Gastro - ix Flashcards

1
Q

Extrinsic pathway of the clotting cascade

How is it measured
Normal value
Affected by

A

PT

14s

Warfarin, liver disease

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2
Q

Intrinsic pathway of the clotting cascade

How is it measured
Normal value
Affected by

A

APTT

34s

Heparin, Hemophilias, VWD

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3
Q

What is the Rockall score used for?

A

UGIB
Determines risk of re-bleeding + death

(1) Risk of rebleeding/mortality pre-endoscopy
(2) Risk of rebleeding/mortality post-endoscopy.

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4
Q

What does the Rockall score include?

A

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
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5
Q

What is the glasgow Blatchford score?

A

Screening tool to assess the likelihood that a person with an acute UGIB will need to have medical intervention

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6
Q

What does the Glasgow Blatchford score include (8)?

A
Blood urea nitrogen
Hb
SBP
HR
Malaena
Syncope
Hepatic disease
Cardiac disease
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7
Q

Achalasia ix

A

• 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

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8
Q

Barrett’s oesophagus ix

A
  • 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)
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9
Q

Oesophageal cancer ix

A

• 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

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10
Q

Gastritis ix

A

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
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11
Q

Peptic ulcer disease Ix

A

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
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12
Q

ALARMS symptoms

A
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
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13
Q

GORD ix

A

• 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

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14
Q

GLASGOW scale

A

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

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15
Q

Oesophageal spasm ix

A

Crockscrew appearance on barium swallow

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16
Q

Anal fissures ix

A
  • Do not attempt a DRE – extremely painful

* Diagnosis is clinical + further Ix only required if there are features of underlying pathology

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17
Q

Rectal prolapse ix

A

• 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

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18
Q

Haemorrhoids ix

A

• 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

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19
Q

Appendicitis ix

A

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
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20
Q

Alverdo scoring system for appendicitis

Symptoms
Signs
Laboratory findings

Results

A

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

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21
Q

Ix to confirm obstruction

A

AXR

Small bowel >3cm
Large bowel >6cm

If large bowel >9cm - risk of imminent perforation + need for surgery

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22
Q

Colon cancer ix

A
Bloods
•	FBC
   Anaemia if bleeding
•	LFTs
   Liver is the first site of metastasis of colorectal cancer (enterohepatic circulation)
•	U&amp;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
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23
Q

Volvulus ix

A

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

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24
Q

Choledocholithiasis ix

A

EUS/MRCP

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25
Q

Gallstones/biliary colic ix

A

• 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

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26
Q

Cholecystitis ix

A
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
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27
Q

Acute cholangitis ix

A
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

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28
Q

Mallory Weiss tear ix

A

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

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29
Q

Toxic megacolon ix

A

AXR >6cm

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30
Q

When should flexible sigmoidoscopy be used instead of colonoscopy toi investigate UC?

A

When there is a high risk of perforation

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31
Q

UC ix

A
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

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32
Q

Crohn’s disease ix

A
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

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33
Q

What is Truelove’s and Witt’s severity index and what does it include (6)?

A

Classifies severity of UC

Includes

  • Number of stools
  • Blood in stools
  • Anaemia
  • Pulse rate (>90)
  • Fever (>37.8)
  • ESR/CRP (>30mm/h)
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34
Q

Cirrhosis ix

A

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

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35
Q

Cirrhosis ix

A

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

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36
Q

Signs of portal HTN on UC/CT/MRI

A
Ascites
Splenomegaly
Increased diameter of the portal vein (>13mm)
Collateral vessels
Hepatocellular carcinoma
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37
Q

Signs of portal HTN on UC/CT/MRI

A
Ascites
Splenomegaly
Increased diameter of the portal vein (>13mm)
Collateral vessels
Hepatocellular carcinoma
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38
Q

What is the child-pugh-turcotte classification?

A

It estimates the prognosis in those with cirrhosis

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39
Q

What does the child-pugh-turcotte classification include?

A
  • Serum albumin
  • Serum bilirubin
  • INR
  • Ascites
  • Encephalopathy
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40
Q

Tumour markers

Breast cancer
Ovarian cancer
Pancreatic cancer
Biliary cancer (cholangiocarcinoma)
Prostate cancer
Colorectal cancer
Hepatocellular carcinoma
Non seminomatous germ cell tumours
A
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
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41
Q

Tumour markers

Breast cancer
Ovarian cancer
Pancreatic cancer
Biliary cancer (cholangiocarcinoma)
Prostate cancer
Colorectal cancer
Hepatocellular carcinoma
Non seminomatous germ cell tumours
A
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
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42
Q

Cholangiocarcinoma ix

A

• 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)
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43
Q

Liver abscess ix

A

• 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
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44
Q

Liver abscess ix if amoebiasis is suspected

A

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

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45
Q

Liver failure ix

A
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
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46
Q

Wernicke’s encephalopathy ix

A
  • 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

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47
Q

What does thumb printing on XR, CT mean?

A

Submucosal oedema or haemorrhage

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48
Q

First line ix for acute mesenteric ischaemia +findings

A
  • 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)

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49
Q

Intestinal ischaemia ix + findings

A

• 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)

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50
Q

Investigations to investigate causes of intestinal ischaemia

A
  • ECG, Echo - AF, arrhythmias, MI (predispose to acute mesenteric ischaemia)
  • Coagulation panel - underlying coagulopathy
  • AXR
51
Q

Chronic mesenteric ischaemia ix

A
  • 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)

52
Q

Ischaemic colitis ix

A

• 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)

53
Q

SBO ix

A

• 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

54
Q

LBO ix

A

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

55
Q

PSC ix bloods

A

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
56
Q

PSC imaging ix

A

• 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

57
Q

Best single test for screening household contacts of HBV infected individuals to determine need for vaccination

A

Anti-HBc

58
Q

What is transient elastrography?

A

Non-invasive test that has a high diagnostic accuracy for the detection of cirrhosis

59
Q

HAV ix

A

• 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
60
Q

HBV ix

A
  • 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

61
Q

HCV ix

A
  • 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
62
Q

HDV ix

A

Anti-HDV antibody

63
Q

HEV ix

A

Hepatitis serology

64
Q

HBsAg -ve
Anti-HBc -ve
Anti-HBs -ve

A

Susceptible

65
Q

HBsAg -ve
Anti-HBc +ve
Anti-HBs +ve

A

Immune due to natural infection

i.e. became infected with HBV in the past, cleared the virus and is now immune

66
Q

HBsAg -ve
Anti-HBc -ve
Anti-HBs +ve

A

Immune due to Hep b vaccination

67
Q

HBsAg +ve
Anti-HBc +ve
IgM anti-Hbc +ve
Anti-HBs -ve

A

Acutely infected

68
Q

HBsAg +ve
Anti-HBc +ve
IgM anti-Hbc -ve
Anti-HBs -ve

A

Chronically infected

69
Q

HBsAg -ve
Anti-HBc +ve
Anti-HBs -ve

A
4 possibilities
resolved infection
false positive anti-HBc thus susceptible
low level chronic infection
resolving acute infection
70
Q

Presence of HBsAg

hep B surface ag

A

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

71
Q

Presence of anti-Hbs

hep b surface ab

A

Recovery + immunity from HBV

Also develop in people who have been successfully vaccinated against HBV

72
Q

Anti-HBc

total hepatitis B core ab

A

indicates previous ongoing infetion with HBV in an undefined time frame
appears at the onset of symptoms in acute HB and persists for life

73
Q

IgM anti-HBc

IgM antibody to hep B core antigen

A

Presence indicates acute infection

positivity indicates recent infection with hep B (<6m)

74
Q

Autoimmune hepatitis ix

A

• 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)

75
Q

Auto-antibodies in AI hepatitis

A

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)

76
Q

PBC ix

A

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

77
Q

Alcoholic hepatitis biopsy result

A

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

78
Q

Biliary dilation diagnosis

A

US

>6 mm CBD diameter

79
Q

Acute pancreatitis ix

A

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

80
Q

Chronic pancreatitis ix

A
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)

81
Q

Peritonitis

FBC
U+E
ABG

A

FBC - increased WCC
U+Es - increased Na, decresaed K
ABG - acidosis

82
Q

To diagnose peritonitis in people with ascites the ascitix fluid should contain (spontaneous bacterial peritonitis)

A

> 250 polymorphonuclear (neutrophils) cells/μL

83
Q

Why do we need to administer Mg with thiamine?

A

Mg serves as a co-factor in enzymes that need thiamne pyrophosphate

84
Q

What does elevated urea and normal creatinine indicate?

A

Active GI bleeding

85
Q

Alcoholic hepatitis ix

A

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

86
Q

Gastric cancer ix

A

• 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

87
Q

NASH/NAFLD ix

A

• 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

88
Q

Courvoiseir’s sign

A

Painless palpable gallbladder unlikely to be due to gallstones - think pancreatic cancer, cholangiocarcinoma (in distal cystic duct tumours)

89
Q

What is Rigler’s sign?

A

Sign of perforated bowel

Air outside bowel + air inside bowel - lining of bowel looks very clear

90
Q

Diverticulitis ix

A

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

91
Q

Hernia ix

A

Clinical

US – 1st line

92
Q

Intestinal obstruction ix

A
•	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

93
Q

Acute intestinal/mesenteric ischaemia ix

A

• 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

94
Q

Chronic mesenteric ischaemia ix

A

• 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
95
Q

Anti-Hbc

A

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

https://d1yboe6750e2cu.cloudfront.net/i/1cfb524d7810124d77d48071a78aff6cb8fbb366

96
Q

Anti-HbS

A

VacSination

or recovery + immunity from HBV

97
Q

HbsAg

A

HBV is here now
acute/chronic infection
active infection
>6m - chronic infection

98
Q

HbeAg

A

Infective

99
Q

Wilson’s disease ix

A
  • 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
100
Q

Haemochromatosis ix

A
•	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

101
Q

HCC ix

A

• 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

102
Q

Pancreatic cancer ix

A
•	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
103
Q

Hiatus hernia ix

A

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
104
Q

Gastroenteritis ix

A
  • 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
105
Q

HBV antibodies present

HBsAg, Anti-HBs, HBeAg, Anti-HBe, Anti-HBc

Acute HBV
Chronic HBV - high infectivity
Chronic HBV - low infectivity
Recovery
Immunized
A

https://d1yboe6750e2cu.cloudfront.net/i/1cfb524d7810124d77d48071a78aff6cb8fbb366

see infectious diseases 2 meded ppt for table

106
Q

Proctoscopy vs rigid proctoscopy

A

Proctoscopy - visualisaiton of anus

Rigid proctoscopy - visualisation of rectum

107
Q

Boerhaave’s perforation radiological findings

A

CXR
Pneumomediastinum
L sided pleural effusion
Gastrografin swallow

108
Q

Ix if high dysphagia and u suspect cancer or pharyngeal pouch high up

A

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

109
Q

Manometry used for

A

Motility disorders like
Achalasia
Oesophageal spasm

lower oesophageal sphincter tone
wave of peristalsis in rest of oesophagus

110
Q

Boerhaave’s perforation ix

A

CXR/CT - pneumomediastinum

111
Q

Coeliac disease ix

A

• 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

112
Q

Both liver disease + blocked CBD (obstructive jaundice) can cause patients to have prolonged blood clotting times - how to differentiate?

A

• Administering parenteral vitamin K will only correct the problem in obstructive jaundice and not in liver disease

113
Q

Histology in

UC
Crohn's
Coeliac 
Pseudomembranous colitis
Barret's
A

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)
114
Q

Duke’s classification

A

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

115
Q

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
A

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

116
Q

Which marker is the first to be detected after an HBV infection?

A

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)
117
Q

Which marker after HBV vaccination?

A

HBsAb

HBsAb measured after vaccination to evaluate response to vaccine 
HBsAb also found in patients who recovered from HBV
118
Q

Which HBV markers in recovered patients

A

HBsAb, Anti-HBcAg

119
Q

HBeAg meaning

A

Present in both acute + chronic

Indicates high level of infectivity

120
Q

HBcAb meaning

A

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

121
Q

Autoimmune hepatitis antibodies

Type 1 autoimmune hepatitis
Type 2 autoimmune hepatitis
Type 3 autoimmune hepatitis

A

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)

122
Q

AAA ix

A
  • 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

123
Q

AAA monitoring + mx

A

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