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DERS (GIT) > L6- GIT Pathology III (intestines) > Flashcards

L6- GIT Pathology III (intestines) Flashcards

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1
Q

Meckel’s Diverticulum:

  • (1) definition
  • (2) explain the rule of 2’s
  • found on (anti-/mesenteric) border
  • (4) types
A

1- incomplete involution of vitelline duct

2- 2% of normal population (x2 in males), 2in (5cm) in length, 2ft from ileocecal valve

3- anti-mesenteric border

4- True Diverticulum (all GIT layers) or Heterotopia (gastric mucosa or pancreatic tissue)

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2
Q

Meckel’s Diverticulum:

  • (1) common Sxs
  • (2) potential complications
A

1- asymptomatic

2- hemorrhage / peptic ulcer, intestinal obstruction, diverticulitis, perforation, fistula

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3
Q

Malabsorption syndromes:

  • (1) definition
  • (2) clinical presentation
  • (3) are impaired
A

1- defective absorption in fats, fat soluble / other vitamins, proteins, carbs, electrolytes, minerals, water

2- chronic diarrhea, steatorrhea

3- digestion, absorption

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4
Q

Celiac Sprue:

  • (1) alternate names
  • mostly presents in (2- race/age) population
  • in atypical presentations in adults, (3) maybe noted
  • all intestinal changes are reversible upon (4)
  • (5) is a important long-term risk
A 
1- gluten-sensitive enteropathy, non-tropical sprue
2- whites, 1-10 y/o
3- Fe deficient anemia
4- gluten free diet
5- T-cell lymphomas
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5
Q

Celiac Sprue mostly affects (1) segment with (2) changes

A

Proximal Intestine:

  • villous atrophy (typical)
  • inc intraepithelial lymphocytes
  • inc lymphocytes, macrophages, plasma cells in lamina propria
  • elongated, hyperplastic crypts
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6
Q

Celiac Sprue pathogenesis

A

1) gluten –> gliadin upon contact with brush border
2) gliadin converted to deamidated gliadin by tTG
3) APC attaches to deamidated gliadin via HLA-DQ2/DQ8
4) APC complex activates T cell
5) IFN-γ production
6) activation of B-cell to create Anti-gliadin Anti-endomysium, Anti-tTG Igs

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7
Q

Celiac sprue:

  • Ig’s against (1)
  • HLA-(2) are heavily involved
  • (3) is an important component for pathogenesis and diagnosis
A

1- (anti-) gliadin, tTG, endomysium

2- HLA-DQ2, HLA-DQ8

3- tTG = tissue transglutaminase

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8
Q

Celiac Sprue histology:

include all changes

A
  • villous blunting
  • inc lamina propria in chronic inflammation
  • crypt hyperplasia
  • intraepithelial lymphocytosis = >30 lymphocytes per 100 enterocytes (normally <20)
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9
Q

Celiac sprue diagnosis investigations

A
  • malabsorption documentation (IDA)
  • SI biopsy
  • reversal of changes after gluten-free diet
  • Serology: Anti-gliadin, Anti-endomysial, Anti-tTG
  • HLA genotyping: majority DQ2, sometimes DQ8
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10
Q

Tropical Sprue:

  • occurs to people living or after visiting (1) in a (2) time-frame
  • involves (3) part of SI in comparison to celiac sprue
  • (4) SI appearance
A

1- Puerto Rico, Caribbean
2- mos-yrs after visit
3- entire SI, mainly proximal SI in celiac’s
4- may appear normal, can appear like celiac’s

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11
Q

Tropical sprue, aka (1):

-pathogenesis is related to (2), therefore (3) are effective in treatment, which is one distinguishing factor from (4)

A

1- post-infectious sprue
2- superimposed bacterial infection on pre-existing SI injury (although unknown cause)
3- antibiotics
4- celiac’s

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12
Q

Whipple disease:

  • caused by (1), described as (2)
  • affects (3) parts of the body
  • affects (males/females) more
A

1- Tropheryma whippelii
2- Gram+ sickle shaped bacteria
3- (systemic disease) intestines, joints, CNS
4- males (10:1)

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13
Q

Whipple disease:

  • (1) is seen in H&E, PAS stain
  • (2) is seen on EM
  • (3) may be present in affected areas
  • (4) Tx
A

1- mucosa laden with distended macrophages (a sheet on macrophages) in lamina propria PAS-positive granules
2- rod shaped bacilli
3- granulomatous inflammation
4- antibiotics

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14
Q

Giardia (lamblia):

  • described as (1) with (2) forms present in the GIT
  • usually acquired due to (3), where (4) and (5) are big risk factors for getting the disease
A

1- protozoa gut pathogen with flagellum
2- trophozoites, cysts (shed in the GIT)
3- drinking contaminated water with cysts
4- areas of poor sanitation, crowded areas
5- immunosuppression

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15
Q

Cryptosporidium:

  • causes (1) in a normal host
  • causes (2) in a (3) patient
  • (4) appearance on histology
A

1- self-limiting infection
2- chronic diarrhea
3- AIDS

4- small blue intracellular spheres lying at the top of brush border cells (enveloped by thin layer of host cytoplasm)

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16
Q

obstructional bowel disease is most common in (1) area GIT with either a (2) or (3) cause

A

1- SI
2- Mechanical: hernias, intestinal adhesions, intussusception, volvulus
3- Non-mechanical / pseudo-obstruction: failure of propulsion due to SM disorder or paralysis or local nerve dysfunction

17
Q

list the mechanical causes of intestinal obstruction

A
  • herniation
  • adhesion
  • intussesception
  • volvulus
18
Q

(1) is the most common cause of intestinal obstruction in children, even though there is no (2). If left untreated, (3) may occur.

A

1- intussusception
2- underlying anatomic defect
3- obstruction and infarction

19
Q

Intestinal Obstruction:

  • (1) clinical features
  • (2) clinical complications
  • (3) investigations / lab testing
A

1- abdominal pain, abdominal distension, vomiting, constipation
2- infarction, peritonitis, electrolyte derangement
3- X-Ray, US, electrolytes

20
Q

list the types of Ischemic Bowel diseases

A
  • mucosal infarction: up to muscularis mucosa
  • mural infarction: mucosa and submucosa
  • transmural infarction: all 3 wall layers involved
21
Q

list the causes for Ischemic Bowel disease

A

Hypoperfusion: acute or chronic

Acute vascular obstruction:

  • severe atherosclerosis
  • AAA
  • hypercoaguable states / oral contraception
  • embolizations of cardiac vegetations / aortic atheromas
22
Q

Ischemic Bowel disease:

  • (1) first phase, (2) second phase of pathogenesis
  • (3) and (4) aspects of intestinal vascular anatomy also contribute to distribution of ischemic changes
A

1- initial hypoxic injury
2- reperfusion injury

3- watershed zones (spleni flexure, sigmoid-rectal junction)
4- patterns of intestinal microvessels

23
Q

Ischemic Bowel disease:

  • mainly affects (1) part of the GIT in a (diffuse/discontinuous) fashion
  • mucosa often appears (3), and he bowel wall has markedly (4)
A

1- any level of the gut
2- discontinuous / segmental and patchy
3- hemorrhagic and ulcerated
4- thickening due to edema

24
Q

Ischemic Bowel disease:

  • damage is most pronounced in (1) or (2) events
  • (3) of the muscularis propria occurs in days 1-4 and may be associated with (4)
A

1- acute arterial thrombosis
2- transmural infarction

3- coagulative necrosis
4- purulent serositis and perforation

25
Q

Ischemic Bowel disease:

  • mainly affects (young/old) population
  • (2) acute Sxs from transmural infarction
  • (3) prognosis
A

1- older adults

2- sudden severe abdominal pain/tenderness, n/v/d, bloody/melanotic stool, shock, diminished/absent bowel sounds, board-like rigidity of abdominal wall

3- depends on underlying cause + severity of injury

26
Q

Acute Appendicitis:

  • (1) definition, with (2) present 50-80% of the time with a (3) pathogenesis
  • if (2) is not present, there is a (4) pathogenesis
A

1- inflammation
2- underlying obstruction
3- obstruction + continued secretions (mucus fluid) –> inc intraluminal P –> collapse of draining veins –> ischemic injury –> bacterial proliferation -> inflammation / edema

4- unclear

27
Q

Acute Appendicitis:

  • normally affects (young/old) individuals
  • (2) clinical presentation
  • (3) clinical complications
A

1- young

2- periumbilical –> RLQ pain w/ tenderness (McBurney’s), n/v, mild fever, leukocytosis (neutrophilia)

3- perforation, peritonitis, periappendiceal abscess, liver abscess, bacteremia

28
Q

list appendix tumors

A
  • carcinoid
  • adenoma
  • adenocarcinoma
  • mucocele
29
Q

describe a mucocele (appendix)

A

dilated appendix filled with mucus from:

  • obstructive appendix
  • mucinous cystadenoma / cystadenocarcinoma
30
Q

_______ is a abdominal tumor with peritoneal involvement by mucinous implants, mostly in the appendix

A

Pseudomyxoma peritonei

-also found in ovary, pancreas, colon

31
Q

describe the range / grade of pseudomyxoma peritonei (appendix)

A

Low-grade (LAMN- low grade appendiceal mucinous neoplasm): abundant mucin, scan low-grade neoplastic epithelium

High-grade (mucinous adenocarcinoma): abundant malignant epithelial cells, signet ring cells can be present

32
Q

Hirschsprung disease:

  • more in (males/females)
  • (2) common associated condition
  • (3) part of the GIT is always affected
A

1- -males (4:1)
2- down syndrome (10%)
3- rectum

33
Q

______ is most common congenital intestinal obstruction

A

Hischsprung disease:

-absent ganglion cells in Messner submucosa and Auerbach / myenteric plexuses

34
Q

Hirschsprung disease definition / pathogenesis

A

absence of ganglion cells in:

  • meissner submucosa plexus
  • auerbach myenteric plexus

i) defect in migration / survival of neuroblasts
ii) congenital absence of ganglion cells
- functional obstruction
- dilation proximal to obstruction (megacolon)

35
Q

Hirschsprung disease:

  • (1) clinical features
  • (2) Dx
  • (3) complications
A

1- *delayed passage of meconium, constipation, abdominal distention (right after birth)

2- *rectal biopsy

3- enterocolitis, perforation / peritonitis

36
Q

Diverticular disease (diverticulosis / diverticulitis):

  • common in (1) geographic area
  • mostly in (2) age population
  • commonly affects (3) part of GIT
  • (4) defintion / description
A

1- western world
2- >60 y/o (50% of cases)
3- sigmoid colon
4- flask-like mucosal pouches extending from lumen thru colonic wall

37
Q

diverticulosis (/diverticulitis) pathogenesis

A
  • LACKS dietary fiber –> substantial bowel contractions + inc intraluminal pressure
  • herniations of colonic wall at focal defects

DERS (GIT) (21 decks)

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