Interne geneeskunde Flashcards
1
Q
Standard ‘Liver Function’ Tests
A
Bilirubin Aspartate Aminotransferase (AST) Alanine Aminotransferase (ALT) Gamma Glutamyltransferase (GGT) Alkaline Phosphatase (ALP) Albumin
2
Q
Which test reflect liver function?
A
prothrombin time
albumin
bilirubin
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
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)
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
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)
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)
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)
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)
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
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)
12
Q
Hepatic Encephalopathy: Precipitating Factors
A
GI haemorrhage, infections, renal/electrolyte disturbances, psychoactive medication, excessive dietary protein acute deterioration of liver function
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.
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
15
Q
hepatitis symptoms
A
Non-specific symptoms: Malaise, fever, headaches Anorexia, nausea and vomiting Right upper quadrant abdominal pain Dark urine Jaundice
16
Q
Acute Hepatitis
A
o Usually symptomatic o Inflammation of the liver o Raised ALT / AST o Jaundice o Clotting Derangement
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
18
Q
ACUTE HEPATITIS: CAUSES
A
Infections
o Hep A, B, C, D, E
o EBV, CMV, Toxoplasmosis
Toxins Drugs Alcohol Autoimmune Wilsons Haemochromatosis
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
20
Q
Which hepatitis virus is associated with high mortality rates during pregnancy?
A
Hep E (4 genotypes - associated with GT 1)
21
Q
sAg - Surface antigen
A
marker of current infection (HBV)
sAg present = infected
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
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
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
25
eAb – e antibody
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
26
```
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
```
Acute Hepatitis B infection (IgM positive = acute)
Patient must be tested for HIV and Hep C as well
27
```
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
```
Prior infection but it has been cleared
28
```
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
```
Chronic Hepatitis B infection (IgM negative = chronic), highly infectious (eAg positive), Carrier
29
```
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
```
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
30
Prevention of HBV
Education (safe sex, injecting etc.)
Screening of pregnanct women / doctors
Protect blood supply & hospital supplies
Immunisation:
31
Which forms of hepatitis have chronic carriage?
HBV, HCV, and HDV
HEV in immunosuppressed patients
32
Acute Pancreatitis Diagnosis
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
33
Causes of acute pancreatitis
Gallstones – important to rule out because it can be treated to prevent recurrence of pancreatitis
Alcohol
Trauma/ ERCP
Other - drugs/ high lipids/ autoimmune/ viral
34
Initial management of acute pancreatitis
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
35
Investigations acute pancreatitis
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
36
Differential Diagnosis for severe abdominal pain and elevated serum amylase
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)
37
Possible outcomes after pancreatitis
May be diabetic
May require creon pancreatic enzyme supplements
May require restorative surgery
Significant impact on quality of life
If gallstones- needs gallbladder removed
38
causes of injury to the liver
```
Drugs or toxins including alcohol
Abnormal nutrition/metabolism
Infection
Obstruction to bile or blood flow
Autoimmune liver disease
Genetic/deposition disease
Neoplasia
```
39
Cirrhosis
= End-stage liver disease
Definition is three-fold:
o Diffuse process with
o Fibrosis
o Nodule formation
40
Clinical approach to liver disease
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
41
Histology of Acute hepatitis
Diffuse hepatocyte injury seen as swelling.
“spotty necrosis”
inflammatory cell infiltrate
42
Causes: Acute cholestasis or cholestatic hepatitis
o Extrahepatic biliary obstruction
o Drug injury e.g. antibiotics
Histology: brown bile (bilirubin) pigment +/- acute hepatitis
43
Acute versus chronic hepatitis histology
histology can look similar
Fundamental difference = chronic may have already progressed to have some degree of fibrosis
Can be visualised using Masson stain
44
which liver diseases may develop fibrosis and progress to cirrhosis
o Fatty liver disease (steatosis and steatohepatitis)
o Chronic hepatitis
o Chronic biliary/cholestatic disease
o Genetic/deposition disease
45
Hepatitis B pathology
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
46
Chronic biliary/cholestatic disease causes:
o Primary biliary cirrhosis (PBC)
| o Primary sclerosing cholangitis (PSC)
47
Genetic/deposition liver disease
| y
Haemochromatosis (iron)
Wilson’s disease (copper)
Alpha-1-antitrypsin deficiency (lack of secretion therefore accumulates in hepatocytes)
48
Histology: Chronic biliary/cholestatic disease
o Focal, portal-predominant inflammation and fibrosis with bile duct injury
mainly affects portal tracts and bile ducts
granulomas in PBC
49
Specific causes of diffuse liver disease
```
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
```
50
Drug-induced liver disease
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!
51
Von Meyenberg complex
(= simple biliary hamartoma)
benign
52
Haemangioma
benign blood vessel tumour
| Biopsy avoided because of risk of bleeding
53
Hepatic adenoma
o Rare
o Mainly young women, often associated with hormonal therapy
o Risk of bleeding and rupture so excision if large
54
Hepatocellular carcinoma
Most common primary liver tumour
Usually arises in cirrhosis and associated with elevated serum AFP (alpha feto-protein)
Screening available for patients with cirrhosis
55
Aims of histopathology in general
o Establish disease diagnosis and severity
| o Predict outcome and guide treatment
56
Acute hepatitis Presentation + Causes
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
Causes of fatty liver disease
o Alcohol
o Non-alcoholic
• Type II diabetes
• obesity
• hyperlipidaemia
o Drugs
• Methotrexate
• Amiodarone
• Steroids
58
Chronic hepatitis Clinical definition + causes
Liver inflammation (abnormal LFTs) for at least 6 months
o Viral hepatitis B
o Autoimmune
o rarely drug injury
59
Grade vs stage in liver disease
grade: degree of inflammation
– Guides treatment
Stage: amount of fibrosis
– Prognosis (& guides treatment)
60
Hepatitis C pathology
often mainly in portal tracts, as chronic inflammation with lymphoid aggregates
61
Primary biliary cirrhosis (PBC)
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
Primary sclerosing cholangitis (PSC)
o Rare, associated with ulcerative colitis
| o Risk of progression to cholangiocarcinoma
63
Budd-Chiari syndrome
Primary hepatic vascular disease
hepatic vein thrombosis
64
causes of Liver abscess
May arise from ascending cholangitis
| parasitic disease
65
Cholangiocarcinoma
adenocarcinoma of bile ducts
either intra- or extra-hepatic (i.e. can be a primary liver tumour)
66
causes of Lithogenic (stone forming) bile
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
Acute Cholecystitis presentation
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
Mucocoele of Gallbladder
Distention of gallbladder due to an inappropriate accumulation of mucus
Previous irritation around the neck of the gallbladder causing fibrosis and obstruction
69
common place for gallstone obstruction
ampulla of vater
slight narrowing at the ampulla of vater
obstruction here irritates the pancreas
70
Potential complications of acute pancreatitis
pseudocyst
pancreatic fistula
pancreatic necrosis
Pancreatitic Abscess
71
Pancreatic Abscess
Potential complication of acute pancreatitis
Infected pancreatic necrosis
Avascular haemorrhagic pancreas acts like a good culture medium
Treatment: drainage or necrosectomy plus antibiotics
72
Pancreatic pseudocyst
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
Differential of Pancreatic Cysts
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
most common Carcinoma of Pancreas
Ductal adenocarcinoma
associated with perineural invasion
Heterogenous tumours with wide range of mutations => No standard effective therapy
75
risk factors for Carcinoma of Pancreas
Germline mutations (e.g. BRCA) account for small proportion of patients,
but SMOKING is by far the biggest risk factor
76
Signs and Symptoms of Carcinoma of Pancreas
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
Whipple’s Resection
for tumours of head of pancreas
78
Commonest functional Pancreatic Neuroendocrine Tumour
insulinoma --> causes hypoglycaemia
79
Reflux oesophagitis (GORD)
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
Candida oesophagitis
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
Barrett's oesophagus
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
Oesophageal cancer
Squamous carcinoma - associated with smoking/drinking
Adenocarcinoma - associated with GORD and obesity
83
causes of acute gastritis
```
o Alcohol
o Medication e.g. NSAIDs
o severe trauma
o burns (Curling's ulcers)
o surgery
```
84
causes of chronic gastritis
o A: Autoimmune
o B: Bacterial (H pylori)
o C: Chemical
85
Autoimmune gastritis
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
Types of H. pylori-induced gastritis
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
Consequences of peptic ulceration
Haemorrhage
Perforation of underlying vessels - haematemesis
Fibrosis (leading to stenosis)
88
causes of chemical gastritis
o bile reflux
o NSAIDs
o Ethanol
o oral iron
89
Gastric cancer
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
Diffuse gastric cancer
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
Upper gastrointestinal bleeding - presentation
* Haematemesis
* “coffee ground” vomiting
* Melaena
Due to a bleeding source from oesophagus, stomach or duodenum
92
Causes of upper GI bleeding
```
Peptic ulcer
Oesophagitis
Gastritis
Duodenitis
Varices
Malignancy
Mallory-weiss tear
```
93
Management of upper GI bleed
```
ABCs
Resuscitate
• IV access for fluids/blood
• (check bloods, esp Hb & urea)
• lie flat & give oxygen
```
Risk assessment & timing of endoscopy:
• High risk: emergency endoscopy
• Moderate risk: admit & next day endoscopy
• Low risk: out-patient management?
94
Endoscopic therapy for upper GI bleed
* 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
What to do about Aspirin & NSAIDs in patients with upper GI bleed
continue aspirin - lifesaving CV treatment
discontinue NSAIDs - not crucial
96
When to administer Blood products in upper GI bleeding
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
Treatment of varices
* endoscopic banding
* Transjugular intrahepatc porto-systemic shunt (TIPS) - decompresses the high pressure portal vein
* B-Blocker drugs
98
Management of Acute variceal bleeding
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
Variceal bleeding management vs ulcer bleeding
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
Variceal Bleeding Primary Prophylaxis:
• Beta-blockers or Banding
same for prevention of rebleeding
101
Types of Alcoholic Liver Disease
Pathologic changes can be divided into 3 groups (with some overlap):
1) Fatty liver (steatosis)
2) Alcoholic hepatitis +/– hepatic fibrosis
3) Cirrhosis
102
Hepatic alcohol metabolism
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
ALCOHOLIC HEPATITIS microscopy
Fatty liver
```
Hepatocyte abnormalities:`
o Ballooning (sub-lethal cell injury)
o Mallory bodies in cytoplasm
o Necrosis
o Neutrophil polymorph infiltration (inflammation)
```
Fibrosis
104
Name 4 causes of Inflammation in the Intestines
IBD - Crohn's/UC
Infection
Coeliac disease
Ischaemia
105
Coeliac Disease
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
Ulcerative colitis Symptoms:
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
Ulcerative colitis extra-intestinal manifestations:
```
migratory polyarthritis
sacroiliitis
ankylosing spondylitis
erythema nodosum
clubbing of fingertips
primary sclerosing cholangitis
pericholangitis
cholangiocarcinoma (rare)
uveitis
```
108
Possible complications of Ulcerative colitis
```
perforation
toxic megacolon
iliac vein thrombosis
carcinoma
lymphoma
```
109
UC treatment (general)
local or systemic steroids
colectomy in uncontrollable disease
Regular colonoscopy with biopsy to detect
precancerous dysplastic changes.
110
Crohn’s Disease
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
Symptoms of Crohn’s Disease
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
Possible complications of Crohn’s Disease
Fibrosing strictures (common in terminal ileum)
Fistula
Malabsorption
Toxic megacolon
Carcinoma (but lower risk than in U.C.)
113
Adenoma-Carcinoma Sequence
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
CRC Risk factors
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
Poor prognostic features in CRC
Vascular invasion – increases risk of haematogenous spread
Perineural invasion
Involved margin – incompletely excised tumour
116
CRC symptoms
o PR bleeding
| o Change in bowel habit
117
pathogenesis of IBD
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
Taking an history in suspected IBD
Stool frequency, consistency, urgency, blood
Abdo pain, malaise, fever
Weight loss
Extraintestinal symptoms (joint, eyes, skin)
Travel
Family Hx
Smoking
119
Investigations in suspected IBD
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
Treatments common to UC & Crohn’s
Coricosteroids
Thiopurines
Biologics
121
Role of corticosteroids in treating IBD
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
Mesalazine
Anti-inflammatory
Induction of remission in mild –moderate UC
maintenance of remission in UC
Maintenance therapy may reduce cancer risk
123
Thiopurines
Azathioprine and mercaptopurine are unlicensed for IBD therapy
Effective as maintenance therapy for UC and Crohn’s
Steroid sparing agent
124
Which form of IBD is methotrexate used for?
Crohn's
125
Acute Severe Colitis
admit to hospital
treat with IV steroids
126
Surgery in IBD
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
causes of acute abdomen
burst
blocked
inflamed
lost its blood supply
combination
or: extra-abdominal causes!
- Myocardial infarction
- Pneumonia
128
Which inflammatory conditions can be imaged well with AXR?
colitis
not useful for appendix, diverticulitis, cholecystitis, pancreatitis,
PID
CT usually first choice
129
which imaging modality is best for suspected cholecystitis?
ultrasound
130
when would you use CT/USS for imaging of the bowel?
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
what imaging modality would you choose for suspected bowel perforation?
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
rigler’s sign
If you can see gas inside an outside the
| bowel you must have a perforation = rigler’s sign
133
Commonest causes of obstruction (GI)
Hernia
Adhesions
Tumour (only visible on CT)
134
what imaging modality would you choose for suspected bowel obstruction?
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
what imaging modality would you choose for suspected bowel ischaemia?
AXR usually non-specific. Positive signs usually mean advanced ischaemia
CT first choice test but <60% sensitive
136
Why not just CT everyone?
RADIATION DOSE - increased cancer risk
may find “COINCIDENTALOMAS” - unnecessary anxiety
137
when would you used plain films for imaging the gut?
Plain radiographs primary role for
1) suspected perforation (CXR)
2) obstruction (AXR)
