Digestive System

Question 1

1. What does GERD stand for?

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

Answer 1

Gastroesophageal reflux disease
The return of stomach contents into the esophagus because of relaxation of the lower esophageal sphincter can occur spontaneously and the gastric contents are usually neutralized and cleared within minutes.
Development of GERD: If occurrence of the above is frequent, and the contents are highly acidic, contain bile salts and pancreatic enzymes, esophagitis can occur.
Gastroparesis (slowing of movement of food from the stomach, can also add to the factors causing GERD)
Most frequent clinical manifestation is heartburn (burning sensation under the sternum). Dyspepsia (upset stomach) may also occur.
Long-term inflammation can lead to fibrosis and precancerous lesions.

Question 2

1. Define dyspepsia.

Answer 2

Dyspepsia (upset stomach)

Question 3

1. What is a peptic ulcer?

Answer 3

A peptic ulcer is a break in the protective mucosal lining of the lower esophagus, stomach or duodenum.

Question 4

1. What are two similarities between duodenal ulcers and gastric ulcers? (thinking question)
2. What are three differences between duodenal ulcers and gastric ulcers? (include the pattern of pain) (thinking question)

Answer 4

Risk factors: Infection with H. pylori and chronic use of NSAIDs
Intermittent pain in upper abdomen

DU
Pain begins 2-3 hr after eating (empty stomach), and is relieved rapidly by ingestion of food or antacids.
GU
Pain frequently occurs immediately after eating.
GU
Gastric ulcers tend to be more chronic
GU
Tends to develop in older people
DU
Occurs in younger people

Question 5

Define melena, hematemesis

Complications of duodenal ulcers

Answer 5

Hematemesis - vomiting of blood, either bright red or “coffee ground” appearing (slightly digested blood)

Melena - black foul smelling stools from digestion of blood

Question 6

1. Describe ulcerative colitis.

1. Describe the development of ulcerative colitis

Answer 6

Chronic inflammatory disease that causes ulceration of the colonic mucosa, most commonly in the rectum and sigmoid colon. The area of ulceration is continuous.

Inflammation of the mucosa results in edema and thickening of the wall of the tract.
Destruction of the mucosa causes bleeding, pain and an urge to defecate, even if colon is empty (= tenesmus). Frequent bloody diarrhea is the common symptom (more than one per day up to 10-20 per day in severe cases).
Fluid loss, bleeding and inflammation produce dehydration, weight loss, anemia and fever.
Extreme cases can develop toxic megacolon, an abrupt increase in diameter of colon (within 1 to a few days) that could rupture.

Question 7

1. Define tenesmus.

Answer 7

urge to defecate, even if colon is empty

Question 8

1. What is the common symptom of ulcerative colitis?

Answer 8

Abdominal pain and bloody diarrehea

Question 9

1. How is ulcerative colitis treated?

Answer 9

Treatment may involve drugs to decrease the inflammatory response, and IV administration of fluid for dehydration and malnutrition

Question 10

1. What are 3 similarities between Crohn disease and ulcerative colitis?

Answer 10

Both inflammatory disease of the intestine
Both associated with altered immune response
Both common symptoms are diarrhea (with tenesmus), accompanied by weight loss and abdominal pain.
Toxic megacolon may also occur (less than with U.C.)
Treatments are similar

Question 11

1. What are 3 differences between Crohn disease and ulcerative colitis?

Answer 11

Chron’s - Affects both large and small intestine (rectum is seldom involved) Tissue injury results in granulomas developing in the intestinal wall.
UC - Affects colon, mucosa, rectum. Ulcers.
C- Inflammation of the entire width of the intestinal wall (from serosa to mucosa) occurs, sometimes in patches (skip lesions)
UC - Only mucosa and continous

Question 12

1. What is celiac disease?

2. Describe the development of celiac disease, its main clinical manifestation and primary treatment.

Answer 12

Malabsorptive disease that, where the mucosa fails to absorb digested nutrients
Also called sprue or gluten-sensitive enteropathy
Appears in children when gluten containing substances are added to the diet
Development: T-cell mediated autoimmune disorder: Persons with the disease show an intense immune reaction to gluten (gliadin), the protein component of cereal grains. The inflammation brought on by the immune reaction damages small intestinal villous epithelium, interfering with absorption, causing systemic problems (e.g., malabsorption of calcium causes seizures/tetany)
Diarrhea with fatty stools is main clinical manifestation
Primary treatment is removal of gluten from diet.

Question 13

1. Define portal hypertension and its cause.

Answer 13

abnormally high blood pressure in the portal venous system
caused by disorders that obstruct blood flow through the portal venous system or vena cava.
Long term hypertension may cause varices (distended, tortuous collateral veins that are formed to connect portal vein and systemic veins). Rupture of these can cause life-threatening hemorrhage.
Most common clinical manifestation is vomiting of blood from hemorrhaging esophageal varices (melena may also occur).

Question 14

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

Answer 14

If there is increased pressure in the portal system (usually caused by changes within the liver), collateral veins develop between veins that drain into the portal vein and veins that lie nearby and drain directly into the inferior vena cava.
This allows blood to bypass the liver, but the collateral veins that develop cannot withstand the pressure of the blood coming through the portal system.
They swell and distend (varicose veins = “varices”).
If these lie within the esophageal wall (and they commonly do), they are easily ruptured and life threatening hemorrhage can result.

Question 15

1. Define ascites and describe two causes for ascites.

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

Answer 15

Ascites: accumulation of fluid in the peritoneal cavity (916).
Can be caused by decrease in serum protein production by the liver, which lowers osmotic pressure of capillaries, resulting in more retention of fluid in the tissues, which then seeps into peritoneal cavity
Portal hypertension also contributes to this, as it increases pressure in capillaries in the abdominal area.
Fluid in abdominal cavity pushes on diaphragm, causing breathing difficulties.
Treatment can include paracentesis (drainage of abdominal cavity, using a needle) to remove fluid and relieve breathing, but this must be done with caution (to avoid hypotension and shock), and ascites will re-occur if liver problem isn’t fixed.

Question 16

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

Answer 16

Liver dysfunctions and collateral vessels that shunt blood past the liver allow toxins to remain in bloodstream and reach the brain (most hazardous is ammonia, which the liver converts to urea).
Neurotransmission is affected.
Individuals display personality changes, loss of memory, confusion, flapping of hands (asterixis) possibly worsening to coma.

Question 17

1. Define asterixis, icterus.
2. Describe two causes of icterus that are related to liver disease.
3. Why may the feces be light in colour and 4. Where does jaundice often occur first?

Answer 17

Flapping of hands
Jaudice
RBC are broken down in the spleen and the liver. One of the breakdown products of RBC is bilirubin, which the liver can process and excrete in the bile.
Icterus (jaundice) is the green/yellow tinge to skin caused by hyperbilirubinemia (high concentrations of bilirubin in the plasma)
These high concentrations of bilirubin in the blood can have 3 causes: too many RBC being broken down, obstructions within the liver interfering with the processing of bilirubin, or obstructions of the common bile duct, with the result that the liver cannot excrete processed bilirubin into the bile.
To repeat, therefore, the causes of jaundice that are related to liver disease are:
Loss of liver cell’s ability to remove and process bilirubin so that it can be excreted in the bile. Bilirubin accumulates in the plasma.
Extrahepatic obstruction to bile flow, which causes the processed form of bilirubin (normally excreted with the bile) to accumulate in the liver and thus enter the bloodstream. Depending upon the amount of obstruction, feces can appear light in colour and urine may appear dark.
Yellow discolouration occurs first in sclera of the eye, and then the skin.

Question 18

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

Answer 18

Spleen enlarges due to portal hypertension (hypertension in portal vein causes shunting of blood into the splenic vein)
Formed elements take longer to filter through the enlarged spleen, leading to increased rate of removal.
Result = anemia, thrombocytopenia, leukopenia

Question 19

1. Name and describe the viral strains involved in hepatitis.

Answer 19

Five usual strains of viruses: A (infectious hepatitis), B (serum hepatitis), C, D and E
All can cause acute hepatitis, and HBV and HCV can also cause chronic liver disease and liver cancer.

Question 20

1. Describe the effects of acute hepatitis.
2. How is the type of virus determined for a case of hepatitis?
3. Describe the stages of disease of a typical acute hepatitis infection.

Answer 20

Acute hepatitis causes destruction of hepatocytes, scarring and hyperplasia of hepatic macrophages. If intrahepatic ducts are damaged, obstruction and jaundice can occur. Damage is more extensive with HBV and HCV.
Determinative test for specific type of hepatitis is based on antibody assay.
Prodromal phase: begins 2 weeks after exposure and ends with jaundice. Marked by fatigue, vomiting, headache, cough, low-grade fever. Disease very infectious during this stage.
Icteric phase: begins after prodromal, lasts 2-6 weeks. Jaundice, dark urine, clay-colored stools, liver is enlarged and tender – palpitation causes pain.
Recovery phase: 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 2-12 weeks after onset of jaundice.

Question 21

1. What are the conditions that show a chronic case of hepatitis?

Answer 21

Persistence of clinical manifestations and liver inflammation after acute stages of HBV and HCV infection.
Liver function tests remain abnormal for longer than 6 months and HBV surface antigen persists.
Risk factor for cirrhosis and liver cancer.

Question 22

1. Define cirrhosis and name 3 causes.
2. What disorders can result from cirrhosis?
3. Describe two mechanisms of damage in the liver that cause these disorders.
4. What is the treatment for cirrhosis?

Answer 22

An irreversible inflammatory, fibrotic liver disease, caused by direct damage and inflammation from many disorders (HBV/HCV infection, excessive alcohol consumption, autoimmune hepatitis, prolonged exposure to drugs or toxins (hepatotoxin = a toxin that can harm the liver), etc.)
A multiple system disease, causing hepatomegaly, splenomegaly, ascites, portal hypertension, hepatic encephalopathy and esophageal varices.
Structural changes result from initial injury and resultant inflammation (fibrosis caused by release of inflammatory mediators by leukocytes and activation of fibroblasts).
Liver metabolism is altered, and liver structure is altered by blockage of channels necessary for liver function.
No specific treatment – rest, vitamin supplements, good nutrition, management of complications, (cessation of drinking, if applicable), possible liver transplant (depends upon cause)

Question 23

1. Define hepatotoxin.

Answer 23

Hepatotoxin = a toxin that can harm the liver

Question 24

1. Name 4 clinical manifestations of liver failure.

1. Define: fetor hepaticus, purpura, petechiae, spider angioma, epistaxis.

Answer 24

Fetor hepaticus – chronic musty odor of the breath
Anemia, thrombocytopenia, leukopenia
Loss of clotting factors (made by the liver) lead to purpura (purple discoloration >5mm), petechiae (purple discoloration < 5mm), spider angioma (appearance of radiating blood vessels on skin surface), epistaxis (nose bleeds)
Hemolysis, caused by changes in the RBC membrane lipids
Hepatorenal syndrome – kidney failure (oliguria) generally due to decreased blood volume brought about through bleeding, loss of fluid, vasodilation resulting from liver failure
Hepatic encephalopathy

Question 25

1. Define cholelithiasis. and cholecystitis

Answer 25

Gallstones.

Cholecystitis: which is inflammation of the gall bladder

Question 26

1. Describe the two types of gallstones.

1. What causes the pain associated with gallstones?

Answer 26

Cholesterol (most common) which form in bile that is supersaturated with cholesterol produced by the liver. The stones can either lie dormant or become lodged in the cystic or common duct, causing pain when the gallbladder contracts. This can then cause “cholecystitis”, which is inflammation of the gall bladder.
Pigmented which form from increased levels of a type of bilirubin, which binds with calcium, They are associated with chronic liver disease.

Question 27

1. Describe the development of acute pancreatitis.
2. Describe the subsequent development of severe acute pancreatitis.
3. Describe chronic pancreatitis.

Answer 27

Acute: mild disease that usually resolves spontaneously, but sometimes develops into severe acute.
Characteristic feature is ongoing abdominal pain.
Outflow of pancreatic digestive enzymes is obstructed, causing: 1) accumulation of pancreatic secretions and 2) pathologic activation of enzymes within the pancreas. This results in autodigestion, leading to vascular damage, necrosis, edema, inflammation.
Severe form involves release of inflammatory cytokines into the bloodstream, which causes whole body reactions, leading to serious consequences, including chronic pancreatitis.

Chronic pancreatitis: caused by irreversible structural or functional impairment of the pancreas.
Most common cause is chronic alcohol abuse.
Risk factor for pancreatic cancer.