Disorders of the GI Tract Pt.1 Flashcards

1
Q

Gastrointestinal Wall Structure

A

4 Layers: (deep) Mucosa, Submucosa, muscularis externa, and serosa (superficial)
3 Parts of Mucosa: Muscous epithelium, Lamina propria, muscle layer
2 Parts of muscularis externa: Longitudinal Muscle layer, circular muscle layer

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2
Q

What does it mean when we describe IBS as a functional disorder?

A

Characterized by chronic abdominal pain, but there are no structural or biochemical causes that can explain the symptoms.

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3
Q

Describe the “hallmark” symptoms of IBS

A

There is abdominal pain relieved by defecation with changes in stool consistency and frequency.

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4
Q

Name the different categories IBS can be listed as

A

IBS(D): diarrhea is predominant
IBS(C): constipation is predominant
IBS(A->alternating) or (M->mixed): stool patterns alternate between constipation and diarrhea
IBS(P): pain is predominant

W>M

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5
Q

Positive diagnosis for IBS

A

Continuous or recurring abdominal pain or discomfort for 12 weeks

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6
Q

What type of foods are recommended to be avoided for those with IBS?

A

Refined grains, processed foods (chips and cookies), coffee, carbonated drinks, high protein diets, dairy products (cheese) and alcohol.

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7
Q

Drugs that help with IBS

A

IBS-D: Anticholinergics-> Levsin, Lomotil, Elavil

IBS-C: Chloride channel activators (draws sodium and water into lumen)-> Amitiza, Linzess

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8
Q

What are the two inflammatory disorders that fall under this category (IBD)?

A

Crohn’s disease and Ulcerative colitis

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9
Q

Recall the common manifestations of IBD.

A

arthritis, skin lesions, inflammatory conditions of the eye like uveitis, and blood disorders including anemia and hypercoagulability

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10
Q

Know what NOD2 is and its role in Crohn’s disease

A

NOD2 (nucleotide oligomerization domain 2) is an intracellular protein that binds to PAMPs on bacteria. This triggers an immune response.

In Crohn’s Disease, NOD2 is mutated. This causes an increase in bacterial growth leading to more inflammation.

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11
Q

What is IL-23 and what does it do?

A

This is a potent activator for Th17 (proinflammatory).

Defects in IL-23 means you have less of a chance to develop Crohn’s and UC

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12
Q

What is the typical age of onset for Crohn’s disease and does it more often affect men or women?

A

Typically effects people in their 20s.

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13
Q

Give a description for the following as it relates to Crohn disease: granulomatous lesion, skip lesion, transmural lesion, “cobblestone” appearance, fistula, and abscess.

A

Granulomatous Lesion: localized swelling that is comprised of an aggregation of
immune cells (mostly macrophages)
Skip Lesion: patchy areas of inflammation or even wounds that represent intestinal tissue damage
Transmural Lesion: affects all the layers of the GI tract
Cobblestone appearance: longitudinal and circumferential fissures that develop in the mucosa
Fistula: Openings

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14
Q

What kinds of tests are used to diagnose Crohn’s disease?

A

Endoscopy, stool cultures (looking for elevated calprotectin), and CT scans

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15
Q

Why is a nutritious diet especially important in the treatment of Crohn disease?

A

patients may experience nutrition deficiencies due to diarrhea, steatorrhea and other malabsorption problems.

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16
Q

Why is it necessary for those with Crohn disease to avoid excessive consumption of fats?

A

fat aggravates the diarrhea

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17
Q

What are elemental diets and total parenteral nutrition and when would they be indicated for Crohn disease patients?

A
  • elemental diet includes foods that are nutritionally balanced and bulk and residue free. It is usually composed of amino acids, fats, sugars, vitamins, and minerals.
  • parenteral nutrition: nutrition is not ingested but is delivered via a gastric feeding tube or intravenous line.
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18
Q

Ulcerative Colitis

A
  • 3rd decade
  • confined to the rectum and colon
  • spreads proximally
  • affects the mucosal layer primarily
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19
Q

Define the terms ulcerative proctitis, proctosigmoiditis, pancolitis,
and pseudopolyps

A

Ulcerative proctitis: affects only the rectum
Proctosigmoiditis: affects rectum and sigmoid colon
Pancolitis: affects the entire colon
Pseudopolyps: due to inflammation process, the mucosal layer forms tongue-like projections resembling polyps

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20
Q

In those with UC, what do stools typically contain?

Why is it highly recommended that UC patients have annual or biannual colonoscopies?

A
  • Contains blood and mucous

- This is recommended because UC patients are more at risk to develop cancer

21
Q

What type of foods should be avoided in those with UC? What are the Tx’s

A

avoid food with caffeine, lactose, spicy foods, fatty foods and gas-forming foods.

Tx: removal of the rectum and entire colon.

22
Q

Name 3 main classes of microbial agents that can cause infectious enterocolitis. Infectious enterocolitis is most spread by which route?

A
  • viruses, bacteria and protozoa

- fecal-oral route

23
Q

Norovirus, enteric adenovirus and rotavirus

A

Norovirus: responsible for the majority of cases of nonbacterial food borne gastroenteritis in all age groups
Enteric Adenovirus: primarily affects infants
Rotavirus: infections are most severe in children younger than 5
-symptoms of this is vomiting, watery stool, and severe dehydration

24
Q
  • What are the names of the 2 vaccines that can be used to prevent a rotavirus infection?
  • What is intussusception?
A
  • Rota teq (5 strains, live attenuated oral)
  • Rotarix (monovalent, live attenuated oral)

Intussusception: when a section of the small intestine telescopes inside another portion

25
Q

Describe 3 pathogenic mechanisms for enterocolitis caused by bacteria.

A
  1. ingestion of preformed toxins present in contaminated food. This is called food poisoning but it is NOT an infection (Clostridium botulism)
  2. infection by toxigenic organisms that proliferate in the gut lumen and produce enterotoxin. This IS an infection. (Clostridium difficile)
  3. infection by invasive organisms that proliferate in the lumen and destroy mucosal epithelial cells. This is also an infection. (E. Coli)
26
Q
  • Give 3 main complications related to a bacterial enterocolitis infection.
  • Which is more severe in general, bacterial or viral enterocolitis?
A
  • dehydration, sepsis, and perforation.

- Bacterial infections are more severe

27
Q

Clostridium difficile

A

gram-positive spore forming bacteria that converts to a vegetative form in the colon.

28
Q

Normally C. difficile is non-invasive. What must happen to develop C. difficile colitis?

A

If C. diff out competes the good flora in the gut then it can germinate.

29
Q

What does the C. difficile toxin do to the colon?

A

Toxin A and toxin B target enterocytes in the gut. This causes an inflammatory response. Overtime it causes watery diarrhea, cramping, blood in stool, and dehydration.

30
Q

How is C. difficile transmitted from person to person?

A

fecal-oral route

31
Q

Other than treatment with broad-spectrum antibiotics, what other factors increase the risk for development of C. difficile-associated diarrhea?

A

gastrointestinal surgery, prolonged stay at healthcare facilities, underlying diseases, immunocompromising conditions, and aging.

32
Q

What is pseudomembranous colitis that can form with a C. difficile infection.

A

This occurs with severe inflammation. Inflammatory cells, fibrin, and necrosis line the lumen of the colon, giving the appearance of a membrane (looks like plaque)

33
Q

When did C. difficile infections start to become a major problem?

A

When broad spectrum antibiotics were starting to be used.

34
Q

What are 2 important diagnostic findings that are consistent with a C. difficile infection?

A

history of antibiotic use and lab tests that confirm C. difficile toxins in the stool

35
Q

What is the first important step in the treatment of C. difficile colitis?

A

Discontinuation of antibiotics that the patient was on.

36
Q

Which 2 antibiotics may be used to eradicate the C. difficile?

A

metronidazole and vancomycin

Another option is a fecal transplant. This is when healthy fecal is transplanted to someone with C. diff to help combat the bad bacteria.

37
Q

What does the term enterohemorrhagic mean?

A

bacteria’s ability to damage the intestine resulting in bloody diarrhea

38
Q

What does virulent mean?

A

something is capable of causing a disease that is severe or harmful in its effects

39
Q

Where is E. coli 0157:H7 mainly found?

A

Found in feces of healthy livestock

40
Q

Give an example of how fruit or other foods may become contaminated. Explain why it is necessary to cook hamburger all the way through but not so when cooking steak?

A

Feces is used as fertilizer for crops and can cause infections in people who eat those crops.

It is important to cook hamburger all the way through because feces may have touched and stayed on the meat of a cow.

41
Q

What are ways you may become infected by E. coli 0157:H7 via water?

A

It can survive in water and can be contracted by drinking even a very little amount.

42
Q

What are two locations that have increased risk for person-to-person transmission of E.coli 0157:H7?

A

nursing homes and daycare centers.

43
Q

What are the main locations of the enterocytes that are infected by E. coli 0157:H7?

A

distal ileum and colon

44
Q

Describe the 9 steps of pathogenesis for an E. coli 0157:H7

A
  1. Attachment of bacterial fimbriae to enterocyte
  2. Bacterial TIR is translated to enterocyte
  3. TIR and intimin of bacteria bind firmly
  4. Release of shiga toxins
  5. Binding of shiga toxins to Gb3/Gb4 receptors
  6. Shiga toxins enter enterocytes and stop protein synthesis
  7. Enterocyte damage and death leading to bloody diarrhea
  8. Shiga toxin enters circulation
  9. Damage to RBCs, platelets, kidneys, brain and possibly death
45
Q

What brings about DIC and thrombocytopenia?

A
  • DIC: disseminated intravascular coagulation. The shiga toxins and mesh like work from platelet can cause kidney failure. This can cause more urea in the blood.
  • Thrombocytopenia: Gb3/Gb4 are on platelet membranes and the shiga toxins bind. This activates more platelet formation, therefore those platelets cannot be used for actual blood clots
46
Q

What is HUS? What is the mechanism by which this infection causes kidney damage?

A

simultaneous occurrence of microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury
-Gb3/Gb4 receptors on the cells of the kidney. Shiga toxins bind to it and induce cell death. The cell death activates platelets. This creates a sort of mesh like plug, that damages any RBCs that pass by.

47
Q

To which patient age group is HUS often the most devastating?

A

HUS mostly affects children.

48
Q

Why can neurological manifestations like stroke, seizures, coma, and hemiparesis occur?

A

Gb3/Gb4 is expressed in brain tissue and shiga can also bind there. the Microthrombi (mesh from platelets) can cause clots

49
Q

Tx for E. Coli 0157:H7

A

Support and a lot of rehydration. Antibiotics and antidiarrheic’s not recommend because they increase HUS. Because antibiotics kill the bacteria and it is not flushed out by diarrhea.