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GI Pathology Flashcards

1
Q

What is hereditary haemochromatosis?

A

An autosomal recessive disorder of iron metabolism leading to iron overload.

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2
Q

What causes hereditary haemochromatosis?

A

Mutation in the HFE gene - often a homozygous C282Y mutation.

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3
Q

What are the complications of hereditary haemochromatosis?

A 
Liver - cirrhosis
Skin - bronzing
Pancreas - diabetes
Heart - restrictive cardiomyopathy
Joints - arthritis
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4
Q

What causes iron deficiency anaemia (IDA)?

A

In young women - menstruation +/- pregnancy

In men and post-menopausal women - GI bleed until proven otherwise.

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5
Q

What is sideroblastic anaemia?

A

Disorder in which Eb take in iron but don’t convert it to haem (can be caused by an ALA-S2 mutation) hence there are large stores of iron bound to haemosiderin in mitochondria.

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6
Q

What are the causes and risk factors of peptic ulcer disease?

A

Causes

  • H. Pylori
  • NSAIDs
  • Zollinger-Ellison syndrome (gastrin secreting tumour)

Risk factors

  • Smoking
  • Alcohol excess
  • Radiation therapy
  • Stomach cancer
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7
Q

What are the effects of H. Pylori infection in the different parts of the stomach?

A

In the antrum - increased risk of peptic ulcers.

  • G cells are most abundant here.
  • H. Pylori produces urease which converts urea to ammonia.
  • The ammonia neutralises the environment, both allowing the bacteria to survive and also the G cells to detect a high pH, therefore gastrin production is stimulated.
  • This increases HCl volume –> increased ulcer risk.

In the body/pylorus - increased risk of gastric cancer.

  • Parietal cells are abundant here.
  • HCl is being neutralised and so can’t act on parietal cells are effectively.
  • This causes parietal cell atrophy and so increased risk of gastric cancer.
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8
Q

How do NSAIDs cause peptic ulcers?

A

Inhibit COX pathway, therefore inhibiting the production of PGs and so there is a decreased protection of the gastric mucosa.

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9
Q

How can H. Pylori be diagnosed?

A
  • C urea breath test
  • Stool test (H. Pylori antigen)
  • Serum test (blood, urine, saliva for antibody)
  • Biopsy (with histology or CLO test)
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10
Q

What is the C urea breath test?

A

Usually C14 isotope used to prevent radiation exposure.

  • Patient drinks a solution containing urea.
  • The urease in the stomach will break down the urea to ammonia and CO2.
  • They then breath out and C02 levels are measured.

HIGH CO2 - signifies H. Pylori infection

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11
Q

What is the CLO test?

A

Endoscopy is done and a biopsy is taken.
The biopsy tissue is then placed in a solution/gel of urease and pH indicator
- If H. Pylori is present, ammonia will be formed and the pH will increase.

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12
Q

When is a biopsy carried out to diagnose H. Pylori?

A

In patients over 55 or those with red flag signs.

  • dysphagia
  • signs of GI bleed (such as maleena)
  • persistent vomiting
  • weight loss
  • IDA
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13
Q

What does maleena suggest?

A

Upper GI tract bleed

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14
Q

How is peptic ulcer disease treated?

A

Lifestyle changes
- stop NSAIDs and smoking, increase exercise.

Pharmacology
- Triple therapy - PPI/H2R antagonist plus 2 antibiotics - amoxycillin, clarithromycin or metroniazadole.

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15
Q

What is the mechanism of action of PPIs, and an example of one?

A

Omeprazole

  • Inhibits the proton pump on parietal cells therefore decreasing the amount of H+ pumped into the lumen.
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16
Q

What is the mechanism of action of H2R antagonists, and examples of them?

A

Cimetidine and ranitidine.

Block the H2 receptor on parietal cells, therefore decreasing the amount of HCl.

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17
Q

How is the oesophagus normally protected from reflux?

A
  • UOS and LOS sphincters.
  • Intra-abdominal oesophagus (diaphragm helps close it)
  • Angle of His/flap valve (angle the oesophagus enters the stomach, forms a flap)
  • Secondary peristalsis
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18
Q

What can cause gastro-oesophageal reflux disease?

A

Impaired defences

  • Low LOS pressure
  • Hiatus hernia
  • Impaired peristalsis (and therefore clearance)
  • Transient lower oesophageal spasm

Increased offences

  • Increased intra-abdominal pressure (pregnancy/obesity)
  • Reduced gastric emptying
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19
Q

What is a hiatus hernia and their types?

A

Protrusion of the stomach through the diaphragmatic hiatus, into the chest.

Sliding - gastro-oesophageal junction slides through hiatus.

Rolling - fundus of stomach protrudes alongside GOJ through hiatus

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20
Q

How does the stomach protect itself from gastric acid?

A

Pre-epithelial

  • Mucous-HCO3 barrier
  • Surfactant - prevent water solue tble materials entering the epithelium
  • Rapid cell turnover.

Sub-epithelial

  • Good mucosal blood flow removing waste and supplying nutrients
  • PGs protect mucosa and help maintain blood flow.
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21
Q

What are the symptoms of GORD?

A

Most common - heartburn and acid regurgitation

Other - night wakening, dysphagia, chest pain

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22
Q

What are the complications of GORD?

A

Initially, oesophagitis - may cause strictures.

May progress to Barrett’s oesophagus - premalignant change of mucous from simple squamous to simple columnar.

This may then progress to an adenocarcinoma.

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23
Q

How can GORD be treated?

A

Prevention - lose weight, avoid smoking and alcohol, prop head up at night.

Pharmacotherapy

  • antacids
  • alginates
  • prokinetics
  • PPIs
  • H2R antagonists
  • surgery
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24
Q

What are the side effects of H2R antagonists?

A
  • Diarrhoea
  • Headache
  • Dizziness
  • Fatigue
  • Rash
  • Cimetidine may cause gynaecomastia and constipation.
  • Tachyphylaxis can also occur.
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25
Q

What is tachyphylaxis?

A

Rapid decrease to the response of a drug after long-term exposure to that drug.

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26
Q

What are the side effects of PPIs?

A 
Headache
Rash
Diarrhoea
Infections with C. Difficle
Interactions with cytochrome P450 (may interfere with warfarin)
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27
Q

What are antacids?

A

Generally Al and Mg salts that act as symptom control in mild disease.

  • they increase the pH of gastric secretions
  • they decrease pepsin activity
  • some bind bile salts
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28
Q

What are the side effects of antacids?

A

Al salts - constipation
Mg salts - diarrhoea

Some also have high Na and so should be avoided in renal and cardiac disease.

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29
Q

What do alginates do?

A

Often combined with antacids. Act as foaming agents and so create a mechanical barrier to stomach contents.

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30
Q

Give an example of pro kinetic drugs.

A

Metroclopramide
Domperidone
Erythromycin

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31
Q

What do prokinetic drugs do?

A

Increase gastric emptying and increase LOS pressure.

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32
Q

What are the side effects of prokinetic drugs?

A

Diarrhoea
Hyperprolactinaemia
Drowsiness

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33
Q

What surgical methods can be used to treat GORD?

A

Surgical fundoplication
- part of stomach wrapped round to create a tighter sphincter
Linx procedure
- beads around the sphincter

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34
Q

What is the difference between Crohn’s and UC with regards to the location and clinical presentation?

A

Distribution

  • Crohn’s - anywhere from mouth to anus
  • UC - large intestine - always rectum

Clinical Presentation

  • Crohn’s - patients are thin and potentially malnourished with diarrhoea and abdominal mass and pain
  • UC - patients usually have bloody diarrhoea, weight loss and pain
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35
Q

What is the distribution of inflammation in Crohn’s vs UC?

A

Crohn’s - skip lesions and asymmetrical inflammation

UC - uniform and symmetrical inflammation

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36
Q

What is the effect of UC and Crohn’s on the bowel wall thickness?

A

Crohn’s - thickened ‘cobblestone’ bowel wall - deep ulcers and swelling
UC - thin bowel wall - loss of vascular pattern

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37
Q

How does diet affect UC and Crohn’s?

A

Crohn’s - remission can be achieved with enteral feed, followed by exclusion diet.

UC - unaffected by diet

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38
Q

How does smoking affect UC and Crohn’s?

A

Crohn’s - associated with smokers

UC - associated with non-smokers

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39
Q

What is acute-postoperative ileus, and how long does it last on average in the small and large intestine?

A

Constipation and intolerance of oral intake in the absence of mechanical obstruction post-surgery (physiological).

  • Small intestine - 0-24 hours
  • Large intestine - 48-72 hours
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40
Q

What are risk factors of acute-postoperative ileus?

A 
Peri-operative opioids 
Peri-operative complications
Open surgery
Prolonged abdominal/pelvic surgery
Delayed enteral nutrition
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41
Q

What is Ogilvie’s Syndrome and its management?

A

Large bowel PNS dysfunction that is commonest post cardiothoracic/spinal surgery

Managed by gut rest, IV fluids, surgery and nasogastric/colonoscopic tubes.

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42
Q

What drugs affect colonic motility?

A

Decrease

  • Opiates
  • Anticholinergics
  • Loperamide (for diarrhoea)

Increase

  • Stimulant laxatives
  • Prucalopride (constipation)
  • Linaclotide (IBS constipation)
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43
Q

What can cause incontinence?

A

Excessive rectal distension

  • acute/chronic diarrhoea
  • chronic constipation

Anal sphincter weakness

  • muscle damage
  • damage to pudendal nerve
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44
Q

What can cause constipation?

A

Hirschrung’s Disease
- obstructive defecation

Rectocoele
- weakness in rectal wall –> prolapse

Anal fissure
- painful tear in anal canal

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45
Q

What is achalasia?

A

Failure of the LOS to relax –> dilated oesophagus with no peristalsis or synchronised contractions.

Food can be forced down with large amounts of water but regurgitation is common.

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46
Q

How can achalasia be treated?

A
  • Rigiflex balloon dilatation of LOS.
  • Laparoscopic Haller’s myotomy
  • Per oral endoscopic myotomy (POEM)
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47
Q

What is scleroderma?

A

A connective tissue disorder resulting in a weak LOS.

- Absent peristalsis and severe oesophagitis with really bad acid reflux.

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48
Q

What is Nutcracker’s Oesophagus and its symptoms?

A

Sphincters are normal but peristalsis pressure is too high.

Leads to dysphagia, odynophagia and chest pain.

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49
Q

What is diffuse oesophageal spasm?

A

Lower oesophagus contractions are too fast and aren’t synchronised.

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50
Q

What causes gastroparesis?

A

Can be idiopathic
Opiates
Post viral
Longstanding diabetes with microvascular disease.

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51
Q

What are the symptoms of gastroparesis?

A

Nausea and vomiting
Weight loss
Abdominal pain

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52
Q

How can gastroparesis be managed?

A

Diet - small meals frequently

Cure/manage underlying cause

Medication - pro kinetics

Endoscopic - Botulinum toxin injection to pyloric sphincter –> temp relaxation.

Gastric electrical stimulation - like a pacemaker - improves n&v

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53
Q

What is the most toxic part of gluten?

A

a-gliadin

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54
Q

Are females or males more likely to suffer from coeliac disease?

A

Females

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55
Q

What gene is the most commonly affected in coeliac disease?

A

HLA-DQ2

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56
Q

What other gene can give rise to coeliac?

A

HLA-DQ8

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57
Q

What is the infection hypothesis?

A

Infection with adenovirus 12 in genetically susceptible individuals may cause coeliac as the peptide on a-gliadin is similar to that within the E1b portion of the virus. This leads to cross-reactivity with a-gliadin and development of coeliac disease.

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58
Q

How can a-gliadin cause coeliac disease in genetically susceptible individuals?

A

Exposure to TTG (IgG and IgA) from damaged epithelium causes deamination of glutamine residues.
This enables bonding to HLADQ2 and activation of pro-inflammatory T cell response.

59
Q

How does coeliac disease present in infants?

A

Usually presents aged 4-24 months, after cereals have been introduced.
Impaired growth, diarrhoea, vomiting and abdominal distension.

60
Q

How does coeliac disease present in older children?

A 
Anaemia 
Short stature
Pubertal delay
Recurrent abdominal pain
Behavioural disturbance
61
Q

How does coeliac disease present in adults?

A 
Symptomatic - bloating, flatulence, diarrhoea
Chronic/recurrent IDA
Reduced fertility/amenorrhoea
Osteoporosis 
Nutritional deficiency
Neurological/psychiatric symptoms
Unexplained increased AST/ALT
62
Q

What histological changes occur in coeliac disease?

A

Loss of villous height (flat or short&broad)
Mucosal inflammation
Hypertrophy of crypts
Increased IEL and plasma cells.

63
Q

How can coeliac disease be diagnosed?

A

Serology - IgA and IgG
Endoscopy - scalloping and paucity of folds, mosaic pattern, prominent submucosal blood vessels.
Biopsy from distal duodenum (must be on gluten rich diet)

64
Q

What is the Marsh Classification and what does it determine?

A

The severity of inflammation.

Marsh 3a-3c shows mild atrophy-absence of villi.

65
Q

What diseases are associated with coeliac?

A

Dermatitis herpetiformis

Other AI diseases - T1DM, Addison’s, thyrotoxicosis

66
Q

What are complications of coeliac?

A

Functional hyposplenism

Osteoporosis

Refractory coeliac disease

Malignancy

  • Adenocarcinoma of small bowel
  • Enteropathy associated T cell lymphoma (EATL)
67
Q

What are the two types of refractory coeliac disease?

A

Type I - loss of villous height but normal immunophenotype

Type II - loss of villous height with abnormal immunophenotype

68
Q

What are other causes of villous atrophy?

A 
IgA deficiency
Crohn's 
Giardisis 
Lymphoma 
NSAIDs
69
Q

What are 3 types of diarrhoea in relation to their causes?

A

Secretory

  • high vol high secretions
  • enterotoxins, laxatives, congenital defects

Inflammatory

  • low vol high frequency
  • Crohn’s, IBD, UC, infectious diseases (salmonella, shigella)

Osmotic

  • high vol
  • laxatives, antacids, Orlistat (lipase inhibitor), pancreatic insufficiency
70
Q

What are the pathogenic mechanisms of diarrhoea?

A

Toxin mediated
- toxins produced prior to/after consumption

Damage to intestinal epithelial surface

Invasion across intestinal epithelial barrier

71
Q

What is the pathogenesis of bacterial gastroenteritis?

A

Release toxins and invasion.

72
Q

What is the pathogenesis of viral gastroenteritis?

A

Local invasion, cytopathic effects and cell destruction.

73
Q

What is the pathogenesis of protozoal gastroenteritis?

A

Invasion and secretory products.

74
Q

What are the 3 types of toxins and give examples of each.

A

Neurotoxins
- S. aureus and B. aureus

Cyotoxins
- E. Coli, shigella, H. Pylori

Secretory enterotoxins
- E. Coli, salmonella, shigella dysentery

75
Q

How can diarrhoea be classified with respect to time?

A

Acute, watery
Acute, bloody
Dysentery (blood and mucous)
Persistant (14 days+)

76
Q

Is n&v common in gastroenteritis?

A

Nausea is, vomiting isn’t - vomiting suggest pre-formed toxin (S. aureus or B. aureus) if there is a sudden onset within 6-12 hours.
Also may be norovirus.

77
Q

What late complications can occur in campylobacter infection?

A

Guillian-Barre syndrome

Reactive arthritis

78
Q

How does E. Coli 0157:H7 infect?

A

Produces shigella toxin, causing enterocyte death.

79
Q

What is the classical triad of conditions in haemolytic uraemic syndrome? What causes this?

A

Shigella toxin in the blood.

  • Acute renal failure
  • Thrombocytopenia
  • Microangiopathic haemolytic anaemia
80
Q

What is a life-threatening complication of C. Difficle infection?

A

Pseudomembrane colitis - pussy, swollen and infected colon.

81
Q

What antibiotics are prescribed to treat C. Diff infection?

A

Metroniazadole and vancomycin.

82
Q

What are non-intestinal manifestations of infectious diarrhoea?

A

Botulism (descending weakness)

Guillan Barre Syndrome (ascending weakness)

83
Q

Who should be prescribed antibiotics for infectious diarrhoea?

A

Those who are critically ill (sepsis), have significant co-morbidities, or in certain cases, such as C. Diff infection.

84
Q

What are the clinical signs of haemolytic uraemic syndrome?

A

Bloody diarrhoea, abdominal tenderness

Fever is rare.

85
Q

How is C. Diff infection detected?

A

C diff antigen + toxin test.

86
Q

What is Wilson’s Disease?

A

Inherited disorder of copper metabolism leading to deposition of copper in the liver, brain and tissues.

87
Q

What is a glycogen storage disease? What is the most common type?

A

Inherited metabolic disorders that leads to an absence or deficiency of the enzymes responsible for the breakdown of glycogen.

Type 1 - most common - deficiency of G-6-Pase, which can lead to anaemia.

88
Q

What is an OTC (ornithine transcarbamylase) deficiency and its effects?

A

Inherited disorder causing hyperammonaemia.

Ammonia affects NS and can cause confusion, failure to thrive and learning disabilities.

89
Q

What can occur in patients with hepatic mitochondrial damage?

A
  • Micro-vesicular steatosis
    due to inhibitor of B-
    oxygenation
  • Insufficient ATP generation
    due to interference with
    oxidative phosphorylation
  • Excess ROS with lipid
    peroxidation
    impairment of resp chain
  • Apoptosis
90
Q

Why can people show signs of mitochondrial dysfunction due to inherited enzyme deficiencies in adulthood?

A

Inter-current stress or disease can aggravate and cause the enzyme deficiency to have adverse effects.

91
Q

What can paracetamol overdose cause?

A

Glutathione depletion (important antioxidant) and cell death, resulting in acute hepatitis.

92
Q

What is centrilobular necrosis?

A

Necrosis of centrilobular tissue of the hepatic lobule - this is zone 3 therefore oxygenation is poor. Ischaemia affects this zone first.

93
Q

What can cause and aggravate centrilobular necrosis?

A

Cause

  • sepsis
  • shock-induced ischaemia
  • congestive HF
  • toxicity from drugs/poisons

Aggravate

  • malnutrition
  • infection
  • fasting
  • exercise
94
Q

What does a metabolic crisis often present as?

A

Mimics signs of sepsis.

  • severe vomiting and failure to thrive
  • recurrent vomiting episodes and encephalopathy with acidosis
  • progressive retardation or seizures with hepatomegaly
  • hepatomegaly with/without jaundice and failure to thrive or grow normally
95
Q

What are the biochemical findings of acute onset liver failure due to inherited metabolic disease?

A 
Hypoglycaemia
Metabolic acidosis
Elevated transaminases
Hyperammonaemia 
Prolonged prothrombin time
Decreased serum albumin 
Leucocytosis
Raised acute phase reactants
96
Q

What are the risk factors for gallstones?

A 
Female
Fat
Forty 
Fertile 
Fair (caucasian > non-caucasian)

Low fibre diet and IBD

97
Q

What types of gallstones can occur?

A

Cholesterol stones
- large, oval and solitary (single)

Bile pigment stones

  • multiple, irregular and hard
  • associated with chronic haemolysis

Mixed stones
- most common

98
Q

What events occur in the pathogenesis of gallstones?

A

Cholesterol supersaturation
- high levels of cholesterol cause supersaturation of bile.

Biliary stasis
- during periods of fasting/starvation

Increased bilirubin secretion

These processes often occur together.

99
Q

What is biliary colic and its signs and symptoms?

A

A gallstone impacted in the GB - usually in the neck or Hartmann’s Pouch.

Leads to epigastric/RUQ pain
Vomiting
Provoked by eating

100
Q

What is acute cholecystitis and its signs and symptoms?

A

Stone impacted in the GB leading to GB wall inflammation/oedema and development of bacterial infection.

Leads to pain, n&v, fever and abdominal tenderness.

101
Q

What is empyema?

A

Pus-filled GB

102
Q

What is a mucoceole?

A

Distension of the GB due to mucus

103
Q

What causes cancer of the gallbladder?

A

Recurrent episodes of gallstones without cholecystectomy leading to polyps and then primary GB cancer.

104
Q

What are the complications of gallstones in the common bile duct?

A

Post-hepatic obstruction jaundice.
Cholangitis (infection of bile duct)
Pancreatitis

105
Q

If jaundice is visible in the sclera, what does this suggest about total bilirubin levels?

A

> 30 umol/L

106
Q

If jaundice is visible in the skin, what does this suggest about total bilirubin levels?

A

> 100 umol/L

107
Q

What are normal total and conjugated bilirubin levels for adults?

A

Total - <21 umol/L

Conjugated - <7 umol/L

108
Q

What causes pre-hepatic jaundice?

A
  • Increased haemolysis - sickle cell anaemia
  • Tropical disease (yellow fever, malaria)
  • Side effects of quinine-based anti-malarials
109
Q

What is physiological jaundice of the newborn and how is it treated?

A

After birth, newborns must destroy foetal Hb and replace it with adult Hb. This increased haemolysis is too much for the undeveloped liver to cope with and so jaundice develops.

Treated by phototherapy.

110
Q

What is haemolytic disease of the newborn and how is it treated?

A

Rh incompatibility between the mother and foetus, leading to increased haemolysis.

Treated by high-dose phototherapy and blood transfusion

111
Q

What is a life-threatening side effect of haemolytic disease of the newborn?

A

Kernicterus - bilirubin crosses the immature BBB and is deposited in the basal ganglia and brainstem. May lead to brain damage if untreated.

112
Q

What can cause hepatic jaundice?

A

Impaired uptake of bilirubin.

Impaired conjugation of bilirubin.
- Gilbert’s

Impaired transport of conjugated bilirubin into bile canaliculi

  - Primary biliary cirrhosis 
  - Liver damage
113
Q

What is Gilbert’s Disease and what LFTs are indicative of this condition?

A

Impairment of bilirubin conjugation - decreased glucornyl transferase activity.

Increased unconjugated and decreased conjugated bilirubin.
Increased ALP

114
Q

Why can a person suddenly develop jaundice due to Gilbert’s Syndrome?

A

Jaundice is more pronounced when a person is tired, has been fasting, or has another illness (such as influenza)

115
Q

What is primary biliary cholangitis (PBC) and what LFTs/blood tests are indicative of this condition?

A

Autoimmune destruction of small bile ducts.

Increased IgM
Increased ALP
Increased ALP and GGT (cholestatic pattern)
Positive anti-mitochondrial Ab

116
Q

What is post-hepatic jaundice and its causes?

A

Obstruction of the cystic, hepatic or common bile duct.

Most common causes are:
- Pancreatic cancer in head of
pancreas
- Choledocholithiasis (gallstones)

Other causes:

  • Pancreatitis
  • Cholangiocarcinoma
  • Portal lymphadenopathy
  • Benign bile duct stricture
117
Q

What does non-painful jaundice suggest?

A

Head of pancreas cancer.

118
Q

What symptoms may occur if gallstones are present in the cystic duct?

A

Pain on eating lipids or proteins due to contraction of the GB.

119
Q

What symptoms may occur if gallstones are present in the common bile duct?

A

Steatorrhoea (fatty faeces)
Grey faeces (no bile means no stercobilin)
Post-hepatic jaundice

120
Q

What symptoms may occur if gallstones are present in the duodenal papilla?

A

Malnutrition
Acute pancreatitis

(plus steatorrhea, grey faeces, jaundice)

121
Q

What is crucial to remember when operating in patients with post-hepatic jaundice?

A

Vitamin K must be administered prior to surgery to prevent haemorrhage - lack of bile salts means fat-soluble vitamins can’t be absorbed as easily.

122
Q

How does urine look in those with hepatic and post-hepatic jaundice and why?

A

Dark urine due to conjugated bilirubin in urine.

123
Q

What do faeces look like in the 3 different types of jaundice?

A

Pre-hepatic and hepatic - normal

Post-hepatic - grey (lack of stercobilin)

124
Q

How can gallstones be diagnosed and treated?

A

Diagnosis - US +/- MRCP

Treatment
If cholangitis - antibiotics

If gallstones - ERCP (extracting stones with balloon)

To prevent recurrence - cholecystectomy

125
Q

What is acute pancreatitis?

A

An acute inflammatory condition caused by enzyme-mediated digestion.

126
Q

What can cause acute pancreatitis?

A 
Gallstones
Alcohol
Tumour
Steroids 
Mumps
Autoimmune
Scorpion venom
Hypercalcaemia/hyperlipidaemia
ERCP
Drugs
127
Q

What are the symptoms of acute pancreatitis?

A 
Pain
N&amp;v
Fever
Hypotension
Shock with multi-organ failure
128
Q

What are the biochemical feature of acute pancreatitis?

A

Increased amylase, lipase, elastase and triglycerides.

Decreased albumin and calcium

129
Q

What is chronic pancreatitis?

A

Irreversible pancreatic damage causing destruction of both endocrine and exocrine functions.

130
Q

What can cause chronic pancreatitis?

A 
Alcohol 
Repeated attacks of acute pancreatitis
Trauma
Hereditary 
Idiopathic
131
Q

What are the clinical signs of chronic pancreatitis?

A

Recurrent abdominal pain radiating to the back

Diabetes mellitus

Weight loss and steatorrhea (late signs of malabsorption)

132
Q

What tests are available for assessing pancreatic damage?

A 
Serum and urinary amylase
       - urinary to exclude 
         macroamylasaemia
Serum lipase 
       - more specific
133
Q

What can cause hyperamylasaemia?

A 
Pancreatitis
Pancreatic disease
Ectopic pregnancy 
Tumours
Drugs
Macroamylase
134
Q

What is macroamylase?

A

Complexes of amylase and IgA/IgG that can’t be filtered through the kidney and so show high amylase levels in blood.

135
Q

What pancreatic function tests are available?

A

Secretin-pancreozymin test

  • measures pancreatic enzymes
  • gold standard

Lundh test
- measures [bicarb], amylase or trypsin activity following a meal.

136
Q

What is the best marker of pancreatic insufficiency?

A

Faecal elastase <200 ug/g of stool.

137
Q

What are the causes of portal hypertension?

A

Pre-hepatic - portal vein thrombosis

Hepatic - PBC, cirrhosis

Post-hepatic - right HF, IVC obstruction

138
Q

What complications can occur due to portal hypertension?

A 
Varices
- internal oesophageal varices
- caput medusae 
- haemorrhoids
Ascites
Splenomegaly 
Hyper-dynamic circulation
Hepatic encephalopathy
139
Q

How can portal hypertension be diagnosed?

A
  • Duplex doppler US

- MRI/CT

140
Q

How can ascites be treated?

A

For ascites

  • restrict Na to <2g/day
  • diuretic therapy
  • paracentesis (directly removing fluid)
141
Q

How can varices be prevented?

A

Non-selective B-blockers such as propranolol.

142
Q

How is an acute variceal bleed managed?

A

1) Resuscitation
2) Urgent endoscopy to confirm diagnosis
3) Injection sclerotherapy/variceal banding
4) Vasoconstrictor therapy
5) Balloon tamponade

143
Q

How are recurrent variceal bleeds managed?

A

TIPSS
- transjugular intrahepatic porto-systemic shunt

DSRS
- distal spleeno-renal shunt

144
Q

How is end-stage liver disease treated?

A

Liver transplantation

GI Pathology (4 decks)

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