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Paediatrics (Y4) > 12- Paediatric Gastroenterology (2/2) > Flashcards

12- Paediatric Gastroenterology (2/2) Flashcards

1
Q

Inflamamtory bowel disease background

A

Inflammatory bowel disease is the umbrella term for the two main diseases that cause inflammation of the GI tract:
- Ulcerative colitis
- Crohn’s disease.

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2
Q

UC vs Crohns

A
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3
Q

pathophysiology of IBD

A

They both involve inflammation of the walls of the GI tract due to autoimmune activity and are associated with periods of remission and exacerbation.

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4
Q

RF for IBD

A
  • Age <30
  • Whites highest risk
  • Family history
  • Cig smoking
    -> Crohns
    ->UC- Non smoker
  • NSAIDs medication
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5
Q

general presentation of IBD

A

Suspect inflammatory bowel disease in children and teenagers presenting with perfuse diarrhoea, abdominal pain, bleeding, weight loss or anaemia. They may be systemically unwell during flares, with fevers, malaise and dehydration.

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6
Q

Extraintestinal manifestations of IBD

A

o Finger clubbing
o Erythema nodosum
o Pyoderma gangrenosum
o Inflammatory arthritis
o Primary sclerosing cholangitis (UC)

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7
Q

investigations for IBD

A
  • blood tests
  • stool tests
  • simple imaging
  • endoscopy
  • detailed imaging
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8
Q

blood tests for IBD

A
  • FBC- anaemia
  • U and E- deranged electrolytes due to AKI due to GI losses
  • CRP – active inflammation
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9
Q

stool tests for IBD

A
  • Stool cultures- exclude infective colitis
  • Faecal calprotectin- raised in active disease and negative in irritable bowel or IBD in remission, but not specific to IBD and shouldn’t be used if blood is present as the presence of blood requires further investigation
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10
Q

simple imaging for IBD

A

AXR
- Used less commonly but used if suspicion of toxic megacolon and can be useful to assess for proximal constipation
- Strings of kantour- Crohns
- Lead pipe colon- UC

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11
Q

endoscopy for IBD

A

OGD and colonoscopy- gold standard
- Flexible sigmoidoscopy- safest test in bloody diarrhoea
- Colonoscopy- needed to look for more proximal disease
- Capsule endoscopy- useful to view small bowel mucosa

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12
Q

detailed imaging for IBD

A
  • Acute complications
  • CT/ MRI enterography when looking for small bowel crohns, fistulas or to map the extent of small bowel crohns
  • MRI rectum is image perianal crohns
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13
Q

general managements for IBD

A
  • MDT
  • Monitor growth and pubertal development
    -> Dietician
    -> Careful steroid use
  • Management involves inducing remission during flares and maintaining remission when well
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14
Q

features of UC

A

Ulcerative colitis
Inflammatory bowel disease characterised by diffuse inflammation of the colonic mucosa
It affects the rectum and extends proximally : distal (proctitis), left sided (splenic flexure) and extensive (beyond splenic flexure)
- Can be up to 40 bloody stools a day
- Blood and mucous= affecting mucosa
- Weight loss -> inflammation uses a lot of calories and diarrhoea can make you lose appetite
- Mild lower abdominal pain
- Normal temp
- Painful red eye-? extraintestinal problem
- Nocturnal symptoms
- Urgency
- Tenesmus
- X-ray- lead pipe colon

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15
Q

pathophysiology of UC

A
  • Chronic inflammatory infiltrate of lamina propria
  • Crypt abscesses (Neutrophilic exudate in crypts)
  • Crypt distortion (bottom image)
    o Irregular shaped gland with dysplasia
    o Darker crowded nuclei
  • Reduced numbers of goblet cells
  • Pseudo polyps can develop after repeated episodes
    o Inflammation then healing
    o Nonneoplastic
    o More common in UC ( vs Crohns)
  • Loss of haustra
    o Inflammation reduces the appeared of haustra on imaging
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16
Q

loss of haustra in UC

A
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17
Q

features of crohns

A
  • Diarrheal – non bloody
  • Mildly anaemic
  • Low grade fever
  • Weight loss
    o Any inflammations stops us absorbing things-> diarrhoea -> weight loss
    o Osmotic pressure drawing water out into the lumen
  • Unlikely to have bleeding
    o Deeper but less widespread
  • Tender mass RLQ
    o Terminal ileum common site
  • Mild perianal inflammation -> fistulas and strictures
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18
Q

pathophysiology of Crohns

A
  • Skip lesions
  • Hyperaemia- red and inflamed
  • Mucosal oedema  cobblestones are oedematous
  • Transmural inflammation
    o Thickening of bowel wall
    o Narrowing of lumen
  • Granuloma formation -> pathognomonic for crohns
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19
Q

management of UC: inducing remission

A

Mild to moderate disease

  • First line: amino salicylate (e.g. mesalazine oral or rectal)
  • Second line: corticosteroids (e.g. prednisolone)

Severe disease

  • First line: IV corticosteroids (e.g. hydrocortisone)
  • Second line: IV ciclosporin
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20
Q

maintaing remission of UC

A
  • Aminosalicylate (e.g. mesalazine oral or rectal)
  • Azathioprine
  • Mercaptopurine
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21
Q

surgery for UC

A
  • Only affects colon and rectum therefore pan proctocolectomy will remove all disease
    o Permanent ileostomy or something called a J-pouch
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22
Q

Crohns inducing remission

A
  • First line: steroids e.g. oral prednisolone or IV hydrocortisone
  • Second line: immunosuppressant medication
    o Azathioprine
    o Mercaptopurine
    o Methotrexate
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23
Q

Crohns maintaining remission

A

First line:
* Azathioprine
* Mercaptopurine
Alternatives:
* Methotrexate
* Infliximab
* Adalimumab

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24
Q

surgery for Crohns

A
  • Resection not as useful as in UC due to Crohn’s being able to spread everywhere
  • When the disease only affects the distal ileum it is possible to surgically resect to prevent further flares
  • For strictures and fistulas
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25
Q

jaundice

A

clinical manifestation of increased bilirubin the blood
- Yellow discolouration of sclera and the skin

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26
Q

bilirubin metabolism

A

When Hb goes to the Spleen it is broken down into haem and globin
1) Globin
2) Haem
- Converted to biliverdin (unconjugated)
- Transported via albumin to the liver
- Liver conjugates bilirubin to make it water soluble
- Can enter entero- hepatic circulation
- Can travel down to duodenum and stay in the gut
- Oxidised to stercobilin – makes faecal matter brown
- Can go to the kidney and be excreted as urobilinogen

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27
Q

causes of jaundice

A

Pre-hepatic
Hepatic
Post-hepatic

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28
Q

pre-hepatic jaundice

A

1) Too much break down of HB –>haem
- Haemaglobinopathies
* Sickle cell
* Thalamasemia
* Spherocytosis
2) Haemolysis
3) Too much demand for liver e.g. newborn
4) Liver cant conjugate it all
5) Therefore some bilirubin is unconjugated

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29
Q

hepatic causes of jaundice

A
  • Liver function down (reduced hepatocyte function)
  • Reduced conjugating ability of the liver
  • Causes
    1) Chronic liver disease
    2) Acute liver damage
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30
Q

post-hepatic causes of jaundice

A
  • Any obstructive condition to the bile duct -> if any part of excretion pathway is obstructed e.g. gall stones
    - Most common jaundice
  • Type of bilirubin likely to be raised is conjugated -> water soluble -> goes through blood stream to the kidney
  • More bilirubin excreted by the kidney
  • Therefore discolouration of the urine
  • Dark urine, pale stools
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31
Q

causes of post-hepatic jaundice

A
  • Gall stones**
  • Inflammation which causes scarring or narrowing of the biliary tree
  • Enlargement of the head of the pancreas** (pancreatic carcinoma) ->painless jaundice (red flag)
  • Intrahepatic obstruction within the liver**
  • Inflammation/ oedema
  • Tumour e.g. hepatocellular carcinoma (compression locally)
    - Cirrhosis- no expansile
  • Compresses veins – portal hypertension
  • Also compresses bile ducts in liver
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32
Q

jaundice blood levels

A

> 25-30 mmol/L

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33
Q

jaundice in children

A
  • Rare outside neonatal period
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34
Q

presentation of jaundice in neonates

A
  • Yellow skin/ eyes
  • Dark urine
  • Fatty light poo
  • Itching
35
Q

types of jaundice in babies

A
  • unconjugated jaundice
  • intrahepatic (conjugated/unconjugated)
  • cholestatic
36
Q

unconjugated jaundice

A

Due to excess bilirubin production, impaired liver uptake, or conjugation.
Causes:
- Haemolysis (spherocytosis, G6PD deficiency, sickle cell anaemia, thalassaemia, HUS).
- Defective bilirubin conjugation (Gilbert syndrome, Crigler–Najjar syndrome).

37
Q

intrahepatic (conjugated/unconjugated) jaundice

A

Due to hepatic damage +/- cholestasis.

Causes
1) Infectious
* Viral, bacterial hepaitits
2) Toxic
* Paracetamol overdose
3) Metabolic
* Tyrosinaemia type 1
* Wilsons
* A1-antitrypsin deficiency
* Hypothyroidism
* Autoimmune hepatitis

38
Q

cholestatic (obstructive) jaundice

A

Due to bile tract obstruction
- Biliary atresia
- Primary sclerosing cholangitis (think IBD)
- Choecysitic
- Cystic fibrosis

39
Q

History and examination for jaundice

A

Full history
- Medication
- Fx
- Overseas travel, blood transfusion, pale stools, dark urine

Examination
- Vitals
- Conscious level
- Hepatic stigmata
- Pallor
- Hepatomegaly
- Splenomegaly
- Ascites
- Peripheral oedema

40
Q

bloods investigations for jaundice

A
  • FBC, blood film, reticulocyte count.
  • Coagulation studies.
  • U&E, SBR (total and conjugated), LFT, albumin, total protein, TFT.
  • Viral serology (hepatitis A, B, C, EBV, CMV), blood culture, leptospira and toxoplasma antibody titres.
  • IEM screen, ammonia, copper studies (serum copper increase, decrease, or normal, serum caeruloplasmin decrease in Wilson’s disease), blood glucose, A1-antitrypsin level, galactose-1-uridyl-phosphatase level.
  • Immunoglobulins, anti-nuclear antibody, smooth muscle and liver/ kidney antibodies (autoimmune hepatitis)
41
Q

imaging investigation for jaundice

A

Abdominal US, abdominal CT/MRI, biliary scintigraphy, e.g. hepatoiminodiacetic acid [HIDA] scan)

42
Q

Management of jaundice

A
  • Remove or treat underlying cause.
  • Correct blood glucose if it is low.
  • Correct any clotting abnormalities.
  • Phototherapy may be helpful only if jaundice has a significant unconjugated component, e.g. Crigler–Najjar syndrome.
  • Treat any associated anaemia if due to haemolysis.
  • Treat liver failure as appropriate.
43
Q

acute hepatitis background

A
  • General term for inflammation of the liver
  • Can be acute or chronic
44
Q

pathophysiology of acute hepatitis

A
  • Virus
    o ABCDE
  • Drugs
    o Overdose with paracetamol
    o halothane
    o Reyes syndrome (aspirin therapy)
  • Alcohol
  • Genetic disorders
    o Wilsons diseases
  • Autoimmune
    o May present with acute hepatitis
    o Rheumatoid, coeliac
45
Q

presentation of acute hepatitis

A
  • fever
  • fatigue
  • malaise
  • anorexia
  • nausea
  • arthralgia
  • right upper quadrant abdominal pain
  • jaundice +/– hepatomegaly
  • splenomegaly
  • adenopathy
  • urticaria
46
Q

presentation of acute hepatitis

A
  • fever
  • fatigue
  • malaise
  • anorexia
  • nausea
  • arthralgia
  • right upper quadrant abdominal pain
  • jaundice +/– hepatomegaly
  • splenomegaly
  • adenopathy
  • urticaria
47
Q

investigations for acute hepatitis

A
  • LFTs : raised AST/ALT (x2-100) and bilirubin
  • Decreased blood glucose
  • Viral serology
  • Blood culture
  • Paracetamol level
  • Serum immunoglobulin, complement (C3,4),
    positive autoimmune antibodies (anti-smooth muscle, anti-mitochondrial
  • Serum Copper, caeroluoplasmin, 24hrs urinary copper (Wilson disease)
48
Q

Hep A

A
  • Faecal oral/Food-borne
  • Spread through contaminated water and unwashed food
  • 2-6 wks incubation
  • Least likely to damage the liver
  • Usually mild and resolves within months
49
Q

Hep B

A
  • Blood born
  • Spread via contaminated blood, needles or bodily fluid
  • Mother to baby
  • Chronic disorder
    o Liver cancer
    o Cirrhosis
  • Vaccine, no cure
50
Q

Hep C

A
  • Blood born
  • Spread via contaminated blood, needles or bodily fluid
  • Mother to baby
  • 6 wks-6 months
  • Chronic disorder
    o Liver cancer
    o Cirrhosis
  • Cure, no vaccine
51
Q

Hepatitis D

A

Only found in those infected with hepatitis B

52
Q

Hepatitis E

A

o Faecal oral transmission
o Endemic in india

53
Q

other organisms that cause hepatitis

A

Other organisms
- Epstein barr visus (EBV: common in adolescents), TORCH organisms (neonatal hepatitis), HIV, CMV (immunocompromised)

54
Q

management of acute hepatitis

A
  • Alcohol avoidance in teenagers
  • ## Treat the cause
  • Antivirals (HepB not usually used unless fulminant or >12 yo
  • Fulminant (life threatening) will require referral to intensive care and possible liver transplantation
  • Maintain glucose if Reyes syndrome
  • Prevention Prophylactic vaccines for Hep B ad A
  • Post exposure prophylaxis pooled serum immunoglobulin for Hep A, CMB, Hep B
55
Q

antivirals used in chronic hepatitis

A

Interferon, entecavir, and tenofovir DF are recommended for treatment of chronic HBV

56
Q

long term risks of acute hepatitis

A

There is a long-term risk of:
- chronic hepatitis (HAV 0%; HBV 5–10%; HCV 785%);
- cirrhosis
- hepatocellular carcinoma (HBV and HCV);
- glomerulonephritis (circulating immune-complexes).

57
Q

Chronic liver failure background

A

Chronic liver failure is the result of long-term inflammation that leads to scarring of healthy liver tissues (fibrosis). Inability to:
- Synthesise clotting factors, albumin
- Breakdown bilirubin (jaundice)
- Storing glycogen
- Immune function etc
- Excretion of toxins

58
Q

causes of chronic liver failure

A
  • Chronic hepatitis (after viral hepatitis B or C).
  • Biliary tree disease, e.g. biliary atresia.
  • Toxin-induced, e.g. paracetamol, alcohol.
  • A1-antitrypsin deficiency.
  • Autoimmune hepatitis.
  • Wilson’s disease (age >3yrs).
  • Cystic fibrosis
  • Alagille syndrome or non-syndromic paucity of bile ducts.
  • Tyrosinaemia.
  • Primary sclerosing cholangitis.
  • PN-induced.
  • Budd–Chiari syndrome.
59
Q

presentation of chronic liver disease

A
  • Jaundice (not always)
  • GI haemorrhage
    o Portal hypertension and variceal bleeding
  • Pruritis
  • Anaemia
  • Enlarged hard liver
  • On-tender splenomegaly
  • Hepatic stigmata
60
Q

stigmata of decompensated liver disease

A

o Spider naevi
o Ascites
o Gynecomastia
o Palmar erythema
o Bleeding and bruising

61
Q

investigations for chronic liver disease

A
  • bloods
  • metabolic studies
  • abdominal IS
  • Uooer GI endoscopy
  • liver biopsy
  • EEG
62
Q

investigations for chronic liver disease

A
  • bloods
  • metabolic studies
  • abdominal IS
  • Uooer GI endoscopy
  • liver biopsy
  • EEG
63
Q

bloods for chronic liver disease

A
  • FBC (Hb decreased if GI bleeding, decreased WCC and platelets (hypersplenism)
  • LFT (increased bilirubin and AST/ALT (x2-10), albumin <35g/L)
  • Coagulation – prothrombin time increase
  • Decreased glucose
  • U&E (d Na+, d Ca2+, i PO43 –, increased alkaline phosphatase if biochemical rickets).
  • Viral serology or PCR for hepatitis B and C.
  • Increased IgG, d complement (C3, C4), autoimmune antibodies
64
Q

metabolic studies for chronic liver disease

A
  • Sweat test (cystic fibrosis); A1-antitrypsin level and phenotype.
  • Decreased Serum copper and caeruloplasmin (Wilson’s disease).
  • Increased 24hr urinary copper (Wilson’s disease).
65
Q

Abdominal US for chronic liver disease

A
  • Hepatomegaly.
  • Echogenic liver.
  • Splenomegaly.
  • Ascites.
66
Q

upper GI endoscopy for chronic liver disease

A
  • Oesophageal or gastric varices.
  • Portal hypertension related gastritis.
67
Q

liver biopsy in chronic liver disease

A
  • Histology, enzymes, electron microscopy
68
Q

why EEG in chronic liver disease

A

to confirm chronic encephalopathy if suspected

caused by ammonia build up

69
Q

management of chronic liver failure involves

A

TREAT UNDERLYING CAUSES

  • Nutritional support
    -Drug therapy
  • Oesophageal varices management
  • Ascited
  • Encephalopathy
  • Liver transplantation
70
Q

which scoring system is used to determine prognosis and treatment in chronic liver disease

A

Child Pugh

71
Q

nutritional support in chronic liver disease

A
  • Increase protein, increased energy, higher carbohydrate diet
  • Fat soluble vitamins ADEK
72
Q

drug therapy in CLD

A
  • Prednisolone +/– azathioprine for autoimmune hepatitis.
  • Interferon-A +/– ribavirin for chronic viral hepatitis.
  • Penicillamine for Wilson’s disease.
  • Colestyramine may be useful to control severe pruritis.
  • Vitamin K and FFP- coagulopathy
73
Q

oesophageal varices management in CLD

A

Endoscopy I.e. sclerotherapy or surgery

74
Q

management of ascites in CLD

A
  • Fluid and Na+ (salt) restriction (2/3 maintenance and 1mmol/kg/day, respectively)
  • Spironolactone (1-2mg/kg 12 hourly)
  • Consider IV 20% albumin if ascites is resistant
75
Q

management of encephalopathy

A

Reduce GI ammonia absorption by oral or rectal lactulose, neomycin or soluble fibre pectin

76
Q

liver transplantation and CLD

A

e.g. for Wilsons and Alpha1-antitryspin deficiency

77
Q

Alpha1 -antitrypsin deficiency
Background

A

Alpha1-antitrypsin is a serum protease inhibitor responsible for control- ling inflammatory cascades.

  • It is the commonest genetic cause of liver disease in children, with autosomal dominant inheritance.
  • Prevalence is 1:2000 to 1:7000.
  • Genetic variants are identified by enzyme electrophoretic mobility as medium (M), slow (S), or very slow (Z).
    –> S is associated with 760% Alpha1-antitrypsin level of normal;
    –> Z 715%.
  • Normal genotype is designated PiMM. Only PiZZ individuals are at risk of liver disease.
78
Q

presentation of alpha1-antitrypsin defieciency

A
  • Cholestasis in infancy, may progress to liver failure.
  • Cirrhosis can occur in late childhood to adult. Chronic liver disease affects 25% of patients in late adulthood.
  • Pulmonary emphysema is the commonest presentation in adulthood
79
Q

pathophysiology of AAT

A

deficiency of AAT leads to reduced inhibition of neutrophil elastase and inflammation-mediated destruction of alveolae.

80
Q

investigations for AAT

A

Diagnosis
* Serum A1-antitrypsin level decreased
* Phenotyping by enzyme isoelectric focusing

81
Q

management of AAT

A
  • Supportive treatment of liver complications.
  • Strongly advise against smoking.
  • Liver transplant for end-stage liver failure.
82
Q

Wilsons disease Background

A

A rare autosomal recessive disorder leading to toxic accumulation of cop- per in the liver and, subsequently, other tissues especially the brain and eye.

83
Q

presentation of wilsons

A
  • Kayser–Fleischer rings (copper deposition in Descemet’s membrane of the eye)
  • Hepatic problems usually present in childhood (hepatitis, cirrhosis, fulminant hepatic failure).
  • Adolescents/young adults usually present with neurological disease.
84
Q

investigations for Wilsons

A
  • Serum copper and caeruloplasmin d.
  • 24hr urinary copper excretion >100microgram (normal <40microgram).
  • Molecular genetic testing—Wilson’s disease gene (ATP7B) mutation.

Paediatrics (Y4) (42 decks)

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