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ACP GI and HBP system, Urogenital system > BAP38 - Non-neoplastic diseases of small and large bowels > Flashcards

BAP38 - Non-neoplastic diseases of small and large bowels Flashcards

1
Q

In ischemic bowel disease, which layer of the bowel is most prone to ischemia? Why?

A

The mucosa, as it is furthest away from the blood supply

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2
Q

In ischemic bowel disease, there is a hypoxic injury phase and a reperfusion injury phase. Briefly describe what happens in each phase.

A

Hypoxic injury: little damage

Reperfusion injury phase:
o ↑O2 supply > ↑ROS
o ↑influx of leukocytes and complements > ↑inflammation

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3
Q

Watershed zones like end of arterial supplies are prone to damage. Give 2 examples.

A
  1. Splenic flexure: between SMA and IMA

2. Rectosigmoid junction: between IMA and internal iliac artery

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4
Q

What are the 3 types of infarction in ischemic bowel disease? (briefly describe)

A
  1. Mucosal
  2. Mural - mucosal + submucosal
  3. Transmural - all layers
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5
Q

What is the pathophysiology for mucosal, mural and transmural infarction in ischemic bowel disease?

A

Mucosal + Mural:

  • Systemic hypoperfusion (shock)
  • Localized anatomical defects

Transmural:
- Acute occlusion of a major mesenteric injury > infarction

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6
Q

Which of the following about ischemic bowel disease is incorrect?
A. If mucosal/mural infarction is not resolved, it will progress to transmural infarction
B. Patients will experience abdominal pain and melena in all 3 types of infarction
C. Patients with transmural infarction have high mortality (>50%)
D. Patients with transmural infarction may experience sepsis and shock

A

All of the above

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7
Q

Etiology of ischemic bowel disease can be classified into luminal, mural and extramural. Give examples of each of them (5)

A
  1. Luminal
    - Embolism: AF as MC factor, - - - Thrombosis (Virchow triads)
  2. Mural
    - Atherosclerosis
    - Vasoconstriction: secondary to shock or vasoconstrictors (phenylephrine, noradrenaline)
  3. Extramural
    - Anatomical defects: volvulus, hernia
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8
Q

Which anatomical site is most vulnerable to arterial embolism? Why?

A

SMA, greatest velocity of blood flow + most acute angle off the aorta

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9
Q

What are hemorrhoids?

A

Variceal dilations of anal/perianal venous plexus

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10
Q

Which of the following about hemorrhoids is incorrect?

A. Constipation is a risk factor
B. Pregnancy is a risk factor
C. Portal hypertension is a rare risk factor
D. Patients experience pain in all types of hemorrhoids
E. Patients may experience rectal bleed and pruritus

A

D: only in external and thrombosed hemorrhoids!

A: because it causes increase venous pressure

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11
Q

What are the differences between external and internal hemorroids? (6)

A

Location:

  • Ex: below the dentate line
  • In: above the dentate line

Epithelium

  • Ex: squamous epithelium
  • In: Columnar epithelium

Pain

  • Ex: pain if thrombosed
  • In: no pain
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12
Q

Internal hemorrhoids can be further divided into which 4 grades?

A

Grade 1: no prolapse
Grade 2: prolapse that can be reduced spontaneously
Grade 3: prolapse that can be reduced manually
Grade 4: prolapse that cannot be reduced

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13
Q

What is the definition of angiodysplasia (vascular ectasia)?

A

AVM (arteriovenous malformation) characterised by tortuous dilatations of submucosal and mucosal veins

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14
Q

Where is the MC site for angiodysplasia in the GI tract?

A

Caecum and ascending colon (80%) > jejunum and ileum (15%)

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15
Q

Which of the following about angiodysplasia is incorrect?

A. It is associated with end-stage renal failure (ESRF)
B. It is a common cause for LGIB
C. It can be due to degenerative causes
D. It can be due to mechanical causes like peristalsis
E. All recurrent bleeding caused by angiodysplasia is self-limited

A

E
- 15% experience massive bleeding

D: Mechanical: peristaltic contraction > intermittent obstruction and dilatation of submucosal veins, venules, capillaries > loss of precapillary sphincter function > AVM

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16
Q

What are the 2 types of infective enterocolitis?

A
  1. Intestinal tuberculosis

2. Pseudomembranous colitis

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17
Q

In infective enterocolitis, patients present with diarrhoea, sometimes ulceration and inflammation in intestine. It can be caused by? (3)

A
  1. Bacteria (Vibrio, difficile)
  2. Virus (rotavirus)
  3. Parasites
18
Q

In intestinal tuberculosis, _____________ can be identified by Ziehl-Neelsen stain (+) because it is an acid fast bacilli. TB-PCR can be used as rapid diagnosis.

A

Mycobacterium tuberculosis

19
Q

What can be seen in the caseating granuloma in intestinal tuberculosis?
(3)

A
  1. Necrotic center
  2. Epithelioid histiocytes
  3. Langhans giant cells
20
Q

In pseudomembranous colitis, the pseudomembrane is composed of?

A

Layer of inflammatory cells + debris overlying sites of mucosal injury

21
Q

Pseudomembranous colitis is caused by toxins of?

A

Clostridium difficile

22
Q

How can pseudomembranous colitis be treated?

A

G+ rods, obligate anaerobe

  1. Antibiotics (clindamycin, severe: metronidazole, oral vancomycin as last resort)
  2. Faecal microbiota transplantation (FMT)
23
Q

Which of the following are possible etiologies for IBD? (inflammatory bowel disease)

A. Genetics: NOD2 (not in HK) gene mutation
B. Mucosal immune response: Th1/2/17 cells
C. Epithelial defects: defective tight junctions
D. Gut microbiota: metronidazole helpful in maintaining remission of CD

A

All of the above

24
Q

In patients with ___________ , there will be abdominal pain, diarrhea with blood and mucus.

A

Ulceraltive colitis

(+/- blood and mucus) for patients with Crohn’s disease

25
Q

Where are the sites that Crohn’s disease affect?

What lesions do they produce?

A

Whole GIT, most common in terminal ileum and caecum ;

Skip lesions

26
Q

Where are the sites that Ulcerative colitis affect?

What lesions do they produce?

A

Rectum +/- colon;

Continuous lesion

27
Q

Crohn’s disease produces ____________ inflammation; with __________ appearance due to the deep linear ulcer and fissures formed.
Is there any fibrosis?
Is there any stricture?
Is there any serositis?

A

transmural;
cobblestone

Yes
Yes
Yes (serositis = local peritonitis)

28
Q

Ulcerative colitis involves _____________ inflammation. The ulcer is _________ and _________ without any fissures.
___________ may be present if severe, which are regenerating mucosa.

A

mucosal/ submucosal;
superficial, broad-based;
pseudopolyps

29
Q

Ulcerative colitis:
Is there any fibrosis?
Is there any stricture?
Is there any serositis?

A

Minimal fibrosis
No stricture
No serositis

30
Q

Comment on the activity and chronicity of ulcerative colitis and Crohn’s disease.

A

Active chronic inflammation

Activity: cryptitis, crypt abscess
Chronicity: glandular distortion, branching, atrophy, epithelial metaplasia

31
Q

Which of them, UC/ Crohn’s disease produces a non-caseating granuloma in 35% of patients?

A

Crohn’s disease

UC: no granuloma

32
Q

Suggest a complication for Crohn’s disease related to its MC site.

A

Macrocytic anemia: B12 deficiency if terminal ileum is affected

33
Q

Suggest a complication of UC.

A

IDA

Toxic megacolon

34
Q

Malignancy risk is higher in Crohn’s/ UC?

A

UC
associated with:
- Chronicity: after 8-years > higher risk
- Extent: Pancolitis > Proctitis
- Activity: increase risk in more severe and frequent inflammation

35
Q

List some extra-intestinal manifestation in both Crohn’s disease in UC.
(A PIE SAC)

A
  • Aphthous ulcers
  • Pyoderma gangrenosum
  • Iritis
  • Erythema nodosum
  • Sclerosing cholangitis
  • Arthritis (enteropathic)
  • Clubbing
36
Q

What are true and false diverticula?

A

True: outpouchings of ALL layers from a tubular structure, e.g. Meckel’s diverticulum;

False: herniation of mucosa and submucosa through muscularis propria into subserosal region e.g. diverticulosis coli

37
Q

Pathogenesis of • Diverticular disease is where there is • Outpouching at the weakest point where _____________enter between antimesenteric and mesenteric taeniae. The outpouching is also facilitated by ______________.

A

Vasa recta;

increased intraluminal pressures (constipation +/- low-fibre diet)

38
Q

Diverticulitis MC site is? Why?

A

Sigmoid colon

  • increased luminal pressure
  • reduced luminal diameter
39
Q

Which of the following about diverticulitis is incorrect?
A. Pateints may present with vagal abdominal distension
B. It is the most common cause of LGIB
C. Peritonitis is one of the complications
D. Stricture and fistula are possible complications

A

All of the above are correct

40
Q

Solitary rectal ulcer
A. can be multiple
B. is always an ulcer
C. is also called mucosal prolapse syndrome
D. affects all age
E. presented as rectal bleed, tenesmus, mucosal discharge

A

All except B

can be non-ulcerated

41
Q

Solitary rectal ulcer/ mucosal prolapse syndrome mimics __________ grossly.

A

CA rectum

ACP GI and HBP system, Urogenital system (10 decks)

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