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Year 2 > Malabsorptive conditions > Flashcards

Malabsorptive conditions Flashcards

1
Q

What is malabsorption

A

Failure to fully absorb nutrients wither because of the destruction to epithelium or due to a problem in the lumen meaning food can’t be digested

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2
Q

Before malabsorption is diagnosed, what needs to be ruled out

A

Insufficient intake must be rules out to ensure it is actually malabsorption

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3
Q

How can pancreatic disorders cause malabsorption

A
  1. Pancreas produce most enzymes for digestion such as amylase
  2. Pancreatitis damages glands meaning no enzymes are released
  3. Cystic fibrosis blocks pancreatic duct due to excess mucus meaning enzymes fail to be released
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4
Q

Name two ways defective bile secretion can result in malabsorption

A
  1. Biliary obstruction

2. Ileal resection (we reabsorb bile salts in the terminal ileum so if removes bile uptake will decrease)

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5
Q

What other factor causes malabsorption

A

Bacterial overgrowth

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6
Q

How does coeliac’s disease cause malabsorption

A

Villi are short if present at all, villous atrophy and crypt hyperplasia

Lots of lymphocyte sin epithelium

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7
Q

How does Crohn’s cause malabsorption

A
  1. Inflammatory damage to lining of bowel = cobblestone mucosa with significant reduction in absorptive SA
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8
Q

What is Giardia lambda and how does it cause malabsorption

A
  1. Extensive surface parasitisation of villi and microvilli

2. Parasites coat surface of cilli and food can’t be absorbed

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9
Q

How does disaccharidase deficiency cause malabsorption

A
  1. Cannot break down lactose in milk into glucose which can then be absorbed. Undigested lacrosse passes into colon where bacteria eat it and produce CO2 (gas and diarrhoea)
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10
Q

What is abetalipoproteinaemia

A

Lack of transporter protein to transport lipoprotein across cell

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11
Q

What defective epithelial transport conditions result in malabsorption

A

Abetalipoproteinaemia

Primary bile acid malabsorption (Mutations in bile acid transporter protein)

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12
Q

What lymphatic diseases can result in malabsorption

A

Lymphatic obstruction

  1. Lymphoma
  2. TB
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13
Q

What is coeliac’s disease

A

Condition in which there is inflammation of the mucosa of the upper small bowel the improves when gluten is withdrawn from diet (relapses when gluten is reintroduced)

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14
Q

Pathophysiology of coeliac’s disease

A

T-cell mediated autoimmune disease of small bowel in which prolamin intolerance causes villous atrophy and malabsorption

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15
Q

What are prolamins

A

Groups of plant storage proteins

Component of gluten proteins

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16
Q

What prolamin are found inn wheat

A

Gliadin

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17
Q

What prolamin is found in barley

A

Hardens

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18
Q

What prolamin is found in rye

A

Secalins

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19
Q

When should you suspect Coeliac’s disease

A

Diarrhoea, Weight loss or Anaemia (iron or B12 deficient with no cause)

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20
Q

What gender does Coeliac’s effect

A

males and females

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21
Q

Causes of coeliac’s

A

Gluten

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22
Q

Risk factors for Coeliac’s

A
  1. Autoimmune dieases: Type 1, Thyroid and Sjorgren’s
  2. IgA deficiency
  3. Breast Feeding
  4. Age of introduction to gluten into diet
  5. Rotavirus infection in infancy increases risk
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23
Q

What part of the gluten in wheat is toxic

A

Prolamin a-GLIADIN

24
Q

What is Prolamin a-GLIADIN resistant to

A

Digestion by pepsin and chymotrypsin because of high glutamine and proline content

25
Q

How does prolamin a-GLIADIN trigger immune responses

A

By remaining in the intestinal lumen

26
Q

What happens to gliadin peptides

A

Pass through epithelium and are deaminated by tissue transglutaminases = increases their immunogenicity

27
Q

How do gliadin peptides trigger inflammation

A

Bind to antigen-presenting cells after deamination

APC interacts with CD4+ T cells in LAMINA PROPRIA via HLA class II molecules

T cells then produce pro-inflammatory cytokines and initiate cascade

28
Q

What HLA class II molecules does gliadin interact with

A

DQ2 or DQ8

29
Q

How do DQ2 AND DQ8 EFFECT T CELLS

A

Activate the gluten-sensitive T cells

30
Q

End product of inflammatory cascade in Coeliac’s

A

Metaloproteinkinases and inflammatory mediators that cause:

VILLOUS ATROPHY
CRYPT HYPERPLASIA
Intraepithelial lymphocytes

^ Causes malabsorption

31
Q

What structure of the GI is primarily effected in Coeliac’s

A

Proximal small bowel mucosa

32
Q

How does Coeliac’s result in anaemia

A

Damage to mucosa means B12, folate and iron can’t be absorbed

33
Q

How does the severity of the mucosa change as we approach the ileum

A

Mucosal damage decreases as gluten is broken down into small non-toxic fragments

34
Q

Clinical Presentation of Coeliac’s

A
  1. 1/3 are asymptomatic (detected on routine blood tests)
  2. Stinking stools/fatty stools (steatorrhoea)
  3. Diarrhoea
  4. Bloating
  5. Abdo pain
  6. Nausea + vomiting
  7. Angular stomatitis
  8. Weight loss
  9. Fatigue
  10. Anaemia
  11. Osteomalacia
  12. Dermatitis hepetiformis
35
Q

What is angular stomatitis

A

Inflammation of one or both corners of the mouth

36
Q

What is osteomalacia

A

Softening of bones due to impaired bone metabolism due to lack of phosphate, calcium and fit D leading to osteoporosis

37
Q

What is dermatitis hepetiformis

A

Red raised patches, often with blisters thet burst on scratching, commonly seen on elbows, knees and buttocks

38
Q

How is Coeliac’s disease diagnosed

A

Maintain gluten for at least 6 weeks before testing to get correct results:

FBC
Duodenal biopsy (GOLD STANDARD)
Serum antibody testing

39
Q

What should be seen on blood tests for Coeliac’s

A
  1. Low Hb
  2. Low B12
  3. Low ferritin
40
Q

How does a duodenal biopsy help with diagnosing coeliac’s

A
  1. See villous atrophy
  2. Crypt hyperplasia
  3. Increased intraepithelial WCC
  4. IgA serum
41
Q

On gluten free diet would we see villous atrophy and crypt hyperplasia on duodenal biopsy

A

No

42
Q

Name two IgAs looked for in serum antibody tests for coeliac’s

A
  1. Endomysial antibody

2. tTG (Tissue transglutaminase antibody

43
Q

How is Coeliac’s treated

A

Lifelong gluten-free diet (no prolamins)
Correction of vitamins and mineral deficiencies
DEXA scan to monitor osteoporotic risk

44
Q

What would a gluten-free diet look like

A
  1. Eliminate wheat, barley and rye
  2. Oats can be tolerated (no flour which can contaminate them in production
  3. Meat, dairy, fruits and veg are gluten-free
45
Q

Complications of coeliac’s

A
  1. Diet may not improve things (non-responsive coeliac’s disease)
  2. Anaemia
  3. Secondary lactose intolerance
  4. T-cell lymphoma
  5. Increased risk of malignancy (gastric, oesophageal, bladder, breast and brain) due to increased cell turnover
  6. Osteoporosis
46
Q

What is Tropical Sprue

A
  1. Severe malabsorption (of two or more substances) with:
    Diarrhoea
    Malnutrition
47
Q

Where is tropical sprue seen

A

Visitors or residents to tropical areas where disease is endemic (most of asia, carribbevn, puerto rico and parts of SA)

48
Q

What is the cause of tropical sprue

A

UNKNOWN but patients improve on antibiotics

49
Q

What happens to the GI tract in tropical sprue

A

Villous atrophy (malabsorption)

50
Q

Describe the onset of tropical sprue

A

Acute and occurs either a few days or many years later being in the tropics

51
Q

Clinical presentation of tropical sprue

A
  1. Diarrhoea
  2. Anorexia
  3. Severe malabsorption
  4. Weight loss
  5. Abdominal distention
  6. Chronic diarrhoea
52
Q

How is tropical sprue diagnosed

A
  1. First we need to exclude acute INFECTIVE causes of diarrhoea (Giardia intestinal - produces similar symptoms)
  2. Blood tests
  3. JEJUNAL biopsy
53
Q

What should blood tests show for tropical sprue

A
  1. Anaemia due to malabsorption of B12, folate and iron
54
Q

What should a jejunal biopsy show for tropical sprue

A
  1. Jejunal mucosa is abnormal showing partial villous atrophy (complete atrophy in coeliac)
55
Q

How is tropical sprue treated

A
  1. Leave area
  2. FOLIC ACID and antibiotics daily
  3. Severe cases: resuscitation with fluids and electrolytes for dehydration and nutritional deficiencies should be corrected and B12 given
  4. Excellent prognosis
  5. Mortality is only associated with water and electrolyte depletion particularly in epidemics
56
Q

What antibiotic is given for tropical sprue

A

TETRACYCLINE

57
Q

What is inflammatory bowel disease

A
  1. CHRONIC AUTOIMMUNE CONDITIOINS

Year 2 (155 decks)

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