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Gastroenterology Flashcards

Coeliac disease Primary biliary cholangitis & Primary sclerosing cholangitis

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USMLE® Step 1 flashcards
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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25
Q

Prognosis & Complications - PSC

A

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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26
Q

Presentation - PSC

A

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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27
Q

Diagnosis - PSC

A

Lab markers: ALP, AST/ALT, Auto- antibodies - Anti-smooth muscle & anti-nuclear antibodies, pANCA (80% of patients)

Gold standard: MRCP (bead on the string)

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28
Q

Treatment - PSC

A

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
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29
Q

Definition: PBC (primary biliary cholangitis)

A

Chronic, progressive autoimmune condition leading to destruction of small intrahepatic bile ducts

True autoimmune condition

30
Q

Prevalence: PBC

A

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
Q

__ antibody is thought to target lipoid acid, especially _ _ _ , on biliary epithelium in PBC

A

Anti-mitichrondrial antibodies

Pyruvate dehydrogenase E2

32
Q

Prognosis - PBC

A

Slow progression and remission induced
Average survival 15-20 yrs from diagnosis

Complications: Hepatocellular carcinoma & osteoporosis

33
Q

Complications - PBC

A

HCC,

Osteoporosis

34
Q

What is the theory linking immune tolerance in middle aged women and PBC

A

Theory: reduced immune tolerance leads to targeting of small interlobular bile ducts. Leading to chronic inflammation and cirrhosis

35
Q

Diagnostic Criteria - PBC

A

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
Q

Treatment - PBC

A
  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
Q

Presentation - PBC

A

50-60% asymptomatic.

Main symptoms: fatigue, pruritus

Others: Jaundice, hyperpigmentation
& Other auto-immune conditions

38
Q

HPC questions for diarrhoea (4 weeks)

A

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
Q

What is used to classify stool type?

A

Bristol stool chart

40
Q

Defintion: diarrhoea

A

Passage of 3 or mroe loose/ liquid stools per day. Colour, difficult to flush away (steatorrhea - malabsorption), timing & blood
bristol: 7

41
Q

Link between hypothyroidism and streatorrhea

A

Thyroxine replacement. Hyperthyroidism can lead to steatorrhea.

42
Q

Medication causing diarrhoea

A

Thyroxine - overdose,
Omeprazole (PPI),
Metformin

43
Q

Findings on examiation

A

?Pain - location or general, guarding
?abdominal mass - malignancy
?dehydration or malnutrition - may need to stay in hospital

44
Q

Differential diagnosis - Diarrheoa - acute (4 weeks with no improvement) and first episode

A

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
Q

Investigation - Acute Diarrhoea

A

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
Q

2 main types of LGI endoscopy

A

Flexible sigmoidoscopy (rectum to splenic flexure) or colonoscopy (rectum to caecum. TI)

47
Q

Indications of LGI endoscopy (sigmoidoscopy and colonoscopy)

A

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
Q

Which sedations are normally used for endoscopy procedures

A

low dose midazolam and fentanyl

49
Q

Possible risk - colonscopy

A

Discomfort
Bleeding - rare
Perforation - rare
Incomplete procedure

50
Q

What is used to diagnose IBS

A

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
Q

What are the common LGI findings?

A

Infection, IBD, ICS colon cancer, diverticulitis, Coeliac disease

52
Q

Acute Hepatitis vs cirrhosis: Definition

A

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
Q

Acute hepatitis w/ necrosis: causes

A
  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
Q

Acute hepatitis: Prognosis & complication

A

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
Q

Wilson’s disease: Pathology

A

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

56
Q

Wilson’s disease: Symptom onset

A

Symptom onset: 10-25 years

First sign:

  • Children: liver disease
  • Young adults: Neurological disease
57
Q

Wilson’s disease: Presentation from excess copper deposition

A

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
Q

Wilson’s: Inx

A

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
Q

Wilson’s: Management

A

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
Q

Achalasia: Pathology

A

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
Q

Achalasia: Prevalence

A

Achalasia typically presents in middle-age and is equally common in men and women.

62
Q

Achalasia: Presentation

A

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
Q

Achalasia: Inx

A

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
Q

Achalasia: Treatment

A

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
Q

Anal Fissure: Pathology

A

Longitudinal or elliptical tears of the squamous lining of the distal anal canal.

Acute: < 6 weeks
Chronic: > 6 weeks.

66
Q

Anal Fissure: Risk factors

A

Constipation
IBD
STI eg HIV, Syphillis, Herpes

67
Q

Anal fissure: Prevention

A

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
Q

Anal Fissure: Management

A

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
Q

Gastroenteritis: Causative pathogen and presentation

A

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

70
Q

Gastroenteritis: Incubation period of causative agents

A

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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