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Pathophysiology - Gastrointestinal > Pathology of Non-Neoplastic Diseases of the Large Intestine > Flashcards

Pathology of Non-Neoplastic Diseases of the Large Intestine Flashcards

1
Q

Tell me whether each structure between the cecum and the rectum is peritoneal or retroperitoneal?

A 
Cecum - peritoneal
Ascending colon - retroperitoneal
Transverse colon - peritoneal
Descending colon - retroperitoneal
Sigmoid colon - peritoneal
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2
Q

Give the blood supply from the cecum to the anus

A

SMA - Proximal duodenum to distal 1/3 of transverse colon

IMA - Distal 1/3 of traverse colon to proximal rectum above pectinate line (superior portion supplied by superior rectal artery, branch of IMA).

Internal iliac artery - above the pectinate line via the middle rectal artery, and below the pectinate line via the the inferior rectal artery

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3
Q

Where are the villi and plicae circulares located in the colon?

A

Villi and plicae circularis are NOT in the colon -> mucosa is flat and smooth with deep crypts
-> plicae semilunares can be seen as mucosa folds which are not circumferential

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4
Q

How does the lamina propria of the colon differ from the stomach?

A

There are NO lymphatics in the lamina propria of the colon -> metastasis cannot occur if tumor only extends to LP

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5
Q

What is the outer longitudinal muscle on the outside and what sometimes juts out of the wall?

A

Outer muscle - taenia coli (three thick bands)

Jutting out of serosa / adventitia = epiploic appendages, made of adipose tissue

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6
Q

How does the function of colon differ from small intestine?

A

Much more mucous secretion for lubrication -> many more goblet cells

Absorption of Na+ and Cl- with loss of K+ and HCO3-

Production of vitamin K and fermentation of polysaccharides

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7
Q

What is cloacal dysgenesis sequence?

A

A rare syndrome of imperforate anus associated with confluence of rectum, vagina, and urinary bladder in a urogenital sinus

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8
Q

What causes Hirschsprung disease?

A

Abnormal arrest of the cephalad to caudal migration of neural crest cells in wall of colon -> aganglionic colon of Auerbach and Meissner plexuses causes tonic contraction
-> increased risk with down syndrome

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9
Q

How does Hirschsprung disease appear grossly and what is the treatment?

A

Colonic dilatation and hypertrophy proximal to segment of bowel without innervation

-> remove denerved segment -> need to have a pathologist in on the procedure checking for when you’ve biopsed regular colon with actual ganglion cells

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10
Q

What is the easy way to microscopically diagnose Hirschsprung disease?

A

Preganglionic nerve fiber hypertrophy can be seen which stains very intensely for acetylcholinesterase
-> much easier than simply saying that ganglion cells are absent, because it could just be your sample or cut

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11
Q

What are the two types of biopsy used for diagnosis of Hirschsprung and when are they used?

A
  1. Suction biopsy - absence of Meissner plexus can be seen - only takes submucosal
  2. Full-thickness biopsy - allows for visualization of Auerbach’s plexus as well, must be done with surgery -> done if suction biopsy inconclusive
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12
Q

What are the clinical manifestations of Hirschsprung disease?

A

In neonates - abdominal distension and failure to pass meconium in children

Chronic constipation in children

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13
Q

What is thought to the etiology of inflammatory bowel disease? What two diseases does this encompass?

A

Immune dysregulation in response to intestinal flora
-> probably due to a Th1-mediated delayed type hypersensitivity reaction

  1. Crohn’s disease
  2. Ulcerative colitis
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14
Q

Who tends to get inflammatory bowel diseases? Include their relationship to smoking.

A

Whites in their 20s or 30s

Becoming more prevalent in the West (hygiene hypothesis)

Crohn’s - smoking for any length of time is a strong risk factor

Ulcerative colitis - continued smoking lowers risk

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15
Q

What are two antibodies which can slightly help differentiate between Crohn’s and ulcerative colitis?

A

atypical p-ANCA - more typical of ulcerative colitis

anti-Saccharomyces cervisiae antibodies - more typical of Crohn disease

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16
Q

What is the distribution of damage in Crohn’s disease in terms of location?

A

Can happen in any portion of the GI tract, but especially the terminal ileum

Patchy involvement with skip lesions (skips segments)

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17
Q

How does Crohn disease appear grossly?

A

Firm segments of bowel with serosal “creeping fat” due to transmural inflammation which is very sticky, and the development of deep, narrow, linear ulcers giving a “cobblestone” effect

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18
Q

How does Crohn disease appear microscopically?

A

Transmural fibrosis and chronic inflammation, sometimes with noncaseating granulomas which would be pathognomonic

Inflammation will be patchy even on a microscopic level. Ulcers will progress from superficial to deep and narrow.

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19
Q

What does smooth muscle appear thickened so that the wall is firm and thick in Crohn’s disease?

A

Growth factors from inflammation / fibrosis induce scarring / thickening of wall

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20
Q

What sign is sometimes seen on barium studies of Crohn’s disease and where is it most commonly found?

A

“string sign” due to thickening of smooth muscle and fibrotic strictures

-> most common in terminal ileum

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21
Q

What are the structural complications of Crohn disease?

A

Fissures form in mucosal wall which may progress to: fistula tracts, abscesses, perforations

Fistula tracts may lead anywhere

22
Q

What malabsorption is characteristic of Crohn’s?

A

Terminal ileum damage -
Vitamin B12 deficiency, bile salt deficiency

Leads to chronic anemia

23
Q

What carcinomas does Crohn’s predispose to? What about Ulcerative colitis?

A

Crohn’s - adenocarcinoma of colon and small intestine

Ulcerative - adenocarcinoma of colon only (does not invade small intestine)

24
Q

How does Crohn’s present clinically?

A

Relapsing and remitting episodes of abdominal pain especially RLQ where terminal ileum is, fever, diarrhea, and weight loss

25
Q

What is the distribution of ulcerative colitis?

A

Continuous lesions always starting at the rectum and moving proximally up the colon

26
Q

How does ulcerative colitis appear grossly in active disease and what is a pseudopolyp?

A

Active - superficial, broad-based ulcerations and hemorrhage with intervening inflammatory pseudopolyps

Pseudopolyp - what remains of the mucosa level which as not ulcerated

Loss of haustra on imaging

27
Q

How does ulcerative colitis appear microscopically in active disease?

A

Diffuse mucosal acute inflammation with crypt abscesses (neutrophils in crypts) and chronic inflammation, with superficial ulceration

28
Q

How does ulcerative colitis appear grossly and microscopically in quiescent disease?

A

Grossly - Diffusely flattened and thin mucosa

Microscopically - mucosal atrophy and fibrosis, with chronic inflammation and glandular loss

29
Q

What type of diarrhea characterizes ulcerative colitis? What pattern does this present in?

A

Bloody, pussy diarrhea (think of crypt abscess and inflammation)

Also presents in relapsing and remitting pattern

30
Q

What is the feared complication of ulcerative colitis?

A

Toxic megacolon - knockout of submucosal plexus by inflammatory mediators leads to stasis and functional obstruction of bowel
-> expansion of bowel with risk of perforation / rupture

This is also called fulminant colitis

31
Q

What are the extraintestinal manifestations of both Crohn’s disease and ulcerative colitis?

A

Arthritis - migratory polyarthritis, sacroiliitis, ankylosing sponylitis

Eyes - Uveitis

Skin - Erythema nodosum (inflammation of adipose)

32
Q

What liver condition are inflammatory bowel diseases causative of?

A

Primary sclerosing cholangiitis - especially associated with ulcerative colitis

33
Q

What is angiodysplasia and who tends to get it?

A

Acquired malformation of mucosal and submucosal capillary beds

Happens in older individuals who had intermittent mechanical obstruction (high wall tension)

34
Q

What are the symptoms of angiodysplasia? How does it look histologically?

A

Lower GI bleeding in an older adult

Histologically - huge dilated submucosal veins which can bleed if there is an erosion

35
Q

Who gets colonic diverticula and what is the pathogenesis?

A

Older adults who have a low-fiber diet

Low fiber diet -> increased peristaltic activity required to propel food -> outpouching of the wall at points of weakness

36
Q

What are diverticula and where do they appear?

A

Outpouchings of the mucosa / submucosa of the colon through the muscularis propria at points where the vasa recta enter (false diverticula)

Appear commonly in the sigmoid colon (where the water has been mostly reabsorbed so poop takes more force to propel)

37
Q

What are the symptoms and complications of diverticulosis?

A

Usually asymptomatic or associated with mild left lower quadrant discomfort

Complications:
Diverticulitis

Diverticular bleeding (painless hematochezia)

38
Q

How does diverticulitis present?

A

Appendicitis-like symptoms in left lower quadrant:
Fever, LLQ tenderness / pain, and neutrophilia

Treat with antibiotics

39
Q

What are the complications of diverticulitis?

A

Pericolonic abscess, fistula, bowel perforation -> peritonitis, and bowel obstruction (inflammatory stenosis)

40
Q

What are the common causes of appendicitis in adults and children?

A

Children / adolescents = most common to get it
-> Lymphoid hyperplasia

Adults -> fecalith obstruction

41
Q

Give the pathogenesis of appendicitis and two less common causes of it?

A

Luminal obstruction causes increased intraluminal pressure -> venous obstruction -> hemorrhagic infarction -> superimposed bacterial infection
(alot like cholecystitis)

  1. Colon carcinoma (older adults)
  2. Enterobius vermicularis (pinworms)
42
Q

What is seen microscopically in appendicitis?

A

Transmural neutrophilic acute inflammatory infiltrate with vascular engorgement, edema, and areas of suppurative necrosis

43
Q

What are the clinical manifestions of appendicitis and some common complications?

A

Periumbilical pain migrating to McBurney point of RUQ, with N/V and fever with left shift.

Complications: rupture leading to peritonitis, sepsis, periappendix abscess

44
Q

Is intestinal obstruction more likely in the small or large intestine and what are the two broad types?

A

More likely in small intestine which is more mobile

  1. Functional obstruction - called an ileus
  2. Mechanical obstruction
45
Q

What are the causes of functional obstruction / ileus?

A

Disruption of intestinal peristalsis (i.e. Hirschsprung)

Risk factors: recent abdominal surgery, opiates, hypokalemia, sepsis

46
Q

What is the most common cause of mechanical obstruction?

A

Formation of adhesions - abnormal fibrous bands between tissues, especially in Crohn’s disease or following surgery

47
Q

When does intussusception occur in adults and children?

A

Adults - associated with intraluminal mass or tumor acting as a lead point

Children - more common -> due to lymphoid hyperplasia (i.e. rotavirus), with terminal ileum telescoping into cecum

48
Q

What is it called when a portion of bowel twists on its mesentery and where does it happen in adults?

A

Volvulus -> happens in sigmoid colon in adults due to long mesentery

(coffee bean sign on X-ray)

49
Q

What do obstructions normally cause symptomatically?

A

Normally just abdominal pain, distention of bowel, constipation, and even diarrhea if peristalsis increases to compensate.

Obstipation - ability to pass gas or stool

50
Q

What are the medical management options for obstructions and when is surgery indicated?

A

Functional obstruction / ileus - Fluid resuscitation, bowel rest, and nasogastric tube decompression

Surgery indicated when: intestinal ischemia is a complication, or when the problem is mechanical

Pathophysiology - Gastrointestinal (24 decks)

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