- a condition in w/c the stomach contents return into the esophagus b/c relaxation of the lower esophageal sphincter can occur spontaneously

- the gastric contents are usually neutralized and cleared w/in minutes

- if frequent occurence, and the contents are highly acidic, contain bile salts and pancreatic enzymes, esophagitis can occur

- slowing of movement of food fr. the stomach, can also add to the factors causing GERD

- heartburn or burning sensation under the sternum

- dyspepsia or upset stomach

- long-term inflammation can lead to fibrosis and precancerous lesions

- a break in the protective mucosal lining of the lower esophagus, stomach, or duodenum

- can be single or multiple; acute or chronic; superficial (erosions) or deep

- infection w/ Helicobacter pylori

- chronic use of NSAIDs

- alcohol

- smoking

- advanced age

- chronic diseases: emphysema, rheumatoid arthritis, cirrhosis, obesity/diabetes

- occur w/ greater freq. than other types of peptic ulcers; tend to develop in younger people

- infection w/ H. pylori

- chronic use of NSAIDS

- result in allowance of acid and pepsin in the duodenum to penetrate the mucosal barrier and cause ulceration

- chronic intermittent pain in the epigastric area

- pain begins 2-3hr after eating (empty stomach) and is relieved rapidly by ingestion of food or antacids

- bleeding - causes hematemesis

- melena

- perforation - destruction of all layers of duodenal wall

- obstruction of the duodenum or stomach outlet - fr. edema or scarring

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

- black foul smelling stools fr. digestion of blood

- aimed at relieving the causes and effects of hyperacidity

- clearing of H. pylori w/ antibiotics and proton pump inhibitors

- surgical resection if ulcers are bleeding or have perforated the wall

- tend to develop in older people (55-65 yrs)

- about 1/4 as common as duodenal ulcers

- tend to be more chronic than duodenal ulcers

treatment: is longer

- H. pylori infection

- chronic use of NSAIDs

- intermittent pain in upper abdomen

- but pattern of pain is different: pain frequently occurs immediately AFTER eating

- Ulcerative colitis

- Crohn disease

- chronic inflammatory disease that causes ulceration of the colonic mucosa, most commonly in the rectum and sigmoid colon

- the area of ulceration is continuous

causes: yet unknown

- age (20-40 yrs)

- family history

- associated w/an altered immune response

- 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; frequent bloody diarrhea is the common symptom ( >1 per day up to 10-20 per day in severe cases)

- fluid loss, bleeding, and inflammation produce dehydration, weight loss, anemia, and fever

- involve drugs to decrease the inflammatory response

- IV administration of fluid for dehydration and malnutrition

- surgical resection may become necessary

- an inflammatory disease of the intestine - small & large; rectum is seldom involved

- inflammation of the entire width of the intestinal wall occurs (fr. serosa to mucosa), sometimes in patches (skip lesions)

- tissue injury results in granulomas developing in the intestinal wall

- family history

- altered immune response

- often asymptomatic for years

- most common is diarrhea w/ tenesmus, accompanied by weight loss and abdominal pain

- toxic megacolon (less than w/ ulcerative colitis)

- individual may be anemic if the ileum is involved - can't absord vit. B12

- malabsorptive disease - 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

- T-cell mediated autoimmune disorder

- person w/ the disease show an intense immune rxn to gluten (gliadin), the protein component of cereal grains

- the inflammation brought on by the immune rxn damages small intestinal villous epithelium, interfering w/ absorption, causing systemic problems

- eg. malabsorption of calcium causes seizures/tetany

1. portal hypertension

2. ascites

3. hepatic encephalopathy

4. jaundice (icterus)

5. splenomegaly

- abnormally high blood pressure in the portal venous system

- caused by disorders that obstruct blood flow thru 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

- vomiting of blood fr. hemorrhaging esophageal varices (melena may also occur)

- distended, tortuous collateral veins that are formed to connect portal vein and systemic veins

- if there's an increased pressure in the portal system usually caused by changes in the liver, collateral veins develop bet. 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 can't withstand the pressure of the blood coming thru the portal system

- they swell and distend (varicose veins = varices)

- if these lie w/in the esophageal wall (commonly do) they are easily ruptured and life threatening hemorrhage can result

- accumulation of fluid in the peritoneal cavity

- paracentesis to remove fluid and relieve breathing, but this must be done w/ caution to avoid hypotension and shock

- ascites will re-occur if liver problem isn't fixed

- liver dysfxns and collateral vessels that shunt blood past the liver allow toxins to remain in bloodstream and reach the brain (most hazardous is ammonia, w/c the liver converts to urea)

- neurotransmission is affected

- personality changes

- loss of memory

- confusion

- flapping of hands (asterixis) possibly worsening to coma

- rbc are broken down in the spleen and the liver; breakdown products is bilirubin w/c the liver can process and excrete in the bile

- icterus is the green/yellow tinge to skin caused by hyperbilirubinemia - high conc. of bilirubin in the plasma

- yellow discolouration occurs first in sclera of the eye, and then the skin

- excessive breakdown of RBC

- obstructions w/in the liver interfering w/the processing of bilirubin

- obstructions of the common bile duct, w/the result that the liver can't excrete processed bilirubin into the bile

1. 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

2. extrahepatic obstruction to bile flow, w/c causes the processed form of bilirubin (normally excreted w/the bile) to accumulate in the liver and thus enter the bloodstream; depending upon the amnt. of obstruction, feces can appear light in colour and urine may appear dark

- spleen enlarges due to portal hypertension

- hypertension in portal vein causes shunting of blood into the splenic vein

- formed elements take longer to filter thru the enlarged spleen, leading to increased rate of removal

- result = anemia, thrombocytopenia, leukopenia

- decrease in serum protein prod. by the liver, w/c lowers osmotic pressure of capillaries, resulting in more retention of fluid in the tissues, w/c then leaks/seeps into peritoneal cavity

- portal hypertension also contributes to this, as it increases pressure in capillaries in the abdominal area

- five usual strains of viruses: A (infectious hepatitis), B (serum hepatitis), C, D and E - all can cause acute hepatitis

- HBV and HCV can cause chronic liver disease and liver cancer

- co-infection w/ HBV, HCV, HDV and HIV can occur b/c the route of transmission is the same - body fluids = more rapid progression of liver disease

- causes destruction of hepatocytes, scarring and hyperplasia of hepatic macrophages

- if intrahepatic ducts are damaged, obstruction and jaundice can occur; damage is more extensive w/ HBV and HCV

- causes abnormal liver fxn test results (assay of compounds released/affected by the liver)

- 3 stages: prodromal, icteric and recovery phase

1. prodromal phase

- begins 2 weeks after exposure and end w/ jaundice

- marked by fatigue, vomiting, headache, cough, low-grade fever

2. icteric phase

- begins after prodromal, lasts 2-6 weeks

- jaundice, dark urine, clay-colored stools, enlarged and tender liver - palpitation causes pain

3. recovery phase

- begins w/ resolution of jaundice and most symptoms, about 6-8 weeks after exposure

- liver remains large and tender, and returns to normal fxn 2-12 weeks after onset of jaundice

- persistence of clinical manifestations and liver inflammation after acute stages of HBV and HCV infection

- liver fxn tests remain abnormal for longer than 6 months and HBV surface antigen persists

- cirrhosis and liver cancer

- an irreversible inflammatory, fibrotic liver disease

- caused by direct damage and inflammation fr. many disorders:

- HBV/HCV infection

- excessive alcohol consumption

- autoimmune hepatitis

- prolonged exposure to drugs or toxins

- hepatomegaly

- splenomegaly

- ascites

- portal hypertension

- hepatic encephalopathy

- esophageal varices

1. structural changes

- results fr. initial injury and resultant inflammation

- fibrosis caused by release of inflammatory mediators by leukocytes and activation of fibroblasts

2. altered liver metabolism

- altered by blockage of channels necessary for liver fxn.

- rest

- vitamin supplements

- good nutrition

- management of complications

- possible liver transplant

1. fetor hepaticus

- chronic musty odor of the breath

2. anemia, thrombocytopenia, leukopenia

3. loss of clotting factors lead to purpura, petechiae, spider angioma, epistaxis

4. hemolysis

- caused by changes in the RBC membrane lipids

- kidney failure (oliguria) generally due to decreased blood volume

- caused by:

- bleeding

- loss of fluid

- vasodilation resulting fr. liver failure

1. cholesterol (most common)

- form in bile that is supersaturated w/ cholesterol produced by the liver

- stones can either lie dormant or become lodged in the cystic or common duct

- causes pain when the gallbladder contracts

- causes cholecystitis

2. pigmented

- form fr. increased levels of a type of bilirubin, w/c binds w/ calcium

- associated w/ chronic liver disease

- outflow of pancreatic digestive enzymes is obstructed

- causing:

- accumulation of pancreatic secretions

- pathologic activation of enzymes w/in the pancreas

- this results in:

- autodigestion

- vascular damage

- necrosis

- edema

- inflammation

- involves release of inflammatory cytokines into the bloodstream

- causes whole body rxns, leading to serious consequences, including chronic pancreatitis

- caused by irreversible structural or fxnl impairment of the pancreas

- caused by:

- chronic alcohol abuse

- risk factor for pancreatic cancer

- often asymptomatic

- abdominal pain and jaundice

- pain occurs 30mins to several hrs after eating a fatty meal, caused by the lodging of one or more gallstones in the cystic or common duct