Gastro - ix Flashcards
Extrinsic pathway of the clotting cascade
How is it measured
Normal value
Affected by
PT
14s
Warfarin, liver disease
Intrinsic pathway of the clotting cascade
How is it measured
Normal value
Affected by
APTT
34s
Heparin, Hemophilias, VWD
What is the Rockall score used for?
UGIB
Determines risk of re-bleeding + death
(1) Risk of rebleeding/mortality pre-endoscopy
(2) Risk of rebleeding/mortality post-endoscopy.
What does the Rockall score include?
Broken into an initial (pre-endoscopy) and final (post-endoscopy) score
Look at haematemesis + melaena for table
Intial Age <60 0 60-79 1 >80 2 Shock (BP+HR) HR >100 1 SBP <100 2 Co-morbidities HF, IHD 2 Renal failure, liver failure DIC 3
Final Stigmata of recent haemorrhage 2 Dx Mallory Weiss tear 0 Other dx 1 Malignancy of the UGIT 2
What is the glasgow Blatchford score?
Screening tool to assess the likelihood that a person with an acute UGIB will need to have medical intervention
What does the Glasgow Blatchford score include (8)?
Blood urea nitrogen Hb SBP HR Malaena Syncope Hepatic disease Cardiac disease
Achalasia ix
• Barium swallow
Bird’s beak appearance
• Manometry - gold standard for dx of achalasia
To distinguish achalasia from other motility disorders
a) high resting pressure in the lower oesophagus/cardiac sphincter, b) incomplete relaxation, c) absent peristalsis
• CXR
Dilated oesophagus behind the heart
May show aspiration pneumonia
Barrett’s oesophagus ix
- Endoscopy - metaplastic changes in the endothelium, “velvety epithelium”
- Histological - visible columnisation (normal: squamous epithelial lining, abnormal: metaplastic columnar epithelium can become invasive adeocarcinoma of the oesopahgus)
Oesophageal cancer ix
• OGD + biopsy any lesion seen
• Barium swallow
Rat’s tail appearance of the oesophagus
- Grade tumour histopathologically
- Stage tumour by CXR, CT, PET
• EUS (endoscopic US) used less commonly
Standard pre-treatment test
Can identify all the histological layers of the oesophagus + there by confirm the T-stage with 90% accuracy
Can identify abnormal or enlarged mediastinal and coeliac axis lymph nodes, and enable cytological examination by FNA
Crucial in planning treatment, particularly prior to durgery
Most accurate modality for local + regional staging (consistently better than CT, PET, MRI)
If there is no evidence of metastatic disease on PET-CT + patient is candidate for surgery
Provides useful info about intramural vs transmural disease + local lymph node involvement
Gastritis ix
1st line investigations:
• H pylori testing –> 13C urea breath test / stool antigen test
• FBC – ?iron deficiency anaemia
Investigation to consider: • Endoscopy • Biopsy • Serum vitamin B12 N/L AI gastritis
Peptic ulcer disease Ix
under 55 or no red flag symptoms
• H pylori testing
13C urea breath test
stool antigen test
• FBC – ?iron deficiency anaemia
over 55 or red flag symptoms or failed treatment or bleeding ulcer
• OGD + biopsy + urease testing
Warning sings >55+ o Chronic blood loss o Persistent vomiting o Epigastric mass o unexplained, persistent, recent-onset diarrhoea o Previous peptic ulcer disease o Previous gastric surgery o Pernicious anaemia (RF for linitis plastica - gastric carcinoma w liver mets) o NSAID use o Early satiety o FHx of gastric carcinoma
ALARMS o Anorexia o Loss of weight o Anaemia (iron deficiency anaemia) o Rectal bleeding o Melaena/Haematemesis o Swallowing difficulty (progressive dysphagia) o Suspicious barium meal
ALARMS symptoms
o Anorexia o Loss of weight o Anaemia (iron deficiency anaemia) o Rectal bleeding o Melaena/Haematemesis o Swallowing difficulty (progressive dysphagia) o Suspicious barium meal
GORD ix
• 1st line Ix
8 week trial PPI trial
• OGD
o If symptoms do not improve w therapeutic 8-week trial
o if pt >55
o If patient has ALARMS symptoms
o Annual endoscopic surveillance – looking for Barrett’s Oesophagus
• Ambulatory pH monitoring - can demonstrate exposure to oesophageal acid
if ph <4 for >4h –> GORD
• Combined impedance pH testing - can quantify exposure to oesophageal acid
GORD
first line ix OGD
in pt <55 or without red flag symptoms –> trial PPIs before proceeding with investigations
GLASGOW scale
Scoring mechanism used clinically for assessing severity + prognosis of pancreatitis
Based on results within 48h of admission
mnemonic: PANCREAS
PaO2 <8kpa or <60mmHg Age >55 years Neutrophilia >15x10^9 WBC/L Calcium <2.0mM Renal funcction: Urea >16mM Enzymes LDH >600 U/L or AST >200 U/L Albumin <32g/L Sugar >10mM (in non-diabetics)
if score >3 (incl 3) - severe pancreatitis likely, consider admission to ICU
Oesophageal spasm ix
Crockscrew appearance on barium swallow
Anal fissures ix
- Do not attempt a DRE – extremely painful
* Diagnosis is clinical + further Ix only required if there are features of underlying pathology
Rectal prolapse ix
• Imaging
o Barium enema +/- colonoscopy – evaluate the entire colon prior to surgery + exclude any other colonic lesions
o Rigid Proctosigmoidoscopy – asses the rectum for additional lesions
• Anal physiology tests
o Used to distinguish between mucosal and full-thickness prolapse
o Anal sphincter manometry, electromyography of the anal sphincter, defecography, continence tests, pelvic floor, nerve stimulation tests (Pudendal nerve studies)
• Haemorrhoid
o Differentiated by the presence of symmetrical circumferential folds/concentric rings of mucosa occurring in rectal prolapse
Assess underlying conditions
• Sweat Cl- test - CF
• Stool + microscopy cultures - GI infection
Haemorrhoids ix
• Proctoscopy
Pink mucosal swellings
• Rigid/flexible sigmoidoscopy/Colonoscopy
To exclude other pathology
Definitive test is colonoscopy
Flexible sigmoidoscopy combined with a barium enema to assess proximal colon in high-risk patients
• FBC – anaemia or infection
If concerned that the patient has experienced significant prolonged rectal bleeding + signs of anaemia are present
• DRE
Appendicitis ix
1st line Ix
• FBC
Increased WCC (polymorphonuclear leukocytes)
Increased CRP
• CT AP
o Abnormal appendix (diameter >6mm) / calcified appendicolith in association with peri-appendiceal inflammation / appendiceal wall thickening / peri-appendiceal fat stranding / appendiceal wall enhancement
• Abdominal ultrasound
- Urinalysis to exclude UTI
- Urinary pregnancy test - exclude ectopic pregnancy
2nd line Ix
• Urinalysis
• Alvarado scoring system
4-6 – CT investigation
>7 appendicectomy
Alverdo scoring system for appendicitis
Symptoms
Signs
Laboratory findings
Results
Symptoms - MAN
- migratory RIF pain
- Anorexia
- N+V
Signs - TRF
- Tenderness in RIF
- Rebound tenderness in RIF
- Fever >38
Laboratory findings - LS
- Increased WCC (2) >10
- Shift to the L of the neutrophils
5-6 possible
7-8 probable
>9 very probable
CT 4-6
Appendectomy >7
Ix to confirm obstruction
AXR
Small bowel >3cm
Large bowel >6cm
If large bowel >9cm - risk of imminent perforation + need for surgery
Colon cancer ix
Bloods • FBC Anaemia if bleeding • LFTs Liver is the first site of metastasis of colorectal cancer (enterohepatic circulation) • U&Es • CEA (not used for diagnosis but to monitor treatment, relapse, recurrence of disease) • FOBT – used as a screening test
Imaging
• Colonoscopy – GOLD STANDARD FOR DIAGNOSIS OF COLORECTAL CANCER
• CT scan CAP
Staging
• Liver USS
Staging
• Barium enema
Apple core stricture
Volvulus ix
Bloods
• FBC - low Hb, high WCC if sepsis, gangrene
• U+E
Dehydration
Sepsis (high lactate)
Acidosis
Hyponatraemia, hyperkalaemia, metabolic acidosis, raised U +Cr, hypochloraemia, lactic acidosis
Imaging
• Upper GI contrast studies - diagnostic test
• AXR (ordered in ED)
Sigmoid volvulus 65% - Coffee bean shape in RUQ, assosciated with large bowel dilation
Caecal volvulus 30% - caecal embryonic sign in LUQ, assosciated with small bowel dilation
• Erect CXR – if perforation is suspected
Choledocholithiasis ix
EUS/MRCP
Gallstones/biliary colic ix
• US abdo
Shows gallstones + sludge in the gallbladder
Dilated bile duct in choledocholithiasis
Allows measurement of the diameter of the CBD
Bloods
• FBC - raised WCC due to inflammation from a complication of cholelithiasis – acute cholecystitis, cholangitis, pancreatitis
• LFTs - raised ALP due to obstruction of the cystic or bile duct
• Serum lipase + amylase
o Pancreatitis is a complication of cholelithiasis
Cholecystitis ix
Imaging • RUQ US – initial test of choice o Thickened bladder wall (>3mm) o Distended gallbladder o Pericholecystic fluid/air o Gallstones o Positive sonographic Murphy’s sign
• HIDA (hepatobiliary iminodiacetic acid) scanning + MRI – helpful in cases where the US dx is unclear
o HIDA directly shows cystic duct obstruction
Bloods • FBC - raised WCC • Raised CRP • LFTs Cholestatic picture Raised ALP, GGT, bilirubin
Acute cholangitis ix
Imaging • US abdo to visualise stones • ERCP First line Ix Direct observation of bile duct stone or other obstruction Therapeutic – can be used for biliary stone extraction • Contrast CT abdo – second line • MRCP – third line
Bloods
• FBC - raised WCC
• LFTs - raised conjugated bilirubin (obstructive jaundice) + raised ALP + N LFTs
• Raised amylase - Indicates involvement of the lower part of the CBD (next to the pancreas)
• Blood cultures - Bacteria are usually gram-negative
Mallory Weiss tear ix
Imaging
• OGD
Diagnostic test
Needs to be performed within 24h – tears heal rapidly
• Angiography
If OGD is no available/is contra-indicated
Bloods
• FBC
• Coagulation studies + platelet counts to detect coagulopathies + thrombocytopenias
• Urea - High in patient with ongoing bleeding, part of the Glasgow-Blatchford Bleeding score
• LFTs - to rule out liver disease (+ hence oesophageal varices, gastric varices)
• ECG + cardiac enzymes – if myocardial ischaemia is suspected as a result of blood loss
Toxic megacolon ix
AXR >6cm
When should flexible sigmoidoscopy be used instead of colonoscopy toi investigate UC?
When there is a high risk of perforation
UC ix
Bloods • FBC (low Hb, high, WCC) • High ESR/CRP • Low albumin • B12/folate deficincy (malabsorption) • Fe deficiency (bleeding, malabsorption) • Anaemia of chronic disease
Stool
• Stool culture
To exclude infectious colitis/diarrhoea
C. Difficile has a higher prevalence in pt with IBD
CMV considered in severe or refractory colitis – reactivation is common in pt with IBD on immunosuppression
• Faecal calprotectin
Disitnguishes between inflammatory (IBD) + non-inflammatory (IBS) causes of diarrhoea
Conc in faeces correlates well with severity of intestinal perforation
AXR
• To rule out toxic megacolon + perforation
o Signs of toxic megacolon: abdominal tenderness + distention, tachycardia, fever, anaemia, transverse colon >6cm
Colonoscopy - not to be performed on an acute setting due to risk of perforation [Flexible sigmoidoscopy performed if there is risk of perforation]
Determines severity
Histological confirmation
Detection of dysplasia (UC pt at higher risk of colonic adenocarcinoma)
Gross uniform inflammation with a clear cut off point between normal and abnormal bowel
Indicated in UC pt who are not responding well to treatments
Biopsy
Inflamed crypts filled with fibrin and polymorphonuclear leukocytes
DCBE
Mucosal ulceration with granular appearance + filling defects (due to pseudopolyps)
Narrowed colon
Loss of haustral pattern – leadpipe appearance
Crohn’s disease ix
Blood • FBC (low Hb, high WCC, high plt) • High ESR/CRP • Low albumin • B12/folate deficiency (malabsorption) • Fe deficiency • Anaemia of chronic disease
Stool • Culture To exclude infective colitis/diarrhoea C. diff esp if Hx of recent Abx use Y enterocolitica – if RIF pain
• Faecal calprotectin
Disitnguishes between inflammatory (IBD) + non-inflammatory causes of diarrhoea (IBS)
Conc in faeces correlates well with severity of intestinal perforation
AXR
• To exclude toxic megacolon
• To assess CD severity
Colonoscopy
• Can help differentiate UC + CD
• Defines presence + severity of morphological recurrence + predicts clinical course
• Useful for monitoring malignancy + disease progression
• Histological confirmation
Biopsy
• Non-caseating granulomas in the bowel wall mucosa
Transmural chronic inflammation with infiltration of macrophages, lymphocytes, plasma cells
DCBE
• String sign of Kantor
• Rose thorn ulcers
• Cobblestone mucosa
What is Truelove’s and Witt’s severity index and what does it include (6)?
Classifies severity of UC
Includes
- Number of stools
- Blood in stools
- Anaemia
- Pulse rate (>90)
- Fever (>37.8)
- ESR/CRP (>30mm/h)
Cirrhosis ix
Bloods
• FBC
Low Hb – occult bleeding
Macrocytosis – alcohol abuse
Thrombocytopenia (<150, normal 150-450 x 10^9/L)
Most sensitive + specific laboratory finding for dx of cirrhosis in the setting of chronic liver disease
• LFTs
o Raised AST, ALT
o Elevation of ALT>AST - viral hepatitis
o Elevation of AST>ALT - alcoholic hepatitis
o Bilirubin normal at the start but as cirrhosis progresses, serum levels rise
Low Na
Low albumin
Prolonged PTT
Tests to consider
• Abdo US/CT/MRI
o Can detect signs of advanced cirrhosis + complications of cirrhosis (e.g. portal HTN)
o Signs of portal HTN: ascites, splenomegaly, increased diameter of the portal vein (>13mm), collateral vessels, hepatocellular carcinoma
• CXR
o Might show elevated diaphragm + pleural effusion
• Upper GI endoscopy
o Presence of gastro-oesophageal varices
• Transient elastography/acoustic radiation force impulse imaging
o Used to diagnose cirrhosis for people with NAFLD + advanced liver fibrosis
• Liver biopsy
o Most specific + sensitive test for dx of cirrhosis
o If liver elastography not suitable
o Not necessary in pt with advanced liver disease + typical clinical/laboratory/radiological findings of cirrhosis - ascites, coagulopathy, shrunken nodular-appearing liver
Cirrhosis ix
Bloods
• FBC
Low Hb – occult bleeding
Macrocytosis – alcohol abuse
Thrombocytopenia (<150, normal 150-450 x 10^9/L)
Most sensitive + specific laboratory finding for dx of cirrhosis in the setting of chronic liver disease
• LFTs
o Raised AST, ALT
o Elevation of ALT>AST - viral hepatitis
o Elevation of AST>ALT - alcoholic hepatitis
o Bilirubin normal at the start but as cirrhosis progresses, serum levels rise
Low Na
Low albumin
Prolonged PTT
Tests to consider
• Abdo US/CT/MRI
o Can detect signs of advanced cirrhosis + complications of cirrhosis (e.g. portal HTN)
• CXR
o Might show elevated diaphragm + pleural effusion
• Upper GI endoscopy
o Presence of gastro-oesophageal varices
• Transient elastography/acoustic radiation force impulse imaging
o Used to diagnose cirrhosis for people with NAFLD + advanced liver fibrosis
• Liver biopsy
o Most specific + sensitive test for dx of cirrhosis
o If liver elastography not suitable
o Not necessary in pt with advanced liver disease + atypical clinical/laboratory/radiological findings of cirrhosis - ascites, coagulopathy, shrunken nodular-appearing liver
Signs of portal HTN on UC/CT/MRI
Ascites Splenomegaly Increased diameter of the portal vein (>13mm) Collateral vessels Hepatocellular carcinoma
Signs of portal HTN on UC/CT/MRI
Ascites Splenomegaly Increased diameter of the portal vein (>13mm) Collateral vessels Hepatocellular carcinoma
What is the child-pugh-turcotte classification?
It estimates the prognosis in those with cirrhosis
What does the child-pugh-turcotte classification include?
- Serum albumin
- Serum bilirubin
- INR
- Ascites
- Encephalopathy
Tumour markers
Breast cancer Ovarian cancer Pancreatic cancer Biliary cancer (cholangiocarcinoma) Prostate cancer Colorectal cancer Hepatocellular carcinoma Non seminomatous germ cell tumours
Breast cancer - CA 15-3, CA27-29 Ovarian cancer - CA 125 Pancreatic cancer - CA 19-9 Biliary cancer (cholangiocarcinoma) CA 19-9, CA125, CEA Prostate cancer PSA Colorectal cancer CEA Hepatocellular carcinoma AFP Non seminomatous germ cell tumours AFP, bHCG, LDH
Tumour markers
Breast cancer Ovarian cancer Pancreatic cancer Biliary cancer (cholangiocarcinoma) Prostate cancer Colorectal cancer Hepatocellular carcinoma Non seminomatous germ cell tumours
Breast cancer - CA 15-3, CA27-29 Ovarian cancer - CA 125 Pancreatic cancer - CA 19-9 Biliary cancer (cholangiocarcinoma) CA 19-9 Prostate cancer PSA Colorectal cancer CEA Hepatocellular carcinoma AFP Non seminomatous germ cell tumours AFP, bHCG, LDH
Cholangiocarcinoma ix
• Abdo US first line
o To identify malignant vs benign lesions
o Mass lesion
o Dilated Intrahepatic ducts
• Contrast MRI
o Optimal imaging for dx of cholangiocarcinoma
• MRCP, ERCP, PTC
o Show site of obstruction
o ERCP/PCT can be used to obtain samples for biopsy or cytological analysis
• Tumour markers
o CA 19-9
o CEA
o CA-125
• Serum o Bilirubin raised o ALP raised o GGT raised o ALT – mildly elevated, o PTT – prolonged obstruction of the CBD/hepatic duct - subsequent reduction in fat-soluble vitamins (A, D, E, K)
Liver abscess ix
• Liver US
o Variably echoic lesion
o Biliary tree examination
o Guides aspiration + drainage
• Contrast CT abdo
o Gas within lesion - bacterial abscess
o Guides aspiration + drainage
• Gram stain + culture of aspirated abscess fluid
- FBC, ESR, CRP – raised
- LFT - raised ALP, Hypoalbuminaemia
- Blood cultures
- PTT, APTT - Aspiration contraindicated in the presence of abnormal clotting
Liver abscess ix if amoebiasis is suspected
o Serum ab test
o Stool Ag detection test (may contain cysts or trophozoites)
o Ag testing/PCR of aspirated abscess fluid for Entamoeba histolytica
Liver failure ix
Blood • FBC Leucocytosis - ?infection Iron deficiency anaemia Thrombocytopenia – chronic liver disease Raised INR (>1.5)
• LFTs
Raised transaminases
Normal ALP
Raised bilirubin
• U+Es
Raised U + Cr
Metabolic derangements in potassium, phosphate, magnesium
- ABG – metabolic acidosis in paracetamol overdose
- Arterial blood lactate – important prognostic indicator in paracetamol-associated ALF
• Low
o Pseudocholinesterase
o Glucose
• High
o Ammonia levels
o Lactate
o Creatinine
• Blood cultures – pt very susceptible to infection
• Viral serology
o Antihepatitis A IgM, antihepatitis B core IgM, hep B surface antigen, antihepatitis C IgG, antihepatitis E IgM
o May indicate infection that ppt hepatic failure
• Autoimmune hepatitis markers
o Antinuclear antibody (ANA), anti-smooth-muscle antibody, quantitative immunoglobulins (IgG)
• Test for specific conditions – Wilson’s disease, paracetamol levels (urine toxicology screen)
Imaging
• Doppler US
o Budd-Chiari syndrome – ?hepatic vein thrombosis
o Hepatic surface nodularity - ?cirrhosis
• CT/MRI
o Demonstrates hepatic anatomy
o Excludes other pathology (particularly patients with massive ascites, obesity, under consideration for transplantation)
- Head imaging – cerebral oedema
- EEG – level of encephalopathy
- Liver biopsy
Wernicke’s encephalopathy ix
- Diagnosis is clinical
- Therapeutic trial of parenteral thiamine (pabrinex) -Treated as an emergency
- Blood thiamine + its metabolites
- Blood magnesium - Mg deficiency may impair the therapeutic benefit of thiamine (Mg serves as a co-factor in enzymes that need thiamine pyrophosphate)
Investigate causes
• BM glucose
• Serum ammonia - exclude hyperammonaemia that causes hepatic encephalopathy (Wernicke’s is due to B1 deficiecy)
• Urinary + serum drug screen – to exclude concomitant intake by the patient
• Blood alcohol level
Monitor complications
• U+E - If condition goes unnoticed –> Hypotension + lactic acidosis - renal dysfunction + electrolyte abnormalities
MEDED
• ECG – pt may have cardiac abnormalities, do one before + after treatment
• CT – may help identify lesions resulting from the disorder
• Neuropsychological test – to determine severity of mental deficiencies
What does thumb printing on XR, CT mean?
Submucosal oedema or haemorrhage
First line ix for acute mesenteric ischaemia +findings
- CT angiogram
o Shows arterial blockage due to emboli or thrombus
o Evidence for extent of bowel compromise from ischaemia
o Stratification of patients to identify those who would benefit from mesenteric angiography from those who require primary surgery
o If findings are non-specific and non-diagnostic for colonic ischaemia – colonoscopy may be required
Bowel wall thickening, dilation
Thumb-printing sign suggestive of submucosal oedema or haemorrhage
Gas in ectopic places – Pneumatosis intestinalis, Portal venous gas
Occlusion of the mesenteric vasculature
Streaking mesentery
Solid organ infarction
• AXR (in advanced disease)
o Gasless abdomen
o Thickening of the bowel wall
o Pneumatosis (air within the bowel wall due to necrosis)
Intestinal ischaemia ix + findings
• FBC
o Leucocytosis
o Anaemia bc of melaena that exacerbates ischaemia
• ABG/lactate level
o Acidosis + increased serum amylase
o Degree of acidosis aids in determination of the severity of the illness
• CT angio • Sigmoidoscopy/colonoscopy (The best test to establish the diagnosis of colonic ischaemia) Mucosal sloughing Mucosal petechiae Submucosal haemorrhagic nodules, erosions, or ulcerations Submucosal oedema Luminal narrowing Necrosis Gangrene
• AXR (in advanced disease)
o Gasless abdomen
o Thickening of the bowel wall
o Pneumatosis (air within the bowel wall due to necrosis)
Investigations to investigate causes of intestinal ischaemia
- ECG, Echo - AF, arrhythmias, MI (predispose to acute mesenteric ischaemia)
- Coagulation panel - underlying coagulopathy
- AXR
Chronic mesenteric ischaemia ix
- FBC, LFT, U+Es - malnutrition, dehydration
- Mesenteric duplex US - first line ix, non-invasive method of demonstrating arterial blood flow, affected by obesity, respiratory movements
- Arteriography - gold standard to show site of arterial blockage or stenosis
• AXR (in advanced disease)
o Gasless abdomen
o Thickening of the bowel wall
o Pneumatosis (air within the bowel wall due to necrosis)
Ischaemic colitis ix
• Colonoscopy - blue, swollen mucosa sparring the rectum
• Abdo XR - abnormal segment outlined with gas
• Barium enema - thumb printing in early phase
o Mucosa may then return to normal or progress with similar appearance to Crohn’s
o May then resolve spontaneously or progress to narrowing of the intestine +/- sacculation of the antimesenteric border
• CT, MRI, angiography
• AXR (in advanced disease)
o Gasless abdomen
o Thickening of the bowel wall
o Pneumatosis (air within the bowel wall due to necrosis)
SBO ix
• Upright + supine AXR
Small bowel dilation >3cm
o Help determine whether patient has a partial or complete SBO + whether the obstruction is simple or complicated
o Partial SBO: gas throughout the abdomen and into the rectum
o Complete SBO: no distal gas, staggered air-fluid levels
o Complicated SBO: free air under the diaphragm (perforation), thumb-printing (ischaemia)
o Poor sensitivity so might need a CT scan when AXR is inconclusive (determine underlying cause, extent + location of obstruction)
• U+E
o Dehydration: increased urea + electrolyte imbalance
LBO ix
Bloods
• FBC
o Increased WCC – infective or inflammatory cause, complication e.g. perforation
o Microcytic anaemia – malignancy
• U&Es
o Elevated urea or creatinine
o Deranged from dehydration, fluid shifts, sepsis
o Colon normally absorbs NaCl + H2O and secretes K + HCO3 - this is disrupted in the obstructed colon - may produce hypokalaemia
- Serum amylase/lipase – can be elevated with any significant intra-abdominal event
- Coagulation studies – coagulopathy may be present in sepsis from perforation
Imaging
• Erect CXR – indicates perforation
• Plain AXR o Dx confirmed by colonic dilation o 3/6/9 rule o Small bowel <3cm o Large bowel <6cm o Sigmoid colon <9cm
Ix to consider
• Contrast enema
o Performed after initial assessment to confirm dx
o Bird’s beak in colonic volvulus
o Contra-indicated if perforation or peritonitis are suspected
PSC ix bloods
Bloods
• ALP – N or Increased
• GGT – increased
o Indication of bile duct injury +/or obstruction
o Supports liver origin of elevated ALP rather than bone
• AST, ALT – mildly elevated
• Bilirubin – N or ncreased, predominantly conjugated
• Albumin – N in early-stage disease, low in advanced liver disease/pt w active IBD
• FBC
o Indication of liver dysfunction due to advanced liver disease + suggestive of portal HTN
o N or thrombocytopenia +/- anaemia, leukopenia
• PTT – N or prolonged
o Indication of liver synthetic function
o Vitamin K deficiency due to malabsorption from cholestasis
- No auto-antibodies specific to/diagnostic of PSC
- But there may be – hypergammaglobulinaemia, raised IgM levels, perinuclear antineutrophil cytoplasmic ab (p-ANCA), anticardiolipin (aCL) ab, antinuclear ab
PSC imaging ix
• Abdo US
o Non-invasive initial test to ix for bile duct abnormality
o May also provide evidence of more advanced liver disease
o Can’t diagnose/exclude PSC – no adequate evaluation of the biliary tree
o Abnormal (dilated) bile ducts (+/- cirrhotic liver, ascites, splenomegaly)
• MRCP
o Standard procedure to visualise the intrahepatic + extrahepatic bile ducts
o Preferred to ERCP
o Normal/multi-focal intrahepatic +/or extrahepatic strictures and dilatations +/- dominant biliary stricture (bead like appearance as a result of stricture formation)
• ERCP
o When MRCP is non-diagnostic or when therapeutic intervention is anticipated (e.g. brush cytology to evaluate for co-existing malignancy, extraction of bile duct stones, dilation of prominent bile duct strictures)
o Risk of procedure-related complications – pancreatitis, bacterial cholangitis, bleeding, liver abscess, perforation
o During interventional procedures accessing the biliary tract, brush cytology should be performed to rule out cholangiocarcinoma
• MRI – to exclude other disease + evaluate the biliary system
• Liver biopsy – rarely diagnostic + may be useful for staging PSC
o Polymorph infiltration of bile ducts
Best single test for screening household contacts of HBV infected individuals to determine need for vaccination
Anti-HBc
What is transient elastrography?
Non-invasive test that has a high diagnostic accuracy for the detection of cirrhosis
HAV ix
• IgM anti-hepatitis A virus serology (HAV) – detected 5-10 days before symptom onset + remains elevated for 4-6 months
• IgG anti-hepatitis A virus serology (HAV) – levels begin to rise soon after IgM levels + stay elevated throughout the person’s lifetime
o +ve result – prior infection or recent disease should be interpreted along with results of IgM anti-HAV + clinical features
o In the absence of IgM it indicates past infection or vaccination rather than acute infection
- Raised ALT + AST but ALT>AST (about 4 weeks after exposure)
- Raised Bil (rises soon after ALT + AST)
- Raised blood U + Cr in fulminant hepatitis
HBV ix
- LFTs - raised ALT, AST, ALP, Bilirubin, albumin
- FBC – microcytic anaemia, thrombocytopenia – portal HTN resulting from HBV related cirrhosis
• HBsAg (HB surface antigen)
o Establishes dx + indicates active infection
o 4 weeks after exposure to the virus – mean time from exposure to detection is 30 days
o Presence for >6m implies chronic HBV infection
• Anti-HBs (antibody to HBsAg)
o Appears several weeks after HBsAg has disappeared
o Detectable in those immunised with HB vaccine
o Provides life-long immunity, suggestive of resolved infection
o Alone imply vaccination
• IgM + IgG Anti-HBc (antibody to HB core antigen)
o IgM anti-HBc - appears within weeks, remains detectable for 4-8 months (acute infection)
o IgM anti-HBc - During the window between disappearance of HBsAg + appearance of Anti-HBs IgM Anti-HBc is the only way to make dx of acute HBV infection
o Not very reliable marker for acute infection as it can become positive in acute flares or acute reactivation
o Does not provide immunity
o IgG anti-HbC - chronic infection
o Best single test for screening household contacts of HBV infected individuals to determine need for vaccination
o Imply past infection
Chronic hepatitis can be divided into HBeAg+ve or HBeAg-ve disease
• HBeAg
o Found in the serum in the early part of acute HBV infection
o Usually disappears at or soon after the peak in ALT
o Its presence >3 months after onset of illness indicates a high likelihood of development of chronic HBV infection
• Ab to HBeAg
o Seroconversion from HBeAg to ab to HBeAg - useful indication of clearance of virus, suggestive of treatment-related clearance of HBV
o Seroconversion can be a temporary phenomenon – should be analysed in association with the serum HBV DNA level
• HBV DNA
o Measured by PCR
o Assesses candidacy for antiviral therapy + monitors response to therapy
• Patients with chronic hepatitis B are positive HBsAg for at least six months or positive HBsAg and negative IgM to HBcAg.
https://d1yboe6750e2cu.cloudfront.net/i/1cfb524d7810124d77d48071a78aff6cb8fbb366
HCV ix
- Hep C antibodies
- Enzyme immunoassay (EIA)
- Nuclei acid amplification tests (NAATs) – used to confirm early infection/viremia in a patient with positive EIA/assess the effectiveness of anti-viral therapy
- Serum aminotransferases – ALT may be elevated + used to measure disease activity
- Viral genotyping – every patient in order to determine the dose + duration of therapy + to estimate the most appropriate regimen
- Liver biopsy – not used to diagnose HCV, useful in staging fibrosis + degree of hepatic inflammation
HDV ix
Anti-HDV antibody
HEV ix
Hepatitis serology
HBsAg -ve
Anti-HBc -ve
Anti-HBs -ve
Susceptible
HBsAg -ve
Anti-HBc +ve
Anti-HBs +ve
Immune due to natural infection
i.e. became infected with HBV in the past, cleared the virus and is now immune
HBsAg -ve
Anti-HBc -ve
Anti-HBs +ve
Immune due to Hep b vaccination
HBsAg +ve
Anti-HBc +ve
IgM anti-Hbc +ve
Anti-HBs -ve
Acutely infected
HBsAg +ve
Anti-HBc +ve
IgM anti-Hbc -ve
Anti-HBs -ve
Chronically infected
HBsAg -ve
Anti-HBc +ve
Anti-HBs -ve
4 possibilities resolved infection false positive anti-HBc thus susceptible low level chronic infection resolving acute infection
Presence of HBsAg
hep B surface ag
Indicates that the person is infectous
can be detected in the serum in high levels during an acute or chronic hep B infection
Ag used to make HBV vaccine
Presence of anti-Hbs
hep b surface ab
Recovery + immunity from HBV
Also develop in people who have been successfully vaccinated against HBV
Anti-HBc
total hepatitis B core ab
indicates previous ongoing infetion with HBV in an undefined time frame
appears at the onset of symptoms in acute HB and persists for life
IgM anti-HBc
IgM antibody to hep B core antigen
Presence indicates acute infection
positivity indicates recent infection with hep B (<6m)
Autoimmune hepatitis ix
• Biopsy
- most important dx procedure, essential to establish dx, evaluate disease severity, determine need for treatment
- Interface hepatitis with portal mononuclear and plasma cell infiltrate
• Inflammatory changes (histology)
- Very raised aminotransferases
- Mildly to moderately increased bilirubin, GGT, ALP
- Prolonged PTT, decreased albumin
- IgG predominant polyclonal hypergammaglobulinemia
- Exclusion of viral/drug-induced/metabolic liver disease
• Presence of circulating auto-antibodies
Type 1
o Antinuclear ab (ANA)
o Smooth muscle ab (SMA)
Type 2
o Anti-liver cytosol 1 (anti-LC1)
o Anti-liver-kidney microsomal-1 ab (anti-LKM-1)
o Perinuclear antineutrophil cytoplasmic auto-antibody (pANCA)
o Antiphospholipid antibodies
o Anti-single-stranded DNA (anti-ssDNA antibodies)
o Anti-double-stranded DNA (anti-dsDNA antibodies)
o Anti-soluble liver antigen or liver/pancreas (anti-SLA/LP)
Auto-antibodies in AI hepatitis
Type 1
o Antinuclear ab (ANA)
o Smooth muscle ab (SMA)
Type 2
o Anti-liver cytosol 1 (anti-LC1)
o Anti-liver-kidney microsomal-1 ab (anti-LKM-1)
o Perinuclear antineutrophil cytoplasmic auto-antibody (pANCA)
o Anti-liver-kidney microsomal-1 ab (anti-LKM-1)
o Anti-soluble liver antigen or liver/pancreas (anti-SLA/LP)
o Anti-liver cytosol 1 (anti-LC1)
o Antiphospholipid antibodies
o Anti-single-stranded DNA (anti-ssDNA antibodies)
o Anti-double-stranded DNA (anti-dsDNA antibodies)
PBC ix
Bloods
• N FBC
• Raised IgM
• Raised ESR
• LFTs
o Raised ALP + GGT – suggests presence of cholestasis
o Bilirubin – N at first, rises as disease progresses
o PTT + Albumin – N until a late stage
o Prolonged PTT – suggestive of impaired liver synthetic function compatible with the presence of advanced liver disease or can reflect vitamin K malabsorption in the context of cholelithiasis
- Raised cholesterol, lipid, HDL (therefore no raised risk of CHD)
- TSH might also be raised
• Autoantibodies- immunofluorescence + ELISA
o Antimitochondrial antibody (95%) – diffuse staining throughout the cytoplasm [FIRST LINE IX]
o Antinuclear antibody (35%)
PBC – staining of multiple dots within the nucleus + nuclear rim staining
Autoimmune hepatitis + SLE – diffuse nuclear staining
o Other antibodies, esp related to thyroid
Imaging
• Liver US - to exclude obstruction as a result of cholestasis e.g. stones – always should be done before a dx of PBC is made
• Cholangiography - to exclude PSC
• Transient elastography - to evaluate degree of liver fibrosis
• Liver biopsy
o To show cholestatic picture when autoantibodies are not diagnostic
o To differentiate PBC from autoimmune hepatitis
o PBC– chronic nonsuppurative cholangitis of the interlobular + septal bile ducts, bile duct lesions (biliary ductular cell disruption with inflamed portal tracts), granulomata formation, ductopenia (bile duct loss) w/ progressive biliary fibrosis
o Autoimmune hepatitis – interface hepatitis
Alcoholic hepatitis biopsy result
Necrosis of liver cells with infiltration of leukocytes (neutrophils) and the presence of Mallory bodies within the hepatocytes
o Centrilobular ballooning
o Degeneration and necrosis of hepatocytes
o Steatosis
o Cholestasis
o Giant mitochondria
Biliary dilation diagnosis
US
>6 mm CBD diameter
Acute pancreatitis ix
1st investigations to order
o Serum amylase/lipase
Ratio of serum lipase: amylase – if >5 favour alcoholic pancreatitis
Serum amylase >5x above normal (>1000U/L)
Serum lipase >2x above normal (>300 U/L)
Amylase levels usually rise within hours of onset of pancreatitis but fall back to normal within 3–5 days. Lipase has a longer half-life and thus may be a more suitable marker if the patient presents late
o AST/ALT
If >3 times the upper limit – gallstone disease as aetiology
• Acute pancreatitis is diagnosed based on clinical findings + serum lipase/amylase BUT if there is concern regarding pancreatic necrosis (i.e. CRP >200) CT abdo performed to detect complications
o US abdo (mild pancreatitis)
First line for pancreatitis
Can reveal gallstones
May show pancreatic inflammation, calcification, fluid collections
o ABG
Hypoxaemia
Disturbances in acid/base balance
o FBC
Raised WCC
Raised HCT (dehydration) or decreased HCT (haemorrhage)
o Raised CRP
CT - if you want to look for evidence of pancreatic necrosis + asses degree of damage to the pancreas (after dx of acute pancreatitis has been made)
AXR - calcifications, sentinel loop (localised ileus/dilation of the bowel from nearby inflammation), gas cut off sign
Chronic pancreatitis ix
o CT abdo - FIRST LINE Pancreatic calcifications, Focal/diffuse enlargement of the pancreas Ductal dilation Vascular complications
o Low Faecal elastase – good marker of pancreatic EXOCRINE function
Only synthesised + excreted by the pancreas
Direct correlation bn elastase in stool + in pancreatic fluid (bc it is stable in transit through the GIT)
Low stool elastase - high sensitivity for pancreatic compromise
Specificity compromised in patients with disease of the small bowel e.g. coeliac disease, Crohn’s, short gut syndrome
o Blood glucose – may be increased
o Amylase will be normal
o Fecal elastase will be low
Imaging o CT abdo - FIRST LINE Pancreatic calcifications, Focal/diffuse enlargement of the pancreas Ductal dilation Vascular complications
o Abdominal x-ray
Pancreatic calcifications
o Abdominal US
Done if CT is unavailable
Hyperechoic foci with post-acoustic shadowing
Structural/anatomical changes incl cavities, duct irregularity, contour irregularity of head/body, calcification
o MRCP + ERCP
Beading of the pancreatic duct + larger calcifications
Early (duct dilation), late (duct strictures)
Peritonitis
FBC
U+E
ABG
FBC - increased WCC
U+Es - increased Na, decresaed K
ABG - acidosis
To diagnose peritonitis in people with ascites the ascitix fluid should contain (spontaneous bacterial peritonitis)
> 250 polymorphonuclear (neutrophils) cells/μL
Why do we need to administer Mg with thiamine?
Mg serves as a co-factor in enzymes that need thiamne pyrophosphate
What does elevated urea and normal creatinine indicate?
Active GI bleeding
Alcoholic hepatitis ix
LIVER
• Elevated AST, ALT, AST>ALT + AST:ALT >2
• Elevated GGT
• Elevated bilirubin (both conjugated + unconjugated)
o Reflects impaired metabolic function of the liver in the absence of biliary obstruction+ has prognostic utility in ALD
• Low albumin
• Elevated serum PTT/INR - Used to evaluate synthetic function of the liver
o Elevated in advanced liver cirrhosis or liver failure
o Elevated PT has a prognostic utility in ALD patients
Blood
• FBC
o Low Hb – iron deficiency, GI bleeding, folate deficiency, haemolysis, hypersplenism
o High MCV
o High WCC – infection, alcoholic hepatitis-related leukaemoid reaction
o Low platelets – may be secondary to alcohol induced BM suppression, folate deficiency, hypersplenism
• U+Es, Mg, PO43-
o Low Na – advanced liver cirrhosis
o Low K, Low PO43- - common causes of muscle weakness in ALD
o Low Mg – can cause persistent hypokalaemia, may predispose patients to seizures during alcohol withdrawal
o High U + N Cr - active GI bleeding
o High U + High Cr - hepatorenal syndrome
• Low folate
o Increased requirements for folate in hepatic disease + decreased intake
IMAGING
• Liver US
o Used to screen for hepatocellular carcinoma every 6-12 months in ALD patients with cirrhosis
• Liver biopsy
o Necrosis of the liver cells and infiltration of leucocytes (neutrophils) with the presence of Mallory bodies within the hepatocytes
o Centrilobular ballooning
o Degeneration and necrosis of hepatocytes
o Steatosis
o Cholestasis
o Giant mitochondria
o In the context of a history of alcohol abuse is diagnostic but is not absolutely indicated in all patients
Gastric cancer ix
• Upper gastrointestinal endoscopy + biopsy required to confirm dx (multiple ulcer edge biopsies)
o If gastric lesion is suspicious and biopsy is negative, a repeat biopsy is necessary
o PPIs should be withheld after endoscopy to avoid misdiagnosis (prescribed because early disease has features of dyspepsia without weight loss,
o anaemia, dysphagia)
• To determine stage
o CT CAP – determines presence/absence of metastatic disease
o EUS – staging, FNA of regional nodes, used to asses operability in the absence of metastatic disease
o CXR
o PET scan more sensitive than CT for distant metastases
NASH/NAFLD ix
• Liver biopsy + histopathological analysis
o Definitive diagnosis
Bloods
• FBC
o Hypersplenism - anaemia, thrombocytopenia
• LFTs o AST, ALT - increased, ALT>AST o ALP – increased o GGT – increased o Total bilirubin – begins to increased with decompensated disease
- Lipid panel - high cholesterol, LDL, triglycerides, HDL
- PPT + INR - prolonged indicates impaired/decompensated liver synthetic function
- Serum albumin - decreased indicates impaired liver synthetic function
- Iron studies – many will have increased transferrin saturation, increased ferritin
Imaging
To define extent + course of disease
Steatosis - focal or diffuse
Steatohepatitis - diffuse
• US
o Hyper-echogenic, bright image
• CT/MRI to monitor course + extend of disease
Courvoiseir’s sign
Painless palpable gallbladder unlikely to be due to gallstones - think pancreatic cancer, cholangiocarcinoma (in distal cystic duct tumours)
What is Rigler’s sign?
Sign of perforated bowel
Air outside bowel + air inside bowel - lining of bowel looks very clear
Diverticulitis ix
Bloods
• Uncomplicated diverticular disease – initial blood haematology normal
• Diverticulitis/abscess - High WCC + CRP
• Bleeding - increased platelet count, anaemia, check clotting, cross-match if bleeding
• Do not perform colonoscopy/barium enema on an acute setting - risk of perforating the inflamed colon
• CT
In an acute setting
Evidence of diverticular disease + complications
• Barium enema
Chronic diverticular disease
Saw-toothed appearance of lumen
If you do it in an acute presentation, it can increase the risk of perforation
• Acute diverticulitis
o AXR – small/large bowel dilation, ileus, pneumoperitoneum, bowel obstruction, soft tissue densities, abscesses
o Erect CXR – pneumoperitoneum
o Abdo US – considered if CT can’t be obtained
• Flexible sigmoidoscopy/colonoscopy
When diagnosis of diverticular disease is unclear and cancer/bowel ischaemia is suspected
• Angiogram/isotope-labelled RBC nuclear scan
Used in acute bleeding if it’s too profuse to enable identification using colonoscopy
Hernia ix
Clinical
US – 1st line
Intestinal obstruction ix
• Plain AXR + CT o Dx confirmed by colonic dilation o 3/6/9 rule o Small bowel <3cm o Large bowel <6cm o Sigmoid colon <9cm o ?Volvulus, ?malignancy
• Erect CXR – indicates perforation
o Riegler’s sign
• FBC
o Increased WCC – infective or inflammatory cause, complication e.g. perforation
o Microcytic anaemia – malignancy
• U&Es
o Elevated urea or creatinine
o Hypokalaemia - Colon normally absorbs NaCl + H2O and secretes K + HCO3
- Serum amylase/lipase – can be elevated with any significant intra-abdominal event
- Coagulation studies – coagulopathy may be present in sepsis from perforation
Ix to consider
• Contrast enema
o Performed after initial assessment to confirm dx
o Bird’s beak in colonic volvulus
o Contra-indicated if perforation or peritonitis are suspected
• Check hernial orifices
o Femoral hernia is at high risk of obstruction
o Inguinal hernia is at lower risk but much more common
Acute intestinal/mesenteric ischaemia ix
• CT angiogram
o FIRST LINE IX WHEN ACUTE ISCHAEMIA IS SUSPECTED
o Shows arterial blockage due to emboli or thrombus
Bowel wall thickening, dilation
Thumb-printing sign suggestive of submucosal oedema or haemorrhage
Gas in ectopic places – Pneumatosis intestinalis, Portal venous gas
Occlusion of the mesenteric vasculature
Streaking mesentery
Solid organ infarction
• Sigmoidoscopy/colonoscopy
o If findings are non-specific and non-diagnostic for colonic ischaemia on CT
o Not necessary to perform in an acute abdomen with planned emergent operative intervention
Mucosal sloughing or friability
Mucosal petechiae
Submucosal haemorrhagic nodules, erosions, or ulcerations
Submucosal oedema
Luminal narrowing
Necrosis
Gangrene
AXR
o Air-fluid levels, bowel dilation, bowel wall thickening, pneumatosis
To investigate causes
• ECG, Echo - AF, arrythmias or acute MI
• Coagulation panel - Coagulopathy - RF for further thrombosis
• Abdo XR
o Rules out other causes (perforation, megacolon)
o May indicate aetiology of ischaemia e.g. distal obstruction
• FBC
o Leucocytosis
o Anaemia bc of melaena that exacerbates ischaemia
• ABG/lactate level
o Acidosis + increased serum amylase
Chronic mesenteric ischaemia ix
• Mesenteric duplex US
First line ix
Non-invasive method of demonstrating arterial blood flow
Affected by obesity, respiratory movements
Decreased or lack of blood flow through proximal mesenteric vessels
Can’t assess distal mesenteric blood flow + non-occlusive aetiology of ischaemia
Affected by obesity, respiratory movements
• Arteriography /MR angiography/Mesenteric angiography
Gold standard to show site of arterial blockage or stenosis
Narrowing/obstruction of mesenteric vasculature
Decreased bowel wall enhancement
o Overall, CT angio is better than MRI for dx of chronic mesenteric ischaemia – higher resolution, faster scans
AXR
o Air-fluid levels, bowel dilation, bowel wall thickening, pneumatosis
- FBC, LFT, U+Es - malnutrition, dehydration
- Blood on DRE
Anti-Hbc
C aught it in the past
o IgM anti-HBc - During the window between disappearance of HBsAg + appearance of Anti-HBs IgM Anti-HBc is the only way to make dx of acute HBV infection
o Not very reliable marker for acute infection as it can become positive in acute flares or acute reactivation
o Does not provide immunity
o IgG anti-HbC - chronic infection
o Best single test for screening household contacts of HBV infected individuals to determine need for vaccination
o Imply past infection
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Anti-HbS
VacSination
or recovery + immunity from HBV
HbsAg
HBV is here now
acute/chronic infection
active infection
>6m - chronic infection
HbeAg
Infective
Wilson’s disease ix
- LFTs – abnormal
- Increased 24h urine copper (>100 μg/24 h with normal levels being <40μg)
- Increased hepatic Cu deposition
- Increased serum free Cu
- Decreased total serum Cu (paradoxical, not reliable therefore not used)
- Decreased blood ceruloplasmin
- Slit-lamp examination – Kayser-Fleischer rings
- Liver biopsy - increased copper deposition
- DNA testing for ATP7B mutations
Haemochromatosis ix
• Haematics o TIBC – low o Transferrin – low o Transferrin saturation – high o Serum ferritin - high o Serum iron - high
• Serum fasting transferrin saturation
o Phenotypic hallmark of the disorder
o First laboratory test to become abnormal
o >45%
• Serum ferritin
o Most widely used biochemical test for iron overload – high sensitivity
o Acute inflammatory protein – low specificity
o >674 picomols/L (>300 ng/mL) in men
o >449 picmols/L (>200 ng/mL) in women
• HFE genetic testing
o Initial HFE mutation analysis should evaluate C282Y and H63D polymorphisms in all patients with otherwise unexplained increased serum ferritin + increased transferrin saturation
o C282Y mutation homozygosity is the most common genetic abnormality associated with the disease in patients of northern European descent
o Should only be performed in those with increased transferrin saturation
• MRI liver
o Detects + quantifies hepatic iron excess
• Liver biopsy
o The most sensitive + specific test for measuring liver iron content
o Pearl’s stain - haemosiderin deposition in hepatocytes
o No longer necessary to diagnose haemochromatosis, genetic testing is very reliable
• Hand XR o Squared-off bone ends o Hook like osteophytes o Joint space narrowing o Sclerosis o Chondrocalcinosis (radiographic calcification in hyaline +/or fibrocartilage) o Cyst formation
• Echocardiogram
o Should be performed in patients with a raised ferritin level
o Haemochromatosis can lead to cardiomyopathy + conduction abnormalities leading to arrhythmias
o Mixed dilated-restrictive or dilated cardiomyopathy
• Testosterone, FSH, LH assays
o Hypogonadism is the second most common endocrine disorder associated with the disease after diabetes
HCC ix
• Urgent US liver
o Initial imaging test for any patients with cirrhosis to screen for HCC
o Poorly defined margins
o Coarse irregular internal echoes
• LFTs
o Can be used initially to measure the severity of liver disease
o Raised AST, ALT, ALP, bilirubin, low albumin
• PT/INR
• Viral hepatitis panel
• Raised AFP
Tumour marker
A rise in serum AFP in a patient with cirrhosis should raise the suspicion for HCC
• Contrast CT/MRI scan of abdomen
o If there is increased AFP and/or abnormal US with focal liver lesions - order contrast CT/MRI to confirm dx
• US percutaneous liver biopsy
o Not required in the vast majority of patients – diagnosis can be made radiologically
o Well-differentiated to poorly differentiated hepatocytes
o Large multinucleated giant cells having central necrosis
• Staging - CT chest, bone scan
Pancreatic cancer ix
• Abdominal US (pancreas, bile duct, liver) o Primary ix o Pancreatic mass o Dilated bile ducts o Liver metastases
• Pancreatic protocol CT
o All pt w suspected disease on US
o Stage 1 - <2cm
o Stage 2 - >2cm
o Stage 3 – grown into neighbouring tissue
o Stage 4 – metastatic (spreads through blood + lymph)
• LFTs
o Obstructive picture
o Cannot distinguish bn obstructive picture + liver metastases
• Biopsy
o Dx by histology is not required before surgical resection
• Lab findings – not specific therefore not used for dx Raised: o serum amylase o serum lipase o CA19-9 o CEA
Hiatus hernia ix
Investigations
• Barium oesophagram
o Standard criterion test
o Stomach is partially or completely intrathoracic
o Outpouching of barium at lower end of the oesophagus
o A wide hiatus through which gastric folds are seen in continuum with those in the stomach
• CXR
o Diagnostic tool
o Retrocardiac air bubble or normal
o Soft tissue opacity with or without an air-fluid level
o Para-oesophageal hiatus hernia retrocardiac air-fluid level on CXR
- Endoscopy
- Oesophageal manometry – mostly used when surgery is being considered
Gastroenteritis ix
- Stool culture – bacterial pathogens, ova cysts, parasites, toxins
- Blood culture – identification of bacteraemia if present
- FBC, CRP/ESR, U+Es – dehydration (low K in severe D+V)
- AXR – to exclude other cases of abdominal pain
HBV antibodies present
HBsAg, Anti-HBs, HBeAg, Anti-HBe, Anti-HBc
Acute HBV Chronic HBV - high infectivity Chronic HBV - low infectivity Recovery Immunized
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see infectious diseases 2 meded ppt for table
Proctoscopy vs rigid proctoscopy
Proctoscopy - visualisaiton of anus
Rigid proctoscopy - visualisation of rectum
Boerhaave’s perforation radiological findings
CXR
Pneumomediastinum
L sided pleural effusion
Gastrografin swallow
Ix if high dysphagia and u suspect cancer or pharyngeal pouch high up
Barium swallow
as during endoscopy the oropharyngeal and upper oesphageal area are intubated blindly –> if there is a pharyngeal pouch or an upper carcinoma there is risk of injury or perforation
Manometry used for
Motility disorders like
Achalasia
Oesophageal spasm
lower oesophageal sphincter tone
wave of peristalsis in rest of oesophagus
Boerhaave’s perforation ix
CXR/CT - pneumomediastinum
Coeliac disease ix
• FBC + blood smear (increased RCDW)
o Iron deficiency anaemia - microcytic anaemia
o Folate deficiency - macrocytic anaemia, hypersegmented leukocytes
o Low calcium/vitamin D
o Splenic atrophy - Howell-Jolly bodies
• Total IgA levels
o If IgA deficient then pt w coeliac disease will have a false negative IgA-tTG test result
• IgA tissue transglutaminase (IgA-tTG)
o Suggests dx
o Should be performed on a gluten-containing diet
• IgA Endomysial ab
o Greater specificity but lower sensitivity than IgA-tTG
o Perform initially if IgA-tTG is unavailable or if IgA-tTG is weakly positive
• IgG DPG (deamidated gliadin peptides) or IgA/ IgG DPG
o Current test choice for individuals with IgA deficiency
• IgG-Ttg
o Old test choice for individuals with IgA deficiency
• Small bowel – histology (duodenal biopsy) - to confirm
o Villous atrophy
o Crypt hyperplasia
o Presence of intra-epithelial lymphocytes
o Gold standard test to confirm dx
o Should be performed on a gluten-containing diet
• Small bowel – macroscopic
o Atrophy + scalloping of mucosal folds
o Nodularity + mosaic pattern of the mucosa
Need to be on a glutinous diet for at least 6 weeks before testing
Both liver disease + blocked CBD (obstructive jaundice) can cause patients to have prolonged blood clotting times - how to differentiate?
• Administering parenteral vitamin K will only correct the problem in obstructive jaundice and not in liver disease
Histology in
UC Crohn's Coeliac Pseudomembranous colitis Barret's
UC
- Inflammatory infiltrates
- Mucosal ulcers
- Goblet cell depletion
- Crypt abscesses
- Inflamed crypts filled with fibrin + polymoprphonuclear leukocytes
Crohn’s
- Transmural inflammation
- Non-caseating granulomata
- Fistulating ulcers
- Lymphoid aggregates
- Neutrophil infiltrates
Coeliac
- Villous atrophy
- Crypt hyperplasia
- Presence of intraepithelial lymphocytes
Pseudomembranous colitis
- small surface erosions of the superficial colonic crypts
- coupled with overlying accumulation of neutrophils, fibrin, mucus, necrotic epithelial cells –> forming a summit lesion
Barrets’s
- high grade dypslasia
- metaplastic columnar epithelium (used to be squamous)
Duke’s classification
A - confined to the bowel wall
B - invades the bowel wall but no lymph node involvement (beyond muscularis propria)
C - invades the bowel wall + spreads to the lymph nodes
C1 - apical lymph node not involved
C2 - apical lymph node involved
D - distant metastases present
grading of colorectal cancer
A 45-year-old man presents with intermittent difficulty in swallowing for the last 4 months. This is associated with severe retrosternal pain and regurgitation. He has no risk factors or sinister signs for malignancy. What is the most important investigation in this case?
A Barium swallow B Chest X-ray C CT of the chest D Endoscopy E Iron studies
Answer - D
Achalasia – intermittent difficulty swallowing both liquids + solids
Patient most likely has achalasia – barium swallow is diagnostic + will show a birds beak appearance + lack of peristalsis
Dysphagia lasting >3 weeks - endoscopy to exclude malignant stricture
Which marker is the first to be detected after an HBV infection?
HBsAg
Detected within 4 weeks of infection, first marker to be detected If still detected in the serum 6 months after acute HBV – chronic infection NOT found in patients vaccinated against HBV (HBsAb is found in those)
Which marker after HBV vaccination?
HBsAb
HBsAb measured after vaccination to evaluate response to vaccine HBsAb also found in patients who recovered from HBV
Which HBV markers in recovered patients
HBsAb, Anti-HBcAg
HBeAg meaning
Present in both acute + chronic
Indicates high level of infectivity
HBcAb meaning
Present in both acute + chronic
In acute it’s the 2nd marker to be detected after HBsAg
In chronic presence of HBcAb in the absence of HBeAg indicates low infectivity + disease activity
Autoimmune hepatitis antibodies
Type 1 autoimmune hepatitis
Type 2 autoimmune hepatitis
Type 3 autoimmune hepatitis
Type 1 autoimmune hepatitis – ANA, ASMA, anti-soluble liver antigen or liver/pancreas (anti-SLA/LP), pANCA
Type 2 autoimmune hepatitis – anti-liver-kidney microsomal – 1 ab (anti-LKM-1), anti-liver cytosol 1 (anti-LC1)
Type 3 autoimmune hepatitis – anti-soluble liver antigen or liver/pancreas (anti-SLA/LP)
AAA ix
- Bloods
FBC, Clotting, U+Es, LFT
Cross match if surgery planned
Blood cultures, ESR, CRP if infectious/inflammatory AAA suspected
ABG will show metabolic acidosis from the hypovolaemia - Imaging
US - can detect aneurysm can’t tell if it’s leaking or not - first line ix
CT with contrast/CT angiography - can tell if an aneurysm has ruptured
MR angiogrpaphy - if allergic to contrast
psoas sign not visible on AXR -? AAA, pancreatitis, normal
AAA monitoring + mx
Normal diameter of aorta - 2cm
3-4.4 cm - annual US
4.5-5.4cm - US every 3 months
>5.5cm - elective intervention
Early intervention rapidly expanding (>1cm/year) tender symptomatic suspected rupture
