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RCPCH TAS/ AKP > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Features of Osmotic Diarrhoea + causes

A

Excess osmotically active particles in bowel.
Stops when fasted.
Causes: Laxatives (lactulose), malabsorption, damage to mucosa, motility disorder (eg hyperthyroid)

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2
Q

Features of Secretory Diarrhoea + causes

A

Bowel mucosa secretes excess water into the lumen.
Continues when fasted.
Causes: Cholera toxin, electrolyte transport disorders or congenital microvilli atrophy.

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3
Q

Features of Exudative diarrhoea

A

Alteration to membrane permeability and serum proteins –> blood and mucus into lumen, small stool amounts

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4
Q

Causes of Cholera + presentation

A

Vibrio Cholerae
Due to ingestion of contaminated food / water
Secretory diarrhoea - “rice water stools”

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5
Q

Presentation of laxative abuse

A

Weight loss and chronic diarrhoea
Colonoscopy - brown pigementation = melanosis coli due to lipofuscin

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6
Q

How does congenital glucose-galactose malabsorption cause diarrhoea?

A

Recessive –> dysfunction of SGLT1
Impaired uptake of glucose / galactose
Osmotic diarrhoea and life threatening dehydration

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7
Q

Infections that can cause acute liver failure

A
  • <6 months: Sepsis, Hep B, Adenovirus, echovirus, Coxsackie B, HSV
  • > 6 months: Hep A / B / E, EBV, Parvovirus B19
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8
Q

Mechanism of transmission Viral Hepatitis A - E

A

Hep A - Faecal-oral
Hep B - Perinatal / inoculation / sexual
Hep C - Vertical transmission, blood transfusion
Hep D - Depends on Hep B
Hep E - Contaminated water / pork

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9
Q

Viral Hepatitis treatment

A

Hep A - vaccinate contacts.
Hep B - Interferon, entecavir. Vaccine / IVIg if high risk
Hep C - PEG interferon, ribavarin

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10
Q

Serology acute Hep B infection

A

Positive: HbcAb IgM/ IgG, HbsAg, HBeAg
Negative: Anti-HBs, Anti-HBe
High HBV DNA titre

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11
Q

Serology Chronic Hep B infection

A

Positive: HbcAb IgG, HbsAg
Low DNA titre

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12
Q

Serology Hep B vaccination

A

Anti-Hbs only

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13
Q

Serology Cleared Hep B infection

A

Positive: HbcAb IgG, Anti-Hbs

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14
Q

Features of 2 types of food allergy

A

IgE mediated: Eg milk, nuts. Reaction within mins. 1st exposure –> sensitising event.
Non-IgE mediated: eg milk, coeliac. Delayed, N+V, food aversion, faltering growth

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15
Q

What is neonatal haemachromatosis?

A

Alloimmune disorder –> abnormal maternal Ab reaction to foetal liver
Accumulation of iron in liver
Dx: Iron storage outside the liver - salivary glands, pancreas, brain

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16
Q

Features of autoimmune liver disease

A

Rare in children. 3/4 female.
Genetic predisposition - HLA B8/DR3
AI - Activation of inflammatory response –> cytokine release –> macrophage activation –> hepatocellular lysis
AI response to parenchyma = AI hepatitis
AI response to biliary tree = Sclerosing Cholangitis
Anti-smooth muscle antibody
Tx: Steroids, DMARDs, ?transplant

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17
Q

Hepatotoxic drugs

A

Paracetamol
Sodium valproate
Indomethacin
NSAIDs
Abx
Anti-epileptics

18
Q

Pathophysiology of Wilson’s Disease

A

Autosomal recessive - mutation to ATP7B
Reduced converstion apoceruloplasmin to ceruloplasmin
Oxidative damage to cells and accumulation in liver, kidneys, brain
Presentation: Neuro-psych, liver/renal failure

19
Q

Investigation and treatment of Wilson’s Disease

A

Ix: Liver biopsy, pencillilamine challenge –> urinary copper, low serum ceruloplasmin and copper
Tx: Penicillamine / zinc acetate (copper chelator)
+/- liver transplant

20
Q

Pathophysiology Alpha-1-antitrypsin deficiency

A

Autosomal recessive. Defect to SERPINA-1 gene.
Intracellular accumulation of misfolded A1A protein within the hepatocyte endoplasmic reticulum (ER), thus inhibiting its secretion.
Ultimately, this accumulation can result in liver cell injury and death. Increased risk of cancer.
Also lung tissue injury due to uninhibited neutrophil elastase
Presentation: Hepatitis and liver failure, lung disease

21
Q

Investigation and management of alpha-1-antitypsin deficiency

A

Ix: Low plasma alpha-1-antitripsin
Tx: ?liver transplant

22
Q

Features and treatment of fatty liver disease in children

A

Accumulation of fat in hepatocytes
Causes: Methotrexate, PCOS, Turner’s, obesity
Presentation: hepatomegaly and mildly deranged transaminases
Tx: Diet and exercise

23
Q

Presentation hepatoblastoma

A

More <4y
Associations: FHx, Beckwith-Wiedemann, FAP, glycogen storage disorder
Palpable mass, abdo distention, weight loss, vomiting, jaundice
Raised alpha-fetoprotein

24
Q

What is Gilbert’s syndrome and how does it present?

A

AR
Reduced bilirubin glucuronidation
Sx: Transient eps unconjugated jaundice

25
Q

Most common site for intussusception

A

Small bowel - ileocaecal valve

26
Q

What dose stool reducing substances test for?

A

Presence of malabsorption of lactose, fructose and galactose

27
Q

What is short gut syndrome and what are the consequences?

A

Absence of large section of small intestine leading to malabsorption
1. Osmotic diarrhoea
2. Malabsorption –> faltering growth and bile salt depletion, depletion fat soluble vitamins
3. Steatorrhoea
4. Renal oxalate stones
5. Bile salt depletion –> gallstones

28
Q

Which are fat soluble vitamins?

A

A
D
E
K

29
Q

Effects of Vit B12 deficiency

A

Macrocytic anaemia
Demyelinating neuropathy
Pernicious anaemia = lack of intrinsic factors –> not able to absorb B12

30
Q

Vitamin A deficiency presentation

A

Eyes - night blindness, dry, corneal opacification
Growth failure
Immune dysfunction
Thickened skin

31
Q

Presentation of Vit E deficiency

A

Axonal degeneration
Progressive neuropathy
Retinopathy

32
Q

Histology findings in coeliac disease

A

Crypt hypertrophy
Villous atrophy
Intra-epithelial lymphocytosis
Glandular hyperplasia

33
Q

What genetic finding is associated with Coeliac disease?

A

HLA-DQ2/8

34
Q

Serology in coeliac disease

A

IgA Anti-TTG
Low IgA
IgA EMA

35
Q

Crohn’s histology

A

Skip lesions
Patchy erosions / ulcers
Fissures and fistulas
Increased lymphocytes
Transmural inflammation with multiple lymphoid aggregates and granulomas
Abnormalities ‘mouth to anus’

36
Q

UC histology

A

MUCOSA MOST AFFECTED
Changes in colon only
Changed crypt architecture
Chronic inflammatory cells in lamina propria - lymphocytes and plasma cells

37
Q

Treatment of IBD

A

1st line = 6-8 weeks exclusive flavoured polymeric formula diet
Steroids
Immunosuppression

38
Q

What blood results are you likely to see in pyloric stenosis?

A

Low chloride
Low potassium
Low sodium
Metabolic alkalosis

39
Q

Cow’s milk sensitive enteropathy histology in distal duodum

A

Patchy eneropathy
Mild disturbance of crypt villous architecture.
Raised mucosal lymphocyte and eosinophil

40
Q

Eosinophilic oesophagitis treatment if severe

A

Oral elemental diet

41
Q

Definition of GORD on pH studies

A

Probe in LO, monitors pH over 24 hours.
Reflux ep. pH <4 for at least 15 secs.

RCPCH TAS/ AKP (20 decks)

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