Alterations in Digestive function

Question 1

Properties of the esophagus

Answer 1

Has sphincters- lower esophageal sphincter normally remains contracted until food moves down. Alkaline mucosa, muscle walls. Food passes via peristalsis

Question 2

Esophagitis

Answer 2

inflammation of the esophagus usually caused by acid reflux (GERD), monilial infection, herpes virus (trench mouth in children), and ingestion of poisons. S&S= heartburn, upper abdominal pain right after eating, dysphagia, weight loss (from vomiting) and aspiration pneumonia

Question 3

Hiatal Hernia

Answer 3

protrusion of a portion of the stomach into the chest through the esophageal hiatus of the diaphragm, caused by loss of muscle tone, increased abd. pressure, and a distorted angle b/w the esophagus and stomach. S&S= substernal discomfort, regurgitation after eating, interference with lower esophageal sphincter protective mechanism

Question 4

Esophageal cancer

Answer 4

Rare type of cancer associated w/malnutrition, GERD, esophagitis, hiatal hernia, ALCOHOL & SMOKING. S&S= progressive dysphagia (6-8 month), steady chest pain, obstruction due to the tumor, weight loss, impaired nutrition, hemorrhage and sepsis from ulcerating tumor.

Question 5

Properties of the stomach

Answer 5

Has motor, digestive and secretory functions but no absorption occurs here. Digestion of protein begins with pepsin and HCl release, gastrin synthesis and release, intrinsic factor for Vit B12 absorption (which occurs in ileum), and mucous secretion.

Question 6

Gastritis

Answer 6

inflammation of the stomach mucosa that can either be acute or chronic. Acute gastritis is the result of local irritants (drugs/alcohol),and is self-limiting. Chronic gastritis is idiopathic and results in thinning of the stomach wall and decreased secretion of HCl, pepsin and intrinsic factor. Both types cause epigastric pain, N&V, anorexia, belching. Acute may cause hematemesis a/o melena while chronic results in Vit B12 deficiency.

Question 7

Peptic Ulcer

Answer 7

erosions of the GI mucosa that penetrate the muscularis mucosa. Gastric ulcers occur from alcohol, aspirin, and bile salts and histamine is liberated, while duodenal ulcers are the effects of acid, drugs and stress. S&S= nagging abd. pain 2 hours after eating that is relieved by food or antacids, pain at night, weight loss, hematemesis and melena. Complications include intractability, hemorrhage, perforation, and obstruction

Question 8

Stomach cancer

Answer 8

Cancer associated with a genetic predisposition, consumption of preserved/smoked meats, H. pylori infection, nitrate preservatives, presence of atrophic gastritis and pernicious anemia. S&S= insidious/asymptomatic until late, weight loss, abd. pain, anorexia, vomiting, dysphagia, bowel changes, anemia and malaise. Metastasis often to liver

Question 9

Crohn’s disease (Regional enteritis)

Answer 9

a type of chronic Inflammatory bowel disease that affects both lg. and sm. intestines. There are pockets of inflammation (skip lesions, thus, the entire bowel is not inflamed) that cause thickening/stiffening of the mucosa and can affect lymphatic drainage. This causes mild/intermittent/non-bloody diarrhea, colic in lower abd, weight loss, malabsorption and anemia, fever. Complications include obstruction, perforation, ulcers, abscesses and fistulae

Question 10

Appendicitis

Answer 10

inflammation of the appendix causing RLQ pain, constipation and failure to pass gas, fever and leukocytosis. The person will flex their knees to reduce abdominal tension. If the appendix ruptures there is sudden/temporary relief of pain but the patient will require surgery

Question 11

Paralytic Ileus

Answer 11

type of bowel obstruction in which there is loss of autonomic control of motility/peristalsis as a result of abd surgery, hypokalemia, severe trauma, peritonitis or toxic agents/narcotic use. This causes bowel distention, seeping diarrhea, impaction, silent abdomen, vomiting, decreased ECF– hypotension, reduced CO-tissue perfusion, metabolic acidosis, and pain

Question 12

Diverticulosis

Answer 12

abnormal condition in which there are outpouchings of intestinal mucosa, most commonly in the sigmoid colon. Prevalence increases with age and low fiber diet. Asymptomatic but can lead to diverticulitis

Question 13

Diverticulitis

Answer 13

inflammation of a diverticulum from trapped digested food. Majority are asymptomatic but can have intermittent diarrhea, constipation, discomfort in LLQ. Complications include- bleeding, perforation and peritonitis, abscess and fisula formation, and intestinal obstruction

Question 14

Ulcerative Colitis (BD)

Answer 14

idiopathic inflammatory disease of the colon (rectum and sigmoid colon) w/remissions and exacerbations. S&S= abrupt onset of bloody diarrhea, fever, abd pain, weight loss and presence of continuous lesions. Bloody diarrhea and continuous lesions marks diff b/w this and Crohn’s. P. w/10 year hx of this have increased risk for colon cancer.

Question 15

Colorectal cancer

Answer 15

RFs include: low fiber diet, high carb/fat diets, presence of colorectal polyps, prolonged contact of stool with mucosa. Presents w/initially vague symptoms- weight loss and malaise. Left colon- diarrhea, constipation, bright red blood on stool. Right colon- pain, palpable mass in RLQ, anemia, weakness, dark red stools.

Question 16

Cholelithiasis

Answer 16

presence of gallstones, which is the hardening of normally soluble components of bile. There are two types of stones; cholesterol and pigmented. S&S= colic pain, pressure in epigastic area/RUQ that radiates to the shoulders, and N&V. If stone causes obstruction, may lead to jaundice.

Question 17

Cholesterol gallstones

Answer 17

Gallstones that occur when the gallbladder is supersaturated with cholesterol, which crystallizes and forms stones. These are the most common type of stones

Question 18

Pigmented gallstones

Answer 18

gallstones that form when there is an increased amount of bilirubin in the gallbladder, which binds with calcium and hardens

Question 19

Cholecystitis

Answer 19

inflammation and distention of the gall bladder caused by a gallstone that is obstructing the neck of the gallbladder or the cystic duct. S&S= RUQ pain/rebound tenderness, fever, leukocytosis, elevation of serum transaminase and bilirubin on liver function tests. If unresolved, obstruction can lead to empyema or gallbladder gangrenous necrosis.

Question 20

Pancreatitis

Answer 20

autodigestion and necrosis of the pancreas (both exo and endocrine cells) due to activation of hydrolytic enzymes within the pancreas. This can be a result of excessive alcohol intake or biliary tract disease. S&S= constant/severe pain in upper back that is relieved by sitting/leaning- may lead to vascular collapse/shock, jaundice, elevated serum amylase and serum lipase.

Question 21

Jaundice

Answer 21

yellow/green hue of skin due to: increased production of bilirubin (hemolytic jaundice), or an intrahepatic or extrahepatic obstruction (obstructive jaundice), or acute viral hepatits.

Question 22

Bile salts

Answer 22

component of bile responsible for breaking fat particles into smaller sizes. This component is essential for the absorption of fat soluble vitamins. (including Vitamin K which is an factor for clotting).

Question 23

Bilirubin

Answer 23

Excretory product of old RBC degradation that is a component of bile. The liver is responsible for conjugating bilirubin and turning it into a water soluble/exretory form. Unconjugated bilirubin can not be excreted into the intestines.

Question 24

Hemolytic jaundice

Answer 24

Jaundice caused by the excessive breakdown of RBCS in which the supply of unconjugated bilirubin is too great for the liver to process. This is seen in p. w/pernicious anemia, sickle cell disease, and transfusion incompatibilities.

Question 25

Physiologic jaundice of the newborn

Answer 25

also called kernicterus. This is a type of jaundice in which the hepatic enzyme (glucuronyl transferase) system of a newborn is inadequate in conjugating bilirubin and bilirubin levels reach 20mg/dL. Could also be from inhibition of the enzyme by pregnane, which is in breast milk. Treated with white or blue light phototherapy.

Question 26

Obstructive jaundice

Answer 26

decreased excretion of bile into the bile caniculi and bile tract resulting in conjugated hyperbilirubinemia, dark urine, light stools, increased liver enzymes- alk phosphate, SGOT, cholesterol and bile salts, and itching. Causes include hepatitis, cirrhosis, dubin-johnson syndrome, certain drugs, gallstone impaction at common bile duct and pancreatic cancer

Question 27

Hepatitis A

Answer 27

Acute infectious hepatitis with a short-incubation period, mild severity, and good prognosis. Transmission occurs by eating shit particles from contaminated objects. Thus, populations exposed to contaminated food/water, and crowded conditions are high risk groups.

Question 28

Hep B

Answer 28

Severe, chronic, serum hepatitis that has a long incubation period and prognosis that worsens with age and debility. Drug addicts, p’s on hemodialysis and HCPs are at high risk as it spreads through percutaneous/sexual routes and blood/body fluids.

Question 29

Acute viral hepatitis manifestations

Answer 29

Prodromal phase- 2 weeks of nonspecific symptoms (N&V, malaise, fever, tender liver..). Icteric Phase- 2 weeks, jaundice, dark urine, light stool, elevated liver enzymes, tender/enlarged liver.
Recovery phase with resolution of jaundice- enzymes level out, symptoms disappear.

Question 30

Chronic Hepatitis

Answer 30

prolonged infection in which the p. c/o symptoms and viral Ags persist longer than 6 months. This predisposes the p. to cirrhosis and hepatocellular carcinoma

Question 31

Cirrhosis

Answer 31

Fibrosis of the liver into abnormal nodules most commonly the result of chronic alcoholism. The liver can regenerate/less damage will occur if p. stops drinking permanently. Cirrhosis results in altered liver function including– impaired conjugation of bilirubin and bile synthesis, impaired energy, fat, protein,sex hormone, aldosterone, and drug metabolism, impaired plasma protein production, and altered circulation.

Question 32

Impaired conjugation of bilirubin and impaired bile synthesis from cirrhosis will lead to what manifestations?

Answer 32

jaundice, clay stools, dark urine (bilirubin excreted through kidneys), malnutrition, vit. K deficiency and bleeding problems, diarrhea or constipation, pruritus from bile salts in skin.

Question 33

Decreased ability to convert ammonia to urea in p. with cirrhosis can lead to?

Answer 33

hepatic coma, encephalopathy, increased blood ammonia, altered memory, day-night sleep reversal, mental changes, asterixis (liver flap), handwriting/speech changes, fetor hepaticas (sweet odor to breath/urine)

Question 34

Impaired production of plasma proteins (albumin, prothrombin, fibrinogen, clotting factors) in p. with cirrhosis causes?

Answer 34

edema and ascites (loss of plasma colloid osmotic pressure and movement of fluid out of vasculature), increased chance for drug toxicity, bleeding tendencies, and anemia.

Question 35

Altered detoxification of drugs, sex hormones and aldosterone in p. with cirrhosis will lead to?

Answer 35

menstrual disorders, gynecomastia, testicular atrophy, loss of sex characteristics, vascular spiders, palmar erythema, hyperaldosteronism (more edema/ascites), drug rxns and toxicity.

Question 36

Portal hypertension and collateral blood vessel enlargement in ps with cirrhosis will cause what manifestations?

Answer 36

esophageal varices (rupturing of bl vessels and hematemesis), hemorrhoids, and caput medusa (prominent abd veins)

Question 37

Why do ps with cirrhosis present with ascites and edema along with hypotension and hypovolemia?

Answer 37

These manifestations are secondary to increased portal vein pressure, decreased serum albumin (loss of colloid osmotic pressure) and increased aldosterone (more retention)

Question 38

Describe “hepatorenal syndrome” that is present in ps with cirrhosis

Answer 38

Hepatorenal syndrome is the renal symptoms experienced due to alterations in liver function. With cirrhosis there is altered albumin production by the liver which causes a loss of plasma colloid osmotic pressure–decreased blood flow and CO– and decreased kidney perfusion. Thus, the p. will have increased serum creatinine levels, oliguria, and azotemia.

Question 39

Pyloric stenosis (pediatric)

Answer 39

inherited/multifactorial trait in which there is hypertrophy/thickening/hardening of the sphincter muscle resulting in pyloric sphincter obstruction. S&S= fulminating vomit leading to esophagitis, constipation, malnutrition, weight loss, F&E imbalances.

Question 40

Meconium Ileus (pediatric)

Answer 40

Intestinal obstruction caused by meconium which has adhered to the mucosa wall of the small intestine. This causes distention of the proximal intestines and collapse of distal segment. S&S= vomiting, abd distention, hyperactive peristalsis without stool.