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GI/Liver Flashcards

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1
Q

List the layers of the bowel wall

A

4 layers

Mucosa
> Epithelium
> Lamina propria
> Muscularis mucosae

Submucosa

Muscularis propria (or externa)
> Inner circular layer
> Outer longitudinal layer

Subserosa
> Loose, fatty connective tissue

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2
Q

Describe the histological features of ulcerative colitis

A

Diffuse involvement of lower GIT

Predominantly affects left side of colon in a confluence pattern (diffuse)

Terminal ileum can be involved but generally only in severe cases where the whole bowel is involved (pancolitis)

No transmural changes, focused in mucosa

Crypt architectural changes are very marked

Little / no fibrosis

No granulomas

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3
Q

Describe the treatments for ulcerative colitis

A

Mesalazine
> Targets inflammation in GI tract
> 4.8g > 2.4g daily for induction of remission in moderate UC
> 2.4g daily as a maintenance dose
> Reduces frequency of flare ups and severity

Escalation of treatment
> Azathioprine (or mercaptopurine)
» With severe relapse / frequently relapsing disease
» Requiring 2 or more corticosteroid courses in a 12 month period
» Risks
»> Intolerance
»> Lymphoma, NMSC

Biologics

Surgery: cure
> Sub-total colectomy

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4
Q

Describe the complications associated with ulcerative colitis

A

Local
> Haemorrhage
> Toxic dilation aka toxic megacolon

Systemic

> Skin
>Erythema nodosum
> Pyoderma gangrenosum

> Liver
> Sclerosing cholangitis
> Cholangiocarcinoma

> Eyes
> Iritis
> Uveitis
> Episcleritis

> Ankylosing spondilitis

> Malignancy
> Colorectal cancer
» Screening colonoscopy after 10y of disease
» Intervals determined by risk – extent of disease

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5
Q

Describe the features of Crohn’s disease

A

Chronic inflammatory condition affecting anywhere from mouth to anus

Risk factors
> Smoking
» Stopping reduces relapse rate, need for immunosuppression and surgery

Peak incidence 15-25y

Features
> Abdominal pain
> Diarrhoea (watery > bloody)
> Commonly affects ileum and right sided colon
> Weight loss
> Fistulae, abscesses, oropharyngeal, gastroduodenal

Extra-intestinal symptoms
> Eyes – episcleritis, uveitis
> Joints – sacroilitis, inflammatory arthropathy
> Skin – erythema nodosum

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6
Q

Describe the pathological and histological features of Crohn’s disease

A

Granulomas – hallmark of Crohn’s

Differences between UC & Crohn’s
> Distribution of inflammation
> Small and large bowel inflammation
> Tends to involve proximal large bowel
> Patchy inflammation resulting in macroscopic “skip lesions”

Type of inflammation
> Transmural process
> Deep ulcerating inflammation

Perianal disease e.g. fistulas / sinus tracts

Macroscopic
> Small bowel strictures
> Narrowed areas with mucosal ulceration

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7
Q

Which investigations are used in the diagnosis of IBD?

A

Abdominal X-ray
> Exclude small bowel obstruction

Ileocolonoscopy
> Apthous ulcers in terminal ileum
> Active illeitis on biopsy

Faecal calprotectin
> Calcium-binding protein, predominantly derived from neutrophils
> Single 20g sample, stable for 5 days
> Useful test to differentiate between IBD / IBS and assess activity in IBD
> Sensitive but not disease specific

Stool cultures

MR / CT enterography
> Show ulceration and inflammation in terminal ileum
> Mucosal enhancement and luminal narrowing

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8
Q

Describe the staging of IBD

A

Montreal classification – staging of disease

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9
Q

What are risk factors for severe disease in IBD?

A

Risk factors for severe disease

Young onset

Smoking

Perianal disease

Stricturing SB disease

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10
Q

Describe the treatment of Crohn’s disease

A

Thiopurines
> Azathioprine and 6-mercaptourine

Biologics
> TNF-alpha antagonists
> Infliximab / adalimumab

Anti-integrins (alpha-4,beta-7)
> Vedolizumab

Anti-interleukin 12/23
> Ustekinumab

Methotrexate

Surgery
> 70% lifetime risk
> Aimed at removing the minimal amount of GI tract (fistulae, strictures, severe inflammation)
> Recurrence common – 50% further surgery

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11
Q

Describe the pathological changes associated with Crohn’s disease

A

Acute
> Acute inflammation
> Ulceration
> Loss of goblet cells
> Crypt abscess formation (neutrophils present)

Chronic
> Architectural changes
> Paneth cell metaplasia
> Chronic inflammatory infiltrates in lamina propria
> Neuronal hyperplasia
> Fibrosis

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12
Q

Describe the presentation, investigations, risk factors and treatment associated with infective colitis

A

Presentation
> Short history of diarrhoea and vomiting
> Abrupt onset and resolution of symptoms
> Systemic upset and fevers prominent

Risk factors
> Travel
> Unwell contacts
> Immunocompromised

Investigations
> Stool sample / CDT
» Need 4 for 90% sensitivity

Treatment
> Conservative if immunocompetent
> Even if bacterial gastroenteritis is confirmed

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13
Q

Describe the presentation and treatment of ischaemic colitis

A

Presentation
> Abrupt onset pain and bloody diarrhoea +/- SIRS
> Hypoperfusion > embolic

Risk factors
> Elderly
> CV disease
> Heart failure
> Constipation
> Female sex
> Smoker

More severe than IBD

Treatment
> Conservative
> IV fluids +/- antibiotics

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14
Q

Describe the assessment, investigations and treatment of severe ulcerative colitis

A

Assessment: Truelove and Witts’ classification

Stool frequency
>8/day
>3 & CRP >45 on day 3 predicts need for colectomy in 85%

Treatment
> IV steroids
> Methylprednisolone
> Hydrocortisone

> If non-responsive to steroids
> Surgery: colectomy
> Rescue medical treatment with
» Cyclosporin
» Infliximab (monoclonal antibody to TNF-alpha)

Investigations
> Stool culture
> Bloods
> Abdominal X-ray
» Essential in severe colitis
» Helps assess disease extent and severity

> > > Megacolon
> Transverse diameter of the colon (usually transverse colon >5.5cm or caecum >9cm)

> > > Toxic megacolon
> Megacolon and signs of systemic toxicity

> Emergency colectomy
> Risk of perforation and peritonitis

Other inpatient investigations
> Endoscopy
> Flexible sigmoidoscopy
> Colonoscopy
> CT scan
» Exclude signs of subclinical perforation

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15
Q

Describe the diagnosis and treatment of coeliac disease

A

Diagnosis

> Serology
> IgA anti-endomysial (immunofluorescence)

> > Anti tTG IgA (quantitative ELISA)

> Duodenal biopsy (second and first part of duodenum)
> Histology: crypt hyperplasia and villous atrophy

Treatments

> Gluten free diet

> Nutritional assessment

> Bone health (FRAX score/DEXA)
> Screen for osteoporosis due to malabsorption of calcium

> If anaemia (iron deficiency or B12/folate), supplementation

> Vaccination (due to increased risk of hyposplenism)
> Pneumococcus
> Meningococcus

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16
Q

Describe the complications associated with coeliac disease

A

Functional hyposplenism

Microcytic anaemia

Osteoporosis

Low BMI

Calcium/ vitamin D deficient

Dermatitis herpetiformis

Increased risk of cancer, specifically lymphoma (T cell) and small bowel adenocarcinoma

IgA deficiency

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17
Q

List the causes of acute hepatitis

A

Infections
> Hepatitis A, B, C, D, E
> EBV, CMV, toxoplasmosis
> Leptospirosis
> Q fever
> Syphilis
> Malaria
> Viral haemorrhagic fever

Toxins

Drugs

Alcohol

Autoimmune

Wilson’s: caeruloplasmin test

Haemochromatosis: assess ferritin & transferrin saturation

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18
Q

Describe the clinical features, diagnosis and treatment of hepatitis A

A

RNA virus

Transmission
> Faeco-oral
> Human reservoir

Virus can survive for months in contaminated water

Virus shed biliary tree into gut

No chronic carriage

Good immunity after infection or vaccination

Clinical features
> Incubation period 2-4 weeks
> Age is main determinant of severity
> Mostly asymptomatic in children <5 years
> Mortality rate 1.5% if >50 year

Diagnosis
> Acute hepatitis A – IgM positive or HAV RNA in blood or stool

> Previous Hep A or vaccinated – IgM positive

Treatments
> No specific treatments
> Maintain hydration, avoid alcohol
> Self-limiting illness
> No role for vaccine or immunoglobulin as treatment

Vaccination
> Hepatitis A vaccine
» Inactivated virus
» 95% efficacy after 4 weeks – 2nd dose gives life protection
» Pre-exposure: travellers, homosexual men, IVDU, chronic liver disease patients
» Post-exposure: outbreak cancer

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19
Q

Describe the clinical features and treatment of hepatitis E

A

RNA virus

Transmission
> Faeco-oral
> Pork products
> Minimal person-to-person

Incubation period - 40 days

Clinical features
> Similar to hepatitis A plus rare reports of neurological effects
> Guillain-Barré syndrome
> Encephalitis
> Ataxia
> Myopathy
> Case fatality rate 1-3%

Treatment – supportive
> No vaccine

Chronic hepatitis E is seen in very immunosuppressed patient e.g. bone marrow transplants
> Treatment – ribavirin

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20
Q

Describe the clinical features and treatments of hepatitis B

A

DNA virus

HBV vaccination in most countries

Transmission
> Vertical transmission (most common) - at birth
> Sexual contact
> Blood transfusions
> Blood, semen

> Incubation: 2-6 months

Acute case fatality rate: 0.5-1%

> Age at time of infection determines severity of acute illness and risk of chronic HBV infection (CHB)

> Infection at birth / young child is usually asymptomatic but leads to chronic infection

> Infection as an adult is usually symptomatic but cleared

Chronic HBV
> Development of chronic liver disease in 25%

Results in
> Cirrhosis
> Decompensation
> Hepatocellular carcinoma (HCC)
> Death

Treatment

Acute HBV
> No treatment
> Usually resolves and infection is cleared

Chronic HBV
> Only treat those with liver inflammation
> Increased ALT or biopsy or fibrosis (on fibroscan or biopsy)

2 types
> Immunomodulatory – interferon
> Suppress viral replication – tenofovir or entecavir

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21
Q

Describe the diagnosis of hepatitis B

A

Lab tests – HBV DNA

Histology - cytoplasmic inclusion – ground glass cytoplasm in hepatocytes

Acute
> SAg – surface antigen
» Marker of infection

> SAb – surface antibody
> Marker of immunity

> Core IgM & IgG – recent infection

> E antigen (eAg) - suggests high infectivity
E antibody (eAb) - suggests low infectivity

Chronic HBV: sAg detectable for >6/12
> Carriers are broadly divided into 2 groups

> > eAg +ve (early disease)
> High viral load
> High risk of CLD and HCC
> Highly infectious

> > eAg –ve (late disease)
> Low viral load
> Lower risk of CLD and HCC
> Less infectious

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22
Q

Describe the clinical features and treatment of hepatitis D

A

ss RNA virus

> Requires HBV to replicate
Transmission same as hep B
Vertical transmission rare

Acquired by
> Co-infection with HBV
> Super-infection of chronic HBV carriers
> Infection only possible in persons who are HBV sAg+

Increases risk of chronic liver disease

Treatment
>Interferon only
> Bulevirtide – suppressive treatment

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23
Q

Describe the clinical features, diagnosis and treatment of hepatitis C

A

RNA virus

Incubation period 6-7 weeks

> 25% of newly infected are symptomatic
30% clear infection
70% chronic hep C
> Cirrhosis
> HCC

Diagnosis
> Screening of high risk groups
» Drug users
» Immigrant from high prevalence countries

> Anti HCV IgG positive = chronic or cleared infection

> PCR or antigen positive = current infection / viraemia

Transmission
> Injecting drugs
> Transfusion + transplant
> Sexual / vertical rare

No vaccine, no post exposure prophylaxis

No reliable immunity after infection

Treatment
> Directly acting antivirals (DAAs)
> Inhibit different stages of the replication cycle
> Cure rates >95% with 8-12 weeks of oral treatment

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24
Q

Describe the causes and histology of chronic biliary disease

A

Causes
> Primary biliary cirrhosis (PBC): anti mitochondrial antibody
> Primary sclerosing cholangitis (PSC): anti-neutrophil cytoplasmic antibody

Histology
Focal, portal predominant inflammation and fibrosis with bile duct injury

Granulomas in PBC

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25
List the clinical features, investigations and treatments associated with autoimmune hepatitis
Clinical presentation > Asymptomatic > Non-specific symptoms >> Fatigue >> General ill health >> Lethargy >> Weight loss >Mild right upper quadrant pain > Acute jaundice arthralgia > Unexplained fever Chronic liver disease Acute or even fulminant hepatic failure Investigations > Elevated AST and ALT > Anti-nuclear antibody (ANA) > Anti-smooth muscle antibody (SMA) > Anti-liver kidney microsomal antibody (LKM) > Raised IgG Treatment > Immunosuppressants >> Corticosteroids: prednisolone, budesonide >> Azathioprine / mycophenolate
26
Describe the clinical features and treatment of primary biliary cirrhosis
Most common chronic cholestatic liver disease 9:1 female to male 90% have anti-mitochondrial antibodies against pyruvate dehydrogenase complex (PDC-E2) in mitochondria LFTs > Elevated GGT & ALP in early disease > Elevated bilirubin in advanced disease Symptoms > Tiredness > Itching > Jaundice Treatment > Ursodeoxycholic acid
27
Describe the clinical features, cause and treatment of haemochromatosis
Iron accumulation in tissues and organs including liver, adrenal glands, heart, skin, gonads, joints, pancreas Presentation > Abnormal LFTs > Chronic liver disease > Polyarthropathy > Adrenal insufficiency > Heart failure > Diabetes > Skin pigmentation – bronzed diabetes Cause > Mutation in HFE gene: autosomal recessive > Homozygous for C282Y mutation > Compound heterozygote for C282Y and H63D Investigations > Raised ferritin and transferrin saturation > Not all hyperferritinaemia is iron (infection) > Liver MRI for iron – liver biopsy Treated with venesection
28
Describe the cause, presentation and treatment of Wilson's disease
Mutation in ATP7B gene: autosomal recessive Failure to transport excess copper into bile leading to copper accumulation Presentation Chronic liver disease <55 years old 5% develop fulminant acute liver failure (often with low ALP and haemolysis) Neurological or psychiatric symptoms Parkinsonism with or without hand tremor Masked facial expressions Slurred speech, ataxia or dystonia Low caeruloplasmin High copper levels Kayser Fleischer rings Treatment Copper chelation – penicillamine or trientine Oral zinc – reduces copper absorption
29
Which enzyme deficiency can result in liver disease?
Alpha 1 antitrypsin
30
Describe the clinical features of alcohol-related liver disease
Alcoholic hepatitis > Excess alcohol within 2 months > Bilirubin >80 micromol/L for less than 2 months > Exclusion of other liver disease > Treatment of sepsis / GI bleeding > AST < 500 (AST:ALT ratio >1.5) Features > Hepatomegaly > Fever > Leucocytosis > Hepatic bruit Glasgow Alcoholic Hepatitis Score (GAHS) Spectrum of alcohol-related liver disease > Hepatitis: liver cell necrosis, inflammation, Mallory bodies, fatty changes > Cirrhosis: fibrosis, hyperplastic nodules > Steatosis: fatty change, perivenular fibrosis
31
Describe the associations of non-alcoholic fatty liver disease and the investigations used
Main associations > Obesity > Type 2 diabetes > Hyperlipidaemia Non-invasive tests of liver fibrosis > APRI > FIB-4 NAFLD Fibrosis score > Takes into account age, BMI, IFG/diabetes, AST/ALT ratio, platelet Fibroscan: transient elastography > F0-F4 Blood tests > Enhances liver fibrosis (ELF) test > FibroTest
32
Describe the main features of liver cirrhosis
End-stage liver disease characterised by Diffuse process > Changes throughout the whole liver Nodule formation > Changes from smoothness to lumps of various sizes Fibrosis > White tissue > Result of chronic inflammation (hepatitis) over many years > Persistence of injury-causing agent > Fibrous scarring and hepatocyte regeneration > Eventually irreversible and cirrhosis develops
33
Describe the consequences of liver failure
Altered intermediary metabolism Impaired synthesis of urea and glycogen (higher risk of hypoglycaemia) Reduced albumin and other transport proteins Coagulation disorders Reduced complement so prone to infection Jaundice Altered xenobiotic metabolism e.g. drugs Circulatory and endocrine disturbances
34
Describe the complications associated with liver cirrhosis
Portal hypertension > Cirrhosis increases resistance to blood flow through liver > Increases pressure in portal circulation causing: >> Portal-systemic shunts and varices >>> There is a junction where portal and systemic circulation meet >>> If pressure is high, portal circulation blood can go back to systemic circulation >>> Varices (vein enlargement) may rupture to give massive haematemesis and precipitate hepatic failure and encephalopathy >> Ascites >>> Increased fluid in abdominal cavity >> Splenomegaly >>> Back pressure is exerted on spleen through portal circulation >>> Spleen is distensible so can accumulate more blood and become enlarged Hepatocellular cancer
35
Describe the pathogenesis of ascites in liver disease
Portal hypertension leads to pressure in splanchnic capillaries and fluid into the peritoneum Portal hypertension also leads to an increase in nitric oxide Results in hypovolaemia and renal artery vasoconstriction, resulting in the activation of RAAS and sodium and water retention
36
List LFTs and what they indicate
- AST: aspartate transaminase; hepatocyte enzyme - ALT: alanine transaminase; hepatocyte enzyme - ALP: alkaline phosphatase: bile duct enzyme (may also be elevated in bone pathology or pregnancy) - GGT: gamma glutamyl transfer: bile duct enzyme - Albumin: decreased albumin indicates chronic liver disease & reduced synthetic function - INR: increased INR indicates decreased synthetic ability of the liver, which produces clotting factors - Bilirubin CRP also indicates inflammation
37
Describe the algorithm used in the diagnosis of liver disease when ALP is elevated
Increased ALP > Increased GGT: perform US or CT >> Dilated ducts: possible stones, strictures or space-occupying lesion; perform percutaneous cholangiography to diagnose sclerosing cholangitis, stricture or stones >> Non-dilated ducts: measure anti-mitochondrial antibody >>> Positive anti-mitochondrial antibody: primary biliary cirrhosis >>> Negative anti-mitochondrial antibody: perform percutaneous cholangiography to diagnose sclerosing cholangitis, stricture or stones > normal GGT: bone disease?
38
Describe the investigations which follow the presence of hepatocyte damage (elevated transaminases)
Serology > Viral serology for hepatitis > Autoantibodies for autoimmune hepatitis Ferritin/iron studies Copper, caeruloplasmin Alpha-1-antitrypsin
39
Describe signs of obstructive jaundice
- Dark urine: conjugated bilirubin - Pale offensive stools (steatorrhoea): lack of conjugated bilirubin products - Pruritus (itchy skin) and excoriation marks: bile salt deposition - Yellow sclerae
40
List causes of prehepatic jaundice
- Elevated haemolysis: > sickle cell anaemia > thalassaemia major > malaria > quinine-based anti-malaria drugs... > neonatal jaundice > haemolytic disease of the newborn
41
List causes of hepatic jaundice
> Gilberts' syndrome: impaired conjugation of bilirubin > Primary biliary cirrhosis: impaired transport of conjugated bilirubin into bile canaliculi > Cirrhosis > Hepatotoxic drugs e.g. paracetamol overdose > Viral hepatitis > Autoimmune hepatitis > Non-alcoholic fatty liver disease
42
List causes of post-hepatic / obstructive jaundice
Biliary obstruction leads to cholestasis - Gallstones - Biliary strictures - Pancreatitis - Pancreatic or bile duct tumours
43
List risk factors for gallstone formation
5 F's: female, fair, fertile, forty, fat Other risk factors: low fibre diet, IBD, family history, Caucasian
44
Describe complications of gallstones
- Biliary colic > no jaundice or fever, LFTs normal > pain epigastrium, RUQ, worse on eating, vomiting is common - Acute cholecystitis > Pain, nausea, vomiting, fever, RUQ tenderness (Murphy's sign) > Raised inflammatory markers, may be abnormal LFTs or jaundice - Empyema - Mucocoele - Cancer
45
Describe Curvoisier's Law
"In the presence of a palpable enlarged gallbladder which is non-tender and accompanied with mild painless jaundice, cause is unlikely to be gallstones" Gallstones cause pain Troublesome gallstones cause chronic inflammation and fibrosis, GB does not distend
46
List stigmata of chronic liver disease
Palmar erythema Fingernail clubbing Gynaecomastia Testicular atrophy Dupuytren's contracture Caput medusae Foetor hepaticus Flapping tremor (hepatic encephalopathy) Lab features > Thrombocytopaenia (pancytopaenia) > Prolonged prothrombin time > Hypoalbuminaemia
47
Describe the assessment of the severity of liver disease
Childs-Turcotte-Pugh score - Considers encephalopathy, ascites, bilirubin, albumin & prothrombin time prolongation - Grade A: 5-6, mild - Grade B: 7-9, moderate - Grade C: 10-15, severe Models for End-stage Liver Disease (MELD) uses bilirubin, INR and creatinine
48
Describe the investigations used in ascites
Diagnostic tap - Cell count > >500 WBC/cm3 and >250 neutrophils/cm3 suggests spontaneous bacterial peritonitis (SBP) > Lymphocytosis suggests TB or peritoneal carcinomatosis - Albumin > Serum ascites albumin gradient (SAAG) = serum albumin MINUS ascites albumin >> SAAG >11g/l = portal hypertension
49
Describe the treatment of ascites
Low salt diet Diuretics > Spironolactone >> Side-effects e.g. gynaecomastia, hyperkalaemia, hyponatraemia, impotence > Furosemide >> Side effects e.g. hyponatraemia Large volume paracentesis
50
Define hepatic encephalopathy, including precipitating factors
Disease caused by the failure of the cirrhotic liver to remove toxins from the blood, which ultimately negatively affects the brain's function Precipitating factors - GI bleeding - Infections - Constipations - Electrolyte imbalance - Excess dietary (especially animal) protein Avoid regular sedation, caution with opiates & avoid hyponatraemia Precipitating factors negatively affect the patient by > Further reducing hepatic or cerebral function > Increasing ammonia levels > Stimulating an inflammatory response
51
Describe the clinical signs and treatment of hepatic encephalopathy
Clinical signs: flapping tremor or asterixis Treatment > Non-absorbable > Disaccharides i.e. lactulose >> Aim for 2-3 soft stools/day > Non (minimally)-absorbable antibiotics: rifaximin >> Gut decontamination: reduces urease and protease activity
52
Describe non-neoplastic focal liver disease
Developmental / degenerative e.g. cysts > Commonest is the Von Meyenberg complex = simple biliary hamartoma > Can resemble metastases by naked eye at operation > No treatment required Inflammatory e.g. abscess
53
Describe the clinical features of hepatic adenoma
Rare Mainly young women, often associated with hormonal therapy Risk of bleeding and rupture so excision if large
54
Describe the clinical features of hepatocellular carcinoma including screening, diagnosis and treatment
Most common primary liver tumour Usually arises in cirrhosis Can occur in pre-cirrhotic liver disease (Hepatitis B) Associated with elevated serum AFP (alpha feto-protein) Screening: 6 monthly US and plasma AFP Diagnosis : 2 cross-sectional scans: CT and MRI with typical features Treatment > Multiple kinase inhibitors: sorafanib, lenvatanib > Radiofrequency / microwave ablation > Transarterial chemoembolisation (TACE) > Resection > Liver transplantation
55
Summarise pharmacokinetic changes in liver disease
Absorption > Decreased absorption and first-pass effect resulting in higher bioavailability Distribution > Reduced plasma protein binding so large fraction of unbound drug Metabolism > reduced activity of phase I & II & CYP enzymes > Delayed clearance by drug metabolising enzymes Excretion > Biliary excretion reduced & reduced renal elimination
56
Describe paracetamol and opioid prescribing in liver disease
Glutathione tissue stores needed to block formation of acetaminophen's toxic metabolite NAPQI > reduced stores in cirrhosis, active alcohol consumption also reduces glutathione stores > half-life of paracetamol may be prolonged up to 2x All opioids can worsen hepatic encephalopathy and should be used cautiously or avoided
57
Describe the composition, diagnosis and management of gallstones
Types Pure > Cholesterol > Bile pigment > Mixed Diagnosis > Abdominal US >> Visualise gallbladder >> Not able to visualise common bile duct due to air in duodenum > X-ray (if sufficient calcium) Management > Conservative > Surgical - cholecystectomy
58
Describe the composition of bile
Composition > 97% water > Cholesterol >> Kept in solution by micelles containing bile acids and phospholipid > Bilirubin pigment > 500mls secreted by liver daily Lithogenic (stone-forming) > Excessive secretion of cholesterol > Decreased secretion of bile salts > Excessive secretion of bilirubin e.g. haemolytic anaemia
59
List causes of acute pancreatitis
Idiopathic Gallstones Ethanol Trauma Steroid use Mumps Autoimmune Scorpion sting Hyperglycaemia and hypertriglyceridaemia ERCP Drugs e.g. azathioprine
59
List complications of pancreatitis
- Fat necrosis - autodigestion - Acute haemorrhagic pancreatitis - Pancreatitic abscess > infected pancreatic necrosis > avascular haemorrhagic pancreas is a good culture medium > drainage or necrosectomy + antibiotics
60
Describe the different types of pancreatic cysts
Intraductal papillary mucinous neoplasm > In continuity with main pancreatic duct or side branch duct > Dysplastic papillary lining secreting mucin Mucinous cystic neoplasm > Mucinous lining, ovarian-type stroma Serous cystadenoma > No mucin production > Almost always benign
61
Describe pancreatic carcinoma including signs and symptoms, and management
Very poor prognosis Stent at ERCP for jaundice Subtypes: ductal adenocarcinoma, most common > Perineural invasion > Pre-malignant PanIN asymptomatic (pancreatic intraepithelial neoplasia) Risk factors: smoking, germline mutations e.g. BRCA Signs and symptoms > Painless obstructive jaundice > New onset diabetes (type 3c) > Abdominal pain due to pancreatic insufficiency or nerve invasion > Tumours in head may obstruct pancreatic duct and bile duct > Double duct sign on radiology Whipple's resection > Only for tumours of head of pancreas > Remove >> Head of pancreas >> Duodenum immediately adjacent to pancreas >> Bile duct >> Gallbladder Neoadjuvant therapy > Folfirinox chemotherapy
62
Describe pancreatic neuroendocrine tumours
Rare May secrete hormones – functional Commonest functional tumour – insulinoma > Presents with hypoglycaemia > 90% are benign Malignant endocrine tumours have a much better prognosis than pancreatic cancer
63
Describe carcinoma of the ampulla of Vater
Presents earlier and smaller than carcinoma of pancreas (causes obstruction) May arise from pre-existing adenoma 25% 5 year survival following Whipple's resection
64
Describe cholangiocarcinoma
Classified as > Intrahepatic >> Needs to be distinguished from metastatic adenocarcinoma (similar histology) and hepatocellular carcinoma > Extrahepatic >> Similar morphology and prognosis to pancreatic carcinoma Treatment > Whipple's resection to remove common bile duct and involve pancreas/duodenum
65
Describe carcinoma of the gallbladder
Rare Gallstones present in 80% of cases Adenocarcinoma Dismal prognosis unless found incidentally in a gallbladder removed for chronic cholecystitis Local infiltration may make gallbladder seem abnormally stuck down at theatre
66
List conditions affecting the oesophagus
- Reflux oesophagitis aka GORD - Infections > Candida albicans - fungus > Herpes simplex virus (immunocompromised) - Inflammation - chemicals > NaOH, caustic soda, iron, bisphosphonates, teracyclines - Oesophageal erosion: viral nuclear inclusions from HSV oesophagitis - Eosinophilic oesophagitis: allergic aetiology, causes dysphagia and food bolus obstruction - Barrett's oesophagus - Oesophageal cancer - Diverticula - Achalasia - Schatzki ring - Systemic sclerosis - Hiatus hernia
67
Describe Barrett's oesophagus including its complications
Metaplastic response to mucosal injury e.g. from long-term GORD Squamous epithelium becomes glandular, usually intestinal with goblet cells Dysplastic epithelium is architecturally and cytologically abnormal > Low grade: cells polarised, nuclei stratified > High grade: polarity lost, nuclei rounder, prominent nucleoli, abnormal mitoses, necrosis Associated with the development of benign strictures but also with oesophageal adenocarcinoma
68
Describe causes of acute gastritis
Alcohol, NSAIDs, severe trauma Burns (Curling's ulcers), surgery
69
Describe autoimmune gastritis including complications
Autoimmune destruction of parietal cells due to auto-antibodies against intrinsic factor and parietal cell antibodies in blood Leads to > Complete loss of parietal cells with pyloric and intestinal metaplasia > Achlorhydria > bacterial overgrowth > Hypergastrinaemia > endocrine cell hyperplasia / carcinoids > Persistent inflammation which can lead to epithelial dysplasia and may lead to cancer
70
Describe the patterns of H pylori infection and how this is treated
Histology > Lamina propria full of plasma cells and lymphocytes > Surface erosion and active inflammation > Helicobacter pylori colonises gastric mucosa causing active chronic inflammation IL-8 from epithelial cells attracts neutrophils Higher IL-8: pangastritis > Hypochlorhydria > Multifocal atrophic gastritis > Intestinal metaplasia > Cancer Lower IL-8: antral gastritis > Hypergastrinaemia > Duodenal ulceration Host/microbe interface > Impaired mucosal defence > NSAIDs interfering with mucosal prostaglandin synthesis > Bile reflux Microbe factors > CagA variants associated with more severe inflammation Treatment: triple therapy, PPI + 2 antibiotics (amoxicillin, clarithromycin)
71
Describe chemical / reactive gastropathy
Morphology > Few inflammatory cells > Foveolar hyperplasia – corkscrew glands > Ectatic mucosal capillaries > Muscle spurs in lamina propria Antrum more than corpus Causes > Bile reflux > NSAIDs > Ethanol > Oral iron
72
Describe intestinal gastric cancer
Strongly associated with chronic gastritis > H pylori > Autoimmune Background atrophic mucosa Chronic inflammation Intestinal metaplasia Dysplasia Various classification schemes > Lauren >> Intestinal or diffuse > WHO >> Papillary >> Tubular >> Poorly cohesive
73
Describe diffuse gastric cancer
Individual malignant cells with mucin vacuoles > Signet ring cells May invade extensively without being endoscopically obvious > Linitis plastica – leather bottle stomach Weaker link with gastritis Metastasis to ovaries - Krukenberg tumour Supraclavicular lymph node – Virchow's node Sister Joseph's nodule – umbilical metastasis
74
Describe hereditary diffuse gastric cancer
CDH1 mutation Penetrance 70-80% Small intramucosal foci of diffuse gastric cancer may be numerous Prophylactic gastrectomy likely to be considered Increased risk lobular carcinoma of breast
75
Describe the presentation and causes of upper GI bleeding
Presentation > Haematemesis > Coffee ground vomiting > Melaena Causes > Peptic ulcer >> Due to acid, H. pylori, NSAIDs > Oesophagitis > Gastritis > Duodenitis > Varices: large high pressure vessels anastomosed with abdominal vessels > Malignancy: ulcerated lesion, rolled edge > Mallory-Weiss tear: tear in oesophageal lining
76
Describe the management of upper GI bleeding
Resuscitation as required > Pulse & BP >> IV access for fluids/bloods >>> Check bloods – especially Hb & urea;High urea due to breakdown of blood into protein in GI tract >>> Lie flat and give oxygen Risk assessment and timing of endoscopy High risk – emergency endoscopy Moderate risk – admit & next day endoscopy Low risk – out-patient management Drug therapy & transfusion
77
Describe the risk scores used in the assessment of upper GI bleeding
Rockall Score > Predicts mortality >> Age >> Shock – pulse & BP >> Comorbidity >> Diagnosis >> Stigmata of recent haemorrhage
78
Describe the Glasgow Blatchford Score (GBS)
Uses > Blood urea and haemoglobin > BP, pulse, melaena or syncope > Background hepatic disease or cardiac failure GBS <=1 > Low risk of poor outcome > Can be discharged for outpatient endoscopy
79
Describe the different options for endoscopic management of an upper GI bleed
Adrenaline injection > Constricts blood vessels and limits blood flow Heater probe > Burn smaller blood vessels > Not suitable for varices Endoscopic clips Haemostatic powders Thrombin, laser Radiological embolisation of bleeding vessel uncontrolled by endoscopy
80
Describe the treatment of upper GI bleeding caused by varices
Resuscitation > Restore circulating volume > Transfuse once Hb <7g/dL Procedures > Endoscopic band ligation > Transjugular intrahepatic portosystemic shunt (TIPS) procedure >> Rescue procedure > Sengstaken tube – balloon tamponade >> Uncontrolled variceal bleeding >> Last minute temporary control of bleeding > Beta blockers e.g. propranolol >> Primary prophylaxis > Cirrhotic patients >> Prophylactic antibiotics early (high risk of sepsis) >> Vasopressors (Terlipressin) early >>> Constrict splanchnic flow and reduce blood entering collateral circulation > Surgical shunt / transection >> Very rarely used, high mortality Prevention of rebleeding > Beta-blocker + repeated band ligation
81
What is the characteristic feature of a hepatocellular carcinoma on a CT scan?
Hypervascularity followed by washout (waiting after contrast has passed) is characteristic of HCC
82
Describe the characteristic features of primary sclerosing cholangitis
Inflammatory condition causing irregularity, narrowing and dilatation of biliary tree Associated with IBD
83
Describe the features associated with Crohn's on MRI enterography
Irregular, thick wall in terminal ileum with ulceration & prominence of fat (hypertrophy), pushing other bowel away Skip lesion with narrowed lumen; abscess in small bowel (T1 W)
84
Describe the prep required for CT colonography
Bowel cleansing and tagging with iodine Bowel distension with CO2 Supine +/- prone CT scans with IV contrast Conventional 2D CT read CGI images for 3D read – virtual colonoscopy
85
Describe the different subtypes of colorectal cancer
Epithelial tumours > Adenocarcinomas > Neuroendocrine neoplasms > Squamous cell carcinoma > Metastatic carcinoma > Adenosquamous carcinoma Non-epithelial tumours > Gastrointestinal stromal tumours (GISTs) > Melanoma > Lymphomas
86
Describe the pathogenesis of colorectal cancer
1. Adenoma – carcinoma sequence > Aka chromosomal instability pathway > Mutation in APC (adenoma polyposis gene – dual function tumour suppressor genes) > Followed by mutation in KRAS > Later mutations in TP53, PIK3CA, loss of 18q > Issues with cell survival, DNA repair, apoptosis 2. Microsatellite instability pathway > Dysfunction in DNA mismatch repair genes (MMR genes) leading to genetic hypermutability > Seen in Lynch syndrome but also some sporadic cancers 3. Aberrant hypermethylation > Epigenetic modification leading to silencing of gene function
87
List risk factors for colorectal carcinoma
Adenomas > Size, number, villous History of IBD – especially ulcerative colitis Increasing age Obesity Sedentary lifestyle High fat / low fibre diet Smoking and alcohol use Family history – polyposis syndromes > Familial adenomatous polyposis – APC gene > Lynch syndrome (HNCC) - mismatch repair defects
88
Describe colorectal polyps giving examples
Polyp – exophytic protuberant growth Examples of bowel polyps > Hamartomatous polyps > Inflammatory polyps > Hyperplastic polyps > Adenomas All colorectal adenomas are dysplastic Adenomatous dysplasia > High grade > Low grade Architecture of adenoma > Villous > Tubulovillous > Tubular
89
Describe the histology of colorectal carcinoma
> Loss of normal architecture > Haphazard arrangement of glands > Tumour invasion through muscularis mucosae – invasive carcinoma Desmoplastic stroma: pink and spindly > Confirms invasive carcinoma Vascular invasion (ENVI – extra-neural vascular invasion) > Vein elastic fibres are stretched around the deposit of colorectal cancer Colon cancer blood marker: carcinoembryonic antigen (CEA)
90
Describe the TNM 8 staging of colorectal carcinoma
T1: enter submucosa T2: invades into muscularis propria T3: invasion through muscularis propria into subserosa T4: invasion of visceral peritoneum and other organs N0: no regional lymph node mets N1: 1-3 regional LN mets N2: 4+ regional LN mets M0: no distant mets M1: distant mets
91
Describe the bowel cancer screening programme
qFIT testing of >50-74 year olds every 2 years If positive refer for colonoscopy Patient education of symptoms - PR bleeding - Change in bowel habit

Phase 3 (14 decks)

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