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Lower GIT Summary
Physiology (PS140)
جامعة طرابلس
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By: Mohimen faraj
Lower GIT
####### Small intestine:
Development defect Gastroschisis: already discussed Omphalocele: already discussed Atresia: no lumen Stenosis: narrow lumen Meckel diverticulum: failure of involution of Omphalomesentric duct role of 2 ~> 2% of population 2 feet from ileocecal valve 2 to 6 cm the length 2 types ~> Gastric Pancreatic Complication: Peptic ulcer, bleeding. Volvulus, intussusception, Vit B12 defect. Hirschsprung: Aganglia, no peristalsis. Upper Segment dilated “megacolon” Acquired megacolon ~> 1)Chagas ~> antibodies against plexus 2)Neoplasia, stricture. “Organic instruction” 3)Diabetes 4)Spinal injury 5)Amyloidosis
Vascular disease
ischemic bowel disease: 1) mucosal infarction 2) mural infarction “mucosa,Submucosa” 3) transmural “All 3 Layers” Mostly occurs at watershed zone “ arterial circulation termination” At splenic flexure , sigmoid, rectum.
####### Types of diarrhea:
- Secretary ~>cells secrete water, more than they absorb “Cholera”
- Osmotic ~> lactase deficiency, viral enterocolitis.
- Malabsorptive ~> excess fat, steatorrhea “fatty diarrhea”
- Exudative
> inflammation> pus, bloody stool. Causes: 1) luminal digestion- Terminal digestion
- Trans epithelial transport
- Lymphatic transport
Malabsorptive syndrome
Chronic diarrhea due to defective absorption.
####### Causes: 1) celiac disease
Immune sensitivity to gluten ~> associated the other immune disease Common, discovered at infancy. Pathogenesis: gluten is seen as antigen presented by CD 50% mutation at HLA DQ2, HLA DQ8. Morphology: Affect proximal small intestine. Crypt hyperplasia Flattening of mucosal villi “reducing absorptive surface” Lymphocytes and other inflammatory cells.
Marsh classification: Clinical features : children ~> irritable, diarrhea, weight loss, muscle waste. Adult ~> diarrhea, iron deficiency, affect jejunum. Diagnosis: Ig A transglutaminase. Ig A,G Deamidated gliadin. Anti endomysial Anti body ~> highly specific low sensitivity Treatment ~> gluten free diet
Cystic fibrosis
Genetic: absence of epithelial cystic fibrosis transmembrane conductance regulator “CFTR” Pancreas enzyme deficiency ~> digestive defect ~> malabsorption.
Environmental enteropathy
Tropical enteropathy, tropical sprue. Endemic, developing countries. Repeated diarrhea “Any part” Unknown, infectious agent ~> respond well to antibiotic More similar to severe celiac disease, than infectious enteritis.
Whipple disease
Multisystemic ~> Intestine “ malabsorption syndrome” CNS ~> headache, and confusion. Joints ~> polyarthritis. Caused by : Tropheryma whippeii ~> Inside MQ, PAS +ve. Clinical features: malabsorption, lymphadenopathic, hyper pigmentation. Treatment : prolonged antibiotic.
Bacterial enterocolitis
Caused by : Vibro cholera Small intestine Campylobacter jejuni Colon Salmonella Both Shigella Both Colstridium difficile Colon E. coli
“Salmonella, Shigella, C jujeni, E. coli”
acute self limited colitis ~> 1) neutrophils ~> Epithelium Lumen Crypts 2) crypt abscess While maintaining the shape and spacing of Crypts.
Vibrio Cholera
Release toxin ~> increase CL secretion ~> causing osmotic diarrhea.
Campylobacter jejuni
Common in developed countries Traveler’s diarrhea
Salmonella, shigella
Invasive bacteria, cause bloody diarrhea. Mostly by food consumption Systemic typhoid fever, enteric fever. Caused by salmonella: 1)Typhi ~> “Endemic” 2)Para typhi ~> “ travelers diarrhea” By contaminated, food or water. 3 Phases:
- acute ~> vomiting, bloody, diarrhea, anorexia, abdominal pain.
- febrile ~> fever, bacteremia.
- rose spots~>Erythematous maculopopular spot“Abdomen, chest”
Systemic dissemination: 1) CNS ~> Encephalopathy, meningitis. 2) CVS ~> endocarditis, myocarditis. 3) Respiratory ~> pneumonia 4) gallbladder ~> cholecystitis 5) sickle cell patients ~> osteomyelitis. Morphology: 1) enlarged Pyers patches in terminal ileum. 2) oval ulcer on the long axis 3) lymphocyte hyperplasia in lymph nodes 4) typhoid nodules “ MQ, lymphocyte” NOTE: salmonella ulcer “Long axis” from T ulcer “ transverse axis”
Colstridium difficile
Pseudomembranous colitis ~> After prolonged Ab therapy C. Difficile ~> Release toxin ~> pseudomembrane.
Parasitic infection
- Entamoeba histolytica
- Giardia lambia
- cryptosporidium parvum
Dysentery
Ulceration of large intestine
- Bacillary
- Amoebic
- Bilharzia
Clinical picture of CD: Transmural fibrosis Stenosis Stricture Clinical picture of UC: Lower abdominal pain Bloody diarrhea Treatment: Surgical resection. Extra intestine manifestation: Clubbing of fingers Erythema nodosum These are mostly in CD ~> Uveitis Sacroiliitis Ankylosing spondylitis Migratory polyarthritis Mostly in UC ~> 1ry sclerosing Cholangitis, pericholangitis. O
Colonic polyps
Classification : 1)Non-neoplastic ~> Inflammatory Hamartoma Hyperplastic 2) Neoplastic “Adenomas” 3) familial polyposis colon Inflammatory polyps Caused by solitary rectal syndrome ~> impairment of anorectal sphincter to relax ~> abrasion ~> ulcer with inflammation. Repeated inflammation produces polyps Hamartoma polyps Two types ~> 1) juvenile “Less than 5” Rectum polyps 3-100 if “>100 risk of malignancy” Rectal bleeding 2) Pentz jeghers syndrome Mucocutaneous hyperpigmentation Colon polyps ~> risk of malignancy Ovaries, uterus, breast, testis, lung, pancreas. Hyperplastic Old age ~> Decrease epithelial turnover Serrated surface ~> delay in shedding No malignancy potential
Adenoma
50% at the age of 50 “screening at that age is recommended” If there is a family history screen 10 years before. Morphology : 3 to 10 cm sessile or pedunculated Epithelial dysplasia Tubular ~> pedunculated, tubular gland Tubulovillus ~> mixed Villous ~> sessile with villi Sessile serrated ~> Adenoma with hyperplastic type Risk Factors ~> More than 4cm , High grade of dysplasia.
5)SMAD2 and SMAD4 mutation SMAD2/SMAD4 Regulated by TGF B 6)Expression telomerase. Microsatellite pathway Herdeitary Non Polyposic colorectal cancer "Lynch syndrome" syndrome because cancer at several sites stomach, Liver, Brain, Uteras, colon. occur at young age, "Right side "more.
- mutation in DNA Repair gene "Mismatch Repair"MSH2, MLH1" Morphology ~> throughout the colon ~> 1) Proximal colon “Rt” Polypoid, exophytic. 2)Distal Colon Annular, napkin ring constriction. Microscopic picture According to glandular mass ~> well to poorly differentiated.
- invasive type “ firm tumor” ~> strong desmoplastic.
- mucinous adenocarcinoma
> mucin ~> Singet ring. Clinical features : Right ~> weakness, fatigue, iron deficiency anemia. Left ~> occult bleeding. Prognosis : depends on> Invasion Lymph node metastasis
APPENDIX
- Inflammation: Acute appendicitis · common in young adult, male.
- Differential Diagnosis 1)mesentric lymphadenitis 3)Ectopic pregnancy 2)Acute salpingitis 4) Meckel diverticulum 5)Ovarin cyst "torsion". 6)salmonella, IBD, ovulation pain Pathogenesis: 1)Stool or fecalith 3) tumors
- gallstone. 4) worms Morphology: Elongated enlarge Erythromatous surface with purulent exudate Dull Serosa Superficial ulceration Congested blood vessels Neutrophil infiltration. Clinical features: Peri umbilical pain, positive Mcburney sign. Nausea, vomiting. Fever Complication Appendix abscess Perforation Peritonitis Adhesion Chronic appendicitis Mucocele
Bleeding per rectum
Local ~> Bilharzia, dysentery “ amoebic”, Tumor, anal fissure, hemorrhoids. General ~> Vit K deficiency Scurvy Hemorrhagic blood disease.
Lower GIT Summary
Course: Physiology (PS140)
University: جامعة طرابلس
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