Common GI Disorders Flashcards

1
Q

What are common GI disorders?

A
Diarrhoea
 Vomiting
 Upper GI bleed
 Irritable Bowel Syndrome (IBS)
 Inflammatory Bowel Disease (IBD)
 Ulcerative Colitis (UC)
 Crohns Disease 
 Coeliac Disease
 Lactose intolerance
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2
Q

What are common causes of diarrhoea?

A
  • 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)

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3
Q

What are the biochemical implications of Diarrhoea?

A

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

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4
Q

What are the biochemical implications of vomiting?

A

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)
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5
Q

What are the biochemical implications of an upper GI bleed?

A

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

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6
Q

What is the nature of IBD/IBS?

A

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

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7
Q

How is an IBS and an IBD diagnosis differentiated?

A

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.

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8
Q

What is coeliac disease?

A

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

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9
Q

What is lactose intolerance?

A
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)

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10
Q

What are common liver disorders?

A

Alcohol:

  • Fatty liver
  • Hepatitis
  • Cirrhosis

Non-alcoholic fatty liver/ steatohepatitis

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11
Q

What is hepatitis?

A

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

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12
Q

What is cholestasis?

A
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
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13
Q

What are gallstones?

A

80% Mainly comprised of cholesterol

20% ‘pigment stones’ of calcium bilirubinate/polymers containing calcium & copper

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14
Q

What is cholangitis?

A

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

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15
Q

What is cholecystitis?

A

Inflammation of the gall bladder

90% cases caused by gallstones

Other causes include infection & tumours (rare)

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16
Q

What are the symptoms of liver and pancreatic cancer?

A

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

17
Q

What is haemochromatosis?

A

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

18
Q

What is Wilson’s disease?

A

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)

19
Q

What is alpha-1 antitrypsin deficiency?

A
A1AT=glycoprotein synthesized by liver
- Protease inhibitor 
- In particular of neutrophil elastase → degrades elastin (lung 
   elasticity)
- Leads to:
     - Respiratory complications
     - Emphysema &amp; 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

20
Q

What is pancreatitis?

A

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

21
Q

What is pancreatic insufficiency?

A

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)
22
Q

What is type 1 diabetes?

A

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