Module 7: Digestive System Disorders

Module #7 – Digestive System Disorders

1. What does GERD stand for?

Gastroesophageal reflux disease (GERD)

2. Describe the development of GERD, its most frequent clinical manifestation and in what the long-term inflammation involved in GERD can result.

return of stomach contents into the esophagus because of relaxation of the lower esophageal sphincter or gastroparesis, by increasing gastric volume and pressure
if reflux is frequent, can cause esophagitis
long-term inflammation can lead to fibrosis and precancerous lesions
Clinical manifestations: heartburn, dyspepsia

3. Define dyspepsia and gastroparesis.

Dyspepsia: indigestion

Gastroparesis: slowing of movement of food from the stomach

4. Be familiar with factors that increase the likelihood of GERD.

Infancy
Increased intra-abdominal pressure
Smoking
Certain foods relax the LES
Individuals with lupus

5. What is a peptic ulcer?

Break down in the protective mucosal lining of the lower esophagus, stomach or duodenum

6. Define melena and hematemesis (know that these can be complications of peptic ulcer disease).

Melena: black-foul smelling stools
Hematemesis: vomiting of blood, bright red, or “coffee ground”

7. Describe three other complications of peptic ulcer disease (other than melena and hematemesis).

Hemorrhage
Perforation
Penetration
gastric/duodenal outlet obstruction

8. Identify and describe the pathophysiology behind the effects of the two high risk factors for the development of peptic ulcers.

Helicobacter pylori passes through the protective mucous layer of the stomach : mucin keeps stomach lining in a spongy-gel like state → h. Bylori releases urease → neutralizes stomach acid → liquifies mucin → h. Pylori can penetrate → stomach acid + pepsin penetrate = ulceration
NSAIDS interfere with prostaglandin synthesis → p. Inhibit acid secretion & stimulate mucous & bicarbonate secretion
- NSAIDS inhibit prostaglandin production → increase acid production → stomach vulernable to injury from acid and enxymes

9. What are two similarities between duodenal ulcers and gastric ulcers?

Caused by h. Pylori & chronic use of NSAIDs

10. What are three differences between duodenal ulcers and gastric ulcers? (include the pattern of pain)

Pain : Gastric - immediately after eating, Duodenal - 2-3 hours after eating
Age: Gastric - older people, Duodenal - younger people
Gastric ulcers are more chronic than duodenal ulcers!!! Duration of treatment is longer too

11. What are the main treatments for peptic ulcers?

Eradicate h. Pylori with antibiotics
Antacids
Proton pump inhibitors
H2 receptor antagonists
Minimally invasive surgery

12. What are the two diseases that make up inflammatory bowel disease?

Ulcerative colitis
Crohn’s disease

13. Describe and differentiate between these two diseases, including:

a. Typical age range affected

UC: 20-40

C: 20-30

b. Regions of the bowel affected and the nature of the inflammatory process

UC: rectum & sigmoid colon

C: large & small intestine

c. The appearance of the inflamed tissues

UC: thick track walls

C: cobblestone

d. Risk factors

UC: age, family history

C: family history

e. Clinical manifestations

Ulcerative Colitis

fluid loss
Bleeding
Inflammation
produce dehydration, weight loss, anemia, fever
Tenesmus (urge to defecate even if colon is empty)
Frequent bloody diarrhea

Crohn’s Disease

Inflammation and granulomas in the intestinal wall
Thickened and inflexible bowels

f. Possible complications

UC: toxic megacolon (abrupt increase in diameter of colon that could rupture)

C: fistulas, abscesses, obstruction

14. Define tenesmus.

Urge to defecate even if the colon is empty

15. What is toxic megacolon?

An abrupt increase in the diameter of the colon that could rupture

16. What is celiac disease?

Malabsorptive disease where the mucosa fails to absorb digested nutrients

17. Describe the development of celiac disease.

T cell mediated immune disorder
Intense immune reaction to gluten
Inflammation damages small intestinal villous epithelium, interfering with absorption of macro and micronutrients

18. Describe the clinical manifestations of celiac disease and the consequences of malabsorption of nutrients in childhood and adulthood.

Failure to thrive
Abdominal pain and bloating
Diarrhea with fatty stools
Malabsorption leading to:
- Osteoporosis, seizures/tetany from lack of calcium
- Anemia from lack of iron
- Short stature from general malnutrition
- Miscarriage, neural tube defects due to lack of folic acid and other nutrients

19. Define portal hypertension and its cause.

Abnormally high blood pressure in the portal venous system
- Caused by: disorders that obstruct blood flow through the portal venous system or vena cava
  - Including: thrombosis of hepatic veins, severe right-sided heart failure, alcoholic cirrhosis
Long term can cause: ascites, splenomegaly, portosystemic shunts, esophageal varices

20. Define ascites and describe two causes for ascites.

Accumulation of fluid in the peritoneal cavity

Caused by:
- Portal hypertension
- Decrease in serum protein production by liver

21. How can ascites be treated? What could happen if fluid is removed too quickly?

Yes it can !
- Paracentesis: drainage of fluid from abdominal cavity using a needle; with caution ( to avoid shock !! )
- Will reoccur if the liver problem is not fixed !!!!

22. Describe the development of varices associated with the portal system, and name the most common clinical manifestation.

Veins that drain from esophagus → hepatic portal vein → esophagus → inferior vena cava
Increased resistance impeding blood to flow from the esophagus → portal system
Blood will bypass the liver
Collateral veins that develop cannot withstand the pressure of the blood coming from the portal system → swell and distend (varicose veins = varices!!!! )

23. Where are two other places where collateral shunts can occur due to portal hypertension? Name the varices that result.

Caput medusae ; abdominal wall
Hemorrhoids ; rectum

24. Describe the development of hepatic encephalopathy and its clinical manifestations.

In liver dysfuncttion, toxins remain in bloodstream and reach the brain
- Because collateral vessels are shunting blood past the liver where ammonia should be converted to urea
Clinical manifestations: personality changes, memory loss, confusion, flapping of hands (asterixis), possibly worsening to coma

25. Define asterixis.

Flapping of hands

26. Define icterus and describe two causes of icterus that are related to diseases of gastrointestinal organs.

The green/yellow tinge to the skin caused by hyperbilirubinemia
RBC are broken down in the spleen and liver → releasing bilirubin, which the liver processes and excretes in bile

27. Why may the feces be light in colour (“clay coloured”) and the urine dark in colour with jaundice?

Bilirubin cannot reach the intestines due to poor liver function = lighter stool
Urine may appear darker to due the presence of bilirubin in the bloodstream

28. Where does jaundice often occur first?

First in the sclera of the eyes!!!

29. Describe why splenomegaly may occur with liver disorders and how blood cell numbers can be affected.

Due to portal hypertension! → causes shunting of blood into the splenic
Formed elements take longer to filter through enlarged spleen → increased rate of removal
Result → anemia, thrombocytopenia, leukopenia

30. Define acute hepatitis and outline some of its common causes and diagnostic features.

Inflammation of the liver caused by one of the 5 virus strains: A,B,C,D,E
Diagnostic features:
- Destruction of hepatocytes, scarring and hyperplasia of hepatic macrophages

31. Name the viral strains involved in hepatitis.

A, B, C, D, E

32. What is the difference between the routes of infection of HAV vs. HBV, HCV and HDV?

HBV, HCV, HDV = through body fluids
HAV = ingestion through contaminated food or water

33. Describe the damage to the liver caused by acute hepatitis.

Destruction of hepatocytes, scarring, hyperplasia of hepatic macrophages

34. How is the type of virus determined for a case of hepatitis?

Test for specific type of hepatitis is based on antibody assay

35. Name and describe the stages of disease of a typical acute viral hepatitis infection.

Prodromal phase = viral inflammatory effects
1. Begins 2 weeks after exposure and ends with jaundice. Marked by fatigue, vomiting, headache, cough, low-grade fever. Very infectious!!!
Icteric phase = effects of liver damage
1. Last 2-6 weeks. jaundice , dark urine, clay coloured stools, liver is enlarged and tender - palpation causes pain (palpation - to assess through touch)
Convalescent phase = healing and repair
1. Begins with resolution of jaundice and most symptoms (about 6 - 8 weeks after exposure), but liver remains large and tender. Liver returns to normal function 4-14 weeks after onset.

36. Define and describe chronic hepatitis, name causative organisms and possible resulting diseases.

Persistence of clinical manifestations and liver inflammation after acute stages of HBV and HCV infection
Causative organisms: HEPBV, HEPCV
Possible resulting diseases: cirrhosis and liver cancer

37. Define cirrhosis, describe its cause and name 3 disorders that can lead to cirrhosis.

Irreversible fibrotic liver disease, caused by direct damage and inflammation
Caused by: HBV/HCV infection, excessive alcohol consumption, prolonged exposure to drugs or toxins (hepatotoxin)

38. Define hepatotoxin.

Prolonged exposure to drugs or toxins

39. What disorders can result from cirrhosis?

Hepatomegaly, splenomegaly, ascites, portal hypertension, hepatic encephalopathy and esophageal varices

40. Describe two types of alterations that occur in the liver during the development of cirrhosis

Liver metabolism
Liver structure
Both are altered by blockage of channels necessary for liver function

41. What is the “treatment” for cirrhosis? (Why is treatment in quotation marks?)

Cirrhosis cannot be cured, however it can be managed!
Management of cirrhosis includes: rest, vitamin supplements, good nutrition, management of complications, cessation of drinking if possible, possible liver transplant

42. Define liver failure.

Inability of the liver to perform its normal synthetic and metabolic function as part of normal physiology (80-90% reduced liver function)

43. Name and describe the clinical manifestations of liver failure.

Can result from acute or chronic diseases

44. Define: fetor hepaticus, purpura, petechiae, spider angioma, and epistaxis.

Fetor hepaticus: chronic musty odor of the breath

Purpura: larger purple or red patches from bleeding under the skin

Petechiae: small red or purple spots caused by tiny blood vessels bleeding

Spider angioma: radiating blood vessels on skin surface

Epistaxis: nosebleeds

45. Define cholelithiasis and cholecystitis

Cholelithiasis: formation of gallstones

Cholecystitis: inflammation of gallbladder - if gallstones obstruct the outlet to the gallbladder

46. From what are most gallstones formed, and what conditions lead to their formation?

Abnormalities in the composition of bile (ex. More cholesterol excreted into bile)
Stasis of bile (gallbladder obstruction)
Inflammation of the gall bladder (causes excessive absorption of water and bile salts)

47. What causes the pain associated with gallstones?

Gallstones can cause pain when they block the flow of bile from the gallbladder.
- This can cause pressure, inflammation, etc resulting in pain

48. What is the significance of the presence of jaundice in the diagnosis of cholelithiasis?

Jaundice indicates that the stone is lodged in the common bile duct since bile backs up into the liver

49. Define acute pancreatitis and describe its characteristic manifestations, underlying pathophysiology, and to what disease it can lead.

Reversible inflammatory process caused by premature activation of pancreatic enzymes
Common manifestation: ongoing abdominal pain
Underlying pathophysiology: outflow of pancreatic digestive enzymes is obstructed causingL
- Accumulation of pancreatic secretions
- Pathologic activation of enzymes within the pancreas
- Results in: autodigestion, leading to vascular damage, necrosis, edema, inflammation
Can develop into severe acute form

50. Define chronic pancreatitis and be familiar with characteristic manifestations. Identify the most common cause and for what condition chronic pancreatitis is a risk factor.

Prolonged, progressive and irreversible destruction of the exocrine and then endocrine pancreas
Manifestations: malabsorption, weightloss, diabetes mellitus
Release of inflammatory cytokines into the bloodstream → systemic effects: nausea, vomiting, anorexia
Most common cause: chronic alcohol abuse
Risk factor: pancreatic cancer