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Peds GI RC > Colon > Flashcards

Colon Flashcards

1
Q

How does the colon rotate in utero

A
  1. physiologic herniation of midgu through umbilical opening out of abdominal cavity
    - starts at 6 weeks ends at 10 weeks
    - midgut rotates 90deg CCW around SMA axis, leaving caudal midgut to left
    - large intestine returns after small intestine and rotates additional 180deg CCW
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2
Q

What is the penctinate line/dentate line

A

-the junction of hindgut endoderm and anal canal protodeum ectoderm

  • anocutaneous line is 2 cm superior to anus
  • anal columnar epithelium changes to stratified squamous
  • 1-2 cm proximal to anus - anal transition zone with columnar, cuboidal and squamous epithelium
  • columns of morgagni: longitudinal folds surrounding dentate line
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3
Q

What happens at the rectosigmoid junction

A
  • the 3 taeniae coli coalesce, forming a longitudinal smooth muscle layer of rectum
  • distal rectum: inner smooth muscle layer forms internal anal sphincter
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4
Q

Which parts of the colon are fixed to the retroperitoneum

A
  • ascending and descending colon

- transverse colon is intraperitoneal and mobile

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5
Q

What are the functions of the colon

A
  • absorption of water/lytes
  • mucous secretion
  • fecal material formation/propulsion/storage
  • residence of microbiota
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6
Q

What are the different SCFA produced by fermentation of CHOs by microbiota and the importance

A
  • acetate
  • butyrate
  • propionate
  • butyrate: important energy source for colonocytes and maintenance of health epithelium
  • metabolism of SCFA by colonocytes provides energy active Na transport
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7
Q

How is Na, K and Cl absorbed in the colon

A
  • Na absorbed against gradient via Na+-K ATP Pump
  • K+ absorbed by active secretion into lumen and passive absorption
  • Cl- absorbed by active transport through exchange via HCO3-Cl- exchanger
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8
Q

What do the endogenous bacteria in your colon do

A
  • important for metabolism of:
  • bile acids
  • bilirubin
  • estrogen
  • cholesterol
  • breakdown of CHO and proteins in the colon

-produce vit K

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9
Q

Are there MMCs in the colon

A
  • no MMCs
  • segmental contractions:
    a) predominant contraction; occurs throughout the day; isolated/bursts; rhythmic/arrhythmic
    b) mainly mixes contents of colon thus facilitating absorption
    c) maximizes intestinal mucosa exposure to luminal contents to enhance absorption of water, lytes and SCFA
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10
Q

What is the Rectal motor complex

A

-rhythmic contractions in cycles of 3-6 per minute (independent of small bowel MMCs) help maintain fecal continence

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11
Q

What is the gastrocolic reflux

A

-colonic mass peristalsis after meals and contraction of rectum in response to distension of stomach by food

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12
Q

What is the gastroileal reflux

A

-cecum relaxes and chyme goes through ICV when food leaves the stomach

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13
Q

What maintains fecal continence and defecation

A

Continence: requires puborectalis muscle and anal sphincter contraction

Defection: requires puborectalis relaxation by sacral parasympathetic nerves

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14
Q

What is the defecation pattern

A

1) high amplitude propagation contraction delivers stool to rectum
2) Rectum distention reflexively relaxes internal anal sphincter due to excitation of sympathetic nerves (rectoanal inhibtory reflex)
3) external sphincter and pelvic floor muscles contract
4) feces contact the anal canal and the sensory nerves distinguish solid/liquid stool and gas, providing the urge to stool
5) if stool is not released, rectum relaxes and the urge subsides (accommodation response) and the stool is retained until a bowel movement occurs
6) bowel movement coordination of increased abdo pressure by valsalva, contraction of rectum, relaxation of puborectalis muscle and opening of the anal canal (initiated voluntarily and then spinal reflexes take control)

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15
Q

How is the rectum different from other parts of the colon

A

1) absence of taeniae coli
2) Columns of Morgani- end in small valve called anal valve
a) btw columns of Morgagni are depressions called anal sinuses = contain anal glands - end at the dentate line
when canal distended the columns, sinuses and valves flatten and mucus is discharged from sinuses to lubricate the passage of stool

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16
Q

What is the internal and external anal sphincter made out of

A

Internal sphincter: smooth muscle, made from inner circular layer of the muscularis externa

external sphincter:

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17
Q

DDX for Constipation

A
  • hypothyroid
  • hypoCa
  • lead toxicity
  • CF
  • Celiac
  • tethered cord, tumors, sacral agenesis, intraspinal problems
  • myopathy and neuropathy
  • HD, neuronal intestinal dysplasia and other myenteric abnormalities
  • anatomic abnormalities
  • psychological etiology
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18
Q

What is the pathophys behind ecoporesis

A
  • large stool volume stretches the rectum and relaxes the IAS
  • sensory feedback is impaired
  • EAS is stressed and shortened
  • prevents ability to contract
  • compromises the preventino of defecation or stool leakage
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19
Q

What is lubiprostone

A
  • locally acting ClC-2 chloride channel activator used to increased fluid secretion into intestines for constipation
  • approved in adults
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20
Q

What is prucalopride

A
  • 5HT4 receptor agonist
  • prokinetic agent that promotes colonic motility and transit
  • improves bowel function and constipation related symptoms
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21
Q

What are the variant types of hirschprung disease

A
  • short segment disease: anorectal junction to splenic flexure
  • long-segment disease: aganglionic segment extends proximal to the splenic flexure
  • total colonic aganglionosis: whole colon affected
  • total enteric aganglionosis: entire small bowel is affected- mostly severe from associated with high-risk morbidity and mortality
  • ultrashort-segment disease: the distal rectum below the pelvic floor and anus are affected
  • zonal or segmental: ganglion cells are present in distal rectum but are absent in proximal segment
  • double-zonal aganglionosis: skip areas in which agnaglionc segments reside between ganglionic ones
22
Q

Treatment for hirschprung enterocolitis syndrome

A

-hydration, rectal washouts and Abx

23
Q

Risk factors for Hischprung enterocolities syndrome

A
  • T21 and other genetic syndromes
  • delay in dx beyond 1 week of age with average reported neonatal age for entercolitis of 16 days
  • major associated congenital anomalies (cardiac, GI, GU or CNS)
  • long segment disease
  • postop complications such as stricture/obstruction
  • family hx of HD
24
Q

How to take samples for HD

A

-2-3 cm proximal to the dentate line - to avoid false-positve results such as distal 1-2 cm of rectum is normally hypoganglionic and include the submucosa

  • Hypertrophic nerve fibers
  • aganglionosis
  • acetylcholinesterase helps identify hypertrophic nerve trunks
  • new calrectinin stain improves histoloigcal accuracy in suboptimal samples
25
Q

Types of surgery for HD

A

Swenson pull-through retains short aganglionic seg

Soave procedure retains portion of affected posterior rectal wall

Duhamel uses surgical clips to anastomose the pull through with rectum

26
Q

Clinical features of Bechets

A
  • mucocutaneous lesions - oral and genital ulcers
  • uveitis/ retinal vasculitis
  • systemic vasculitis (venous?arterial: thrombophlebitis, budd-chiari, pulmonary arterial aneurysm
  • monoarticular arthritis

GI: abdo pain, GI bleed, fever, wt loss, diarrhea, constipation, perforation, fistulas, ischemia, infarction, apthous-like ulcers in esophagus/ileum, pancreatitis and hepatobiliary complications

  • erythema nodosum, pustules, acne-like lesions,
  • aseptic meningitis, meningoencephalitis, cranial nerve palsies, seizures
27
Q

Treatment for GI bechets

A
  • 5-ASA
  • steroids
  • thalidomide
  • IFX
28
Q

How does infectious colitis differ from UC histoloigcally

A

-no significant architecture (chronicity) changes and there are predominantly neutrophils present

29
Q

What is the triad of typhlitis-

A
  • fever
  • abdo pain
  • neutropenia (ANC < 500)

colonic edema, inflammation, thumbprinting, fluid filled cecum

30
Q

Risk factors for acute GVHD

A
  • HLA mismatch
  • unrelated HLA-matched donor
  • increasing dose of total body irradiation
  • female donor to male recipient
  • incomplete GVHD prophylaxis
  • history of herpes infection in donor
31
Q

What are the 3 conditions essential for the initiation and progression of GVHD

A
  1. graft must contain immunologically competent T-cells introduced with the graft
  2. Host must possess transplant alloantigens lacking in the donor graft so that the host appears foreign to the graft
  3. host is capable for mounting an effective immunologic reaction agains the graft mediated by dysregulated cytokines
32
Q

Histological findings on liver and GI tract for acute GVHD

A

Liver: lymphocytic infiltration of bile duct –> extensive bile duct damage

GI: apoptotic bodies in the base of crypts, sometimes accompanied by acute or chronic inflammatory infiltrate, crypt abscess, destruction of surface epithelium, loss of crypts

33
Q

Risk factors for chronic GVHD

A
  • older age of patient
  • peripheral blood stem cells for the graft source
  • use of donor lymphocyte transfusions, and mismatched and unrelated donors
34
Q

GI liver findings of chronic GVHD

A

GI: N/V anorexia, abdo pain, diarrhea, sclerodermatous-like findings

liver: cholestasis with increase ALP and serum bili

35
Q

Histological findings of liver and GI tract for chronic GVHD

A

Liver: small bile duct and ductule destruction with cholestatic and inflammatory changes. portal and bridging fibrosis and loss of small interlobular bile ducts

GI tract: destruction of glands, ulceration or submucosal fibrosis

36
Q

What is the pathogenesis of an anal fissure

A
  1. trauma from overstretching the anoderm

2. hypertonic anal internal and external sphincters –> poor perfusion of posterior anoderm

37
Q

Differential for perirectal abscess

A
  • drug induced or autoimmune neutropenia
  • leukemia
  • HIV
  • DM
  • Crohns
38
Q

What are Hemorrhoids

A

-submucosal varicose veins arising from the superior and middle hemorrhoidal veins that drain into internal pudendal veins

39
Q

What is an internal hemorrhoid vs an external hemorrhoid

A 
Internal: located above dentate line
-originate from superior rectal vein 
-lack somatic sensory innervation
uncommon in children 
-usually with PHTN, CLD but can be with excessive straining

External: located below dentate line
Nerve supply is cutaneous
-pain when thromboses

40
Q

What is are the grades of internal hemorrhoids

A

Grade I: protrude into the anal canal but do not prolapse

Grade II: prolapse on straining and reduce spontaneously

Grade III: prolapse on straining and require manual reduction

Grade IV: prolapse and are irreducible

41
Q

What is the pathogenesis of hemorrhoids

A
  1. Submucosal venous plexus held in place by supportive connective tissue and 3 fibrovascular cushions. When damage, loss support=> hemorrhoidal prolapse
  2. Straining increase venous pressure and hemorrhoidal engorgement
  3. Passage of hard stool = mechanical insult to fibrovascular cushions
  4. Chronic constipation/straining/diarrhea associated with thrombosis of external hemorrhoids
42
Q

What are the classification of rectal prolapse

A
  1. Mucosal prolapse: involves only rectal mucosa, < 2 cm and appears as radical folds at junction with anal skin
  2. Complete prolapse
    a. First degree: full thickness involving mucocutaneous junction, > 5 cm and appears as circular folds
    b. 2nd degree: full thickness not involving mucocutaneous junction, 2-5 cm,
    c. 3rd degree: is internal or occult
43
Q

What are the features of acrodermatits enteropathica

A
  • erythematous and vesiculobullous dermatitis located in the perioral and perianal/genital region
  • alopecia, diarrhea, growth regardation, delayed sexual maturation, hypogonadism, decrease immune function, opthalmic disorders
44
Q

What low lab marker supports dx of zinc deficiency

A
  • low ALP

- Zn2+ is a cofactor for ALP

45
Q

What is the Anal position index

A
  • used to assess anal position

- severe displacement if distance < 10% and anal sphicnter muscle may not completely encircle the anal opening

46
Q

What polyps fall under Hamartomatous polyps

A
  • Solitary juvenile polyp
  • JPS
  • PJS
  • PTEN (Cowden, Borlin, Bannayan-Riley-Ruvalcaba syndrome)
47
Q

Which polyps fall under adenomatous polyps

A
  • FAP
  • Turcot
  • Gardner
  • Lynch syndrome
  • MYH-associated polyposis
48
Q

What is the histology of a solitary junvenile polyp

A
  • dilated cysts filled with mucin

- abundant LP with prominent inflammatory infiltrate

49
Q

What is the pathogenesis of Radiation Enteritis

A

Mechanism: free radical formation -> DNA disruption and cell death
Injury directly related to radiation exposure: dose rate, total dose and fractionation and field size

Acute injury -> histological changes
Damage to small intestine happens in first 12 hours
-over week, cell loss > mitotic ability of crypt cells to regenerate
-villi in small bowel shorten and lose disaccharidases
-Bowel edema and inflammation - decrease absorptive capacity and bile salts

50
Q

Which chemoagents increase risk of radiation enteritis

A
  • 5-FU
  • doxorubicin
  • actinomycin D
  • MTX
51
Q

What are the late effects of radiation enteritis

A
  • result from ischemia
  • obliterative endarteritis and fibrosis -> ulceration, necrosis, perforation and stricture
  • proctitis with associated tenesmus and bleeding
  • stricture from fibrosis
  • bacterial overgrowth
  • Altered bowel motility
52
Q

What can be done as prophylaxis for radiation enteritis

A
  • polygycolic acid mesh sling to raise small bowel out of the radiation field to prevent damage
  • amifostine (cytoprotective) agent
  • sulfasalazine
  • probiotics

Peds GI RC (12 decks)

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