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Gastroenterology Flashcards

Coeliac disease Primary biliary cholangitis & Primary sclerosing cholangitis

1
Q

What are the Dukes Staging System for Bowel Cancer?

A

Dukes A – tumour confined to bowel wall
Dukes B – tumour has gone through wall but not into nodes
Dukes C – tumour involving regional nodes
Dukes D – distant metastases are present

Dukes stage histologically affects prognosis – i.e. 90% alive at 5 years Dukes A, reducing to 10% for Dukes D.

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2
Q

Definition - Coeliac disease

A

Autoimmune condition - immune reaction caused by the exposure to gluten.
Leads to inflammation of the D2 small bowel (jejunum)

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3
Q

Where is the inflammation of the coeliac disease?

A

Jejunum - epithelial cells of intestine. Atrophy of intestinal villi and hypertrophy of crypt cells

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4
Q

When does coeliac normally present?

A

Early chlidhood but can present at any stage

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5
Q

What are the 3 main autoantibodies involved? (qhat is 3rd)

A

Anti-TTG & Anti- EMA (gliadin) & endomysium
Class: IgA.
Relate to disease activity - rise and fall depending on how active disease is.
(Deaminated gliadin peptide - less commonly found)

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6
Q

What is the main complication of coeliac?

think: which cells affected

A

Atrophy of intestinal villi

Effect: malabsorption of nutrients

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7
Q

How can coeliac patients present?

A

Low threshold needed for suspected cases. Many can be asymptomatic

Failure to thrive as children
diarrhoeas
fatigue
weight loss
mouth ulcers
anaemia secondary to iron, B12 & folate deficient
Dermatitis Herpetiformis
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8
Q

Coeliac disease: associated skin manifestation - location and characteristics

A

Dermatitis Herpetiformis

a pruritic, vesicular skin rash caused by IgA deposition in the papillary dermis.
Locations: trunk, elbows and knees

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9
Q

Rare neurological symptoms of coeliac disease

A

peripheral neuropathy
cerebellar ataxia
epilepsy

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10
Q

Which metabolic condition is coeliac closely associated with?

A

T1DM. All new diagnosis will undergo coeliac screen.

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11
Q

2 genes associated with Coeliac

A 
HLA DQ2 (most common)
HLA DQ8
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12
Q

How would IgA deficiency affect coeliac diagnosis? What instead?

A

Anti-TTG & Anti-EMA & endomysium- IgA. If deficient, false negative finding.
All immunoglobulin screen required for all patients.

IgG antibody tests instead (Anti-TTG & Anti-EMA) or endoscopy + biopsy

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13
Q

Expected histological findings - Coeliac biopsy

A

Atrophy of intestinal villi
Hypertrophy of crypt cells
Intraepithelial lymphocytic infiltration

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14
Q

Diagnosis of Coeliac Disease?

What is patient requirement for investigations?

A

All investigations must be done while patient is on gluten diet - to detect antibodies and

Test IgA levels -> Anti-TTG antibodies test
Endoscopy with intestinal biopsy

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15
Q

Complications - Coeliac disease (auto-immune conditions)

A

All autoimmune disease.

T1DM, thyroid disease, Autoimmune hepatitis, Primary biliary sclerosis, Primary sclerosing cholangitis

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16
Q

Complications - UNTREATED coeliac disease

A

Vitamin D deficiency & anaemia (quick manifestation)
Osteoporosis
ulcerative jejunitis
enteropathy associated T-cell lymphoma (lymphoma of small intestine - EATL)
non-Hodgkin’s lymphoma

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17
Q

Treatment - Coeliac disease

A

Lifelong gluten-free diet (curative)

If ingest gluten - relapse of disease

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18
Q

What is the underlying pathogenesis of PSC & PBC?

A

Cholestatic liver disease

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19
Q

What are the differences between Primary sclerosing cholangitis and Primary biliary cholangitis/cirrhosis?

A

Location: intrahepatic & extra hepatic bile duct vs intrahepatic ONLY
Autoimmune: immune mediated vs true autoimmune disease
USDA

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20
Q

What are the differences between Primary sclerosing cholangitis and Primary biliary cholangitis/cirrhosis?

A

Location: intrahepatic & extra hepatic bile duct vs intrahepatic ONLY
Autoimmune: immune mediated vs true autoimmune disease
USDA efficacy: can improve blood results but no proof to prolong progression of disease vs can improve prognosis

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21
Q

What is the imaging finding for PSC? What is the gold standard imaging for diagnosis

A

MRCP - Beads on a string appearance

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22
Q

Definiton - PSC

A

Chronic, progressive condition characterised by the inflammation and scarring of the intrahepatic and extrahepatic bile ducts

Leading to harden and strictures (narrowing) leading to bile obstruction

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23
Q

Prevalance - PSC

A

Rare - 6/100,00 (under-diagnosis),
Male: female 2:1,
Age peak 30-40,
80% associated with IBD (UC)

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24
Q

Pathophysiology - PSC

A 
Immune mediated (not true autoimmune),
Genetic predisposition (HLA B2 (more common) & HLA D3),
Disruption of biliary epithelial (iliac bacterial translocation leading to inflammation)

Chronic cycle of inflammation leading to more scarring -> cirrosis

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Prognosis & Complications - PSC
Average survival - 15 years from diagnosis. Cirrhosis of biliary duct Complications: cholangiocarcinoma (poor prognosis), hepatocellular carcinoma, gallbladder cancer, colorectal cancer & pancreatic cancer
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Presentation - PSC
50% asymptomatic at diagnosis. ``` Fatigue, fever, diarrhoea, non-specific upper abdominal pain, High bilirubin (jaundice, pruritus), fat soluble vitamin deficiency (ADEK), cirrhosis ```
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Diagnosis - PSC
Lab markers: ALP, AST/ALT, Auto- antibodies - Anti-smooth muscle & anti-nuclear antibodies, pANCA (80% of patients) Gold standard: MRCP (bead on the string)
28
Treatment - PSC
No definitive treatment 1. Liver transplants (high recurrence rate), 2. UDCA - limited effect on improving survival/ symptoms. 3. Cholestyramine (bile acid sequestrants) - relief pruritus. 4. Immunosupressants/ antifribrotics (cyclosporine, tacrolimus & methotrexate) - no significant improvement
29
Definition: PBC (primary biliary cholangitis)
Chronic, progressive autoimmune condition leading to destruction of small intrahepatic bile ducts True autoimmune condition
30
Prevalence: PBC
35/100,000 Male: female 1:9 - 1 in 1000 45 yr old women have condition Association with other autoimmune disease: celiac's, sjogren syndrome, thyroiditis. Theory: reduced immune tolerance leads to targeting of small interlobular bile ducts
31
__ antibody is thought to target lipoid acid, especially _ _ _ , on biliary epithelium in PBC
Anti-mitichrondrial antibodies | Pyruvate dehydrogenase E2
32
Prognosis - PBC
Slow progression and remission induced Average survival 15-20 yrs from diagnosis Complications: Hepatocellular carcinoma & osteoporosis
33
Complications - PBC
HCC, | Osteoporosis
34
What is the theory linking immune tolerance in middle aged women and PBC
Theory: reduced immune tolerance leads to targeting of small interlobular bile ducts. Leading to chronic inflammation and cirrhosis
35
Diagnostic Criteria - PBC
Must have at least 2: 1. Elevated ALP 1.5 x upper limit 2. Histological evidence - non suppurative chronic biliary duct destruction 3. Antimitochondrial Ab 1:40 titre (& antinuclear antibodies) Imaging - to exclude PSC & obstruction
36
Treatment - PBC
1. UDCA (ursodeoxycholic acid) - reduces toxicity to biliary epithelium -> decrease inflammation (40% cases resistant) 2. Obeticholic acid (if UDCA failed) - reduces bile acid synthesis and inflammation 3. Cholestyramine - systemic relief of itching 4. Liver transplant - last resort but 20% recurrence
37
Presentation - PBC
50-60% asymptomatic. Main symptoms: fatigue, pruritus Others: Jaundice, hyperpigmentation & Other auto-immune conditions
38
HPC questions for diarrhoea (4 weeks)
Type of stool: loose or watery. Mucus or blood present? Associated symptoms: fever, abdominal pain, nausea and vomiting (infection - gastroenteritis) bloating Triggers: recent travel, recent food Weight loss? Improvement in symptoms over the course? Previous episodes? - if recurrent, less likely to be infection
39
What is used to classify stool type?
Bristol stool chart
40
Defintion: diarrhoea
Passage of 3 or mroe loose/ liquid stools per day. Colour, difficult to flush away (steatorrhea - malabsorption), timing & blood bristol: 7
41
Link between hypothyroidism and streatorrhea
Thyroxine replacement. Hyperthyroidism can lead to steatorrhea.
42
Medication causing diarrhoea
Thyroxine - overdose, Omeprazole (PPI), Metformin
43
Findings on examiation
?Pain - location or general, guarding ?abdominal mass - malignancy ?dehydration or malnutrition - may need to stay in hospital
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Differential diagnosis - Diarrheoa - acute (4 weeks with no improvement) and first episode
Infection - Gastroenteritis IBD - > 2 weeks, Coeliac disease - less likely to be acute onset, IBS - 30 yr old women, Diverticular disease/ diverticulitis - very unlikely for 30.. more likely in > 50-60, colorectal cancer,
45
Investigation - Acute Diarrhoea
Stool sample - signs of infection (C. diff - bloody diarrhoea with Abx use), faecal calprotectin - shows inflammation of bowel, Ova and parasite (if recent hx of travel) Blood test - TFTs, FBCs/ U&Es/ CRP/ TFTs/ Bone profile Coeliac serology +/- OGD wtih D2 biopsy. AXR/cross sectional imaging - if suspected distended or obstruction Lower GI endoscopy - if no obvious cause
46
2 main types of LGI endoscopy
Flexible sigmoidoscopy (rectum to splenic flexure) or colonoscopy (rectum to caecum. TI)
47
Indications of LGI endoscopy (sigmoidoscopy and colonoscopy)
Sigmoidoscopy - rectal bleeding if <40 yrs or no CIBH, bowel scope at 55 yrs, diarrhoea in unwell patients, abnormal imaging & surveillance of pouch/stump (IBD/polyposis) Colonoscopy - iron deficiency anaemia, abnormality on imaging, LGI bleeding, concerns for colorectal cancer, IBD reassessment/surveillance, BCSP (bowel cancer screening program - 60 yrs)
48
Which sedations are normally used for endoscopy procedures
low dose midazolam and fentanyl
49
Possible risk - colonscopy
Discomfort Bleeding - rare Perforation - rare Incomplete procedure
50
What is used to diagnose IBS
Rome Criteria. Recurrent abdominal pain on average at least 1 day/week in last 3 months associated with 3 or more following criteria: 1. related to defecation, 2. associated with a change in frequency of stool, 3. associated with a change in form (appearance) of stool
51
What are the common LGI findings?
Infection, IBD, ICS colon cancer, diverticulitis, Coeliac disease
52
Acute Hepatitis vs cirrhosis: Definition
Acute inflammation of the liver with little/no fibrosis, nodular regeneration or distortion of lobular architecture Cirrhosis: extensive fibrosis, nodular regeneration and therefore distortion of lobular architecture
53
Acute hepatitis w/ necrosis: causes
1. Infection: most common - Hepatitis A. Other viruses causing hepatitis B,C&E, infective mononucleosis (EBV), CMV & yellow fever. Associated with septicaemia & leptospirosis. 2. Chemical poison: Carbon tetrachloride, vinyl chloride, ethylene glycol & similar solvents Toxic drugs: rifampicin & isoniazid, paracetamol, alcohol, halothane, methotrexate, chlorpromide & monoamine oxidase inhibitor 3. Pregnancy (rare)
54
Acute hepatitis: Prognosis & complication
If patient recovers, they will recover entirely Progressive necrosis affecting the entire liver can lead to fulminant hepatic failure/ acute massive necrosis can lead to hepatic coma
55
Wilson's disease: Pathology
Congenital: autosomal recessive disorder (Defect in ATP7B gene on chrom. 13) Excessive copper deposition in tissues causing metabolic abnormalities including increased copper absorption form small intestine and decreased hepatic copper excretion
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Wilson's disease: Symptom onset
Symptom onset: 10-25 years First sign: - Children: liver disease - Young adults: Neurological disease
57
Wilson's disease: Presentation from excess copper deposition
liver: hepatitis, cirrhosis Neurological: - basal ganglia degeneration: particularly in putamen and globus pallidus - speech, behavioural & psychiatric problems are often the first - also: asterixis, chorea, dementia, parkinsonism Kayser-Fleiscer rings Renal tubular acidosis (esp. Fanconi syndrome) Haemolysis Blue nails
58
Wilson's: Inx
Bedside: - Slit lamp -> Kayser-Fleischer rings - Increased 24 hr urinary copper excretion Bloods: Reduced total serum copper Gold-standard diagnostic: Confirmed by ATP7B in genetic analysis
59
Wilson's: Management
penicillamine (chelates copper): traditional first-line treatment Trientine hydrochloride: - Alternative chelating agent - may become first-line treatment in the future Tetrathiomolybdate: - newer agent that is currently under investigation
60
Achalasia: Pathology
Failure of oesophageal peristalsis and of relaxation of the LOS due to degenerative loss of ganglia from Auerbach's plexus i.e. LOS contracted, oesophagus above dilated.
61
Achalasia: Prevalence
Achalasia typically presents in middle-age and is equally common in men and women.
62
Achalasia: Presentation
typically variation in severity of symptoms Dysphagia: BOTH liquids and solids - heartburn - regurgitation of food - may lead to cough, aspiration pneumonia etc malignant change in small number of patients
63
Achalasia: Inx
oesophageal manometry - excessive LOS tone which doesn't relax on swallowing - considered the most important diagnostic test Barium swallow - shows grossly expanded oesophagus, fluid level - 'bird's beak' appearance chest x-ray - wide mediastinum - fluid level
64
Achalasia: Treatment
Pneumatic (balloon) dilation - increasingly preferred first-line option - less invasive and quicker recovery time than surgery patients should be a low surgical risk as surgery may be required if complications occur Surgical intervention with Heller cardiomyotomy - Should be considered if recurrent or persistent symptoms Intra-sphincteric injection of botulinum toxin is sometimes used in patients who are a high surgical risk Drug therapy (e.g. nitrates, calcium channel blockers) has a role but is limited by side-effects
65
Anal Fissure: Pathology
Longitudinal or elliptical tears of the squamous lining of the distal anal canal. Acute: < 6 weeks Chronic: > 6 weeks.
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Anal Fissure: Risk factors
Constipation IBD STI eg HIV, Syphillis, Herpes
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Anal fissure: Prevention
painful, bright red, rectal bleeding Around 90% occur on posterior midline. - if the fissures found in alternative locations then other underlying causes should be considered e.g. Crohn's disease
68
Anal Fissure: Management
Acute ( <1 week): Soften stool - Diet: high fibre diet with high fluid intake - bulk-forming laxatives (1st line): bran, ispaghula husks. Lactulose if not tolerated - Lubricants: petrolein jelly - topical anesthetics - analgesia Chronic - Continue acute management - 1st line: topical GTN - If not effective after 8 weeks: referral for sphincterotomy or botulinum toxin referral
69
Gastroenteritis: Causative pathogen and presentation
Escherichia coli: common in travellers, watery stool & abdominal cramps and nausea Giardiasis: prolonged & non-bloody diarrhoea Cholera: Profuse, watery diarrhoea. severe dehydration -> weight loss.not common in travellers Shigella: bloody diarrhoea with vomitting &abdom pain Staphylococcus aureus: severe vomitting & short incubation period Campylobacter: flu-like prodrome is usually followed by crampy abdominal pains, fever and diarrhoea which may be bloody. May mimic appendicitis Complications include GBS Bacillus cereus: Vomitting < 6hrs (rice) and diarrhoea > 6hrs Amoebiasis: gradual onset bloody diarrhoea, abdominal pain & tenderness lasting for several weeks
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Gastroenteritis: Incubation period of causative agents
1-6 hrs: Bacillus cereus (vomitting rice), Staphylococcus aureus 12-48hr: Salmonella, E.coli 48-72hr: Shigella, campylobacter > 7 days: A§moebiasis, Giardiasis

Medical Conditions (8 decks)

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