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J3 > Interne geneeskunde > Flashcards

Interne geneeskunde Flashcards

1
Q

Standard ‘Liver Function’ Tests

A 
 Bilirubin
 Aspartate Aminotransferase (AST)
 Alanine Aminotransferase (ALT)
 Gamma Glutamyltransferase (GGT)
 Alkaline Phosphatase (ALP)
 Albumin
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2
Q

Which test reflect liver function?

A

prothrombin time
albumin
bilirubin

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3
Q

What tests would you use for Investigation of in CHRONIC LIVER DISEASE?

A

Ultrasound

Blood:
 viral hepatitis screen (chronic forms) - HBV, HCV

 Autoimmune liver disease
o ANA / SMA / LKM (AIH)
o AMA (PBC)
o Immunoglobulins –> elevated IgM can be very suggestive of PBC

 Metabolic liver disease
o Ferritin (haemochromatosis), transferrin saturation
o Caeruloplasmin (Wilson’s Disease)
o alpha 1 anti-trypsin deficiency
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4
Q

What tests would you use for Investigation of ACUTE LIVER INJURY?

A

 Ultrasound

 Acute viral hepatitis - HAV, HBV, (HCV), HEV, CMV (in immunocompromised patients)

 Autoimmune liver disease
o ANA / SMA (=smooth muscle antibody)/ LKM (AIH)
o Immunoglobulins -> specific IgG elevation can be very suggestive of autoimmune hepatitis

 Drug-induced liver injury - Paracetamol levels
o Not always overdose
o toxicity is augmented with alcohol excess or in underweight patients (<50kg)

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5
Q

Most Common Causes of Abnormal Liver Blood Tests

A

FATTY LIVER
o Alcoholic Liver Disease
o Non-alcoholic Fatty Liver Disease (NAFLD)

CHRONIC VIRAL HEPATITIS
o Chronic Hepatitis C

AUTOIMMUNE LIVER DISEASE
o Primary Biliary Cholangitis
o Autoimmune Hepatitis

HAEMOCHROMATOSIS

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6
Q

How can you distinguish between NAFLD and ALD?

A

Can be distinguished clinically

AST/ALT ratio differs:
● <0.8 in NAFLD
Alcoholic Hepatitis
● >1.5 in ALD (AST is preferentially raised, causing a high AST to ALT ratio)

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7
Q

Alcoholic Hepatitis

A

acute reaction to prolonged excessive alcohol consumption

Patients presenting with a history of alcohol excess with new-onset jaundice

Essential Features
o recent excess alcohol
o Bilirubin <80 micromol/l for less than 2 months
o exclusion of other liver disease
o treatment of sepsis/GI bleeding
o young patients (40s/50s)
o AST <500 (AST: ALT ratio >1.5)
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8
Q

Signs of Chronic Liver Disease/Portal Hypertension

A

Ascites

spider naevi

caput medusa

hypersplenism

foetor hepaticus - portosystemic shunting allows thiols to pass directly into the lung

encephalopathy

‘synthetic dysfunction’:
o prolonged prothrombin time
o hypoalbuminaemia.
thrombocytopenia (decreased TPO produced by liver)

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9
Q

Childs-Turcotte-Pugh Score

A

Assessment of Severity of Chronic Liver Disease

Grade A = Compensated liver disease (coping well)

Grade C = Decompensated liver disease (not coping well, likely to result in liver disease)

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10
Q

Assessment of Ascites

A

diagnostic tap

Cell count
 >500 WBC/ cm 3 and/ or >250 neutrophils/cm 3 suggest spontaneous bacterial peritonitis (SBP)
 Inflammatory conditions can also increase WCC
 lymphocytosis suggests TB or peritoneal carcinomatosis

Albumin
 Serum ascites albumin gradient (SAAG) =
o serum albumin MINUS ascitic albumin g/l
 SAAG >11g/l = portal hypertension

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11
Q

Management of Ascites

A

Low salt diet  reduces the degree of sodium retention

Diuretics

  • spironolactone (aldosterone antagonist -> direct negative effect on RAAS)
  • Frusemide (Furosemide)
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12
Q

Hepatic Encephalopathy: Precipitating Factors

A 
 GI haemorrhage,
 infections,
 renal/electrolyte disturbances,
 psychoactive medication,
 excessive dietary protein 
 acute deterioration of liver function
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13
Q

Hepatic encephalopathy

A

caused by the failure of the cirrhotic liver to remove toxins from the blood

this ultimately negatively affects the brains function.

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14
Q

What should you be cautious of with Hepatic encephalopathy ?

A

don’t make it worse!

No:

  • opiates
  • sedatives
  • hyponatraemia

give lactulose to get bowels moving
gut decontamination with antibiotics (non-absorbable) to decrease urease load

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15
Q

hepatitis symptoms

A 
Non-specific symptoms:
 Malaise, fever, headaches
 Anorexia, nausea and vomiting
 Right upper quadrant abdominal pain
 Dark urine
 Jaundice
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16
Q

Acute Hepatitis

A 
o Usually symptomatic
o Inflammation of the liver
o Raised ALT / AST
o Jaundice
o Clotting Derangement
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17
Q

Chronic hepatitis

A

o Usually asymptomatic by this stage
o Hepatitis virus present for more than 6 months
o Jaundice has normally settled by this point
o Variable changes in Liver Function

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18
Q

ACUTE HEPATITIS: CAUSES

A

 Infections
o Hep A, B, C, D, E
o EBV, CMV, Toxoplasmosis

 Toxins
 Drugs
 Alcohol
 Autoimmune
 Wilsons
 Haemochromatosis
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19
Q

Which hepatitis virus can cause neurological effects and what are they?

A

Hep E (4 genotypes - associated with GT 3)

o Guillain-Barre syndrome = ascending flaccid paralysis
o Encephalitis = inflammation of the brain
o Ataxia
o Myopathy

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20
Q

Which hepatitis virus is associated with high mortality rates during pregnancy?

A

Hep E (4 genotypes - associated with GT 1)

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21
Q

sAg - Surface antigen

A

marker of current infection (HBV)

sAg present = infected

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22
Q

sAb – Surface antibody

A

marker of immunity

Only seen in people who have been infected in the past but have cleared the virus

Seen in vaccinated individuals

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23
Q

cAb – Core antibody

A

o Definitely been infected (currently or in the past)

o Check surface antigen to determine if infection is active

o Not seen in vaccinated individuals

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24
Q

eAg – e antigen

A

suggests high infectivity

generally seen in younger patients

eAg +ve (early disease)
o High Viral Load
o High risk of chronic liver disease and HCC
o Highly infectious

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25
Q

eAb – e antibody

A

suggests low infectivity

generally seen in older patients

eAg –ve (late disease)
o Low viral load
o Lower risk of chronic liver disease and HCC
o Less infectious

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26
Q 
29-year-old male, UK born
 Recent holiday in Thailand
 8 weeks later, developed jaundice and “flu”
 Results
o HBV sAg Positive
o Anti-HBV core Positive
o Anti-HB core IgM Positive
A

Acute Hepatitis B infection (IgM positive = acute)

Patient must be tested for HIV and Hep C as well

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27
Q 
45-year-old male
 Born in China, now in UK
 Family history of hepatitis B
 Brother recently died of liver cancer
 Presented to GP anxious after brother’s recent death
 Results
o HBV sAg Negative
o Anti HBV core Positive
A

Prior infection but it has been cleared

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28
Q 
 30-year-old from India
 Tried to give blood and found to be HBV+
 Results
o HB sAg Positive
o Anti-HBc Positive
o Anti-HBc IgM Negative
o HB eAg Positive
A

Chronic Hepatitis B infection (IgM negative = chronic), highly infectious (eAg positive), Carrier

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29
Q 
20-year-old jaundiced medical student
 Results
o HB sAg Negative
o Anti HBV s Positive
o Anti-HB core Negative
o Anti-HBc IgM Negative
o Anti-HAV IgM Positive
A

Acute Hep A infection.

Not infected with Hep B and has never been exposed to the virus. Has been vaccinated for Hep B
has antibodies

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30
Q

Prevention of HBV

A

 Education (safe sex, injecting etc.)
 Screening of pregnanct women / doctors
 Protect blood supply & hospital supplies
 Immunisation:

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31
Q

Which forms of hepatitis have chronic carriage?

A

HBV, HCV, and HDV

HEV in immunosuppressed patients

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32
Q

Acute Pancreatitis Diagnosis

A

2 of 3
 pain in keeping with pancreatitis
• severe pain, presents as an acute abdomen
• central abdominal pain, radiating to back
• May be relieved by leaning forwards
• Often a history of vomiting

 amylase 3 times ULN

 characteristic CT appearance

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33
Q

Causes of acute pancreatitis

A

Gallstones – important to rule out because it can be treated to prevent recurrence of pancreatitis

Alcohol

Trauma/ ERCP

Other - drugs/ high lipids/ autoimmune/ viral

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34
Q

Initial management of acute pancreatitis

A

Assess ABC’s

Fluids – usually volume depleted due to vomiting, decreased intake and systemic inflammation (dry
intravascularly)

Oxygen – high lactate levels due to anaerobic respiration

Organ support

NB: abx not given in GGC due to risk of selecting for fungal/MRSA

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35
Q

Investigations acute pancreatitis

A

Bloods (remember to check serum amylase)

 US to assess for gallstones

 MRCP to assess for CBD stones (US not very good to assess for this)

 CT if diagnostic doubt or concern about complications

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36
Q

Differential Diagnosis for severe abdominal pain and elevated serum amylase

A

 Acute pancreatitis (if amylase is in 1000s)

 Perforated duodenum - raised amylase due to leakage from duodenum

 Ischaemic bowel - leakage of amylase-rich fluid

Cholangitis
Mumps (amylase secreted by parotids)

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37
Q

Possible outcomes after pancreatitis

A

 May be diabetic
 May require creon pancreatic enzyme supplements
 May require restorative surgery
 Significant impact on quality of life
 If gallstones- needs gallbladder removed

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38
Q

causes of injury to the liver

A 
 Drugs or toxins including alcohol
 Abnormal nutrition/metabolism
 Infection
 Obstruction to bile or blood flow
 Autoimmune liver disease
 Genetic/deposition disease
 Neoplasia
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39
Q

Cirrhosis

A

 = End-stage liver disease

Definition is three-fold:
o Diffuse process with
o Fibrosis
o Nodule formation

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40
Q

Clinical approach to liver disease

A

History, symptoms and signs by examination

Blood tests:
• LFTs
• Haematology (synthetic function = PT/Albumin)
• viral and autoimmune serology
• deposition diseases (HH/Wilson’s/A1ATD)

o Radiology: usually at least ultrasound

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41
Q

Histology of Acute hepatitis

A

 Diffuse hepatocyte injury seen as swelling.
 “spotty necrosis”
 inflammatory cell infiltrate

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42
Q

Causes: Acute cholestasis or cholestatic hepatitis

A

o Extrahepatic biliary obstruction
o Drug injury e.g. antibiotics

Histology: brown bile (bilirubin) pigment +/- acute hepatitis

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43
Q

Acute versus chronic hepatitis histology

A

histology can look similar

Fundamental difference = chronic may have already progressed to have some degree of fibrosis

Can be visualised using Masson stain

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44
Q

which liver diseases may develop fibrosis and progress to cirrhosis

A

o Fatty liver disease (steatosis and steatohepatitis)
o Chronic hepatitis
o Chronic biliary/cholestatic disease
o Genetic/deposition disease

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45
Q

Hepatitis B pathology

A

 may look like acute hepatitis plus fibrosis

 Specific feature of hepatitis B virus = ground glass cytoplasm in hepatocytes
o Represents accumulation of “surface antigen”, one of three main HB viral antigens

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46
Q

Chronic biliary/cholestatic disease causes:

A

o Primary biliary cirrhosis (PBC)

o Primary sclerosing cholangitis (PSC)

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47
Q

Genetic/deposition liver disease

y

A

 Haemochromatosis (iron)

 Wilson’s disease (copper)

 Alpha-1-antitrypsin deficiency (lack of secretion therefore accumulates in hepatocytes)

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48
Q

Histology: Chronic biliary/cholestatic disease

A

o Focal, portal-predominant inflammation and fibrosis with bile duct injury

mainly affects portal tracts and bile ducts

granulomas in PBC

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49
Q

Specific causes of diffuse liver disease

A 
 Hepatitis viruses 
 Drug injury
 Autoimmune liver disease
 Extrahepatic biliary obstruction
 Alcohol
 Metabolic syndrome e.g. obesity
 Chronic biliary disease e.g. PBC
 Vascular disease e.g. venous obstruction/drug induced injury
 Genetic/deposition e.g. haemochromatosis
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50
Q

Drug-induced liver disease

A

common and mimics other liver diseases.

Drugs can cause almost any pattern of liver disease

common causes:

  • paracetamol
  • amiodarone
  • methotrexate
  • co-amoxiclav

remember non-prescribed drugs!

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51
Q

Von Meyenberg complex

A

(= simple biliary hamartoma)

benign

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52
Q

Haemangioma

A

benign blood vessel tumour

Biopsy avoided because of risk of bleeding

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53
Q

Hepatic adenoma

A

o Rare

o Mainly young women, often associated with hormonal therapy

o Risk of bleeding and rupture so excision if large

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54
Q

Hepatocellular carcinoma

A

 Most common primary liver tumour

 Usually arises in cirrhosis and associated with elevated serum AFP (alpha feto-protein)

 Screening available for patients with cirrhosis

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55
Q

Aims of histopathology in general

A

o Establish disease diagnosis and severity

o Predict outcome and guide treatment

56
Q

Acute hepatitis Presentation + Causes

A

o Short history of RUQ tenderness, malaise etc
o Elevated AST/ALT (and often Bil)

Causes:
o Viral hepatitis,
o Autoimmune
o drug injury

57
Q

Causes of fatty liver disease

A

o Alcohol

o Non-alcoholic
• Type II diabetes
• obesity
• hyperlipidaemia

o Drugs
• Methotrexate
• Amiodarone
• Steroids

58
Q

Chronic hepatitis Clinical definition + causes

A

Liver inflammation (abnormal LFTs) for at least 6 months

o Viral hepatitis B
o Autoimmune
o rarely drug injury

59
Q

Grade vs stage in liver disease

A

grade: degree of inflammation
– Guides treatment

Stage: amount of fibrosis
– Prognosis (& guides treatment)

60
Q

Hepatitis C pathology

A

 often mainly in portal tracts, as chronic inflammation with lymphoid aggregates

61
Q

Primary biliary cirrhosis (PBC)

A

o Mainly middle-aged women

o Auto-immune disease with serum anti-mitochondrial antibodies (AMA) and high IgM

o No cure but ursodeoxycholic acid eases symptoms and slows progression

62
Q

Primary sclerosing cholangitis (PSC)

A

o Rare, associated with ulcerative colitis

o Risk of progression to cholangiocarcinoma

63
Q

Budd-Chiari syndrome

A

Primary hepatic vascular disease

hepatic vein thrombosis

64
Q

causes of Liver abscess

A

 May arise from ascending cholangitis

 parasitic disease

65
Q

Cholangiocarcinoma

A

adenocarcinoma of bile ducts

either intra- or extra-hepatic (i.e. can be a primary liver tumour)

66
Q

causes of Lithogenic (stone forming) bile

A

Bile becomes lithogenic for cholesterol if there is:

  • excessive secretion of cholesterol
  • decreased secretion of bile salts.

Excessive secretion of bilirubin (eg haemolytic anaemia) can cause its precipitation in concentrated bile in the gallbladder.

67
Q

Acute Cholecystitis presentation

A

 Severe RUQ pain, tenderness and fever

 Leucocytosis and normal serum amylase

 Usually resolves spontaneously (as the stones move) but can progress to empyema, gangrene and
rupture

Initiated by stone obstruction of cystic duct causing supersaturation of bile and chemical irritation

68
Q

Mucocoele of Gallbladder

A

 Distention of gallbladder due to an inappropriate accumulation of mucus

 Previous irritation around the neck of the gallbladder causing fibrosis and obstruction

69
Q

common place for gallstone obstruction

A

ampulla of vater

slight narrowing at the ampulla of vater

obstruction here irritates the pancreas

70
Q

Potential complications of acute pancreatitis

A

pseudocyst

pancreatic fistula

pancreatic necrosis

Pancreatitic Abscess

71
Q

Pancreatic Abscess

A

 Potential complication of acute pancreatitis
 Infected pancreatic necrosis
 Avascular haemorrhagic pancreas acts like a good culture medium

Treatment: drainage or necrosectomy plus antibiotics

72
Q

Pancreatic pseudocyst

A

Potential complication of acute pancreatitis

 Commonly in lesser sac
 High concentration of pancreatic enzymes
 May resolve spontaneously
 May be drained into stomach

 Can be communicating (with pancreatic duct) or
noncommunicating (majority)

73
Q

Differential of Pancreatic Cysts

A

Intraductal papillary mucinous neoplasm – in continuity with main pancreatic duct or side branch duct

  • dysplastic papillary lining secreting mucin
  • Premalignant condition

 Mucinous cystic neoplasm – mucinous lining, “ovarian-type” stroma

 Serous cystadenoma – no mucin production; (almost always) benign

74
Q

most common Carcinoma of Pancreas

A

Ductal adenocarcinoma

associated with perineural invasion

Heterogenous tumours with wide range of mutations => No standard effective therapy

75
Q

risk factors for Carcinoma of Pancreas

A

 Germline mutations (e.g. BRCA) account for small proportion of patients,

 but SMOKING is by far the biggest risk factor

76
Q

Signs and Symptoms of Carcinoma of Pancreas

A

 Painless obstructive jaundice

 New onset diabetes

 Abdominal pain due to pancreatic insufficiency or nerve invasion.

 Tumours in head may obstruct pancreatic duct and bile duct – “double duct sign” on radiology

77
Q

Whipple’s Resection

A

for tumours of head of pancreas

78
Q

Commonest functional Pancreatic Neuroendocrine Tumour

A

insulinoma –> causes hypoglycaemia

79
Q

Reflux oesophagitis (GORD)

A

Acid and digestive enzymes injure squamous epithelium lining oesophagus.

Stimulates an inflammatory response

Increased numbers of inflammatory cells (lymphocytes = chronic inflammatory cells)

basal zone of the squamous epithelium is hyperplastic = attempt at repair

80
Q

Candida oesophagitis

A

Typically see active chronic inflammation with many neutrophils especially near the luminal surface

White plaques

PAS stain confirms spores and hyphae of Candida albicans

81
Q

Barrett’s oesophagus

A

metaplastic response to mucosal injury
o e.g. from long term GORD.

Squamous epithelium becomes glandular, usually columnar with goblet cells

Associated with:

  • benign strictures
  • adenocarcinoma
82
Q

Oesophageal cancer

A

Squamous carcinoma - associated with smoking/drinking

Adenocarcinoma - associated with GORD and obesity

83
Q

causes of acute gastritis

A 
o Alcohol
o Medication e.g. NSAIDs
o severe trauma
o burns (Curling's ulcers)
o surgery
84
Q

causes of chronic gastritis

A

o A: Autoimmune

o B: Bacterial (H pylori)

o C: Chemical

85
Q

Autoimmune gastritis

A

 Autoimmune destruction of parietal cells due to auto-antibodies against intrinsic factor and parietal cell antibodies in blood

Leads to:
o complete loss of parietal cells with pyloric and intestinal metaplasia.

o Achlorhydria & bacterial overgrowth.

o Hypergastrinaemia & endocrine cell hyperplasia /carcinoids.

o Persistent inflammation which can lead to epithelial dysplasia and may lead to cancer.

86
Q

Types of H. pylori-induced gastritis

A

Antral-predominant gastritis - hypergastrinaemia and duodenal ulceration

Pangastritis - hypochlorhydria, multifocal atrophic gastritis, intestinal metaplasia, cancer

patients with higher IL-8 production tend to get pangastritis

87
Q

Consequences of peptic ulceration

A

 Haemorrhage
 Perforation of underlying vessels - haematemesis
 Fibrosis (leading to stenosis)

88
Q

causes of chemical gastritis

A

o bile reflux
o NSAIDs
o Ethanol
o oral iron

89
Q

Gastric cancer

A

Strongly associated with chronic gastritis: H pylori or autoimmune.

Background atrophic mucosa, chronic inflammation, intestinal metaplasia, dysplasia.

Morphologically classified into ‘intestinal’ or ‘ diffuse’
o Intestinal – maintain glandular architecture
o Diffuse – loss of architecture

90
Q

Diffuse gastric cancer

A

 Individual malignant cells with mucin vacuoles (‘signet ring’ cells)

 May invade extensively without being endoscopically obvious = linitis plastica (‘leather bottle
stomach’)

 Metastasis to ovaries (‘Krukenberg tumour’)
 Supraclavicular lymph node (‘Virchow’s node’)
 ‘Sister Joseph’s nodule’ (umbilical metastasis)

91
Q

Upper gastrointestinal bleeding - presentation

A
  • Haematemesis
  • “coffee ground” vomiting
  • Melaena

Due to a bleeding source from oesophagus, stomach or duodenum

92
Q

Causes of upper GI bleeding

A 
 Peptic ulcer 
 Oesophagitis 
 Gastritis 
 Duodenitis 
 Varices 
 Malignancy 
 Mallory-weiss tear
93
Q

Management of upper GI bleed

A 
ABCs
 Resuscitate 
• IV access for fluids/blood
• (check bloods, esp Hb &amp; urea)
• lie flat &amp; give oxygen

 Risk assessment & timing of endoscopy:
• High risk: emergency endoscopy
• Moderate risk: admit & next day endoscopy
• Low risk: out-patient management?

94
Q

Endoscopic therapy for upper GI bleed

A
  • AdrenaIine injection - temporary, constricts blood vessels
  • Heater probe - cauterize vessels
  • Endoscopic clips – obstruct blood vessel to stop bleeding. Falls off about a week later
  • (thrombin, laser)

IV Proton pump inhibitors (PPIs) in Upper GI bleeding reduce rebleeding and mortality if given post-endoscopy

95
Q

What to do about Aspirin & NSAIDs in patients with upper GI bleed

A

continue aspirin - lifesaving CV treatment

discontinue NSAIDs - not crucial

96
Q

When to administer Blood products in upper GI bleeding

A

Restrictive transfusion
• Only transfuse blood once Hb <7-8g/dL

Transfuse platelets if actively bleeding & platelet count <50x10^9/L

FFP if INR>1.5

Prothrombin complex concentrate if on warfarin & active bleeding

97
Q

Treatment of varices

A
  • endoscopic banding
  • Transjugular intrahepatc porto-systemic shunt (TIPS) - decompresses the high pressure portal vein
  • B-Blocker drugs
98
Q

Management of Acute variceal bleeding

A

Resuscitation
• restore circulating volume
• transfuse once Hb <7 g/dL

Diagnosis - endoscopy

Therapy
• antibiotics early
• vasopressors (Terlipressin) early
• endoscopic band ligation
• consider airway protection - can aspirate into lungs

sengstaken tube in uncontrolled bleeding

99
Q

Variceal bleeding management vs ulcer bleeding

A

variceal bleeding differs from ulcers in that you can give two drugs before that improve mortality:

 prophylactic Antibiotics – cirrhotic patients are at risk of infection (immunosuppressed)

 Terlipressin – vasopressin agonist. Constricts blood vessels entering portal vein (specific to gut circulation)

100
Q

Variceal Bleeding Primary Prophylaxis:

A

• Beta-blockers or Banding

same for prevention of rebleeding

101
Q

Types of Alcoholic Liver Disease

A

Pathologic changes can be divided into 3 groups (with some overlap):

1) Fatty liver (steatosis)
2) Alcoholic hepatitis +/– hepatic fibrosis
3) Cirrhosis

102
Q

Hepatic alcohol metabolism

A

 Two main metabolic pathways:

  1. Cytoplasmic alcohol dehydrogenase (ADH)
     Main route for metabolism
     Not inducible
     Polymorphisms – some people cannot process alcohol properly
  2. Microsomal ethanol oxidising system (MEOS)
     In SER
     Uses cytochrome P450:2E1
     Inducible – induced with excess alcohol ingestion

o Both oxidise alcohol to produce acetaldehyde –> acetate –> acetyl-coA
o Acetyl-coA enters krebs cycle in mitochondrion, leading to fatty acid formation

103
Q

ALCOHOLIC HEPATITIS microscopy

A

Fatty liver

Hepatocyte abnormalities:`
o Ballooning (sub-lethal cell injury)
o Mallory bodies in cytoplasm
o Necrosis
o Neutrophil polymorph infiltration (inflammation)

Fibrosis

104
Q

Name 4 causes of Inflammation in the Intestines

A

IBD - Crohn’s/UC
Infection
Coeliac disease
Ischaemia

105
Q

Coeliac Disease

A

 Immunological response to gliadin
 Auto-antibodies formed

 HLA DQ2 and DQ8

 Gluten derived peptide gliadin presented by HLA molecules to helper T cells -> lymphocytic response

  • > epithelial damage -> flattening of villi
  • > less surface area for absorption of nutrients -> malabsorption

 Serum TTG elevated

 Villous atrophy
 crypt hyperplasia
 Intraepithelial lymphocytes

 Manage by removal of gluten-containing foods from diet.

106
Q

Ulcerative colitis Symptoms:

A

 relapsing, bloody mucoid diarrhoea (stringy mucus)

 pain/cramps relieved by defecation

 lasts days/months, then remission for months/years

Extra-intestinal manifestations:
 migratory polyarthritis
 sacroiliitis
 ankylosing spondylitis
 erythema nodosum
 clubbing of fingertips
 primary sclerosing cholangitis
 pericholangitis
 cholangiocarcinoma (rare)
 uveitis
107
Q

Ulcerative colitis extra-intestinal manifestations:

A 
 migratory polyarthritis
 sacroiliitis
 ankylosing spondylitis
 erythema nodosum
 clubbing of fingertips
 primary sclerosing cholangitis
 pericholangitis
 cholangiocarcinoma (rare)
 uveitis
108
Q

Possible complications of Ulcerative colitis

A 
 perforation
 toxic megacolon 
 iliac vein thrombosis
 carcinoma
 lymphoma
109
Q

UC treatment (general)

A

 local or systemic steroids

 colectomy in uncontrollable disease

 Regular colonoscopy with biopsy to detect
precancerous dysplastic changes.

110
Q

Crohn’s Disease

A

 Transmural granulomatous disease affecting oesophagus to anus but discontinuous

 usually involves small intestine and colon with rectal sparing

 less severe in distal vs. proximal colon (i.e. preferential right-sided involvement)

111
Q

Symptoms of Crohn’s Disease

A

 Episodic mild diarrhoea
 Fever
 Pain

 May be precipitated by stress
 if colon affected, may have anaemia
 20% have abrupt onset, resembling acute appendicitis or bowel perforation

112
Q

Possible complications of Crohn’s Disease

A

 Fibrosing strictures (common in terminal ileum)
 Fistula
 Malabsorption
 Toxic megacolon
 Carcinoma (but lower risk than in U.C.)

113
Q

Adenoma-Carcinoma Sequence

A

Adenomas (i.e. benign glandular neoplasms) of the colon are by definition dysplastic, and the majority
are polyps

dysplasia = malignant potential

At some point during the development of a carcinoma, it will have features of dysplasia, but has not yet reached full malignant potential

Identifying and removing adenomas removes the first stage in the sequence and stops it progressing (in
the removed lesion)

114
Q

CRC Risk factors

A

 Adenoma – size, number
 IBD - especially Ulcerative colitis
 Family History
 Other Carcinomas

 Polyposis syndromes:
o FAP (associated with APC gene)
o Lynch syndrome (associated with MMR defects)
115
Q

Poor prognostic features in CRC

A

 Vascular invasion – increases risk of haematogenous spread

 Perineural invasion

 Involved margin – incompletely excised tumour

116
Q

CRC symptoms

A

o PR bleeding

o Change in bowel habit

117
Q

pathogenesis of IBD

A

Aetiology unknown

— “abnormal host response to environmental triggers in genetically susceptible individuals”

— Numerous genetic factors implicated

Smoking
— Increases risk of Crohn’s
— Reduces risk of UC

118
Q

Taking an history in suspected IBD

A

— Stool frequency, consistency, urgency, blood
— Abdo pain, malaise, fever
— Weight loss
— Extraintestinal symptoms (joint, eyes, skin)
— Travel
— Family Hx
— Smoking

119
Q

Investigations in suspected IBD

A

— FBC, ESR
— U&E’s, LFTs
— CRP

Stool cultures + C. Difficile toxin
 IBD predisposes to bacterial GI infections due to broken mucosa and immunosuppression

— Faecal Calprotectin – white cell marker released due to inflammation in the gut (not diagnostic!)

— Abdominal x-ray – rule out toxic megacolon

— Colonoscopy

120
Q

Treatments common to UC & Crohn’s

A

Coricosteroids

Thiopurines

Biologics

121
Q

Role of corticosteroids in treating IBD

A

Rapid induction of remission -> good for getting disease under control
— Slow reducing course
— Prednisolone 40mg daily/1 week
— Reduce by 5mg/ week

— Poor evidence for maintaining remission, poor long-term disease control

Significant side effects

122
Q

Mesalazine

A

Anti-inflammatory

Induction of remission in mild –moderate UC

maintenance of remission in UC

Maintenance therapy may reduce cancer risk

123
Q

Thiopurines

A

Azathioprine and mercaptopurine are unlicensed for IBD therapy

Effective as maintenance therapy for UC and Crohn’s

Steroid sparing agent

124
Q

Which form of IBD is methotrexate used for?

A

Crohn’s

125
Q

Acute Severe Colitis

A

admit to hospital

treat with IV steroids

126
Q

Surgery in IBD

A

UC
— Surgery technically “curative”
— Ileo-anal pouch or ileostomy -> no stoma but still move bowels very frequently

Crohn’s
— Indicated for stricturing, perforation, fistulizing disease
— Sparing as will come back

127
Q

causes of acute abdomen

A

burst

blocked

inflamed

lost its blood supply

combination

or: extra-abdominal causes!
- Myocardial infarction
- Pneumonia

128
Q

Which inflammatory conditions can be imaged well with AXR?

A

colitis

not useful for appendix, diverticulitis, cholecystitis, pancreatitis,
PID

CT usually first choice

129
Q

which imaging modality is best for suspected cholecystitis?

A

ultrasound

130
Q

when would you use CT/USS for imaging of the bowel?

A

US for cholecystitis (and appendicitis if young and slim)

CT first choice otherwise

CT is not sensitive for gallstones → usually don’t see them, needs USS

131
Q

what imaging modality would you choose for suspected bowel perforation?

A

CXR sensitive for free gas

AXR less so - can be very subtle
Don’t do an abdominal film for suspected perforation

CT to confirm and look for cause

132
Q

rigler’s sign

A

If you can see gas inside an outside the

bowel you must have a perforation = rigler’s sign

133
Q

Commonest causes of obstruction (GI)

A

Hernia

Adhesions

Tumour (only visible on CT)

134
Q

what imaging modality would you choose for suspected bowel obstruction?

A

AXR useful

look for:
small and/or large bowel dilatation?
how much gas in colon?
any gas in rectum?
any complications - ischaemia, perforation?

CT to look for cause

135
Q

what imaging modality would you choose for suspected bowel ischaemia?

A

AXR usually non-specific. Positive signs usually mean advanced ischaemia

CT first choice test but <60% sensitive

136
Q

Why not just CT everyone?

A

RADIATION DOSE - increased cancer risk

may find “COINCIDENTALOMAS” - unnecessary anxiety

137
Q

when would you used plain films for imaging the gut?

A

Plain radiographs primary role for

1) suspected perforation (CXR)
2) obstruction (AXR)

J3 (18 decks)

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