What is the purpose of mucus cells? What happens if that layer is disrupted?
They provide a mucous barrier that is highly resistant to acid. It can be damaged by aspirin, alcohol, and NSAIDs. This causes the H+ ions to move into tissues and cause inflammation and damage of the submucosal layer.
What do parietal (oxyntic) cells secrete, where are they found, and what would result from decreased secretion?
- found in proximal fundus of stomach - secrete HCl and intrisic factor - intrinsic factor is important in absorption of B12. With decreased secretion there is a decrease in RBC production and a risk for anemia.
Where are peptic (chief) cells found, what do they secrete, and what do the secretions do?
- found in proximal fundus of stomach - secrete pepsinogen - in the presence of HCl, pepsinogen converts to pepsin, which breaks down proteins
Where are G cells found, and what do they secrete?
- found in antrum of stomach - secrete gastrin - stimulats gastric acid prod and secretion, pepsinogen secretion, increases gastric blood flow, and stimulates smooth muscle contraction and growth of mucosa
How does aspirin work to cause ulcers in the stomach?
Aspirin is a prostaglandin inhibitor. Prostaglandin inhibits gastric secretion, stimulates mucosal blood flow, and promotes bicarb production.
What does ghrelin do?
stimulates secretion of growth hormone stimulates appetite (gastric hormone)
What does cholecystokinin do?
stimulates contraction of gallbladder and secretion of pancreatic enzymes, slows gastric emptying (intestinal hormone)
What does secretin do?
stimulates secretion of bicarb solution from pancreas and liver (intestinal hormone)
What does incretin do?
increases insulin release after high oral glucose load to lower blood glucose
What role does gastric flora play?
break down food, ferment residue, generate short chain FA, synthesize vitamins, absorb Ca Fe Mg, restrict growth of exogenous or opportunisic flora
What do carbohydrates break down into, and where does their digestion begin?
Carbs --> monosaccharides Digestion begins in the mouth with amylase and continues in the intestine with pancreatic and brush border enzymes.
What do lipids break down into, and what breaks them down?
lipids --> FA and glycerol lipase breaks them down
What do proteins break down into , and where does their digestion occur?
proteins --> AA begins in the stomach with pepsinogen and HCl (make pepsin) and continues in the small intestine
What is anorexia, and what factors can influence it?
anorexia - loss of appetite or desire to eat despite the normal physiologic stimuli factors that influence it - hunger, smell, emotions, drugs, disease state
What is nausea, and what is a common cause?
nausea - unpleasant, SUBJECTIVE, conscious sensation resulting from stimulus of the medullary vomiting center common cause - distention of the duodenum
not enough fiber, exercise, or fluids slowed peristalsis (elderly clients or excessive use of opiates) conditions that alter GI motility (spinal cord injuries, MS) medications (opiodids, anticholinergics)
What is GERD?
the backflow of gastric contents into the esophagus through the lower esophageal sphincter
Increases in intra-abcominal pressure (the pressure distal to LES exceeds what it can withstand - related to obesity)
What are some clinical manifestations of GERD?
heartburn, belching, pain (throat, shoulder, back - can be confused with angina), bleeding, hoarseness, cough, dysphagia
GERD is a progressive disease. What may ultimately occur?
After mucosal injury/inflammation, ulceration, scarring, and strictures, Barrett's esophagus may result. This is believed to be a precursor to esophageal cancer.
What are some treatments for GERD?
wt reduction, avoid large meals before bedtime, decrease foods and activities that impair LES tone, avoid activities that increase intra-abdominal pressure (lifting), position of patient, surgical intevention
What is peptic ulcer disease, and what are some clinical manifestations?
it is any disorder of the GI tract (stomach, dodenum) caused by action of acid and pepsin - ranges from slight injury to severe ulceration
It adheres to mucus secreting cells in the stomach and secretes urease. This allows the organism to buffer the acidity of the environment. It also produces an enzyme that degrades mucin and interferes with the stomach's protective barrier.
What is the hallmark sign of IBS?
Abdominal pain relieved by defecation and associated with a change in consistency or frequency of stool
Which two diseases fall under the IBD umbrella?
Chrohn's disease ulcerative colitis
Which disease is ulcerative/exudative, and which is granulomatous? Chrohn's disease ulcerative colitis
UC - ulcerative/exudative CD - granulomatous
Which disease is mucosal, and which is submucosal? Chrohn's disease ulcerative colitis
UC - mucosal CD - submucosal
Which disease has lesions representing a cobblestone pattern, and which has continuous lesions? Chrohn's disease ulcerative colitis
CD - cobblestone UC - continuous lesions
Which disease occurs in the rectum/left colon, and which occurs in the primary ileum and then colon? Chrohn's disease ulcerative colitis
UC - rectum, left colon CD - primary ileum, then colon
In Chrohn's disease, diarrhea is ____ and rectal bleeding is ____. In UC, diarrhea is ____ and rectal bleeding is ____.
In which disease are strictures, fistulas, and abscesses common? Chrohn's disease ulcerative colitis
Which disease increases the risk for cancer? Chrohn's disease ulcerative colitis
What is diverticular disease, and what is the patho?
Outpouchings through the muscular layer of the colon wall caused by high intraluminal pressure on areas of bowl wall weakness
What is the treatment for diverticular disease before/after it becomes diverticulitis
before: controlled by diet after: antibiotic, fluids, electrolytes, surgery is obstruction or fistula develop
What is a mechanical intestinal obstruction, and what are the clinical manifestations?
results from adhesions, tumors, prolonged impacted feces, volvulus, etc
manifestations: increased bowel sounds, ab pain, nausea, constipation, distention, vomiting
What is a paralytic intestinal obstruction, and what are the clinical manifestations?
results from any condition that inhibits peristalsis like use of opioids, anesthetic agents, surgical manipulation, spinal cord and back injuries, or peritonitis
manifestations: absence of bowel sounds, pain, constipation, distention, vomiting
What are some complications of an intestinal obstruction?
edema, ischemia, necrosis, perforation
The liver is a vascular reservoir. What problem may occur in a pt with a liver problem?
bleeding, hypovolemic shock
The liver metabolizes carbs. What may result of decreased liver function?
The liver breaks glycogen -> glucose and synthesizes glucose from AA. If the liver is not working, there will be a decreased ability to respond to hypoglycemia.
What are some protective functions of the liver?
filter and destroy bacteria, detox drugs/alcohol/poisons
What are some hormonal functions of the liver?
metabolize sex hormones, inactivate aldosterone
Describe the process of bilirubin elimination.
Hb -> Heme + Globin Heme - oxidized into biliverdin - "free bilirubin" created - bilirubin attaches to albumin and moves to the liver where it is made more water soluble - it is excreted through the bile duct into the small intestine where it is acted on by bacterial flora and converted into urobilinogen - it is eliminated by feces or put back into circulation to the kidneys and out as urine
What happens if bilirubin is built up, and what is one possible cause?
It circulates back through the kidney and results in coca-cola colored urine. One possible cause is a hemolytic transfusion reaction.
What are normal total bilirubin counts? What level is associated with jaundice?
normal: 0.1 - 1.2 mg/dl jaundice: >20.-2.5 mg/dl
What are causes of pre-hepatic, intrahepatic, and post-hepatic jaundice?
pre-hepatic: RBC destruction causes excess bilirubin because the cells are releasinc excess heme and globin
intrahepatic - failure of the liver to remove and conjugate bilirubin
post-hepatic: obstruction of bile flow
What would you expect to see in serum protein level and coagulation factor times in a patient with jaundice?
serum protein levels - albumin would be decreased because protein is not being synthesized by the liver
coagulation factors - thrombin and prothrombin times increase
What are clinical manifestations of hepatitis during the prodromal (pre-icterus), icterus, and recovery phases?
prodromal - basically just not feeling well - ends with the appearance of jaundice
icterus - jaundice, pruritus, liver enlargement, tenderness, dark urine
recovery - return of appetite, disappearance of jaundice, other symptoms diminish
Which forms of hepatitis can be caused by feces, and which can be caused by blood or other body fluids?
feces - A and E Blood or blood-derived body fluids - B, C, D
Which forms of hepatitis are transmitted fecal-orally, and which are transmitted percutaneously or permucosally?
fecal-oral: A and E percutaneous/permucosal: B, C, D
Which forms of hepatitis are chronic and which are not?
chronic: B, C, D not chronic: A and E
Which forms of hepatitis can be prevented through immunization?
A, B, and D (there is no immunization for Hep D, but protection comes through protection for Hep B)
Which form of hepatitis is the most common cause of chronic hepatitis and is associated with cirrhosis and liver cancer?
What is portal hypertension?
Backup at the hepatic vein due to inability of blood to normally move through the liver
What can result from portal hypertension?
asciets, splenomegaly, portosystemic shunts
What are ascites, and what is the patho behind them?
ascites - fluid buildup in peritoneum
portal hypertension - increased hydrostatic pressure in peritoneal capillaires - fluid retention bc aldosterone is not being inactivated - increased water and Na retention - hypoalbuminemia so fluid is not pulled back into capillaries - body senses vascular volume loss and cause more retention of fluid and Na - leads to the beginning again