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Phase 3 > GI/Liver > Flashcards

GI/Liver Flashcards

1
Q

List 5 functions of the liver

A

Filtration of blood from GI tract

  • Detoxification of blood eg. clears adrenal androgens
  • Drug metabolism
  • Bile production and excretion

Storage

  • Storage of glycogen, minerals, proteins

Synthesis

  • Lipid, protein and carbohydrate metabolism
  • Protein synthesis eg. clotting factors, albumin
  • Thrombopoietin production (TPO): stimulates platalet produciton

Activation

  • Enzyme activation
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2
Q

Which areas of the abdomen is the liver predominantly in?

A

Right hypochondrium and epigastric

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3
Q

Describe the microscopic anatomy of the liver

A
  • Hepatocytes are arranged into lobules (structual units)
  • Each lobule is drained by a central vein which drains into the hepatic vein

At the periphery of each lobule: portal triad which lies in the portal tract

  • Arteriole: branch of hepatic artery entering the liver
  • Venule: branch of portal vein entering the liver
  • Bile duct: branch of the bile duct leaving the liver
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4
Q

What are the two main types of liver disease

A
  • Space-occupying lesions (masses, focal disease)
  • Diffuse liver disease
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5
Q

List 5 causes of liver injury

A
  • Drugs and toxins inc. alcohol
  • Abnormal nutrition/metabolism (eg. obesity)
  • Infection
  • Obstruction to bile/blood flow
  • Autoimmune liver disease
  • Neoplasm
  • Primary Biliary disease eg. primary biliary cholangitis
  • Vascular disease eg. venous obstruction
  • Genetics eg. haemochromatosis
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6
Q

Differentiate between acute and chronic inflammation

A

Acute inflammation: agent causes injury but is then removed

  • Days to weeks
  • Fulminant: defined as severe, acute inflammation rapidly progressing toward liver failure

Chronic inflammation: agent causes injury and then persists

  • Months to years
  • Liver disease: any abnormality in LFTs for >6 months
  • Acute on chronic: chronic liver disease often presents with acute exacerbating plus evidence of underlying chronicity
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7
Q

What is the main target of liver injury?

What is the relationship between different hepatic structures in inflammation?

A
  • Liver injury mainly affects parenchyma ie. hepatocytes
  • Bile ducts or blood vessels are rarely the main target
  • Parenchyma, bile ducts, blood vessels and CT are interdependent, so damage to one leads to damage to the others
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8
Q

What is the clinical approach to liver disease?

A
  • History, symptoms and signs by examination
  • Investigations: LFTs, viral and autoimmune serology, metabolic tests and radiology

^ usually yields diagnosis without biopsy, should at least differentiate space-occupying lesion with diffuse liver disease

  • Avoid liver biopsies due to significant complication rates
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9
Q

List 4 histological patterns that can be seen with diffuse liver disease

A
  • Acute hepatitis
  • Acute cholestasis
  • Fatty liver disease (steatosis and steatohepatitis)
  • Chronic hepatitis
  • Chronic biliary/cholestatic disease
  • Genetic/Deposition disease
  • Hepatic vascular disease
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10
Q

Define cholestasis

A

Reduction in bile flow due to impaired secretion from hepatocytes or obstruction of bile flow through intra- or extrahepatic ducts

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11
Q

What are the features of acute hepatitis and acute cholestasis

A
  • Inflammation
  • Acute bile stasis (more marked in cholestasis)
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12
Q

What are the features of acute hepatitis?

A
  • Inflammation in and affecting the hepatocytes, causing damage
  • Diffuse hepatocyte injury seen as swelling
  • Looks very busy
  • Some cells have died: ‘spotty necrosis’
  • Inflammatory cell infiltrate in all areas (portal tracts, interface and parenchyma)
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13
Q

What are the causes of acute cholestasis (cholestatic disease)?

Describe it’s histology

A
  • Extrahepatic biliary obstruction
  • Drug injury eg. antibiotics

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

  • Inflammation and acute bile stasis
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14
Q

How would you differentiate acute and chronic hepatitis clinically and histologically?

A

Clinically: chronic is >6 month history of abnormal LFTs

Histologically: chronic hepatitis would have presence of fibrosis

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15
Q

Define chronic liver disease

A

Any abnormality in LFTs for >6 months

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16
Q

Which histological patterns are most likely to develop fibrosis and progress to cirrhosis?

A
  • Fatty liver disease
  • Chronic hepatitis
  • Chronic cholestatic disease
  • Genetic/Deposition disease
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17
Q

Describe the pathology of Hepatitis B

What is it’s distinguishing feature?

A
  • Looks like acute hepatitis with addition of fibrosis
  • Specific feature: ground glass cytoplasm hepatocytes (accumulcation of surface antigen)
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18
Q

Where is the target for damage in chronic biliary/cholestatic disease?

What are the causes?

  • What is the histology?
A
  • Damage to the portal tracts, esp. the bile ducts

Causes:

  • Primary biliary cholangitis: autoimmune disease resulting in slow, progressive destruction of small bile ducts of the liver
  • Primary sclerosing cholangitis (PSC): long-term progressive disease of liver and gallbladder characterised by inflammation and scarring of bile ducts

Histology:

  • Focal, portal-predominant inflammation and fibrosis
  • Granulomas
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19
Q

What conditions cause genetic/deposition liver disease?

A
  • Haemochromatosis: excess iron, stained blue, not normally seen
  • Wilson’s disease
  • Alpha-1-antitrypsin deficiency (it’s produced in the liver)
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20
Q

What are the aims of management for diffuse liver disease?

What are the treatment options?

A
  • Reduce symptoms, reduce inflammation and prevent/slow progression of fibrosis

Treatment options:

  • Specific treatment against cause eg. removal of alcohol/drug, optimal diabetic control. antivirals or immunosuppression
  • Supportive treatment eg. for severe acute hepatitis or cirrhosis
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21
Q

What histological pattern(s) can drug-induced liver disease present as?

A
  • Almost any pattern of liver disease
  • Therefore, usually in differential diagnosis esp. with acute hepatitis and acute cholestasis
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22
Q

What are the types of space occupying lesions that cause liver disease?

A

Non-neoplastic:

  • Degenerative/Developmental eg. cysts
  • Inflammatory eg. abscess

Neoplastic:

  • Benign or malignant
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23
Q

Describe the pathology of liver cysts

What is the clinical significance of a liver cyst?

What is the treatment?

A
  • Developmental or degenerative in origin
  • Most common: simple biliary hamartoma
  • Found on the surface of the liver and can resemble metastases by naked eye in operation

Treatment: none

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24
Q

Fill in the blanks

  • Types of liver neoplasms
A
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25
Q

What are the risk factors for a hepatic adenoma?

A

Young, women, often associated with hormone therapy

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26
Q

In which situation is hepatocellular carcinoma likely to arise?

What investigation would you do?

A
  • Usually arises in cirrhosis
  • Associated with elevated serum AFP (alpha feto-protein)
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27
Q

Define cirrhosis

A
  • diffuse process characterised nodule formation and fibrosis
  • End-stage liver disease
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28
Q

What are the signs of chronic liver disease?

A
  • Spider naevi
  • Palmar erythema
  • Loss of male hair pattern
  • Gynaecomastia (reduced clearance of adrenal androgens)
  • Sarcopenia (muscle breakdown)
  • Bruising ( inc. prothrombin time, platelets)
  • Itch (buildup of bile salt under the skin)
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29
Q

What causes easy bruising and itch in chronic liver disease (CLD)?

A

Easy bruising:

  • Reduced production of clotting factors VII - XII, therefore takes longer to activate thrombin ie. longer prothrombin time (PT)
  • Reduced production of TPO (thrombopoietin) which stimulates differentiation of megakaryocytes into platlets

Itch: accumulation of bile salts under the skin

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30
Q

What are the signs of portal hypertension?

A
  • Caput medusa: the appearance of distended and enlarged superficial epigastric veins, seen radiating from the umbilicus across the abdomen
  • Hypersplenism: over-active spleen, regardless of size, due to inc. blood flow to the spleen. Causes thrombocytopenia and pancytopenia
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31
Q

Define decompensated cirrhosis

What are the signs of decompensated chronic liver disease?

A

= Acute deterioration in liver function in a patient with cirrhosis

  • Jaundice
  • Ascites
  • Hepatic flap
  • Peripheral oedema
  • Encephalopathy
  • Bleeding varices
  • Hepatocellular carcinoma
  • Deteriotating synthetic function: high bilirubin, low albumin, high PT
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32
Q

What are the two types of cirrhosis?

A
  • Micronodular: regenerating nodules <3mm and the liver is involved uniformly. Often caused by ongoing alcohol damage or biliary tract disease
  • Macronodular: nodules variable in size and normal acini seen with larger nodules. Often following hepatitis eg. HBV
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33
Q

Describe/Explain the progression of cirrhosis and portal hypertension

A

Cirrhosis leads to increased intrahepatic resistance therefore slower blood flow through the liver and raised portal pressure (portal hypertension) → hypersplenism

Portal HTN leads to porto-systemic shunting → oesophageal-gastric varices and encephalopathy

this shunting leads to vasodilatation causing splanchnic vasodilatation (futher raising portal pressure) and reduced effective circulating volume → hyperdynamic circulation

this leads to compensatory vasopressors (RAAS) causing Na retenion and renal vasoconstriction → ascites and hepato-renal syndrome respectively (progressive kidney failure)

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34
Q

Describe the histology of cirrhosis

A
  • Results from the necrosis of hepatocytes followed by fibrosis and nodule formation
  • Architecture is diffusely abnormal which interferes with liver blood flow and function
  • Clinical perspective: some patients are very well (compensated) and some are very unwell (decompensated)
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35
Q

What are the main complications associated with cirrhosis?

A
  • Ascites
  • Encephalopathy
  • Variceal bleeding
  • Hepatocarcinoma
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36
Q

How does cirrhosis lead to encephalopathy?

A

Failure of the cirrhotic liver to remove toxins from the blood, which ultimately negatively impacts the brain function

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37
Q

What are the best indicators for determining liver function?

A

Best indicators look at synthetic function:

  • Albumin, bilirubin and clotting factors (Prothrombin Time (PT))
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38
Q

How are ascited assessed?

A

Ascites = build-up of fluid in the abdomen

  • Diagnostic tap of the fluid

Cell count

  • WCC >500 or neutrophils >250 suggests spontaneous bacterial peritonitis
  • Inflammatory conditions also inc. WCC

Albumin

  • Low protein ascites: portal hypertension
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39
Q

How are ascites managed?

A
  • No added salt diet
  • Diuretics: spironolactone (blocks aldosterone) or frusemide (loop diuretic)
  • Paracentesis
  • transjugular intrahepatic portosystemic shunt (TIPSS)
  • liver transplant
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40
Q

What is the class, indication and action of furosemide?

A

Class: loop diuretic

Indication: HTN, hyperkalaemia, HF, cirrhosis (fluid retention, ascites), nephrotic syndrome

Action:

  • Na/Cl/K symporter antagonists
  • Act on the thick ascending loop of Henle
  • Increases secretion of Na, Cl, K and water
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41
Q

What are the 3 main causes of liver disease?

A
  • Alcohol
  • Obesity
  • Viral hepatitis
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42
Q

Where are the following produced in the liver and are they produced anywhere else in the body?

Alanine Aminotransferase / Aspartate Aminotransferase

Alkaline Phosphatase

GGT

Bilirubin

Albumin

PT

A

ALT/AST: produced in hepatocytes, also produced in skeletal and cardiac muscle. ALT is more specific to the liver

ALP: produced in canaliculi, also produced from bone (growing bone, pregnancy, Paget’s disease, bone mets, recent fracture)

GGT: produced in all cells, also produced with alcohol/drug metabolism

Bilirubin: hepatocyte function (conjugated), also produced in haemolysis (unconj)

Albumin: hepatocyte synthesis (low in abnormality), also low in infection/inflammation/renal loss (acute phase protein)

Clotting factors: hepatocytes

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43
Q

What investigations determine liver function?

What combination of results suggested liver failure?

A

Function of the liver indicated by:

  • Serum albumin: guide to severity of chronic liver disease (may be normal initially in acute liver disease)
  • Prothrombin time (PT): short half-life therefore is sensitive to both acute and chronic liver disease
  • Bilirubin: normally all unconjugated in serum. Determination of conj. and unconj. bilirubin only necessary in congenital disorders of bilirubin metabolism or to exclude haemolysis

A high bilirubin/PT and encephalopathy indicates <25% function

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44
Q

What are the differentials for abnormal LFTs?

A

MEDIC PINNE HAT

Metabolic

Endocrinological

Degenerative

Inflammatory/Infection (Viral Hep)

Congenital (inc. genetic)

Psychological

Idiopathic

Neurological

Neoplasm

Environmental (exposure to drug/toxin)

Haematological

Autoimmune

Traumatic

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45
Q

Describe the interpretation of LFTs

A
  1. Assess ALT and ALP
    - ALT is raised x10 in hepatocellular damage
    - ALP is raised x3 in cholestasis

(Possible to have a mixed picture of hepatocyte injury and cholestasis)

  1. Look at GGT
    - If ALP is raised, it’s important to look at GGT
    - Raised GGT can be a sign of epithelial biliary damage and bile flow obstruction
    - Raised ALP with raised GGT: highly suggestive of cholestasis
    - Raised ALP with normal GGT: think non-hepatobiliary pathology ie. anything increasing bone formation
    - Isolated GGT elevation: think drug/alcohol cause
  2. Assess synthetic function: bilirubin
    - Isolated bilirubin elevation: think pre-hepatic ie. Gilbert’s disease or haemolysis
    - Ask about urine and stool
  3. Assess synthetic function: albumin and PT
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46
Q

How are urine and stool affected by bilirubin

A

Urine

  • Unconjugated bilirubin = water insoluble therefore elevated levels don’t change urine
  • Conjugated bilirubin = water soluble and makes the urine darker

Stool

  • If bile and pancreatic lipases cannot reach duodenum (post-hepatic jaundice), fat can’t be absorbed and stool appears lighter

So..

  • normal urine and normal stool = pre-hepatic jaundice/cause
  • dark urine and normal stool = hepatic
  • dark urine and pale stool = post-hepatic
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47
Q

Define jaundice

A

Yellowing of the skin due to excess bilirubin pigment, caused by obstruction to the bile duct, hepatocellular damage or increased haemolysis (RBC breakdown)

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48
Q

What investigations would help identify acute liver injury?

A
  • History: days/weeks
  • Ultrasound (cancer, bile ducts, blood vessels)
  • Acute viral hepatitis screen: Hep A/B/C/E virus
  • Autoimmune liver disease
  • Check paracetamol levels
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49
Q

What investigations would help identify chronic liver disease?

A
  • History: >6 months
  • Ultrasound (cancer, bile ducts, blood vessels, portal hypertension) +/- CT/MRCP
  • Liver screen: chronic viral hepatitis (HBV, HCV), autoimmune liver disease, metabolic liver disease
  • Autoimmune liver disease:

IgG goes up with autoimmune liver disease, IgA goes up in alcohol, IgM goes up in primary biliary cholangitis

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50
Q

What are the stages of fatty liver disease?

A

1. Macro-vesicular steatosis with lipid vacuole filling the hepatocyte cytoplasm

  • Steatosis aka fatty change, is abnormal retention of fat within a cell

2. Steatohepatitis: neutrophils and lymphocytes surrounding hepatocytes eith Mallory hyaline

  • A type of fatty liver disease, characterised by inflammation of the liver with concurrent fat accumulation in liver

3. Pericellular fibrosis as well as bands of fibrotic tracts between portal tracts

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51
Q

What is the progression of alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD)

A
  • Types of fatty liver disease
  • Multifactorial
  • Both can lead to end-stage liver disease or develop hepatocellular carcinoma

ALD: alcoholic steatosis > alcoholic hepatitis > alcoholic cirrhosis

NAFLD: steatosis > non-alcoholic steatohepatitis > NAFLD cirrhosis

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52
Q

How is fibrosis of the liver assessed?

A

Fibroscan (non-invasive testing)

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53
Q

What are the main associations with NAFLD?

How is it treated?

A
  • Obesity
  • T2DM
  • Hyperlipidaemia

At higher risk of diabetes and CV death

Treatment: weight loss and reduce metabolic risks

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54
Q

How would ALD and NAFLD be differentiated clinically?

A

ALD: normal BMI and excessive drinking

NAFLD: elevated BMI and no history of alcohol excess

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55
Q

What are the characteristic features of alcoholic liver disease?

What are some of the essential features?

A

- Hepatomegaly +/- fever +/- leucocytosis +/- hepatic bruit (caused by narrowing of artery)

Also seen as disease progresses toward cirrhosis:

  • Malaise, nausea, itch, jaundice, sepsis, encephalopathy, ascites, renal failure, death

Essential features:

  • Excess alcohol within 2 months
  • Bilirubin <80mmol/l for <2 months

- AST:ALT ratio >1.5

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56
Q

Compare NAFLD and ALD

A

NAFLD v ALD

Weight: elevated v variable

Fasting plasma glucose/HbA1c: usually elevated v normal

Reported daily alcohol: below daily v excess

ALT: elevated or normal in both

AST: normal v elevated

AST:ALT ratio: <0.8 v >1.5

GGT: elevated/normal v marked elevated

HDL-Cholesterol: low v elevated

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57
Q

Define acute hepatitis

A

Inflammation of the liver caused by infection with one of the five hepatitis viruses

  • Inflammation begins suddenly and only lasts a few weeks
  • Usually symptomatic (fever, flu, yellow sclera)
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58
Q

Define chronic hepatitis

A
  • Inflammation of the liver for >6 months
  • If viral chronic hepatits: virus has been present for >6 months
  • Common causes: Hepatitis B and C virus (HBV/HCV)
  • Usually asymptomatic by this stage
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59
Q

List 3 causes of acute hepatitis

A
  • Infection: Hep A-E, Malaria, Syphilis,
  • -* Toxins, drugs, alcohol
  • Haemochromatosis
  • Autoimmune
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60
Q

What are the laboratory findings to diagnose viral hepatitis?

A

Detection of specific immune responses (IgM or IgG)

  • Look for antibodies against different viruses
  • IgM: new/acute infection
  • IgG: previous or chronic infection

Viral nucleic acid detection using PCR

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61
Q

What is Hepatitis A (HAV)?

Transmission

Clinical features

A

What: RNA virus

  • Acute hepatitis

Transmission: faeco-oral with a human reservoir

  • Virus can survive for months in contaminated water and sheds via biliary tree into gut

Clinical features:

  • Jaundice, fever, diarrhoea
  • Incubation period: 30 days
  • Age: main determinant of severity (usually asymptomatic in <5yrs)
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62
Q

What is the diagnosis and treatment for HAV?

Are there any prevention strategies?

A

Diagnosis: IgM to Hepatits A or RNA in stool/blood

Treatment: self-limiting

  • Maintain hydration, avoid alcohol

Prevention: vaccine

  • inactivated vaccine, 2nd dose gives life protection
  • Pre-exposure for travellers, MSM, IVDU, chronic liver disease
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63
Q

What is Hepatitis B Virus (HBV)?

Transmission

A
  • DNA virus
  • Chronic or acute

Transmission:

  • Mother to baby transmission (most common)
  • Blood and sex eg. transfusion, sex
  • Organ and tissue transplantation
  • Contaminated needles
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64
Q

What are the clinical features of acute hepatitis B?

What is the importance of the age of acquisition

A
  • Incubation: 2-6 months
  • Fever, jaundice
  • Age at time of infection determines:

Severity of acute illness: younger people have weak immune system so weak immune response mounted therefore will be asymptomatic

Risk of developing chroniv hepatitis B (CHB)

  • Infection at birth: asymptomatic but leads to chronic infection
  • Infection in adults: usually symptomatic but is cleared
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65
Q

What are the complications of hep B?

A
  • Weight loss
  • Abdo pain
  • Fever
  • Cachexia (wasting and weakness of body due to severe chronic illness)
  • Abdo mass
  • Blood ascites

As it progresses:

  • Liver failure
  • Cirrhosis so higher risk of carcinoma (HCC)
  • Decompensation
  • Death
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66
Q

How is Hepatitis B diagnosed?

What do the results mean?

A

sAg - surface antigen, marker of current infection

sAb - surface antibody, marker of immunity (previously infected but not currently)

cAb - either been infected or currently infected, just know patient has come into contact with whole antigen (not from vaccine)

HBV DNA - determines viral load, patient currently infected

eAg - e-antigen, suggests high infectivity

eAb - e-antibody, suggests low infectivity

HBV infection diagnosed if sAg or DNA are detectable

Chronic HBV: sAg detectable for >6 months

Carriers 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, low risk of CLD and HCC, less infectivity

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67
Q

What are the treatment options for acute and chronic hepatitis B?

A

Treatment:

Acute HBV: none (self-limiting)

Chronic HBV:

  • Most don’t require treatment
  • Only treat those with liver inflammation (LFT or biopsy) or fibrosis (fibroscan)
  • Aim of treatment: suppress viral replication and prevent further liver damage
  • Two types of treatment: immuno-modulatory (interferon) or suppress viral replication (Tenofovir)
  • These aren’t curative but reduce risk of complications
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68
Q

Are there any prevention strategies for Hepatitis B?

A
  • Education (safe sex, safe injecting)
  • Immunisation (HBV sAg vaccine): included in immunisation schedule in UK
  • Prevent mother-to-child transmission: HBV vaccine to newborn (6 doses in first year), Tenofovir during last trimester if high viral load
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69
Q

What is Hepatitis C (HCV)?

Transmission

Clinical features

A
  • RNA virus
  • Acute or chronic
  • Most common Hep virus in the UK

Transmission: blood-borne

  • Shared needles, transfusion, transplant

Clinical Features:

  • Incubation: 6-7 weeks
  • Ususlly asymptomatic
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70
Q

What determines the progression from acute to chronic hepatitis C and on to cirrhosis?

A

Spontaneous resolution in 25% of acutely infected patients

Rate of progression related to:

  • Male sex, age >40 at time of acquisition and alcohol >50g/week

Duration of infection:

  • 20% risk of cirrhosis after 20yrs
  • 50% risk of cirrhosis after 50years
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71
Q

How is hepatitis C diagnosed?

A

Diagnosis:

  • Mostly diagnosed through screening high-risk groups (IVDU and immigrants from high prevalence countries) as usually asymptomatic
  • Anti-hcv IgG (antibody) positive = chronic infection or cleared infection

PCR or antigen positive = current infection / viraemia

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72
Q

What is the treatment?

Are there any prevention strategies?

A

Spontaneous resolvement of acute HCV in 25% individuals

Treatment: aim to cure infection

  • 8-12 weeks of oral treatment
  • Direct Acting Antivirals (DAAs) inhibit different stages of the replication cycle

Prevention: no vaccine or exposure prophylaxis

  • No reliable immunity after infection
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73
Q

What is Hepatitis D?

Transmission and acquisition

Complications

Treatment

A
  • ssRNA virus

Transmission: requires HBV to replicate

  • Blood and sex (same as HVB)

Acquisition:

  • Co-infection with HBV
  • Super infection of chronic HVB carriers

Complication: inc. risk of CLD

Treatment: Peg IFN (pegylated interferon (chemotherapy))

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74
Q

What is Hepatitis E (HEV)?

Transmission

Clinical features

A
  • RNA virus
  • Acute infection

Transmission: faeco-oral and pork products

Clinical features:

  • Incubation period: 40 days
  • Diarrhoeal illness (similar to Hep A)
  • Neurological manifestations in some: Guillaine-Barre syndrome, encephalitis, ataxia, myopathy
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75
Q

What is the treatment for hepatitis E?

Are there any prevention strategies?

In what situations would Chronic Hep E arise?

A

Treatment: supportive

Prevention: none, no vaccine

Chronic Hep E develops in immunosuppressed patients or patients who’ve had a bone marrow transplant

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76
Q

Describe the biliary tree pathway

A

Bile drains through left and right hepatic ducts into common hepatic duct

This joins with the cystic duct from the gallbladder to form the common bile duct

Before it enters the duodenum, it joins with the pancreatic duct to form the ampulla of vater

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77
Q

Define cholelithiasis

A

The formation of gallstones

78
Q

What can gallstones be composed of?

A
  • Cholesterol
  • Bile pigment
  • Mixed (cholesterol, pigment, calcium)
79
Q

Describe the pathophysiology of cholesterol gallstones

A

Cholesterol secreted into bile is not water soluble and kept in solution by micelles containing bile acids and phospholipid

  • Excess cholesterol (in relation to bile salts) will crystallise out and form a gallstone
    ie. supersaturated bile
  • This would occur if there was excess cholesterol secretion or decreased bile salt secretion
80
Q

List 3 risk factors for formation of cholesterol gallstones

A

Fat (overweight)

Forty (near forty or above)

Female

Fertile (premenopausal therefore increased oestrogen levels which are thought to inc. cholesterol levels in bile and decrease gallbladder contractions

Fair (caucasians)

Others:

Things that inc. oestrogen: OCP, liver cirrhosis

Things that inc. cholesterol: diet, diabetes

81
Q

Describe the pathophysiology of bile pigment gallstones

A
  • bile pigment = bilirubin, a breakdown product of haemoglobin
  • excessive bilirubin secretion (eg. haemolytic anaemia) can cause it’s precipitation in concentrated bile in the gallbladder
82
Q

Explain the clinical features of gallstones depending on their location in the biliary system

A

80% gallstones are in gallbladder and are asymptomatic

Cystic duct/neck of gallbladder:

  • RUQ pain, usually occuring after meals
  • Crampy in nature
  • no associated jaundice or fever
  • Acute cholecystitis (inflam of GB)

Common bile duct: Biliary obstruction

  • cholestatic jaundice
  • bacterial infection and cholangitis
  • severe RUQ pain

Pancreatic duct: can lead to pancreatitis (severe, constant abdo pain)

Rarely, can perforate through the wall of the inflamed GB into the intestine producing a fistula

83
Q

Describe the pathophysiology and clinical features of acute cholecystitis

A

Pathophysiology:

  • Initially, obstruction of the neck of the gallbladderor cystic duct by an impacted stone, leading to distension and inflammation
  • Inflammation is usually sterile but within 24hours, organisms can grow there
  • occassionly, the inflam subsides quickly leaving the gallbladder distended with mucus (mucocele): slight abdo pain with palpable gallbladder
  • more commonly, inflam is more severe involves whole wall leading to localised perotinitis and acute pain

Clinical Features:

  • severe RUQ pain
  • continuous pain, increasing in intensity over 24 hours
  • can radiate to shoulder and back
  • nausea, vomiting
  • fever and mild jaundice (20%)

- positive Murphy’s sign (right hypochondrium pain worse on inspiration)

84
Q

What is lithogenic bile?

A

Bile that forms gallstones

  • Excess cholesterol or
  • Reduced bile salt or
  • Excess bile pigment
85
Q

List 3 complications of gallstones

A
  • Inflamed gallbladder (cholecystitis)
  • Blockage of common bile duct: severe pain, jaundice and cholangitis
  • Blockage of the pancreatic duct: can lead to pancreatitis (intense, constant abdo pain)
  • Gallbladder cancer
86
Q

How are gallstones identified/diagnosed?

A

Abdominal Ultrasound

Endoscopic ultrasound (EUS)

  • Helps identify smaller stones

MRCP (magnetic resonance cholangiopancreatography)

  • Type of MRI

Operative cholangiogram

  • Used to visualise bile ducts

ERCP (endoscopic retrograde cholangiopancreatography)

  • gallstones diagnosed this way can also be removed in the same procedure

Bloods

  • infection, jaundice, pancreatitis or other complications of gallstones
87
Q

What are the treatment options for gallstones?

A

Asymptomatic: active monitoring

Keyhole cholcystectomy

  • Removal of gallbladder, recommended if stone formation is frequent

ERCP to remove stones from bile duct

88
Q

What LFT results would be seen in prehepatic , hepatic and post-hepatic jaundice?

A

Pre-hepatic: isolated rise in bilirubin (inc. RBC breakdown)

hepatic jaundice: rise in bilirubin, AST and ALT

Post-hepatic jaundice:

  • Early: rise in ALP (bile ducts - cholestasis) and bilirubin
  • Late: also get elevated AST/ALT due to back pressure
89
Q

Define acute pancreatitis

A

Inflammation of the pancreas by enzyme-mediated autodigestion

90
Q

List 4 causes of acute pancreatitis

A

Idiopathic

Gallstones

Ethanol

Trauma

Steroids

Mumps/Metabolic

Autoimmune

Scorpian bites

Hyperlipidaemia, hypercholesterolaemia

ERCP

Drugs eg. OCP, azathioprine, HRT

91
Q

List the symptoms seen with pancreatitis

List 3 examination findings

A

Severe epigastric pain, radiated to back

Worse lying flat

Nausea and vomiting

Fever (chills, temperature etc.)

Examination findings:

  • tachycardic, hypotensive, pyrexia
92
Q

Outline the pathophysiology of acute pancreatitis

A

(dependent on underlying cause)

  • inflammation damages the pancreas and acini (exocrine functional units)
  • acinar cells release digestive enzymes (protease/lipase/amylase) into surroundings rather than the pancreatic ducts causing further damage of surrounding structures and pancreatic tissue
  • autodigestion
  • amylase: measured for diagnosis
  • lipase: fatty necrosis of pancreas
93
Q

List investigations needed to diagnose acute pancreatitis and those to help with diagnosis

A

Need two of:

  • clinical presentation
  • LFTs
  • Ultrasound (to exlucde/confirm gallstones): if positive may need ERCP

To aid diagnosis:

  • FBC (leucocytosis), U&Es, LFTs
  • CRP
  • Amylase
  • Ultrasound
  • Glucose
94
Q

What is the management for acute pancreatitis?

A

Treat underlying cause

Supportive treatment: 48hr monitoring for serious complications

  • IV fluids
  • oxygen
  • analgesia
  • nutritional support
95
Q

List 3 acute and 3 chronic complications of acute pancreatitis

A

Acute:

  • Fatty necrosis
  • pancreatic abscess
  • Haemorrhage (erosion of splenic artery)
  • Portal vein thrombosis
  • acute kidney infection
  • acute respiratory distress syndrome

Chronic

  • chronic pancreatitis
  • exocrine failure and malnourishment
  • endocrine failure and diabetes
  • stones/strictures
96
Q

Describe how fatty necrosis occurs following acute pancreatitis

A

= autodigestion

  • enzymes (lipases) leak into the pancreatic tissue and abdominal tissue leading to fat necrosis
  • yellow fat: damaged
  • vessel necrosis leads to avascular tissue
97
Q

List 3 different types of pancreatic cysts and state their ability to become malignant

A

Intraductal papillary mucinous neoplasm

  • in continuity of main pancreatic duct or side branch
  • dysplastic papillary lining secreting mucin
  • risk of pancreatic cancer

Mucinous cystic neoplasm

  • mucinous lining, ‘ovarian-type’ stroma
  • small porportion can become malignant

Serous cystadenoma

  • many small and some larger cysts
  • no mucin production
  • almost always benign
98
Q

What is the most common cancer of the pancreas?

What is the pre-malignant stage?

Outline the pathology and prognosis

A

ductal adenocarcinoma (exocrine pancreatic cancer)

Pre-malignant stage: pre-malignant pancreatic intraepithelial neoplasm (PanIN) which is asymptomatic

Pathology: perineural invasion

Prognosis: common to present late as symptoms are vague and so 5yr survival is 5%

99
Q

List two risk factors for development of pancreatic carcinoma

A
  • smoking
  • germline mutations eg. BRCA, but these are rare
100
Q

List three signs and symptoms of ductal adenocarcinoma

A
  • Painless obstructive jaundice
  • New onset diabetes
  • Abdo pain due to pancreatic insufficiency or nerve invasion
  • Tumour in head may obstruct pancreatic and biliary duct - double duct sign on radiology
101
Q

How are pancreatic carcinoma’s treated?

A

Whipple’s procedure: tumour in the head of the pancreas

  • Removal of the head of the pancreas, duodenom, GB and bile ducts
  • difficult to get clear resection margins

Neoadjuvant therapy

  • improves margin status and may be associated with longer survival
102
Q

List 3 cancers of the pancreas/biliary tract

A

Ductal adenocarcinoma

Pancreatic neuroendocrine tumour

Carcinoma of ampulla of Vater

Cholangiocarcinoma

Carcinoma of the GB

103
Q

Outline the pathology of pancreatic neuroendocrine tumours

Outline the prognosis

A
  • Sometimes secrete hormones (function tumours)

Commonest functional tumour: insulinoma

  • Presents with hypoglycaemia

Prognosis:

  • 90% are benign
  • Malignant endocrine tumours have better prognosis than pancreatic carcinoma
104
Q

What is a cholangiocarcinoma?

How does it present?

How is it classified?

How is it treated?

A

= Carcinoma of the bile ducts

Present: behave similarly to pancreatic cancers due to obstruction

Classification: intrahepatic/extrahepatic depending on origin

  • intrahepatic cholangiocarcinoma needs distinguished from metastatic adenocarcinoma and HCC

Treatment: Whipple’s procedure to remove common bile duct

105
Q

What is the biggest risk factor for carcinoma of the gallbladder?

A

Gallstones

106
Q

outline the presentation of upper GI bleeds and how they correlate to the position of pathology in the GI tract

A

Haematemesis: vomiting blood

‘Coffee ground’ vomiting: presence of coagulated coffee

Melaena: dark tarry stool, usually diarrhoea

Location:

Oesophagus/Stomach: more likely to present with haematemesis

Duodenum/Below: Melaena

107
Q

List 4 causes of upper GI bleed

A

Peptic ulcer

  • Due to acid, H. pylori or NSAIDs

Oesophagitis

Gastritis

Duodenitis

Varices

Malignancy

108
Q

Why do peptic ulcers need checked to ensure they’ve healed?

What is the aim of treatment of a bleeding peptic ulcer?

A
  • Worried about malignancy

Aim: treat the ulcer but also need to find the bleeding vessel

109
Q

What is the main cause of oesophagitis?

A

Gastric reflux

110
Q

What is a mallory weiss tear?

How does it present?

A

= A tear of the mucous membrane, most common at the gastro-intestinal junction

Presentation: violet vomiting without blood then suddenly get vomiting with blood

  • Non-variceal bleeding
111
Q

Outline the management for upper GI bleeds

A

Resuscitate if required

  • Pulse and BP
  • IV access for bloods/fluids (more fluid resuscitation)
  • Oxygen

Risk assessment and timing of endoscopy

Drug therapy and transfusion

112
Q

What is involved in the risk assessment for upper GI bleeds?

A

To assess risk:

  • Sometimes it’s obvious: severe upper GI bleed identified by clinical assessment (pulse, BP, age, co-morbidities)
  • Endoscopic: rockall score
  • Clinical: admission rockall score (pre-endoscopic score) or Glasgow Blatchford Score (more predictive of mortality and need for endoscopic intervention. GBS <1 identifies those at very low risk of poor outcome). GBS measures blood urea (goes up with GI bleed)

High Risk (haemodynamic instability or severe ongoing bleeding): emergency endoscopy

Moderate risk: admit and next day endoscopy. Most patients need endoscopy within 24hours)

Low risk: out-patient endoscope and management

113
Q

What endoscopic therapy is available for upper GI bleeds?

A

Adrenaline injection: vasoconstriction, tamponade effect however this will wear off

Heat probe

Endoscopic clips: clip the artery

Haemostatic powders

Usually:

  • Dual therapy of adrenaline with either heater probe or endoscopic clips
  • Can follow up with a haemostatic powder
114
Q

What is the pharmacological management for upper GI bleeds

A

IV PPIs

  • Reduce rebleeding and mortality if given post-endoscopically (for 3 days) to high-risk patients who required endoscopic therapy
  • not beneficial pre-endoscope
115
Q

What advice is give to patients on:

Aspirin

NSAIDs

Clopidogrel

Warfarin

A

Aspirin: continue low dose aspirin once haemostasis is achieved and add PPI

NSAIDs: Stop

Clopidogrel: continue

Warfarin: difficult to achieve homeostasis therefore stop until haemostasis is achieved and then assess risks v benefit. Generally aim to restart as soon as possible

116
Q

Define varices

A

Dilated veins in the distal oesophagus/proximal stomach caused by elevated pressure in the portal venous system (typically from cirrhosis). They may bleed but no other symptoms

117
Q

Outline the pathophysiology of varices

A

With cirrhosis there is..

  • The liver is scarred and therefore blood won’t flow as easily through it and increase pressure
  • Also have increased portal inflow due to toxic excretions of the liver causing splanchnic vasodilation
  • Increased pressure in the portal circulation ie. splenic, portal, superior and inferior mesenteric veins
  • Portal vein drains into the liver which comes from splenic and mesenteric veins ie. the entire GI tract drains into the portal veins
  • Poor flow through the portal vein and vasodilation increases portal pressure causing oesophageal veins to dilate (varices)
  • Angiogenesis: production of more veins
118
Q

How are varices diagnosed?

How are bleeding varices managed?

A

Diagnosis: upper endoscopy

Managed:

Primary prophylaxis: beta-blockers or band ligation

Acute bleeding:

  • abx and terlipressin early in A&E
  • Band ligation 1st line for oesophageal variceal bleeding
  • TIPS for uncontrolled variceal bleeding
  • Balloon tamponade (temporary salvage)

Prevention of rebleeding: beta-blocker and repeated band ligation

119
Q

What is TIPS?

What does it do?

What is one risk of TIPS?

A

Transjugular Intrahepatic Portosystemic Shunt (TIPS

  • A shunt between the portal vein and hepatic vein
  • Without TIPS, blood has to pass through microcirculation of the liver and with all the scarring, the blood finds it difficult to flow through

Risk: encephalopathy

120
Q

What is the classical presentation of upper GI cancers?

A

An ulcer which will not heal

  • If an ulcer persists without definite, identifiable cause, think possible cancer
121
Q

List the layers of the oesophagus

A

Mucosa: non-keratinising stratified squamous epithelium and muscularis muscosa

Submucosa

Muscularis propria (2 types of muscle orientation)

Adventitia

122
Q

Outline the pathology of reflux oesophagitis

A
  • acid and digestive enzymes injury squamous epithelium lining oesophagus
  • inc. number of inflammatory cells- basal zone of the squamous epithelium is hyperplastic
123
Q

List 2 infections and 2 inflammatory conditions that can occur in the oesophagus

A

Infections:

  • Candida albicans (candida oesophagitis)
  • Herpes Simplex virus

Inflammation:

  • peptic oesophagitis / GORD (gastro-oesophageal reflux disease)
  • pills (eg. iron, bisphosphonates) can get stuck in the oesophagus, causing damage/ulceration of the lining
124
Q

Outline the pathology of candida oesophagitis

A
  • Active chronic inflammation
  • many neutrophils
125
Q

Which 2 conditions affecting the oesophagus occur more commonly in immunosuppressed patients?

A
  • Candida albicans
  • Herpes Simplex Virus
126
Q

Outline the histology/cytology of Herpes Simplex Virus in the oesophagus

A
  • atypical squamou cells
  • inflammatory exudate and cells slough
  • multi-nucleared giant cells with ground-glass nuclei in epithelial cells
127
Q

Define Barrett’s oesophagus

A

A pre-cancerous condition which is a complication of chronic GORD (gastro-oesophageal reflux disease) involving metaplastic changes to the epithelium that line the distal end of the oesophagus

128
Q

Outline the pathology of Barrett’s oesophagus

A
  • a metaplastic response to mucosal injury eg. from long-term GORD
  • pre-cancerous condition
  • squamous epithelium become glandular, usually intestinal with goblet cells
  • associated with development of benign strictures but also with adenocarcinoma
  • can progress to dysplasia then adenocarcinoma
  • dysplasia can be defined as low- or high-grade
129
Q

Outline the cell changes seen with low grade and high grade dyplasia as seen in Barrett’s oesophagus

A

Low grade

  • Polarity lost
  • nuclei are stratified

High grade

  • polarity lost
  • nuclei rounder and vesicular
  • prominant nucleoli
  • abnormal mitoses
  • necrosis
130
Q

What is the major complication of Barrett’s oesophagus?

A

Dysplasia can progress into adenocarcinoma

131
Q

What is the diagnosis and treatment for Barrett’s oesophagus

A

Diagnosis: screening

  • 4 biopsies taken

Treatment:

  • radiofrequent ablation (endoscopic treatment)
132
Q

What are the two cancer types seen in the oesophagus and list 2 risk factors for each

A
  • Squamous carcinoma: smoking and alcohol
  • Adenocarcinoma: GORD and obesity
133
Q

List 3 causes of acute and 3 causes of chronic gastritis

A

Acute:

  • Alcohol
  • Medication eg. NSAIDs
  • Severe trauma
  • Burns (may cause systemic upset)
  • Surgery

Chronic:

Autoimmune (destruction of parietal cells due to anutoantibodies to intrinsic factor therefore can’t absorb B12)

Bacterial (H. Pylori)

Chemicals eg. NSAIDs, bile reflux

134
Q

Outline the pathophysiology of autoimmune gastritis

A

Autoimmune destruction of parietal cells due to autoantibodies against intrinsic factor and parietal cell antibodies in blood

Leads to:

  • complete loss of parietal cells with pyloric and intestinal metaplasia
  • Achlorhydria (HCl absence in gastric secretions) leading to bacterial overgrowth
  • Hypergastrinemia (excess gastrin which stimulates HCl release) leading to endocrine cell hyperplasia / carcinoids (slow-growing neuroendocrine tumour)
  • Persistent inflammation which can lead to epithelial dysplasia and may lead to cancer
135
Q

Outline the pathophysiology of H. Pylori infection

A
  • H. pylori colonises gastric mucosa causing active chronic inflammation
  • H. Pylori inhabits the gastric glands and produces large amounts of urease (turning urea into ammonium) therefore neutralising the acid

After exposire to H. Pylori, the resulting gastritis can occur in 2 patterns:

  1. Antral-predominant gastritis: hypergastrinemia, hyperchlordria and duodenal ulceration
  2. Pangastritis (more commonly seen with chronic infection): hypochlorhydria, multifocal atrophic gastritis, intestinal metaplasia, cancer
    - In antral-predominant: the glands detect acidity to determine how much to secrete, and with H. pylori no longer detect acidity therefore more gastrin therefore HCl is produced, irritating the stomach and causing gastritis
    - Patients with high IL-8 tend to get pangastritis
    - Peptic ulceration is due to a combination of excess acid secretion and host effects: impaired mucosal defence (eg. NSAID interference with mucosal prostaglandin synthesis) and microbe factors
136
Q

List 3 complicatoins of peptic ulceration

A
  • haemorrhage
  • perforation
  • fibrosis (leading to stenosis)
  • melena (black tarry stools)
137
Q

Outline the pathophysiology of chemical gastritis

List 3 causes of chemical gastritis

A
  • few inflammatory cells
  • surface congestion oedema, elongation of gastric pits
  • reaction hyperplasia/atypia, ulceration
  • Seen in atrum

Causes:

  • Bile reflux
  • NSAIDs
  • ethanol
  • oral iron
138
Q

What is the major complication of pangastritis and antral-predominant gastritis

A

Pangastritis: cancer

Antral-predominant: ulceration

139
Q

What is the strong association with gastric cancer?

A
  • Chronic gastritis: H. Pylori or autoimmune
140
Q

Outline the morphology of gastric cancer

A
  • Atrophic musoca
  • Chronic inflammation
  • Intestinal metaplasia
  • Dysplasia

Classified into intestinal and diffuse

  • Diffuse: individual malignant cells with mucin vacuoles
141
Q

Outline 3 conditions that can be categorised under the umbrella term irritable bowel disease (IBD)

A

Ulcerative colitis

  • causes long-lasting inflammation and ulcers in the innermost lining of the colon (restricted to the colon)

Crohn’s disease

  • inflammation of the GI tract, anywhere from mouth to anus

UC and Crohn’s are both inflammatory colitis

Other forms of colitis eg. infective, ischaemic colitis

142
Q

Outline the epidemiology of IBD

A

Peak incidence: 16-24

Second peak in older generation

143
Q

What is the aetiology of irritable bowel disease

A

Combination of:

  • environment factors eg. diet
  • genetic disposition eg. inflammatory conditions
  • gut microbiome
  • host immune responses (innate, adaptive)
144
Q

Outline the presentation of infective colitis

Identify 2 clues in a patient’s history that may suggest infective colitis

A
  • short history of diarrhoea +/- vomiting
  • abrupt onset +/- resolution of synptoms
  • systemic upset and predominant fever

History:

  • travel
  • unwell contacts
  • immunocompromised
145
Q

Outline the investigations and treatment required for a patient with suspected infective colitis

A

Infections: stool culture (need 4 samples for 90% sensitivity)

Treatment:

  • clears spontaneously
  • treatment usually conservative if immunocompetent
146
Q

Outline the presentation of ischaemic colitis

A
  • Abrupt onset of pain and bloody diarrhoea +/- systemic inflammatory response syndrome (SIRS)

SIRS: two of

  • WCC <4 or >12
  • Temp <36 or >38
  • RR >20
  • HR >90

Hypoperfusion > embolic

  • Hypoperfusion causes segmental colitis
  • blood supply is compromised (usually @ splenic flexure)
147
Q

Outline the investigation and treatment for suspected ischaemic colitis

A

Investigation:

  • CT may show segmental colitis in watershed areas (regions of body receiving dual blood supply from most distal branches of 2 large arteries eg. splenic flexure
148
Q

Define acute severe colitis

What investigation is essential for severe colitis

A

>6 stools per day and systemic upset

Investigations: AXR and Endoscopy

AXR

  • Helps assess extent as severity
  • Megacolon: dianeter >5.5cm
  • Toxic megacolon: perforation / about to perforate. Megacolon and signs of systemic toxicity

Endoscopy

  • flexible sigmoidoscopy is safer and can still diagnose
  • useful for biopsies
  • need to be carried out within 72hrs (ideally 24hrs)
149
Q

Outline the acute and chronic changes with chronic IBD

A

Acute:

  • acute inflammation: inflammatory infiltrate helps determine if UC or Crohn’s
  • Ulceration (and depth of ulceration)
  • Loss of goblet cells
  • Crypt abscess formation

Chronic:

  • Architectural changes: shorter villi, doesn’t invade muscularis layer, can split dilate, brach
  • Paneth cell metaplasia: red granular cytoplasm
  • Chronic inflammatory infiltrate in lamina propria: plasma cells normally distributed superficially in mucosa, but with IBD there is loss of the gradient and plasma cells are seen throughout. Removes idea of infective colitis
  • Neuronal hyperplasia
  • Fibrosis
150
Q

Outline the clinical presentation of ulcerative colitis

A
  • Diarrhoea: often with blood/pus
  • Fever
  • Abdominal pain and cramping
  • Rectal pain and bleeding
  • Urgency to defecate
  • Weight loss and poor appetite
  • Fatigue
151
Q

Outline the histology of ulcerative colitis

A
  • inflammation confined to the mucosa
  • active component: prominent crypt abscess formation
  • degranded gland architecture, gland drop-out, dilation and branching
  • inflamed lamina propria: diffuse inc. in plasma cells and lymphocytes
152
Q

Outline the macroscopic and microscopic features of ulcerative colitis

A

Macroscopic:

  • Diffuse involvement of the colon
  • terminal ileum can be involved but generally only in severe cases where whole bowel inc. caecum is involved

Microscopic:

  • Crypt architectural changes generally very marked
  • little/no fibrosis
  • no granulomas
153
Q

Outline the treatment for ulcerative colitis

A

1st line - mesalazine (5-ASA)

  • effective in inducing remission
  • high dose controls UC quickly
  • topical or oral

2nd line - Azathioprine

  • used for severe relapse/freq. relapsing
  • requiring 2+ corticosteroid courses within 12m period
154
Q

Outline the treatment for acute severe ulcerative colitis

A

Treated with high-dose IV corticosteroids eg. methylprednisolone or hydrocortisone

  • Start early, don’t need to wait for stool culture

If stool freq >8/day or >3/day with CRP >45 - need colectomy or infliximab / ciclosporin

  • Infliximab: TNF-a monoclonal antibody
155
Q

Identidy 3 complications of ulcerative colitis

A

Malignancy (colorectal tumour)

Local complications:

  • haemorrhage
  • toxic dilation (ie. toxic megacolon)

Systemic complications:

  • Skin: erythema nodosum, pyoderma gangrenosum
  • Liver: cholangiitis
  • Eyes: iriitis, uveitis
  • Ankylosing spondylitis
156
Q

What is the commonest colorectal cancer?

A

adenocarcinoma

157
Q

Outline how an adenoma can develop into a carcinoma

A

Adenoma - benign tumour of glandular tissue

  • In hollow organs, the adenoma grows into the lumen: adenomatous polyp

Progressive acquisition/accumulation of mutations

  • Loss/mutation of TSGs occur early eg. TP53 (gene coding for P53)
  • P53 can stall the cell cycle at checkpoints allowing for DNA repair or to initiate apoptosis
  • Mutations of TSGs; point mutations or deletions
  • Activation of proto-oncogenes (eg. RAS genes)
  • Defective DNA repair: mismatch repair genes (eg. MSH2 and MSH6) can be mutated
158
Q

Outline high-grade and low-grade adenomatous dysplasia

A

High grade: characterised by very abnormal architecture with complex glands (joined, fused, brnached)

Low grade: abnormal nuclei, abnormal, mitotic cells with chromatin all bundled together

159
Q

What are the categories used to describe the architecture of adenomas

A
  • Villous (>80% mucosa is villous)
  • Tubulovillous
  • Tubular (<20% of mucosa is villous)
160
Q

List 3 risk factors for developing colorectal carcinoma

A
  • Presence of adenoma (size, number, villous)
  • History of IBD esp. ulcerative colitis
  • Family history eg. polyposis syndromes
161
Q

outline the histology of colon cancer

A
  • ulcerated surface
  • irregular gland architecture
  • pink, inflammatory material at the surfave
162
Q

Outline the features of bowel screening

A

qFIT testing (stool sample)

50-74yr olds every 2 years

+ve result goes to colonscopy

  • Helps pick up polyps before they progress to cancer
163
Q

List 2 risk factors for developing Crohn’s disease

A
  • smoking: stopping smoking reduces relapse rate, need for immunosuppression and surgery
  • peak incidence: 15-24yrs
164
Q

Outline the clinical presentation of crohn’s disease

A
  • abdominal pain
  • diarrhoea (watery > bloody)
  • weight loss
  • fistulae, abscesses (could be oropharyngeal, gastroduodenal)
  • fatigue
  • mouth ulcers
165
Q

Identify 3 extra-intestinal symptoms of crohn’s disease

A

Eyes: uveitis, episcleritis

Joints: sacroiliitis, inflammatory arthropathy

Skin: erythema nodosum, pyoderma gangrenosum

More complications than UC but less likely to develop cancer

166
Q

Outline the investigations for Crohn’s disease

A

Faecal calprotectin (useful to differentiate between IBD/IBS and assess activity in IBD)

MR/CT enterography (extraluminal activity)

Ileocolonoscopy and biopsy

167
Q

Outline the pathology of Crohn’s disease

A

GRANULOMAS

  • Significant proportion don’t have granulomas, but if present, it’s highly suggestive of crohn’s

Microscopy: transmural inflammation (loss of the 5-layer structure)

  • Inflammatory cells infiltrate from mucosa right through the muscularis layer
168
Q

Outline the treatment for Crohn’s

A

Azathioprine (DMARD)

  • maintenance of control
  • reducing course of corticosteroid

Methotrexate

  • induces remission, can be used for maintenance

Biologics

  • TNF-a antagonists: infliximab

Surgery

  • 70% lifetime risk of surgery
  • non-curative
169
Q

Compare and contrast the pathology of ulcerative colitis and crohn’s disease

A

Crohn’s: small and large bowel inflammation

UC: only large bowel involvement

Crohn’s: tends to involve prox. large bowel

UC: tends to extend from rectum and involve LHS of bowel

Crohn’s: patchy inflammation resulting in macroscopic ‘skip lesions’

UC: confluent, diffuse inflammation

Crohn’s: transmural, deeply ulcerating inflammation

UC: inflammation centred on mucosa

Crohn’s: granuloma’s present

170
Q

Outline the assessment of LFTs

A
  1. Look at ALP and ALT
    - elevated x10 ALT: hepatocellular injury
    - elevated x3 ALP: marker of cholestasis (produced from bile canaliculi)
  2. Look at GGT
    - Suggests biliary epithelial damage and bile flow obstruction
    - Elevated in response to damage or alcohol and drugs
    - ALP elevation in absence of elevated GGT: increased bone breakdown
  3. Jaundiced patient with normal LFTs
    - Isolated bilirubin elevation
    - Suggestive of pre-hepatic jaundice eg. Gilbert’s syndrome or haemolysis
171
Q

Outline the pathway of bilirubin following haem breakdown

A

Haem is broken down into iron and unconjugated bilirubin

  • Unconj. bilirubin is lipid soluble and transported to the liver to be conjugated (water soluble)
  • this then is taken to the colon where it becomes urobilinogen
  • 90% of urobilibogen is converted to stercobilin (brown) and excreted in faeces
  • 10% of urobilinogen is taken back to the liver and converted to urobilin (yellow) and excreted in urine
172
Q

Identify 2 causes of pre-hepatic jaundice and outline the changes of bilirubin and how this affects stool and urine

A

Pre-hepatic jaundice = increased RBC breakdown

  • Overwhelms conjugation process in the liver therefore have increased unconjugated bilirubin
  • Unconj. bilirubin isn’t water soluble therefore cannot enter urine so elevated levels have no affect on urine ie. normal urine
  • No bile obstruction (which would cause poor fat breakdown) therefore normal stool (rather than fatty, pale stools)

Causes: Gilbert’s syndrome and haemolytic anaemia

173
Q

Outline hepatic jaundice, the changes seen in bilirubin levels and the changes seen in stool and urine

Give two causes

A

Hepatic jaundice: hepatic injury (dysfunction of hepatocytes) therefore lose conjugation ability

  • Increase in unconjugated bilirubin

In cirrhotic livers, there is compression of intrahepatic portions, causing a degree of obstruction

  • Therefore, increase in inconjugated and conjugated bilirubin
  • Inc. in conjugated bilirubin - dark urine
  • Bile obstruction (only if cirrhosis) - fatty, pale stools

Causes: alcoholic liver disease

  • hereditary haemachromatosis
  • alcoholic hepatitis
  • hepatocellular carcinoma
174
Q

Outline post-hepatic jaundice, the changes seen in bilirubin levels and the changes seen in stool and urine

Give two causes

A

Post-hepatic jaundice: obstruction to biliary drainage

  • inc. in conjugated bilirubin - dark urine
  • bile obstruction - pale, fatty stools

Causes:

  • gallstones
  • cholangiocarcinoma
  • pancreatic cancer
175
Q

What causes dark urine and pale, fatty stools

A

Dark urine: increase in conjugated bilirubin

Pale, fatty stools: bile obstruction causing poor fat breakdown

176
Q

What is a procelain gallbladder and what is it’s primary cause?

A

Porcelain gallbladder: calcification of the gallbladder

Cause: excessive gallstones (the exact cause is unclear)

177
Q

What is Chilaiditi syndrome?

A

A rare condition in which a portion of the colon is abnormally located between the liver and diaphragm

178
Q

What is the pathopneumonic sign of colitis on CXR?

A

Thumbprinting

179
Q

Define pneumoperitoneum

What is it’s pathopneumonic sign?

A

Air in the peritoneual cavity

Pathopneumonic sign: Rigler’s sign (double-walled sign)

180
Q

What would calcification outside of the kidney suggest on CXR?

A
  • Calcified lymph node (TB)
  • Calcification of faecal material
181
Q

Outline the risk factors for a porcelain gallbladder

A

Fat

Forty

Fertile

Female

Fair (caucasian)

182
Q

How do you differentiate between Chilaiditi syndrome and pneumoperitoneum?

A

Both are seen as air under the right hemidiaphragm

Chilaiditi syndrome: air is held within a specific space (the colon) and is confined

Pneumoperitoneum: looks free and not within a particular space

183
Q

What is a hernia and how would it present

A

Hernia: abnormal protrusion of bowel through a weak spot in the abdominal muscles

Presentation:

  • a buldge that is painful, especially on coughing, bending over, laughing
184
Q

How do look for perforation radiologically?

A

CXR - 80% sensitive for free gas

CT used to confirm diagnosis and look for cause

185
Q

How do you look for bowel inflammation radiologically?

A

AXR useful for colitis

US for cholecystitis

CT first choice otherwise

186
Q

Define uroperitoneum

A

urine leakage into the peritoneal space

187
Q

What is the most common cause of free air in the abdomen?

A

Perforated ulcer

188
Q

If an obscured psoas muscle is identified on CXR, what would you want to think about?

A
  • Burst aneurysm (haemorrhage pushing on the psoas muscle)
189
Q

How would you look for obstruction radiologically?

How would the history help identify location of obstruction

A

Radiologically:

  • AXR
  • CT to look for cause

History:

  • More distal: pain, constipation and more distension
  • More proximal: pain, vomiting and less distension
190
Q

Identify 3 common causes of bowel obstruction

A
  • sigmoid volvulus (twists around it’s own mesentery
  • hernia
  • colon cancer
  • gallstone that erodes through GB into intestine
191
Q

What is the 1st choice imaging modality for ischaemia?

A

CT

192
Q
A

Phase 3 (12 decks)

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