IBD up to Peptic Ulcer Disease Flashcards

1
Q

What constitutes IBD?

A

2 conditions:
Ulcerative colitis
Crohn disease (aka Crohn’s)

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2
Q

Etiology of IBD?

A
  • complex trait
  • Genetic susceptibility → is not specific genetic defect (not monogenic problem);
  • Environ trigger → suggested to be bacterial infection
  • IR against normal gut flora
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3
Q

Is IBD autoimmunity?

A

Ahmed says no…b/c is NOT autoimmunity b/c are not self-cells and do not have MHC and HLA genetic defect listed here

Textbook p 892 specifically says it is autoimmunity and that HLA is involved…

For fuck’s sakes.

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4
Q

How does targetting normal gut flora in IBD result in lesions?

A

Here normal tolerance that body has for normal flora is lost…problem here is that these flora have attachments to the lining of the gut (because can’t be free floating or would be swept through with fecal matter) so when bacteria are targeted, so are some of the cells

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5
Q

How is the distribution of lesions different in Crohn’s and Ulcerative Colitis?

A
  • In Crohn’s disease, lesions are “skipped”
  • Ulcerative colitis: has one, continuous lesion that affects only large intestine and rectum

(See figure 37-6)

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6
Q

Describe Crohn’s disease in terms of:

1) Area of intestines affected
2) Layer of intestine affected
3) Nature of lesions
4) Rate of progression

A
  • Primarily affects terminal ileum – others can be affected
  • Primarily affects submucosa – but all layers can be affected
  • Granulomatous skip lesions - cobble stone appearance
  • Slow, non-aggressive progression
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7
Q

Manifestations of Crohn’s disease

A

1) Diarrhea
2) Intermittent abdominal pain
3) Weight loss

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8
Q

Why does diarrhea result form crohn’s?

Intermittent pain?

A

peristalsis affected b/c lining affected, exudate formation

pain with peristalsis and passage of food…if not ingesting food and peristalsis is not ocurring, will not feel pain

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9
Q

Why does weight loss result in crohn’s disease?

A

Most lesions are in small intestine, which is where we absorb our nutrients…these areas are inflamed and damaged, decreasing absorptive surface → nutritional deficiency AND diarrhea means food moving too quickly to be absorbed properly

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10
Q

Ulcerative colitis

1) What areas affected? Layer of intestine?
2) How does progression occur?
3) are lesions skipped?

A

1) Primarily involves mucosa of colon and rectum
2) Spread is proximal from rectum → almost always begins in anus and rectum and progresses over time to spread upwards
3) Continuous lesions

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11
Q

Describe the changes that occur with the lesions and gut in ulcerative colitis

A

o Tissue thickens and becomes inflamed
o Bleeding ulcers
o Edema and congestion within lumen of gut → this occurs in area that is affected, edema develops from exudate formation in these areas

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12
Q

Manifestations of ulcerative colitis?

A
  • Bloody diarrhea (resulting in anemia)
  • Abdominal cramping
  • Weight loss (d/t diarrhea…may not be as significant as with Crohn’s disease)
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13
Q

Why is weight loss in Crohn’s disease tyically more sig?

A

Crohn’s affects small intestine more…where absorption occurs
UC: just about loss of absorptive time r/t diarrhea

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14
Q

Dx of Crohn’s and UC?

A
  • Hx, px
  • differential diagnosis: Exclude GI infection – serology, stool samples. etc
  • Sigmoidoscopy, colonoscopy, biopsy → taken to lab, lab will exclude other problems; looking for polyps, tumours
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15
Q

Tx of Crohn’s and UC?

A
  • Chronic so need to manage both progression of disease and symptoms
  • Based on severity (may only need lifestyle and diet mods)
  • If moderate to severe:
    1) Anti inflm eg: sufasalazine (+ Abx)
    2) Prednisone if non-responsive
    3) Immunomodulator for prevention of progression = Methotrexate
    4) Sx (if need to fix ulcers or do resection)
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16
Q

How/why are sufasalazine and Abx used in tx of Crohn’s and UC?

A
  • sufasalazine is first line therapy, the drug of choice
  • Abx b/c targeting normal flora = partially prophylactic (prevent bacteria invading wall) and limiting flora that are being targeted in general
  • Remember, bacterial infection that triggered disease to develop is not the problem anymore…is not what we’re targeting with Abx
17
Q

How do immunomodulators differ from immunosuppressants and why do we want the earlier in this case?

A

immunosuppressant will suppress immunity, don’t want to do this…instead want to regulate… brings aggressive IR under control

18
Q

What is methotrexate?

A

immunomodulatory, anticancer, anti-folate – prevents DNA replication and cell division) → here trying to regulate defective T cells; dosage will determine what cells are targeted (here lower dose, in cancer higher dose)

19
Q

How do herniations differ from diverticula?

A

• Don’t confuse with diverticula – outpouchings…here is often external pushing through body wall

20
Q

What are herniations?

WHere do they usually occur?

A
  • Organ protruding through retaining structure

* Usually in abdominal cavity

21
Q

Patho of herniations?

A

Need 2 factors:
1) Weakened supporting structure (eg: muscles) – through aging, degenerative change, congenital defect affecting muscles,
o Acquired or congenital – usually acquired (after born at some point over life)
2) Inc intra-abdominal pressure (eg: obesity, pregnancy) → herniation

22
Q

What is a hiatal hernia?

A

• Hiatal hernia = Part of stomach enters thoracic cavity if hiatus enlarges (junction of stomach and esophagus raised up above diaphragm)

23
Q

What is a hiatus?

A

means an opening through which another structure passes (eg: Aperture in diaphragm for esophagus – is “closed” opening…tight around esophagus

24
Q

2 types of hiatal hernias?

A

1) Sliding
2) Paraesophageal or Rolling
* Based on how it occurs

25
Q

Differ between 2 types of hiatal hernias with regard to what happens and symptoms of each

A

1) Sliding =
GEJ (gastroesophageal junction) and upper stomach enter thoracic cavity
o Some asymptomatic
o Others: chest pain, heartburn, reflux

2) Paraesophageal/rolling =
o Non-upper part of stomach enters TC (not distal or pyloric end, greater curvature hasn’t changed)
o GEJ remains below the diaphragm
o Chest pain, dyspnea, fullness after meals (feel full sooner than should)

See fig 37-2

26
Q

Why do chest pain and heartburn result in a hiatal hernia?

A
  • Chest pain r/t displacement of stomach and esophagus
  • Heartburn: d/t gastric content coming into esophagus – ph of HCl = 2, lining of esophagus not equipped for this so becomes irritated
27
Q

Why does reflux not result from a paraesophageal or rolling hiatal hernia?

A

Not sliding straight up, gastric content remains in pouch of stomach, not pushed up into esophagus

28
Q

Why does premature fullness result from a paraesophageal/rolling hernia?

A

because have reduced size of stomach (so stretch receptors activated sooner) and stretch receptors in pouch set off sooner because is small

29
Q

Tx of hiatal hernias?

A
  • Often managed w/o drugs
  • Lifestyle modifications: can’t address pain but can address reflux
    • Drugs (for reflux)
    –> Antacids (neutralizes acid)
    –> H2RA (H2 receptor antagonists)
    –> PPI (proton pump inhibitors) – decreasing acid secretion in the stomach
    • Sx (only ~15% of cases require this) Ex: fundoplication…fundus of stomach taken and wrapped around GEJ (is like boot being laced up)
30
Q

What sort of diet/lifestyle modifications are used to minimize symptoms in tx of hiatal hernia?

A

smaller portions, food that doesn’t aggressively cause acid production; stop eating a few hours before bed, raise head of bed (these prevent reflux)

31
Q

Is prolonged antacid use ok?

A

should not be taken unchecked for long time d/t Ca carbonate…possible kidney stones, etc.

32
Q

Action of H2 receptor agonists?

A

??

33
Q

Inguinal Hernia:
What is it?
What passes through?
How is it corrected?

A
  • Abdominal organ(s) protrude via inguinal ring
  • Peritoneum forms hernial sac - Peritoneum pushed out with the organ (such as cecum)
  • Sac usually contains intestine and omentum
  • Sx correction
34
Q

What is the difference between direct and indirect hernias?

A

(applies to both hiatal and inguinal hernias) – in indirect hernia, hernia occurs through existing aperture; direct = passing through body wall, etc where no aperture exists

35
Q

What kind of hiatal hernia is more prevalent?

A

Sliding = 95%