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GIT > Small & Large Intestine > Flashcards

Small & Large Intestine Flashcards

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1
Q

Name two congenital conditions of intestines.

A
  1. Meckel Diverticulum
  2. Hirschsprung Disease
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2
Q

What is the pathogenesis of Hirschsprung Disease?

A

Absence of neural crest derived ganglion cells within the colon - lacking Meissner Submucosal and Auerbach Myenteric plexus

Hence absence of co-ordinated peristalsis leading to functional obstruction of the affected bowel and proximal dilation

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3
Q

What is the initial sign of Hirschsprung Disease?

A

Failure to pass meconium in immediate postnatal period
- constipation, abdominal distension, bilous vomiting

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4
Q

What are the complications of Hirschsprung Disease?

A

Megacolon –> Perforation –> Peritonitis –> Sepsis
Enterocolitis
Fluid/Electrolyte Disturbances

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5
Q

How can Hirschsprung Disease be treated?

A

Surgical Removal Of Aganglionic Segment

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6
Q

In Ischemic Bowel Disease, infarction may be ___, ___, or _____. What are the underlying causes of each?

A

Transmural (acute vascular obstruction), Mural or Mucosal (secondary to hypoperfusion)

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7
Q

Which part of the bowel epithelium is most vulnerable to damaghe in ischemic bowel disease?

A

Surface epithelium. Patterns of intestinal microvessels: intestinal capillaries run alongside glands from crypt to surface before U-turning to empty into post-capillary venules

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8
Q

How does ischemic colitis appear?

A

Surface epithelial necrosis and normal crypts

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9
Q

State some predisposing conditions for ischemia.

A
  1. Arterial Thrombosis
  2. Arterial Embolism
  3. Venous Thrombosis
  4. Non-Occulsive Ischemia
  5. Misc. (Volvulus, Herniation, Adhesions)
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10
Q

How does malabsorption present normally?

A

Chronic Diarrhoea

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11
Q

Name 3 common chronic malabsorptive disorders.

A

Pancreatic Insufficiency
Celiac Disease
Crohn’s Disease

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12
Q

What is the pathogenesis of Celiac Disease?

A

Immune-mediated enteropathy triggered by ingestion of gluten

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13
Q

3 morphological features seen in Celiac Disease

A
  1. Intraepithelial CD8+ T lymphocytes
  2. Crypt Hyperplasia
  3. Villous Atrophy
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14
Q

Name some
a) Bacteria
b) Viruses
c) Fungi
d) Protozoa and Parasites
that cause Infectious Enterocolitis

A

a) E. Coli, Salmonella, Shigella, V. Cholerae, Campylobacter
b) Rotavirus, Norovirus, CMV, HSV
c) Candida, Aspergillus, Mucormycosis, Histoplasma
d) Entameba histolytica, Giardia lambila, Cryptosporidia Ascaris, Trichuris, Enterobius, Strongyloides, Schistosomiasis

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15
Q

What bacteria causes pseudomembranous colitis?

A

Clostridium Difficile

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16
Q

What are the histological presentations of pseudomembranous colitis?

A

Pseudomembranes composed of an adherent layer of inflammatory cells and debris at sites of colonic mucosal injury, where damaged crypts spew out mucopurulent exudates

17
Q

What are the clinical presentations of pseudomembranous colitis?

A

Fever, Leukocytosis, Abdominal pain/cramps, watery diarrhoea

18
Q

How is diagnosis of pseudomembranous colitis done?

A

Detection of C. Difficule Toxin
Histopathology

19
Q

Where is the commonest site of intestinal TB?

A

Ileocecal region

20
Q

What can intestinal TB cause?

A

Circumferential ulcers (in the direction of lymphatics to mesentery)
Thickening of walls, strictures

21
Q

How can intestinal TB spread?

A

Miliary Spread

22
Q

How does amebiasis present endoscopically?

A

Flask-shaped ulcers with shaggy edges, napkin-like constrictive mass (granulation tissue)

23
Q

Name a complication of amebiasis.

A

Liver Abscesses via portal circulation

24
Q

What is the pathogenesis of acute appendicitis?

A

Lumen Obstruction (fecolith, foreign matter, lymphoid hyperplasia) –> Luminal bacteria multiplication, invasion of mucosa and wall, acute inflammation, necrosis and ulceration –> Perforation (peritonitis, pelvic abscess, subphrenic abscess)

25
Q

What are the histological features in acute appendicitis?

A

Edema and Turgidity
Congestion and Hemorrhage
Fibrinopurulent Exudate
Necrosis, Ulceration

26
Q

What is the pathogenesis of IBD

A

Dysfunctions of gut microbiome
Intestinal epithelial dysfunction\
Aberrant mucosal immune responses

27
Q

Two types of IBD?

A

Crohn’s
Ulcerative Colitis

28
Q

How is IBD treated?

A

Immunosuppression

29
Q

4 features of Crohn’s

A

Transmural Chronic Inflammation with Lymphoid FOllicles
Non-Caseating Granulomas
Discrete Deep Ulcers
Fibrosis

30
Q

4 complications of Crohn’s

A

Stricture
Fissues/Fistulas
Perforation/Peritonitis
malignancy

31
Q

Features of UC?

A

Limited to mucosal surface
Only affects rectum and distal colon (only affects Small intestine if ‘backwash ileitis’)
Inflammatory pseudopolyps

32
Q

Complications of UC?

A

Malignancy
Toxic Megacolon - inflammatory mediators damage muscularis propria and disturb neuromuscular function such that there is massive dilation and perforation risk

33
Q

Compare and COntrast Crohn’s and UC. Divisions are macroscopic, microscopic, clinical.

A
34
Q

What is diverticular disease?

A

Mucosa outpiuching surrounded by fibrous tissue

35
Q

Who usually gets diverticular disease?

A

Elderly due to weakening of muscle wall

36
Q

What are 2 complications of diverticular disease?

A

Acute inflammation (diverticulitis)
- pericolic abscess
- pericolic fibrosis and adhesions
- colovesical fistula
- strictures
- perforation/peritonitis

Erosion of blood vessels
- rectal bleeding
-anemia

37
Q

Name some obstructive lesions of the GIT

A
38
Q

Name some causes of lower GI bleeds.

A
39
Q

What is angiodysplasia? Where does it occur? When does it occur?

A

Malformed submucosal or mucosal blood vessels

Cecum or right colon

After sixth decade

GIT (3 decks)

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