W5. Disease of large and small bowel Flashcards
A. Congenital and neonatal disorders of SI
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
meckels diverticulim
-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
primary malabsortpion syndorme
-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
what is Malabsorption syndrome and types(SI)+clinical features
- nutrients are inadequately absorbed by the GIT
types:
1. primary malabsortption syndromes
2. secondary
clincal features
-weight loss, growth retardation in infants, weakness, anemia
celial disease+classification+etiology
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
secondary malabsorption syndormes
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
microscopic finding and complications of celiac disease
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
collagenous sprue
-end result of celial disease
-total villous atrophy- absent
-see: bands of coll under basal lamina of epi
-fatal
tropical sprue
-tropical areas
-not clear pathogenesis: somethign with enetrotocin form E.coli
-leave are and oral antibiotic
Disachharide deficiency
-lactase
- diarrhea and abd pain
whipple disaes
- 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
Ischmic bowel diesase: what, forms and types
-❖ = 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
macroscopically+ development of ischemi bowel diases
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
complication and clinical feature of ischmeic bowl
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
herediatry cancer syndromes
-Peutz jeghers syndrome
- familial adenomatous polyposis
-lynch syndrome
Peutz jeghers syndrome
- 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
-
Familial adenomatous polyposis -FAP
- 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
lynch syndrome
-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
tumors of small intestine
bening: common–>least
1.leiomyomas,
2. adenomas
3. vascular tumors-hemangioma, lymphangioma
malignant: common–>loeast
-uncommon, rare, 2% of all human malignancic
- carcinoid tumors
2.lymphomas - adenocarcinoma
carcinoid tumor–>neuroendocrine tumor
-from endocrine cells-APUD(apudomas) cell sys
-mucosa of GIT
- Secretory granules: argentaffin and arygyrophil
-types: argentaffin
-fore, mid and hindgut carcinoids
carcinoid syndrome
-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
adenocarcinoma
-who: 55-67 y
clinically: maybe asymptomatic
-early: occult bleeding–>iron def anemia
-advanced: abd pain and ileus via obstruction
-complication: intestinal obstruction, intussusception
Infectous colitis - Large intestisne
-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
pseudomembranous colitis -LI
-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