Common GI Disorders Flashcards
What are common GI disorders?
Diarrhoea Vomiting Upper GI bleed Irritable Bowel Syndrome (IBS) Inflammatory Bowel Disease (IBD) Ulcerative Colitis (UC) Crohns Disease Coeliac Disease Lactose intolerance
What are common causes of diarrhoea?
- Purgatives (MgSO4), malabsorption=e.g ↑glucose, specific
absorptive defect e.g disaccharidase deficiency/lactose intolerance
Secretory:
- Enterotoxins e.g cholera, hormones e.g VIP, metabolites e.g
5HIAA, some laxatives e.g phenolphthalein
Inflammatory
- Damage to intestinal mucosa e.g UC/Crohn’s & infective e.g Shigella
(Dysentary)
What are the biochemical implications of Diarrhoea?
Loss of bicarb: lower GI losses = can cause metabolic acidosis
Dehydration : ↑Urea
Electrolyte disturbances – esp ↓K & ↓Mg
Usually ↓K=↑HCO3 (alkalosis), but in diarrhoea you see ↓K & ↓HCO3
Ix & Rx underlying cause
What are the biochemical implications of vomiting?
Upper GI losses:
- Loss of acid= ↑bicarb, ↓Cl =metabolic alkalosis
- Dehydration can result in low K (2°Hyperaldosteronism - If you’re dehydrated you try to hold on water, reabsorb salt, excrete potassium)
What are the biochemical implications of an upper GI bleed?
Red blood cells released and reabsorbed
↑K (from intracellular release)
↑Urea from protein metabolism (different to raised urea from dehydration, where the Na is also affected)
↑urea:creatinine
What is the nature of IBD/IBS?
Irritable bowel syndrome:
- bowel disorder with no detectable organic cause
- Diagnosis of exclusion
Inflammatory bowel disease:
- Crohn’s:
- Can affect any part of GI tract from mouth to anus
- Most commonly starts in terminal ileum
- Ulcerative colitis:
- Restricted to colon and rectum
- Diagnosis : appearance (endoscopy), symptoms & pattern of
inflammation
- Serology:
- Crohn’s: S. cerevisiae Ab +ve, pANCA Ab –ve
- UC: S. cerevisiae Ab -ve, pANCA Ab +ve
How is an IBS and an IBD diagnosis differentiated?
IBS: Calprotectin NEGATIVE
- calprotectin is a calcium binding protein found in high concs in
neutrophils, with antimicrobial activity.
- During an infection, the inflammation process causes neutrophils to
get localised to the affected area - calprotectin is released from
neutrophils.
- This is not necessary in IBS, but is in IBD, so its presence is a
differentiation tool.
IBD:
- Chron’s : calprotectin POSITIVE
- UC: calprotectin POSITIVE
- Is a monitoring test , not a diagnostic tool as it allows a
gastroenterologist to differentiate whether someone is having a IBS or
IBD flair up as often people suffer from both.
What is coeliac disease?
Gluten sensitive enteropathy
Wheat protein containing gliadin
Gliadin metabolised by tissue transglutaminase
Autoimmune disease
Upon exposure to gliadin → immunological response (affecting the vili) to tissue transglutaminase (& endomysial) [IgA’s - in case someone has an IgA deficiency - if so willl di an IgG test]
Screened by ELISA
Histology to confirm
Must stay on wheat containing diet
throughout diagnosis
What is lactose intolerance?
Lactase deficiency: Most often seen in children Inability to digest lactose Genetic or environmentally induced Bacteria ferment lactose in colon Produce gases and osmotic diarrhoea
Tests:
Faecal reducing substances/TLC
Stool pH (<5.5 - sign of bacterial fermentation)
Lactose tolerance test/ H breath test
Looking for production of any compounds that are reducing sugars
- lactose ———> glucose + galactose (via lactase)
What are common liver disorders?
Alcohol:
- Fatty liver
- Hepatitis
- Cirrhosis
Non-alcoholic fatty liver/ steatohepatitis
What is hepatitis?
Alcohol
Viral A (contaminated food and water), B (bodily fluid), C(bodily fluid - silent killer as it is chronic and lethal but can go undiagnosed and asymptomatic for months), D, E, glandular fever, cytomegalovirus
Severe bacterial infection
Amoebic infections
Drugs & other toxins e.g toadstool poisoning, paracetamol OD
Automimmune
Wilson’s disease/Haemochromatosis
Acute & Chronic presentation
What is cholestasis?
Obstruction of bile flow: - Pregnancy - not fully understood, causes increased risk of still birth - Gallstones - Pancreatic carcinoma
Non-obstructive causes
- Drug induced- e.g ampicillin/erythromycin
- Inherited
- Primary biliary cirrhosis (PBC), PSC – inflammatory conditions
- Total parental nutrition (TPN) - causes this due to lack of mobility
What are gallstones?
80% Mainly comprised of cholesterol
20% ‘pigment stones’ of calcium bilirubinate/polymers containing calcium & copper
What is cholangitis?
Inflammation of common bile duct
(usually infection e.g bacterial but can occur due to roundworm/fluke)
PSC- Primary Sclerosing Cholangitis
Inherited condition
60+% cases are pANCA Antibody +ve
Strongly associated with IBD (85%UC, 15% Crohn’s)
Can cause liver cancer and early death
Typical presentation: ‘Charcot’s triad’:
1: fever/chills/rigor
2: upper right quadrant pain
3: jaundice’
- Biliary obstruction, complete or intermittent
- Mixed hepatocellular & cholestatic picture
What is cholecystitis?
Inflammation of the gall bladder
90% cases caused by gallstones
Other causes include infection & tumours (rare)
What are the symptoms of liver and pancreatic cancer?
Weight loss - due to lack of enzymes required for digestion
Painless jaundice
Liver (& bone) carcinoma often secondary due to metastases
Endocrine tumours of pancreas
Insulinoma (too much insulin. Hypoglyceamia), Glucagonoma, (hyperglycaemia) VIPoma
What is haemochromatosis?
Acquired:
- Repeated blood transfusion
- Excess iron therapy
Hereditary – Autosomal recessive disorder
- Prevalence : 1 in 200 caucasians
- HFE gene on chromosome 6
- Increased intestinal iron absorption
- Resultant deposition into tissues
- Cirrhosis (deposit in liver), diabetes(in pancreas), arthritis (in joints),
hypopituitarism (in pituitary), cardiomyopathy (in heart),
hyperpigmentation (iron stimulates melanin synthesis)
Diagnosis:
- Transferrin saturation, Ferritin → Genetic test (C282Y/H63D) & biopsy
Management:
- Venesection
What is Wilson’s disease?
Autosomal recessive disorder:
- ATP7B gene on chromosome 13
- Encodes ATPase that incorporates copper into caeruloplasmin
(transport protein) and facilitates copper excretion in bile
- Copper accumulates in the liver, brain, kidneys, eyes (Kayser-
Fleisher rings) & other tissues
Presentation:
- Neurological symptoms
- Liver impairment
- Renal tubular dysfunction
- Adolescence=peak of onset
Diagnosis:
- Urinary copper excretion, post penicillamine
- Liver biopsy for copper analysis
Management:
- Chelation therapy (penicillamine)
What is alpha-1 antitrypsin deficiency?
A1AT=glycoprotein synthesized by liver
- Protease inhibitor
- In particular of neutrophil elastase → degrades elastin (lung
elasticity)
- Leads to:
- Respiratory complications
- Emphysema & COPD
Alternative deficiency/mutation:
- A1AT gets trapped in proteosome (doesn’t actually leave the liver) &
polymerises
- Accumulation leads to liver damage & cirrhosis
Not just down to genetics, also environmental isses.
But the genotype SS (MS) leads to lung and ZZ (MZ) leads to liver
MM is normal
What is pancreatitis?
Acute, Chronic & Hereditaryinflammation of pancreas
Acute
- Abdo pain, nausea & vomiting
- At worst can lead to multi-organ failure!
- measure Amylase, Lipase & CRP, U&E, LFT, Calcium (deposits on
tissue) , Blood gases (diabetic ketoacidosis picture)
Chronic:
- Follows acute
- Most commonly due to alcohol (in UK)
- Faecal elastase
Hereditary
Ranson’s criteria:
- Clinical prediction tool for predicting likelihood & severity of pancreatitis
- Parameters. Measure twice:
- On admission: Age, WBC, Glucose, AST, LDH
- Within 48h: Serum calcium, HCT, O2, Urea (after hydration), base
excess, sequestration of fluids
What is pancreatic insufficiency?
Usually due to long term damage to organ
- E.g. Cystic Fibrosis
- Complications
- Malabsorption
- Malnutrition
- Vitamin deficiencies
- Weight loss
- Fatty stools (steatorrhoea)
- Diabetes
Lab Tests:
- Faecal enzymes (e.g elastase)
- IRT Immunoreactive trypsin (newborn screening bloodspots)
Treatment:
- Supplementation (Creon - contains protease, amylase, lipase)
- Insulin (if they also develop DM)
What is type 1 diabetes?
Insulin deficiency
Immune-mediated:
- Auto-antibodies to pancreatic islet cells (Glutamic acid decarboxylase
antibodies GAD)
Genetic & environmental factors involved
Presents in childhood & adolescence
- Polyuria, thirst, weight loss →life threatening DKA
