GIT Flashcards by denzie hurst

Major symptoms and prototypic diseases

Heartburn &amp; Waterbrash
Esophagitis 
Nausea, Vomiting, Hemetemesis
Gastritis, Peptic ulcer, Carcinoma stomach
Diarrhea
Infections; Inflammatory bowel disease (IBD)
Abdominal pain
Acute appendicitis
Rectal bleeding
Colon Cancer

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

reaching

tightning of the body

How well did you know this?

Not at all

Perfectly

projectile vomiting

due to intense pressure in the intracranial , meningitis

nothing to do with the gut

How well did you know this?

Not at all

Perfectly

eosophagus

very thick and not usualy infected unless lots of damage from stomach!! acid or if immune!! system is comprimized

How well did you know this?

Not at all

Perfectly

Infectious esophagitis

Caused by viruses or fungi
Herpesvirus
Candida albicans (fungus)
Usually immunosuppressed patients

How well did you know this?

Not at all

Perfectly

Reflux esophagitis

Reflux of gastric juice into esophagus
Usually secondary to hiatal hernia (compromises lower esophageal sphincter)
Pepsin & hydrochloric acid  chemical inflammation & ulcers

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Nausea, Vomiting, Hemetemesis, Upper abdominal pain

Gastritis
Stomach (Peptic) ulcer
Carcinoma Stomach

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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!!!!

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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)

How well did you know this?

Not at all

Perfectly

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 3. 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 ```