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Study Notes - Gastroenterology > *Intestinal Problems 1 (lectures 1, 2 and 3) > Flashcards

*Intestinal Problems 1 (lectures 1, 2 and 3) Flashcards

1
Q

What is intestinal failure?

A

The inability to maintain adequate nutrition or fluid status via the intestines - can result from a number of things such as obstruction, dysmotiltiy, surgical resection, congenital defect, or disease associated with loss of absorption and is characterised by the inability to maintain protein-energy, fluid, electrolyte, or micronutrient balance

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2
Q

How can IF be classified in terms of time frame?

A

Acute short term = days/ weeks/ months e.g. mucositis post chemotherapy
Chronic long term e.g. short gut syndrome

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3
Q

How many different types of IF are there?

A

3

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4
Q

What types of IF are classified as acute short term?

A

Types 1 and 2

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5
Q

What types of IF are classified as chronic long term?

A

Type 3

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6
Q

What is type I intestinal failure?

A

Self-limiting short term postoperative or paralytic ileus (usually on wards, sometimes HDU/ ITU)

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7
Q

What is type 2 intestinal failure?

A

Prolonged, associated with sepsis and metabolic complications. Often related to abdominal surgery with complications (mainly HDU/ ITU or wards)

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8
Q

What is type 3 intestinal failure?

A

Long term but stable - home parenteral nutrition often indicated (usually seen in wards to home)

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9
Q

How malnourished will a patient with type I intestinal failure be?

A

Normal/ moderately malnourished

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10
Q

Treatment of a patient with type I intestinal failure? (7)

A

Replace fluids, correct electrolytes
Parenteral nutrition if unable to tolerate food/ fluids for greater than or equal to 7 days post op
Acid suppression: PPI
Octreotide (reduces GI secretions)
Alpha hydroxycholecalciferol to preserve Mg
Intensive multi-disciplinary input
Allow some diet/ enteral feeding

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11
Q

What does parenteral nutrition rely on?

A

Venous access e.g. PICC line, tunnelled catheter (central line), vascuport (portacaf) - US guided placement

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12
Q

Parenteral nutrition complications?

A 
Nutrient toxicity
Liver disease
Metabolic disturbance
Physcho-social effects
Inappropriate usage
Sepsis
SVC thrombosis
Line fracture
Line leakage
Line migration
Metabolic bone disease
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13
Q

How long do patients with type 2 IF usually have it for?

A

Weeks/ months

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14
Q

What type of feeding should patients with type 2 IF usually receive?

A

Parenteral +/- some enteral feeding

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15
Q

What are some examples of causes of type 2 intestinal failure?

A

Usually a surgical complication but can be due to crohns, coeliac disease, malignancy, ischaemia, radiation, etc.

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16
Q

What is the treatment of choice for patients with chronic IF? (type III)

A

Home parenteral nutrition

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17
Q

What is another 3 treatment options for patients with type 3 intestinal failure, apart from parenteral nutrition?

A 
Intestinal transplantation (specific indications, long term survival lower than HPN)
Bowel lengthening (not validated yet in adults)
GLP2 (teduglutide) treatment for SBS
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18
Q

What are examples of conditions that can cause type 3 intestinal failure?

A 
Short gut syndrome
Crohns disease
Neoplasia
Vascular
Mechanical
Radiation enteritis
Dysmotiity
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19
Q

What length must the bowel be to be classified as short bowel syndrome?

A

Less than 200cm - insufficient length of small bowel to meet nutritional needs without artificial nutritional support

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20
Q

What length of bowel is indicative that the patient requires HPN for their short bowel syndrome?

A

Less than 50cm of small bowel

Although patients usually need it before due to a poor quality of life e.g. 100cm of small bowel

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21
Q

Do patients who go on HPN usually get weaned off it eventually/

A

Very rarely - there are usually dependent for life

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22
Q

What is the advantages of intestinal transplantion compared to HPN?

A 
Transplantation = survival 5 years = 50-60% and the patient requires a stoma, risk of immunosuppression but eating
HPN = 5 year survival 80% but not eating
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23
Q

What are the main indications of small bowel transplant compared to HPN?

A

Loss of venous access
Liver disease (usually combined with a liver transplant)
Last resort

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24
Q

Do palliative patients tend to get sent home with HPN?

A

Not usually - look at individual cases

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25
Q

What are the 2 causes of ischaemia of the small bowel?

A

Mesenteric arterial occlusion

Non occlusive perfusion insufficiency

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26
Q

What are the 2 causes of mesenteric arterial occlusion?

A

Mesenteric artery atherosclerosis

Thromboembolism from the heart e.g. A fib

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27
Q

What are 4 causes of non occlusive perfusion insufficiency?

A

Shock
Strangulation obstructing venous return e.g. hernia adhesion
Drugs e.g. cocaine
Hyperviscosity

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28
Q

Is bowel ischaemia usually acute or chronic?

A

Usually acute but can be chronic

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29
Q

What part of the small bowel is most sensitive to the effects of hypoxia?

A

The mucosa - most metabolically active part

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30
Q

In non-occlusive ischaemia, when does most of the tissue damage occur?

A

After reperfusion

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31
Q

How is acute ischaemia classified?

A

By degree of infarction caused - mucosal infarct, mural infarct or transmural infarct (depending on the length of time of the ischaemia)

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32
Q

What are the 3 types of outcomes of acute ischaemia depending on the length of time the ischaemia has been present for?

A

Regeneration
Stricture
Gangrene

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33
Q

What type of outcome does mucosal infarct usually have?

A

Regeneration - mucosal integrity restored

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34
Q

What type of outcome does mural infarct have?

A

Repair and regeneration = fibrous stricture

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35
Q

What type of outcome does transmural infarct have?

A

Gangrene - patient death if not resected

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36
Q

Complications of ischaemia of the small bowel? (10)

A 
Fibrosis
Stricture
Chronic ischaemia
Mesenteric angina
Obstruction
Gangrene
Perforation
Peritonitis
Sepsis
Death
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37
Q

What is Meckel’s diverticulum?

A

A tubular structures, 2 inches long, 2 foot above the IC valve in 2% of people due to incomplete regression of vital-intestinal duct (may contain heterotopic gastric mucosa)

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38
Q

Symptoms of a meckels diverticulum?

A

May cause bleeding, perforation or diverticulitis which mimics appendicitis - commonly asymptomatic, incidental finding

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39
Q

Are primary or secondary tumours of the small bowel more common?

A

secondary (metastases) - ovary, colon, stomach

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40
Q

What type of primary tumours of the small bowel are found? (3)

A

Lymphomas
Carcinoid tumours
Carcinomas

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41
Q

What are carcinoid tumours?

A

Slow growing neuroendocrine tumours - different to carcinomas which are epithelial

42
Q

What type of lymphomas are found in the small bowel?

A 
Non hodgkins (rare) e.g. maltomas (B-cell - mucosa-assocaited lymphoid tissue)
Enteropathy associated t-cell lymphomas (associated with coeliac disease)
43
Q

What type of bowel cancer is associated with coeliac disease?

A

T-cell lymphomas (also carcinoma of the small bowel)

44
Q

How are lymphomas of the small bowel treated?

A

Surgery and chemotherapy

45
Q

What is the commonest site of carcinoid tumours of the bowel?

A

Appendix

46
Q

What is the appearance of carcinoid tumours?

A

Small, yellow, slow growing, local invasive

47
Q

What symptoms do carcinoid tumours cause?

A

Intussusception, obstruction
Produce hormone like substances
If metastases to liver occur, a carcinoid syndrome occurs producing diarrhoea and flushing

48
Q

What is carcinoma of the small bowel associated with?

A

Rare - Crohns disease and coeliac disease

49
Q

What does carcinoma of the small bowel look like?

A

Identical to colorectal carcinoma in appearance
Presents late
Metastases to lymph nodes and liver occur

50
Q

What causes vomiting, abdominal pain, RIF tenderness and increased WCC?

A

Appendicitis

51
Q

What causes acute appendicitis? (5)

A 
Unknown
Faecoliths (dehydration)
Lymphoid hyperplasia
Parasites
Tumours (rare)
52
Q

Pathology of acute appendicitis? (5)

A

Acute inflammation (neutrophils)
Mucosal ulceration
Serosal congestion, exudate (yellow surface)
Pus in lumen
Acute inflammation must involve the muscle coat

53
Q

Complications of appendicitis? (5)

A 
Peritonitis
Rupture
Abscess
Fistula
Sepsis and liver abscess
54
Q

What causes coeliac disease?

A

An abnormal reaction to a constituent of what flour, gluten, which damages enterocytes and reduces absorptive capacity

55
Q

What are 3 things that coeliac disease is strongly associated with?

A

HLA-B8
Dermatitis herpetiformis
Childhood diabetes

56
Q

What is the component of gluten that is suspected to be the toxic agent that causes coeliac disease?

A

Gliadin - abnormal immune reaction to this in coeliacs

57
Q

What mediates the immune reaction to gliadin in coeliac disease?

A

T-cell lymphocytes which exist within the small intestinal epithelium “intraepithelial lymphocytes”

58
Q

What is the normal life span of an enterocyte?

A

About 72 hours

59
Q

What causes the fat duodenal mucosa in coeliac disease?

A

Increasing loss of enterocytes due to intestinal epithelial lymphocyte mediate damage = loss of villous structure, loss of surface area and a reduction in absorption

60
Q

What part of the bowel are legions worse in in coeliac disease?

A

Proximal bowel so duodenal biopsy is very sensitive - even if the bowel looks normal

61
Q

What antibodies may be present in the serum = coeliac disease? (3)

A

Anti-TTG
Anti-endomesial
Anti-gliadin

62
Q

Why do patients with coeliac disease sometimes get steatorrhoea?

A

Malabsorption of fats

63
Q

Why do patients with coeliac disease sometimes get gallstones?

A

Reduced intestinal hormone production leads to reduced pancreatic secretion and bile flow (CCK) leading to gallstones

64
Q

What are the effected of malabsorption caused by coeliac disease? (5)

A 
Loss of weight
Anaemia
Abdominal bloating
Failure to thrive
Vitamin deficiencies
65
Q

Complicaitons of coeliac disease apart from malabsorption effects? (4)

A

T-cell lymphomas of GI tract
Increased risk of small bowel carcinoma
Gall stones
Ulcerative-jejenoilitis

66
Q

What is malabsorption?

A

Defective mucosal absorption - caused by defective luminal digestion, mucosal disease, structural disorders

67
Q

What are 5 common causes of malabsorption?

A 
Coeliac disease
Crohns disease
Post infections
Biliary obstruction
Cirrhosis
68
Q

What are 5 uncommon causes of malabsorption?

A 
Pancreatic cancer
Parasites
Bacterial overgrowth
Drugs
Short bowel
69
Q

What 2 questions should be asked when presented with someone who has malabsorption?

A

What is being malabsorbed? (protein, dat, carbohydrate, vitamins and minerals)
What is this reason for this?

70
Q

What are digestive causes of protein malabsorption? (4)

A

Partial or total gastrectomy = poor mixing
Exocrine pancreatic insufficiency
Trypsinogen deficiency
Congenital deficiency of intestinal enterokinase (produced in the duodenum)

71
Q

What are absorptive causes of protein malabsorption?

A 
Coeliac disease
Tropical sprue
Methionine malabsorption syndrome and blue diaper syndrome
Short bowel syndrome
Jejunoilial bypass
Harasnup disease (defects in neutral AA transporters)
Cystinuria I-III
Oculocerebral syndrome of lowe
72
Q

What are fats delivered in post-absorption?

A

Lymphatics

73
Q

What are digestive causes of fat malabsorption?

A

Less time to mix- gastric resection, autonomic neuropathy, amyloidosis
Decrease in micelle formation - decreased bile acid synthesis/ secretion - cirrhosis, biliary obstruction, CCK deficiency, small intestinal bacterial overgrowth
Decreased lipolysis - chronic pancreatitis, CF, pancreatic tumours, low luminal pH, excessive calcium ingestion, co-lipase deficiency

74
Q

What are absorptive causes of fat malabsorption?

A

Decreased chylomicron formation and/ or mucosal absorption - coeliac disease, + other rarer causes

75
Q

What are post-absorptive causes of fat malabsorption?

A

defective lymphatic transport - primary intestinal lymphangiectasia, lymphoma, whipple disease, trauma

76
Q

What is a digestive cause of carbohydrate malabsorption?

A

Severe pancreatic insufficiency (alpha-amylase deficiency)

77
Q

What is an absorptive cause of carbohydrate malabsorption?

A

Primary or acquired lactase deficiency: post-infecitohs lactase deficiency, coeliac disease, crohns disease, other deficiency

78
Q

Causes of vitamin B12 malabsorption?

A

Atrophic gastritis (impaired peptin/ acid secretion)
Deficiency of gastric intrinsic factor
Pancreatic insufficiency
Ileal crohn disease/ resection

79
Q

Cause of folic acid malabsorption?

A

Diseases affecting the proximal small bowel e.g. coeliac, whipple, tropical sprue
Alcoholism

80
Q

Causes of fat soluble vitamins malabsorption?

A

Anything that disrupts fat absorption will result in one/ more deficiency

81
Q

Causes of calcium malabsorption?

A

Selective deficiency can occur with renal disease/ hyperparathyroidism, inborn defect in vitamin D receptor
Disease that reduce intestinal surface area and/ or cause formation of insoluble calcium soaps with long chain fatty cards e.g. coeliac, bile acid deficiency

82
Q

Cause of magnesium malabsorption?

A

Anything causing a reduced mucosal surface area and/ or luminal binding by malabsorbed fatty acids

83
Q

What causes iron malabsorption?

A

Most often GI bleeding, or mucosal surface area decrease

84
Q

What causes zinc malabsorption?

A

Acrodermatitis enteropathica

85
Q

What causes copper malabsorption?

A

Menkes disease

86
Q

What is the primary blood test for coeliac disease?

A

IgA anti-tissue transglutaminase test (biopsy confiramtive)

87
Q

How is lactose malabsorption confirmed?

A

Lactose breath hydrogen test

Oral lactose intolerance test (treated with lactose free diet)

88
Q

What is tropical sprue?

A

Tropical sprue is a malabsorptive disease of the small bowel, characterised by inflammation and villous flattening in the small intestine usually due to colonisation of the intestine by an infectious agent or alterations in the intestinal bacterial flora induced by exposure to another environmental agent

89
Q

How is tropical sprue diagnosed?

A

Biopsy

90
Q

How is tropical sprue treated?

A

Tetracycline

Folic acid

91
Q

What is whipple disease?

A

Whipple disease is a rare bacterial infection that most often affects your gastrointestinal system. Whipple disease interferes with normal digestion by impairing the breakdown of foods, such as fats and carbohydrates, and hampering your body’s ability to absorb nutrients.
Whipple disease also can infect other organs, including your brain, heart, joints and eyes.
It caused by infection by Tropheryma whipplei

92
Q

How is whiles disease diagnosed?

A

Demonstration of T. while in involved tissue by microscopy

93
Q

When do patients with Crohns disease get very severe malabsorption?

A

When they have extensive ill involvement, many resections, enterocolic fistulas and strictures causing small intestinal bacterial overgrowth

94
Q

What is a risk factor for infection with the parasite Giardia lamblia?

A

Travel to areas where the water supply may be contaminated, swimming in ponds

95
Q

Diagnosis of Giardia lamblia infection?

A

Stool examination for ova and parasites (3 separate stool samples increase the yield of positive examinations)

96
Q

Treatment of Giardia lamblia?

A

Metronidzole for 1 week

97
Q

Symptoms of small bowel bacterial overgrowth?

A

Diarrhoea, steatorrhoea, macrocytic aneamia (B12)

98
Q

Causes of small bowel bacterial overgrowth?

A

Diverticula, fistulas and strictures related to Crohns disease, bypass surgeries functional stasus

99
Q

Treatment of small bowel bacterial overgrowth?

A

Low cobalamin and high folate levels
Aerobic and/ or anaerobic colonic-type bacteria in a jejunal aspirate
Best established by a schilling test

100
Q

Treatment of a small bowel bacterial overgrowth?

A

Surgical correction of an anatomical blind loop

Tetracyclines for 2-3 weeks

101
Q

What causes easy bruising?

A

Vitamin C deficiency - scurvy

Vitamin K deficiency

102
Q

What is acrodermatits enteropathica?

A

An autosomal recessive condition that causes impaired zinc uptake - premolar rash - need lifelong zinc supplements

Study Notes - Gastroenterology (42 decks)

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