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GI 2 Pathology--Chapt 16 and 17 > Chapter 17 part 5--Small Intestine > Flashcards

Chapter 17 part 5--Small Intestine Flashcards

1
Q

Disease processes common to the small intestine and colon

A

-bc of their roles in nutrient and water transport and their interface with diverse food and microbial Ags, the intestines are involved by processes like malabsorption, infectious, inflammatory and neoplastic processes

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2
Q

What are the most common causes of intestinal obstruction?

A
  • Tumors, infarctions and strictures (due to for ex: CD) account for 10-15% of obstructions
  • 80% are attributable to 4 entities: Hernias, Adhesions, Volvulus and Intussusception
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3
Q

Hernias–hernia sac

A
  • Peritoneal wall defects permit peritoneal sac protrusion in which bowel segments can be trapped (external herniation!!!)
  • subsequent vascular stasis and edema lead to incarceration!
  • vascular compromise leads to STRANGULATION
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4
Q

Locations of hernias

A

-femoral and inguinal canals, umbilicus, and surgical scars

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5
Q

Most common cause of intestinal obstruction worldwide

A

Hernias!!

-also the 3rd most common cause in US

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6
Q

Adhesions are

A
  • residua of localized peritoneal inflammation (peritonitis) following surgery, infection, endometriosis, or radiation
  • healing leads to fibrous bridging bw viscera
  • congenital adhesions also rarely occur
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7
Q

Most common cause of intestinal obstruction in the US??

A

-Adehesions!!

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8
Q

Complications of adhesions

A

-internal herniation (within peritoneal cavity), obstruction and strangulation

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9
Q

4 major causes of intestinal obstruction

A

1) herniation of a segment in the umbilical or inguinal regions
2) adhesion between loops of intestine
3) volvulus
4) intussusception

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10
Q

Volvulus

A
  • complete twisting of a bowel loop about its mesenteric vascular base leading to vascular and lumina obstruction with infarction
  • occurs most often in redundant loops of sigmoid colon followed by cecum and small bowel
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11
Q

Intussusception

A
  • occurs when an intestinal segment (usually small bowel) telescopes into the immediately distal segment
  • Peristalsis propels the invaginated segment along with its attached mesentery, resulting in obstruction, vessel compression, and infarction
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12
Q

Intussusception in children vs adults–causes

A
  • infants and children: spontaneous or ROTAVIRUS infxn
  • adults: point of traction is usually a tumor!!
  • in children under 2 years, intussusception is the most common cause of intestinal obstruction!!!
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13
Q

Ischemic Bowel Disease

A
  • abundant collateral supply throughout GI tract allows bowel to usually tolerate slowly progressive loss of blood supply
  • BUT abrupt compromise of any major vessel can cause infarction of severe meters in intestine
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14
Q

Watershed zones

A

-between major branches (e.g., splenic flexure bw superior and inferior mesenteric artery circulations) are most vulnerable for infarction

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15
Q

Infarction damage ranges; what cells are more susceptible to infarction??

A
  • ranges from mucosal infarction to transmural infarction
  • bc they are at the end of the capillary network, the epithelial cells at the tips of villi are more susceptible to ischemia than crypt epithelial cells!!
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16
Q

Important causes of ischemia of bowel=

A
  • Atherosclerosis
  • Aortic aneurysm
  • Hypercoagulable states
  • Embolization
  • Vasculitis
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17
Q

Hypoperfusion also associated with?

A
  • cardiac failure, shock, dehydration, vasoconstrictive drugs
  • Mesenteric venous obstruction or thrombosis due to hypercoagulability, masses or cirrhosis can also cause ischemic disease
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18
Q

Pathogenesis of ischemic bowel disease

A
  • An initial hypoxic injury occurs at onset of vascular compromise (although intestinal epithelium is relatively resistant to transient hypoxia)
  • subsequent repercussion leads to an influx of inflammatory cells and mediators causing majority of damage
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19
Q

Ischemic bowel disease morphology–Mucosal infarction

A

-Patchy mucosal hemorrhage but with normal serosa

20
Q

Ischemic bowel disease morphology–Mural infarction

A
  • Complete mucosal necrosis, with variable necrosis of submucosa and muscularis propria
  • Distribution is typically segmental without serositis!!
21
Q

Ischemic bowel disease morphology–Transmural infarction

A
  • involved segments are hemorrhagic and has associated serositis
  • Coagulative necrosis of muscular propria with perforation develops within 1-4 days
22
Q

Microscopic morphology of Ischemic bowel disease

A
  • atrophy and sloughing of surface epithelium but preserved crypts can be hyper proliferative
  • Extent of inflammation and edema depends on duration of injury
  • Superimposed bacterial infection can induce pseudomembrane formation
23
Q

Chronic vascular insufficiency in Ischemic Bowel disease results in what?

A

-fibrosis of lamina propria and occasionally structure formation

24
Q

Clinical features of Ischemic Bowel Disease–in who? what are the symptoms?

A
  • typically occurs in older individuals with coexisting cardiac or vascular disease
  • ischemic bowel presents with severe abdominal pain, bloody diarrhea or gross melon, abdominal rigidity, nausea and vomiting
  • Right sided colonic disease has more severe course and coexisting COPD is a poor prognostic indicator
25
Q

Treatment of Ischemic bowel disease and prognosis

A
  • Surgery is indicated in unto 10% of cases

- with appropriate management, 30-day mortality is 10-20%

26
Q

Aangiodysplasia lesions–what are they

A
  • tortuous, ecstatic dilations of mucosal or submucosal veins occurring in 1% of population
  • most common in the cecum or ascending colon, after age 60
  • accounts for 20% of major episodes of lower GI bleeding
27
Q

Causes for Angiodysplasia

A
  • partial, intermittent venous occlusion

- cecal or right colonic predilection derives from the greater wall tension in those owing to larger diameter

28
Q

What is malabsorption?

A

-defective absorption of fats, fat and water-soluble vitamins, proteins, carbs, electrolytes, minerals and water

29
Q

Symptoms of malabsorption

A
  • diarrhea, flatus, abdominal pain, and muscle wasting

- classic hallmark=steatorrhea!!=excessive fecal fat and greasy, malodorous stools

30
Q

Clinical consequences of malabsorption (due to various deficiencies)

A
  • Anemia and mucositis (pyridoxine, folate or vitamin B12)
  • Bleeding (vitamin K)
  • Osteopenia and tetany (calcium, magnesium, vitamin D)
  • peripheral neuropathy (vitamins A or B12)
31
Q

Most common causes of malabsorption in the US

A
  • celiac disease
  • pancreatic insufficiency
  • CD
32
Q

Pathogenesis of malabsorption

A
  • Intraluminal digestion
  • Terminal digestion
  • Transepitheial transport
  • Lymphatic transport
33
Q

Intraluminal digestion

A

-Emulsification and initial enzymatic breakdown

34
Q

Terminal digestion

A

-Hydrolysis within enterocyte brush border

35
Q

Transepithelial transport

A

-through enterocytes

36
Q

Lymphatic transport

A

-of absorbed lipids

37
Q

What is diarrhea?

A
  • increased stool mass, frequency, or fluidity usually exceeding 200g/day
  • severe cases can exceed 14 L/day and be fatal without fluid restoration
38
Q

Dysentery

A

-Painful, bloody, small-volume diarrhea

39
Q

Categories of diarrhea

A
  • Secretory
  • Osmotic
  • Malabsorptive
  • Exudative
40
Q

Secretory diarrhea

A

-isotonic with plasma and persists during fasting

41
Q

Osmotic diarrhea

A
  • Unabsorbed luminal solutes (e.g., due to lactase deficiency) increase osmotic pull of fluid
  • stool is more than 50 most hyperosmolar relative to plasma and abates with fasting
42
Q

Malabsorptive diarrhea

A
  • abates on fasting
43
Q

Exudative diarrhea

A
  • due to inflammatory disease

- purulent, bloody stools persist during fasting

44
Q

Cystic fibrosis

A
  • due to absence of the epithelial cystic fibrosis transmembrane conductance regulator (CFTR)
  • causes defective bicarb, sodium and water secretion resulting in defective luminal hydration
45
Q

Results of cystic fibrosis

A

-ocassionally causes intestinal obstruction but more commonly (80% of cases) results in formation of pancreatic intraductal concretions and causes pancreatic duct obstruction, low grade chronic auto digestion of pancreas with eventual exocrine pancreatic insufficiency

46
Q

Tx for failure of nutrient absorption in CF

A

-oral enzyme supplementation

GI 2 Pathology--Chapt 16 and 17 (14 decks)

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