W5. Disease of large and small bowel Flashcards

1
Q

A. Congenital and neonatal disorders of SI

A

Diverticulum disease:
- diverticulosis and diverticulitis
-Diverticulum-blind puch leading of alimentary canal, lined by mucosa that communicates with gut lumen
-types: congentital(true, all layers), aquired(musel misiing)

who: vesten, >60y
where: sigmoid colon is common
cliniccally: 80% is asymptomatic, other: cramping, discomfort, distention, alternating constipation and diarrhea
complications: hemoorhage, perforation w abscess, fistual into bowel/bladder, obstruction and ahdesions

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2
Q

meckels diverticulim

A

-true
-Most prevalent congenital abnormality of GI tract, in 2%
- Etiology: due to persistence (failure to involute) of proximal vitelline duct
➢ Usually 20 cm proximal to ileocecal valve on antimesenteric side of bowel

Symptoms: usually asymptomatic but also abdominal pain of unknown etiology
➢ Complications: perforation, enteroumbilical fistula, peptic ulceration, hemorrhage
(often massive in children), carcinoid and other tumors

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3
Q

primary malabsortpion syndorme

A

-cause is in the enterocytes
-Due to primary deficiency of the absorptive mucosal surface and associated enzymes

-ex: celial diases, collagenous sprue, tropical sprue, whippple disease, dissacc deficiency

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4
Q

what is Malabsorption syndrome and types(SI)+clinical features

A
  • nutrients are inadequately absorbed by the GIT

types:
1. primary malabsortption syndromes
2. secondary

clincal features
-weight loss, growth retardation in infants, weakness, anemia

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5
Q

celial disease+classification+etiology

A

what:
-gluten sesitive enetropathy
- immune mediated enteropathy
—>atrophy of small intestinal villi

classification:
Type1. in childhood: diarrhea, steatorrhea, weight loss, thrive failure
Type 2: atypical or latent diases in adulthood: fatigue, infertility, iron defi anemia, oestoperesis

Etiology
Genetic factors
- predisposition HLA-DQ2 or HLA-DQ8 encoded COELIAC1 (6p21)
-other: COELIAC2/3

Imuunological factors
Type 1: upreg of CD8+ Tcells
type 2: plasma cell diff–>AB prod

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5
Q

secondary malabsorption syndormes

A

cause is outside the enterocytes
▪ In which mucosal changes result secondary to other factors such as diseases,
surgery, trauma and drugs

ex:
-inadequet/impaired digestion
-inflammatory and neoplastic disorders
-systemic diseases
-inaqequate absorptice surface secondary to surgical proceedures
-CVD
-metbaolic and endocrine disorders

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6
Q

microscopic finding and complications of celiac disease

A

micro:
-reduction in number of circular folds
-Architectural changes of mucosal villi: thick ans short(villoyus atrophy),
Grade
- 1st grade: Marsh 3a
-2nd: 3b –visible villi byt very short and wide, infla cell in mucosa and epi
- 3rd grade-3c: no visible villi,

Complication
-^risk of pri small bowel adenocarcinoma
-^risk of development of non-hodgkin lymphoma
-dermatitis herpetiformis
-lymphocyctic gastritis and colitis

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7
Q

collagenous sprue

A

-end result of celial disease
-total villous atrophy- absent
-see: bands of coll under basal lamina of epi
-fatal

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8
Q

tropical sprue

A

-tropical areas
-not clear pathogenesis: somethign with enetrotocin form E.coli
-leave are and oral antibiotic

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9
Q

Disachharide deficiency

A

-lactase
- diarrhea and abd pain

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10
Q

whipple disaes

A
  • by Actinomycete tropheryma whippeli
    -other organs also
  • malabsorption is main feuture
    -who: more males, 40-50y

clinical:
- weight loss mainly
-lymphadenopathy, arthritis, neuropsychiatric manifestatioj

Macro:
- like celiac:wide and thick mucosa folds, reduced
-yellow white plaques on surface
-foamy macropahes w actinomycetes in propria

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11
Q

Ischmic bowel diesase: what, forms and types

A

-❖ = injury of bowel caused by decreased intestinal blood flow of any cause.
-types: acute and chronic(2 or more compressed arteries)

types:
1. arterial occlusion(50%): large artery
2. non occlusive intestinal ischemia-30%: shock, sepsis, HF, dehydration, drugs
3. thrombosis of mesenteric vv-10%: hypercoagulable state, liver cirrhosis, polycythemia, oral contraceptive
4. starngualtion and torsion: mechanic obstruction

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12
Q

macroscopically+ development of ischemi bowel diases

A

macroscopically:
-MOST involved: splenic flexure, signmoid colon, and left colon
- edematous and diffusely purple
-demarcation
-cloudy serosal surface w inflamamtory exsudate

Development
1. transmural infarction
2. mural infarction: limited to mucosa, submucosa and superficial muscularis
3. ischemic colitis

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13
Q

complication and clinical feature of ischmeic bowl

A

Complication
- paralytic ileus
-perforation–>periotinotis, speticemia
- stricture formation or stenosis

Clinical
- elderly
-^abd pain
-bloody diarrhea
-vomiting , nausea, hematemesis
- more severe-multiple organ dysfunction syndrome

chroninc ontestinal ischemic syndromes
- compression of 2 or moremajor aa
-intestilnal abdominal angina
-fibrosis structure formation and stenossi

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14
Q

herediatry cancer syndromes

A

-Peutz jeghers syndrome
- familial adenomatous polyposis
-lynch syndrome

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15
Q

Peutz jeghers syndrome

A
  • autosomal trait
    -rare
    -LKB1/STK11 gene

Compartments:
1. GI ghematomous polyps: usualli SI
2. Mucocutaneous melanin prigmentation: lipds, oral cavity, plasma, digitis, perianal area,

Signs and symtpt
- abd pain, intesitnal bleeding,a nema, intussusception
- 2-20yeras

complication
- extra interstinal neoplasma–>genital tract

-

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16
Q

Familial adenomatous polyposis -FAP

A
  • numerous adenomatous polyps
    -mostly colorectum
    -tendency to –>adenocarcinoma
    -APC gene
    -assocated w turcot syndrome and gardner syndrome
    -womena dn men

Clinical:
-adenoma not at birth
- 36 y median
-rectal bleeding+anemia, colicky abd pain, diarrhea, mucus discharge

Pathology:
-100/1000 polyps in colon and rectum
-small <5mm sessile polyps

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17
Q

lynch syndrome

A

-autosomal dominant
-defect in a DNA mismatch repair (MMR)
gene.
-characterized by the development of colorectal carcinoma,
endometrial carcinoma(^in women) and other cancers.

clinically
-family history
-colorectal cancer <50y
-proximal right colon
-extracolonic lesions: cancer of endometrium (15-44&), stomcach, renal, brain..

Pathology:
-mucinous, poorly diff adenocarcinoma
-infiltrating lymphocyte

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18
Q

tumors of small intestine

A

bening: common–>least
1.leiomyomas,
2. adenomas
3. vascular tumors-hemangioma, lymphangioma

malignant: common–>loeast
-uncommon, rare, 2% of all human malignancic

  1. carcinoid tumors
    2.lymphomas
  2. adenocarcinoma
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19
Q

carcinoid tumor–>neuroendocrine tumor

A

-from endocrine cells-APUD(apudomas) cell sys
-mucosa of GIT
- Secretory granules: argentaffin and arygyrophil
-types: argentaffin
-fore, mid and hindgut carcinoids

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20
Q

carcinoid syndrome

A

-they MTS: often to liver

Features:
Attacks of flushing of skin of face
* Episodes of watery diarrhea
* Abdominal pain
* Attacks of dyspnea due to bronchospasm
* Right-side heart failure due to involvement of tricuspid and pulmonary valves
and endocardium

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21
Q

adenocarcinoma

A

-who: 55-67 y

clinically: maybe asymptomatic
-early: occult bleeding–>iron def anemia
-advanced: abd pain and ileus via obstruction
-complication: intestinal obstruction, intussusception

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22
Q

Infectous colitis - Large intestisne

A

-Bacteria: campylobacter jejuni, salmonella shigella species, e.coli, yerisnia enetrocolotita
-throuch contaminated food

Pathogenesis
-pathogen–>mucisa/produce enteroxoins
-tissue invasive organism
and toxigenic organisms

Clinically:
- sjapp abd pain, diarrhea(+blood) and fever
- ferdig etter 2-4 w

23
Q

pseudomembranous colitis -LI

A

-caused by overgrowth of clostridium difficile
-composed of fibrin, necrotic epithelium and inflammatory
leukocytes
-epidemiology: destruction of normal gut flora

clinically:
-midl diarrhea
. watery diarrhea, abd pain, crmaping, fever and leukocytosis

cross:
-lesions
-patchy +raised yellow white plaques on mucosa
-congested mucosa+ulcerations

mciro:
-pseudomembrane: fibrin+mucus+infla cells+mucosal epi cells
-focal necrosis of epi cell
- propria: infla cell infiltrate
-submucosa: congested cappilaries,

complication:▪ Toxic megacolon, perforations and death

24
toxic megacolon
-acute form of colonic distention -Characterized by a very dilated colon (megacolon), accompanied by abdominal distention/bloating and sometimes fever, abdominal pain and shock -The dilatation can be either total or segmental
25
Inflammatory bowel disease-chrons disease (what + symptoms
-idiopathic - distal SI -infla in all layers=transmural symptoms: - abdominal pain (lower right quadrant – relieved by defecation), fever, diarrhea usually without blood, abdominal mass, intestinal obstruction, anal and perianal fissures and fistulas - May have extraintestinal manifestation
26
chrons disease grosss feacture+ microscopically
-discontinus/segmental intestine involment -thickened bowel walll+edematous->narrow lumen -creepign fat -early: mucosal ulcer-->deeper-->linear fissures-->fistulas - cobbelstone apperance: nodular swelling, fibrosis +ulceration microscopicallY: -in chronic can find: transmural lymphoid aggregates and granulomas: non caseating
27
chrons complication
- fibrosing strictures and ileus -second most common complications are fistulas to loops of bowel, bladder, vagina and perianal skin -Generalized malabsorption, vitamin B12 deficiency (other complications) ➢ Carcinoma (Lymphoma)
28
inflammatory bowel disease: ulcerative colitis (LI): what and charactertistic
- Chronic inflammatory bowel disease with episodes of bloody diarrhea (in contrast to Chron’s) -continous involvment -characterized by chronic diarrhea and rectal bleeding Characteristic feature -Diffuse (continuous) disease limited to colon + rectum ▪ In rare cases it may involve the distal part of terminal ileum, then we call it Backwash ileitis ➢ Inflammation restricted to mucosa and submucosa (
29
ulcerative colitis: cross feature, mciroscopic and clinical
Gross: - externsive ulceration: surferificial and longitudinal -psuedopolyps -normal wall thickness and serosa Microscopic: -lymphoplasmatic infiltarta in lamina proproa+neutrophils, esoinophils and mast cells -paneth cell metaplasia in left colon -neutrophilic cryptitis and crypt abscess -erosins and ulcers Clinical - 70% have intermitten atacks -Stages of colitis 1. mild colits: rectal bleeding, maybe tenesmus 2. moderate colitis: loss bloody stoll, crampy abd pain, low fever, edeka, 3. severe/fulminant) cilitis: 6-20 bloody bowel saily, fever, anemia, dehrration, extraintestinal symotoms: like chrons - eye infla -skin lesions erythrema nodosom and pyoderma ganrenosum -deep v thrombosis -arthritis-25% complications -toxic megacolon - ^risk for perforation w peritonints -^risk for colorectal cancer
30
Polups of colon and rectum
-a mass that protrudes into the lumen of the gut Division 1. Attachment to bowel wall: sessile or pedunculated 2. histogenesis -spi, hamartomatous, infla, mesenchymal, lymphoid, polypoid endocrine tumors 3. neoplastic potential -bening or malignant
31
hamatomatous polyps
- overgrowths of cells and tissues native to the anatomic location in which they occur.
32
non neoplastic polyps
inflammatory, hamarotmatous, hyperplastic, lymphoid
33
inflamamtory polyps
inflamed and regenerating mucosa that project above the level of the surrounding mucosa,
34
hyperplastic polyps
- localized non dysplastic epithelial proliferation characterized by a superficial serrated architecture and elongated crypts with proliferation confined to the lower portion of the crypt (=epithelial hyperplasia at the base of these crypts). - colon most common - asymptomatic, no malignacy ptentialt
35
lymphoid polyps
-Reactive hyperplasia of lymphoid tissue that is normally also more prominent in the rectum and terminal ileum, gives rise to localized or diffuse lymphoid polyps, also called rectal tonsils.
36
neoplastic polyps
- colorectal adenomas which have potential for malignant change while polypoid carcinoma is the term used for invasive epithelial tumors. ' -Presence of intraepithelial dysplasia -2/3 among individuals older than 65 years -Conventional Adenomas have 3 main variations: ➢ Tubular, villous and tubulovillous -left hemicolin most commoin -asymptomatic mostly
37
Tubular adenoma(adenomatous polyp)
-most common-75% - after 30y, male moslty distal colon and rectum - asymptomatic or rectal bleeding micro - overlying mucosa muscularis -composed of branching tubules embedded in lamina propria - epo cell diminsihied muvus secreting capacity -Atypical epithelium: Abnormal changes in the epithelial cells lining the gland, suggesting the potential for malignancy. -carcinoma in situ
38
Villous adenoma (villous papilloma)
-60y - distal colon and rectum micro: -slender finger like villi form mucosa muscularis - each papilla: fibrovascular stromal core with epi cells around+bening-anaplastic cells -symtoms: rectal bleeding, diarrhea, mucus -MOST dangrous:severe atypia, carcinoma in situ and invasive carcinoma are seen more frequently
39
Carcinoma of colon and rectum
-arises from colonic epithelium -through muscularis mucosae->submucosa - mostly in sigmoid colon and regtum Epidemiology -98% are adenocarcinoma -2nd leading cause of cancer death -after 40+ there is ^risk and doubeles each decade -males -5y survival is 40-60% etiology -diet and lifestyle -chornic infla -gentic factorss clinical: -early are asymptomatic -right sided lesion: silent, but lead to anemia and abd pain -left sided: constipation, decerase of caliber of stooll -rectal bledding : 50% - bowel obstruction -weakness, malaise, fatigue and weight loss, melena
39
tubovillous adenoma(papillary adenoma)
micro: mixed pattern vertical villi and deeper part showing tubular pattern.
40
Sessile serrated adenomas:
-pithelial neoplasms with distinctive serrated epithelial architecture -proximal colon, sessiel/flat lesions -70+ women and smokers -aymptomatic
41
colorectal carcinoma: tumor spread
-➢ May grow to surrounding organs and structures and may cause complications -May go to serosa, and may spread to abdominal cavity and cause peritoneal carcinomatosis -▪ Typical way of spread is the infiltration of lymphatic channels and blood vessels -▪ First involvement in metastasis is regional lymph nodes, then liver and lungs staging -Dukes ABCs staging -Astler-Coller staging -TNM staging
42
adenocarcinoma of colon
-glandular neoplasm=98% - primary colon carcinoma most common gross: Usually single, polypoid or ulcerated mass ➢ Right colon tumors tends to be exophytic, Left colon tumors tends to be annular encircling lesions Right sided tumors cause anemia, weakness and fatigue ➢ Left sided tumors cause change in bowel habits (diarrhea or constipation
42
development of colorectal carcinoma
Most colonic carcinoma develop via the conventional pathway of carcinogenesis also called chromosomal instability pathway(chnages of nr of chromosomes or parts of chromosomes) ➢ These tumors develop from the conventional adenomas, so the tubular and tubulovillous adenomas Adenomas accumulate genetic damage in a stepwise fashion beginning with loss of gatekeeper APC. Chromosomal instability (CIN) is a later event associated with the development of carcinoma APC-->KRAS-->TP53
43
❖ CpG islands methylator phenotype (CIMP) pathway (30% carcinomas)
-➢ (the serrated adenoma – carcinoma sequence) -ain genetic change is the methylation of the tumor suppressor genes, the methylation of the mismatch repair gene HMLH1 may lead to microsatellite instability and that leads to hypermutability of tumor
44
90% of colorectal cancers are
gland forming adenocardcinoma
45
convectional type of adenocarcinoms
necrosis, polygonal shped glands
46
signet ring cell type carcinoma
intracell mucin
47
mucinous adenocarcinoma
extracell prod of mucin
48
errated adenocarcinoma
Characterized by saw shaped appearance of epithelium
49
▪ Micropapillary variant of adenocarcinoma
Not typical for colorectum, more common in breast
50
Cribriform type
Characterized by cribriform glandular structures with central necrosis * This type resembles ductal carcinoma in breast
51
▪ Clear cell variant of carcinoma
very rare
52