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Pathology 205 > GIT > Flashcards

GIT Flashcards

1
Q

Major symptoms and prototypic diseases

A 
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
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2
Q

Heartburn (BURNING SENSATION IN CHEST- IRRITATION FROM ACID OF THE EOSOPHAGUS), and Waterbrash (START SALIVATION) - Esophagitis

A

Causes:
Infections
Reflux of gastric juice
Exogenous irritants & chemicals

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3
Q

reaching

A

tightning of the body

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4
Q

projectile vomiting

A

due to intense pressure in the intracranial , meningitis

nothing to do with the gut

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5
Q

eosophagus

A

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

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6
Q

Infectious esophagitis

A

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

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7
Q

Reflux esophagitis

A

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

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8
Q

Chemical esophagitis

A

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

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9
Q

Major problem with long-standing esophagitis

A

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

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10
Q

Nausea, Vomiting, Hemetemesis, Upper abdominal pain

A

Gastritis
Stomach (Peptic) ulcer
Carcinoma Stomach

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11
Q

Gastritis

A

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

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12
Q

Gastric (Peptic) Ulcer Disease

A 
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!!!!
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13
Q

Peptic ulcers

A

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

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14
Q

Peptic Ulcer DiseaseClinical Features

A 
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

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15
Q

Complications in peptic ulcer disease!!!!

A

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)

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16
Q

Carcinoma of Stomach

A

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)

17
Q

Clinical Features of stomac cancer

A

In addition to nausea, vomiting,bleeding, what are additional symptoms?- night sweat decrease apetite

5-year survival: 10-15%

18
Q

how do you distinguish bening from malignant

A

bening: small clean
malignant: big dirty , everted wall

19
Q

Diarrhea:

A

frequent passage of loose stool: usually cause by infection
Infections
Inflammatory Bowel Disease (IBD)- cronic diarhea
Crohn’s disease
Ulcerative colitis

20
Q

Small Bowel dont need to know for exam

ask questions about volume can tell where the infection is happening

A 
Etiology
E.coli,V.cholerae
Rotavirus
Giardia
Features
Large volume
Watery
No blood
Leukocytes usually none
21
Q 
Large Bowel (Colon)
dont need to know for exam
A 
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)
22
Q

TRAVELER’S

A 
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
23
Q

Inflammatory bowel disease!!!

A 
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.
24
Q

Sites of involvement!!!

A

Crohn’s
Terminal ileum
Anywhere from mouth to anus

UC
Rectum
Extend proximally (goes backwards)up to ileocecal valve

25
Q

Pattern of involvement!!!

A

Crohn’s
Discontinuous with skip areas

UC
Continuous

26
Q

Extent of inflammation in the bowel wall!!

A 
Crohn’s
Full thickness (whole tissue)

UC
Mucosal only usually

27
Q

Complications

A

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

  1. Cancer
28
Q

Abdominal Pain: Acute Appendicitis

A

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

29
Q

What’s happening 2:

A

Blockage (by fecolith, worm etc.) first prevents venous return, causing edema.
Eventually, edema together with bacterial growth, shuts off arterial supply ® gangrene

30
Q

sign of an appendicitis

A

red swollne, pus invades wall, pus proliferates wall

31
Q

what is acute appendicitus

A 
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)
32
Q

Rectal Bleeding

A

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.

33
Q

Neoplastic colonic polyps

A

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

34
Q

Colon Cancer

A

95% of malignancies of bowel
Almost all in colon
50% in rectosigmoid colon

35
Q

Right -sided colon cancer

A

Symptoms late in the course of the disease
Weakness
fatigue
- flat stool

36
Q

Left-sided colon cancer

A

Symptoms often early
Constipation
Flattened stools
Rectal bleeding

37
Q

Survival in Colon Cancer

A

Depends upon stage (local extension in
Bowel wall, spread to regional nodes and
Distant metastases)
dukes staning

38
Q

Treatment and Follow-up of patients

A 
Surgical resection
Chemotherapy or radiation
New genetic treatments
Follow-up
Carcinoembryonic antigen secreted by tumor cells can be looked for in the serum

Pathology 205 (23 decks)

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