GIT Flashcards
Major symptoms and prototypic diseases
Heartburn & Waterbrash Esophagitis Nausea, Vomiting, Hemetemesis Gastritis, Peptic ulcer, Carcinoma stomach Diarrhea Infections; Inflammatory bowel disease (IBD) Abdominal pain Acute appendicitis Rectal bleeding Colon Cancer
Heartburn (BURNING SENSATION IN CHEST- IRRITATION FROM ACID OF THE EOSOPHAGUS), and Waterbrash (START SALIVATION) - Esophagitis
Causes:
Infections
Reflux of gastric juice
Exogenous irritants & chemicals
reaching
tightning of the body
projectile vomiting
due to intense pressure in the intracranial , meningitis
nothing to do with the gut
eosophagus
very thick and not usualy infected unless lots of damage from stomach!! acid or if immune!! system is comprimized
Infectious esophagitis
Caused by viruses or fungi
Herpesvirus
Candida albicans (fungus)
Usually immunosuppressed patients
Reflux esophagitis
Reflux of gastric juice into esophagus
Usually secondary to hiatal hernia (compromises lower esophageal sphincter)
Pepsin & hydrochloric acid chemical inflammation & ulcers
Chemical esophagitis
Accidental or deliberate swallowing of irritants or acids (still a common accident with toddlers who get into the cupboards under the sink and drink whatever they find there)
infection, chemical or reflux
Major problem with long-standing esophagitis
Barrett’s change!!!: (stomach secrease mucous to protect, the eosophagus starts to change so that it can also secreate mucous- can cause cancer because can cause dysplasia(intestinal type epithelium in the esophagus)
Dysplasia
Esophageal cancer
So, Follow-up of patients for dysplasia
Nausea, Vomiting, Hemetemesis, Upper abdominal pain
Gastritis
Stomach (Peptic) ulcer
Carcinoma Stomach
Gastritis
Acute
Erosive gastritis – erosions-superficial defects in mucosa)
Alcohol, Aspirin,Stress,Shock
Chronic
Autoimmune causes
Chronic active
Infectious: (Helicobacter pylori)- on the road to developing gastric peptic disease
Gastric (Peptic) Ulcer Disease
In stomach or duodenum Caused by acid damage to epithelial lining Etiology: Helicobacter pylori infection Non-steroidal antiinflammatory drugs (NSAIDS) Stress Zollinger Ellison syndrome most common site is duedenum!!!!
Peptic ulcers
Location:
Lesser curve of stomach
Proximal duodenum
Appearance:
Sharply punched-out defects of mucosa extending into deep layers- looks very clean!!! because of enzymes - if dirty and everted edges( cancer)
Bottom consists of granulation tissue and scar tissue
Peptic Ulcer DiseaseClinical Features
Duodenal Ulcer Pain 1 – 2 hours !!!after eating Pain alleviated by alkali or food May see melena ± iron loss Melena: Digested blood in stool
Gastric ulcer
Pain but no such typical relation to food
Complications in peptic ulcer disease!!!!
1: Hemorrhage(blood in vomit)
2: Penetration (erode into pancreas)-
3: Perforation (erode into peritoneum)
Spillage of acid contents - peritonitis
4: Scarring - contracture -stenosis -obstruction (low apetite and getting full really fast)
Carcinoma of Stomach
Higher incidence in Japan and Chile
Related to nitrosamines, smoked fish & chronic atrophic gastritis
4 types recognized
Polypoid (comes to attention- get full)
Fungating (late to clinical attention- die)
Ulcerated
Diffusely infiltrating (late to clinical attention)
Clinical Features of stomac cancer
In addition to nausea, vomiting,bleeding, what are additional symptoms?- night sweat decrease apetite
5-year survival: 10-15%
how do you distinguish bening from malignant
bening: small clean
malignant: big dirty , everted wall
Diarrhea:
frequent passage of loose stool: usually cause by infection
Infections
Inflammatory Bowel Disease (IBD)- cronic diarhea
Crohn’s disease
Ulcerative colitis
Small Bowel dont need to know for exam
ask questions about volume can tell where the infection is happening
Etiology E.coli,V.cholerae Rotavirus Giardia Features Large volume Watery No blood Leukocytes usually none
Large Bowel (Colon) dont need to know for exam
Etiology E.coli, Shigella sp. Norwalk virus Entameba Features Small volume Mucoid Blood common Many leukocytes (only travel a few centimeters so are still intacks)
TRAVELER’S
IN UP TO 70% TRAVELLERS TO DEVELOPING COUNTRIES 50% WITH IN FIRST TWO WEEKS VARIABLE SYMPTOMS ETIOLOGY 80% BACTERIAL: E. Coli, Campylobacter, FEW ARE VIRAL: Norwalk, Rota RARE PROTOZOAL: Giardia, Entamoeba
- need broad spectrum anti biotic- profilatric or could take pepto a little bit every day
1 month after return from trip is still travelers diarhea
Inflammatory bowel disease!!!
Chronic inflammation (more than 2 weeks) of the bowel wall 2 main categories: Crohn’s disease Ulcerative colitis Distinction based upon many factors Anatomic location of the disease Extent of inflammation in the bowel wall Diagnosis is based upon excluding infections as a cause of diarrhea.
Sites of involvement!!!
Crohn’s
Terminal ileum
Anywhere from mouth to anus
UC
Rectum
Extend proximally (goes backwards)up to ileocecal valve
Pattern of involvement!!!
Crohn’s
Discontinuous with skip areas
UC
Continuous
Extent of inflammation in the bowel wall!!
Crohn’s Full thickness (whole tissue)
UC
Mucosal only usually
Complications
Crohn’s Disease: Malabsorption
Fistulae and sinuses (getting stuff in the abdominal cavity- inflammation)
Perforation and peritonitis
Scarring and adhesions and intestinal obstruction (blocks the food by scarring
ulser grows from inside lumen to outside- can get poop leaking out all the time
UC:
1. massive Bleeding (
2. Megacolon: -Thin, dilated, paralytic colon (cannot function properly)
trying to rebuild but keeps getting destroyed - can lead to cancer
- Cancer
Abdominal Pain: Acute Appendicitis
What’s happening: Appendix has a peripheral arterial blood supply and a luminal venous return
pain in right upper quadrant
looks a lot like fallopian tube prego
What’s happening 2:
Blockage (by fecolith, worm etc.) first prevents venous return, causing edema.
Eventually, edema together with bacterial growth, shuts off arterial supply ® gangrene
sign of an appendicitis
red swollne, pus invades wall, pus proliferates wall
what is acute appendicitus
Acute Bacterial Infection Common in children & adolescents Clinical Fever Leukocytosis Abdominal pain Starts at umbilicus Moves to RLQ (McBurney’s point – 1/3 of distance from anterior superior iliac spine to umbilicus. Site of tenderness in acute appendicitis)
Rectal Bleeding
Colon cancer and its precursor lesions (adenomatous polyps or adenomas)
Polyps in the GIT can be non-neoplastic (e.g. inflammatory) or neoplastic.
Multistep model of carcinogenesis is well applicable to adenoma-carcinoma sequence in colon.
Neoplastic colonic polyps
Sporadic( will lead to cancer)- need to be removed
Familial (e.g Familial Adenomatous Polyposis- FAP)- entire colon is full of the polyps- genetic- remove the entire colon when a teenager
Colon Cancer
95% of malignancies of bowel
Almost all in colon
50% in rectosigmoid colon
Right -sided colon cancer
Symptoms late in the course of the disease
Weakness
fatigue
- flat stool
Left-sided colon cancer
Symptoms often early
Constipation
Flattened stools
Rectal bleeding
Survival in Colon Cancer
Depends upon stage (local extension in
Bowel wall, spread to regional nodes and
Distant metastases)
dukes staning
Treatment and Follow-up of patients
Surgical resection Chemotherapy or radiation New genetic treatments Follow-up Carcinoembryonic antigen secreted by tumor cells can be looked for in the serum
