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253-Green Patho > GI INFLM > Flashcards

GI INFLM Flashcards

1
Q

What is diverticular disease?

3 Types?

A

• Diverticular disease refers to the mucosal layer of the colon herniating through muscluaris externa layer (like a pouch) Often multiple diverticula and sometimes multiple sites

3 Types include
diverticulosis, diverticular bleeding, and diverticulitis

NOTE
Diverticula (pl) Diverticulum (singular)

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2
Q

Prevalence of Diverticular Disease?

A

• (5-10% > 45yrs) AND (80% > 85yrs) have Diverticular disease

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3
Q

Etiology/RIsk Factors of DD

A
  • Poor diet, not well balanced (specifically low fibre)
  • Inactivity
  • Poor bowel habits (specifically constipation)
  • Ageing
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4
Q

What areas of the colon might be most effected in DD?

A

• Effects Normal weak points near areas of blood vessel entry

Also common in areas of high intra luminal pressure (sigmoid colon is common)

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5
Q

What is the trigger for herniation in DD?

A

• Accumulated gut content increases intra luminal pressure causing mucosa layer herniating through muscularis externa layer causing a bowel protrusion

(i.e constipation)

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6
Q

If a diverticulum develops near a blood vessel, what complication might arise?

A

• If problem arises near vessel entry, damage will lead to reduced blood flow to area, also potential increase risk of bacterial growth/invasion

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7
Q

Diverticulosis VS Diverticulitis

Key difference and MNFTS

A

Diverticulosis
• Non inflamed out pouchings
• MNFTS
o Aysymptomatic

Diverticulitis
• Inflamed out pouchings
• MNFTS
o Dull pain, nausea, vomiting, low grade fever

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8
Q

What is it called if a diverticulum is cut off from the rest of the gut

A

Strangulation

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9
Q

Tx for Diverticular Disease

A
  • Focus on ET and risks (diet, exercise, bowel habits)

* SX for complications of obstruction or perforation

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10
Q

What is IBS?

A

a functional GI disease is order characterized by a variable combination of chronic or recurrent intestinal symptoms not explained by structural or biochemical abnormalities.

Major issue is the symptoms
• GI Motility Disorder
• MNFTS are Variable (mild to debilitating)
• No obvious abnormality of structure or function

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11
Q

Etiology of IBS

A

Etiology is unclear.
• Sometimes linked to diet, stress, smoking, lactose intolerance

IBS often includes a search for triggers

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12
Q

3 possible pathologies for IBS?

A
  • Malabsorption of fermentable CHO (carbohydrates) and polyols (sugar alcohols) ex. Sorbitol. Unabsorbed then pass to colon where they are processed by gut flora causing flatulence
  • Alteration of CNS regulation of GI motor and sensory fx
  • Molecular signaling defect for serotonin
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13
Q

How might serotonin be related to IBS MNFTS?

A

• Serotonin actions and IBS MNFTS have parallels

o Serotonin facilitates perfusion, secretions, motility and pain and the GI tract is main site of synthesis

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14
Q

MNFTS of IBS?

A

• TEXT: Hallmark is abd pain relieved by defecation and an associated change in consistency and frequency of stools

CLASS:
• Diarrhea AND/OR constipation
• Abdm discomfort and pain
• Flatulence (common caused by bacteria processing carbs), nausea
• Mucoid stool (irritated gut will inc mucous production, not generally beneficial)

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15
Q

DX of IBS?

Scopes?

A

• Generally largely based on pt presentation
o Work up is not precise, Dx by exclusion and MNFTS

• Requires exclusion of organic disease (large number of potential labs and scopes)

o Endoscopy (Upper GI- through mouth  as far as       duodenum)
o Colonoscopy (lower GI tract)
o Sigmoidoscopy (similar to colon, but not as far, simpler, less prep)
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16
Q

Non pharmaceutical TX IBS

A

• Based on severity, type and triggers
• Avoid offending foods (identify triggers and eliminate)
o Works for mild to moderate IBS

• Reduce emotional stress

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17
Q

Pharmaceutical tx of IBS

Abx WHY?

A

• Drugs only in severe cases
o Anti-spasmodic (modulon)
o Antidiarrheal/ or laxative
o Abx with caution (i.e. when necessary, short term, specific low dose)
• ABX may control numbers of normal flora to rebalance concentrations

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18
Q

What is peritonitus

A

• Inflm of peritoneum

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19
Q

Most common etiology of peritonitis?

A

•Bacterial (esp. E Coli) or chemical irritation (bile, Hydrochloric acid) of the peritoneal serous membrane from contents that have escaped GI tract

20
Q

Peritonitis

Offending agent enters abdm cavity via?

A 
o Perferated ulcer
o Ruptured appendix
OR
• Pelvic Inflm disease PID (bact enter through vagina, uterus, Fallopian tube, ova to ABD cavity
OR
o	Colonoscopy (inotrogenic)
21
Q

What sort of exudate is present during peritonitis?

A

Thick and sticky exudate

Why thick?
Ahmed says thickness simply d/t to str and location

22
Q

Pathogenesis of peritonitis

Two disadvantages of peritoneal inflm?

A
  • Peritoneum is large structure allows easy spread across broad area
  • Mesenchyme heavily vascularized allowing for rapid absorption of toxins
23
Q

Two advantages to the thick exudate?

A

o Thick exudate forms
• Limits spread of bacteria (localization)
• Seals perforation

24
Q

What is ileus?

A

refers to the cessation of peristalsis

• CNS limits GI motility during peritonitis (compensatory action and is intentional)

25
Q

Three Key MNFTS of Peritonitis?

A

• Fluid shift (electrolyte imbalance)
o Ileus, fluid and air retained, Inc intra lumina pressure (GI), inc fluid sec in the gut (mucous)

• Alt perfusion
o Blood shunted to site of inflm

• Dyspnea
o Pain cause pt to limit breathing movements (larg infm abd strc)

NOTE- Can be severe leading to shock d/t volume of fluid involved

26
Q

Tx for peritonitis?

A
  • IV Abx
  • Fluids and electrolytes
  • Anti-inflm
  • Sx if indicated
27
Q

What is Appendicitis?

A

• Acute inflm of appendix WALL

28
Q

Which age group are most at risk of appendicitis

A

• Peaks 20-30yrs but common in 5-30yrs

29
Q

What is the etiology of appendicitis?

A

Idiopathic

30
Q

Two Theories of appendicitis etiology

?

A

Sometimes apparent on post-mortem, but not always

o Fecalith (hard small fecal pellet) obstructs cecum (opening to appx)
o Twisted appendix or bowel
31
Q

Pathophysiology of appendicitis

A

• Appendix lumen obstruction -> drainage into cecum blocked -> inc intra luminal pressure (as mucous secretion continues)-> exceeds venous pressure (of veins in walls, close veins) -> venous stasis (no blood return, blocks blood in)-> ischemia -> necrosis -> bact invasion of appendix wall

32
Q

What is the major complication of appendicitis?

A

Perforation (of an inflm bag of angry bacteria in your abdomen potential for peritonitis)

33
Q

How will pain MNFTS over time in appendicitis?

Other MNFTS?

A
  • Acute epigastric or periumbilical pain (referred pain)
  • Pain increases
  • Then colicky pain over 12 hrs (spasmotic, starts/stops)
  • Localizes to LRQ (rebound pain, pt will be guarding)
  • Ends with Mcburney point (Halfway along a line between iliac crest to umbilicus)

May also see some:
• Nausea
• Inc Temp and WBCs

34
Q

Dx of appendicitis

A
  • Hx and Px
  • Ultra Sound
  • CT
35
Q

Tx of appendicitis

A 
• IV Fluids
• Pain MNGMT
• Abx
• Appendectomy within 24-48 hrs
   o Delay may end with perforation and peritonitis
36
Q

Name 2 chronic conditions under the umbrella term IBD

Table 37-1

A
  • Ulcerative colitis (lesion restricted to large intestine and continuous)
  • Crohn disease (lesions found in both small and large intestine, not continuous- AKA skip lesions)
37
Q

Basic Etiological components of IBD?

A

• Complex trait
o Genetic susceptibility (no specific gene)
o Environmental trigger (bacterial infection)

38
Q

How is the IR involved in IBD?

A

o IR against normal gut flora
• Normally normal flora is tolerated by IR
• IN this case the IR targets normal flora
• These bacteria are not just in the lumen, but also in the lining of the gut (IR causes inflm and damage in lining)

39
Q

Is IBD a kind of autoimmunity?

A

o This is not autoimmunity, because flora are not self components, but foreign components that are normally in body

40
Q

Describe regions affected, lesion type and progression of Crohn’s disease

FIG 37-7

A 
• Primarily affects terminal ileum  
   o Other areas possible
• Primarily affects submucosa
   o all layers possible
• Granulomatous skip lesion, lesion takes on cobblestone pattern
• Slow non-aggressive progression
41
Q

MNFTS of Crohn’s

A

MNFTS
• Diarrhea
• Intermittent abdm pain
• Weight loss (decrease in absorptive surface area -> nutritional deficiency

42
Q

Describe regions affected, lesion type and progression of ulcerative colitis

A 
• Primarily involves mucosa of colon and rectum
• Proximal spread from rectum
• Continuous lesion
   o Bleeding ulcers
   o Thickened and inflm and harden
   o Edema and congestion
43
Q

Describe MNFTS of Ulcerative colitis

A
  • Bloody diarrhea
  • Abdm cramping
  • Some Weight loss (less so then crohn’s, but pain and GI irritability limits intake over long term)
44
Q

Dx strategies for IBD

A
  • Hx and Px
  • Exclude Gi infections
  • Sigmoidoscopy, colonoscopy, biopsy
45
Q

What is the tx for mild IBD?

1rst and 2nd line tx for more severe cases?

A
  • Very mild: diet manipulation might be enough)
  • 1rst line- Anti inflm (eg Sulfasalazine) w/ short course of Abx
  • 2nd line – steroids if not responsive
46
Q

What other pharmaceutical tx might be affective at controlling progression of the disease? IBD

A

immunomodulator medication such as methotrexate (anti folate)

NOTE- Med reduces DNA and cell division. Also used in higher doses in cancer treatments

47
Q

In what situations might Sx be required for IBD Tx?

A

Ulcer repair, fistula, drainage, resecting problematic section

253-Green Patho (21 decks)

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