-differentiated, keratinising, good prognosis, spread to inguinal LNs
Canal: above dentate line, spread to pelvic LNs, poorly differentiated, non-keratinising, poor prognosis
Associations with anal cancer
Perianal warts Leukoplakia Lichen sclerosis Bowen's disease Crohn's disease
Signs of decompensated liver failure
Jaundice
Ascites
Encephalopathy
Common liver secondaries
Breast and uterine
Bronchus
GIT
Leading causes of HCC
HBV HCV AI hepatitis Cirrhosis (alcohol, haemachromatosis, PBC) NASH
Ix for HCC
4-phase CT: delayed wash-out of contrast in suspected mass
MRI
Biopsy
Mx of HCC
Resection of solitary tumours under 3cm Liver transplant Percutaneous ablation Tumour embolisation Sorafenib
Cholangiocarcinoma
Biliary tree cancer
~10% of liver primaries
Causes of cholangiocarcinoma
Flukes PSC Biliary cysts HBV HCV DM
Mx of cholangiocarcinoma
70% unsuited to surgery (and many recur anyway)
Stenting improves quality of life
Transplant rarely indicated
Prognosis of cholangiocarcinoma
~5/12
Liver tumour DDx
Malignancy (primary or secondary) Haemangioma (don't require treatment; avoid biopsy!) Adenoma (treat if symptomatic or >5cm) Cysts Focal nodular hyperplasia Fibroma
Causes of liver adenoma
Anabolic steroids
OCP
Pregnancy
AI hepatitis
Inflammatory liver disease of unknown cause; autoAbs against hepatocyte surface Ags
Predominantly affects young or middle-aged women
~40% present with acute hepatitis (remainder with gradual jaundice or are asymptomatic)
Dx of AIH
Diagnosis of exclusion
Based on increased IgG levels, +ive autoAbs and histology from biopsy (mononuclear infiltrate of portal and periportal areas, piecemeal necrosis +/- fibrosis or cirrhosis)
Type I AIH
80%
Anti-smooth muscle Abs (ASMA), may have ANA
Good response to immunosuppression
Type II AIH
Commoner in Europe, more often seen in children
More commonly progresses to cirrhosis, less treatable
Anti-liver/kidney microsomal type 1 Abs (LKM1)
ASMA and ANA -ive
Type III AIH
Like type I but ASMA and ANA -ive
Abs against soluble liver Ag (SLA) or liver-pancreas Ag
Mx of AIH
Prednisolone 30mg/d PO for 1/12, decreasing by 5mg/month to maintenance dose of 5-10mg/d
Can sometimes be stopped after 2 years but relapse may occur
Azathioprine can be used as steroid-sparing agent
Liver transplant if decompensated cirrhosis or failure to respond to medical therapy (but recurrence may occur)
Associations of AIH
Pernicious anaemia UC Glomerulonephritis AI thyroiditis AI haemolysis DM PSC
PBC
Interlobular bile ducts are damaged by chronic AI granulomatous inflammation causing cholestasis which may lead to fibrosis, cirrhosis and portal HTN
Dx of PBC
AMA (anti-mitochondrial Abs) are hallmark
Complications of PBC
Cirrhosis
OP
Fat-soluble vitamin malabsorption due to cholestasis
HCC
Mx of PBC
Colestyramine for pruritis
UCDA (secondary bile acid)
End-stage: liver transplantation (once jaundice develops, survival is
PSC
Progressive cholestasis with bile duct inflammation and strictures
Complications of PSC
Increased risk of cancers: bile duct, gall bladder, liver, colon (do yearly colonoscopy + U/S)
Ix for PSC
AMA -ive
ANA, SMA, ANCA may be +ive
ERCP: many strictures with characteristic “beaded’ appearance
Biopsy: fibrous, obliterative cholangitis
Mx of PSC
Liver transplant for end-stage
UCDA (may protect against colon cancer, improve LFT)
Colestyramine for pruritis
Abx for bacterial cholangitis
Overlap syndrome of AIH
PSC, IBD
Hydatid
Cystic hydatid disease is a zoonosis caused by eating eggs of dog parasite e.g. Echinococcus granulosus
Sx of hydatid cysts
Liver: hepatomegaly, obstructive jaundice, cholangitis
Lung: dyspnoea, chest pain, haemoptysis, anaphylaxis
CNS: space-occupying lesions
Bone: osteolytic
Hydatid cyst Mx
Surgical referral to excise/drain cysts (some favour hepatic resection) with PAIR approach (puncture, aspirate, inject hypertonic saline, re-aspirate)
Albendazole pre- and post-drainage
Amoebic liver abscess
Often single mass in R lobe containing “anchovy-sauce” pus
Dx of amoebic liver abscess
Increased WCC
LFT normal or cholestatic picture
PCR
U/S or CT +/- aspiration (don’t rely on microscopy)
Mx of amoebic liver abscess
Metronidazole for acute amoebic abscess
Diloxanide furoate for 10 days to destroy gut cysts or in chronic disease
Causes of liver abscess
Pyogenic: streptococcus, staphylococcus, gut microbes
Amoebic
Fungal
NB Can occur following haematogenous spread of bacteria through portal vein post-abdominal infection (e.g. appendicitis, diverticulitis)
Toxic megacolon
Acute form of colonic distension
Characterised by a very dilated colon (megacolon), accompanied by abdominal distension, and sometimes fever, abdominal pain, or shock
Caused by IBD, infection (e.g. C. diff, Entamoeba histolytica, Shigella)
Mx of toxic megacolon
NGT for bowel decompression IVFs Steroids if IBD is underlying cause Consider Abx to prevent sepsis If decompression is not achieved or the patient does not improve within 24 hrs: colectomy
