CONDITIONS AFFECTING

ABSORPTION DISORDER IN TRANSPORT AND

• Chron’s disease and ulcerative colitis ELIMINATION
- Chronic inflammatory bowel disease
- Cobble stone appearance leading to malabsorption and losses of • Intussusception
protein from lesion - One part of the intestine slips into the another part (lumen)
- S/S: diarrhea, steatorrhea, fever, fatigue, malaise, weight loss and - Problem in transport of GI contents
RLQ abdominal pain.
- Not relieve by defecation • Adhesions
- Mgt: Weight patient daily; increase CHON; increase caloric diet; - Loop of intestine become adherent and heal slowly or scar
colonoscopy (chron’s disease); sigmoidoscopy (ulcerative colitis) after abdominal surgery

• Cystic Fibrosis • Volvulus

- Production of thick tenacious secretions that stick to the walls of the - Bowel twists and turns upon itself
pancreatic and bile ducts
• Hernia
• Celiac disease - Protrusion of intestine through a weakened area in the
- affects the proximal (mainly duodenum and jejunum) small intestine; abdominal wall
abnormal mucosa, and permanent intolerance to gluten (substance
seen in rice, oats, barley) • Hirschsprung disease
- leads to atrophy of intestinal villi, malabsorptions of fats, iron, and - Dilate and atonic colon caused by the absence of autonomic
calcium parasympathetic ganaglionic (less nerve cells) cells.
- S/S: mushy light, foul-smelling stools, explosive flatus, steatorrhea,
weight loss, fatigue, anorexia, anemia and bruising (cannot absorb
nutrients for blood components)

• Lactose intolerance
- Inability to absorb lactose d/t a deficiency in lactose from the small
intestine
- Can be inherited (no lactose) or acquired (destruction of intestinal
mucosa)
- S/S: pain, diarrhea, flatulence, osteoporosis, dental caries
- Mgt.: eliminate milk products, commercial lactose, calcium
supplements
- Note: Milk cannot be digested-ferment-will form gas
 • Alcohol induced
- Stimulation of hydrochloric acid and secretin stimulates the
exocrine function of the pancreas.
PANCREATITIS - Alcohol also causes edema of the duodenum and ampulla of
Vater. (lesser absorption and accumulation of bile in pancreas
• Reflux of duodenal contents
- Inflammation of the pancreas - General loss of muscle tone caused by alcohol ingestion,
causes reflux into the pancreas and activate pancreatic secretion
• Acute pancreatitis: can be classified into:
- Non Hemorrhagic: edema and inflammation are confined to Auto digestion and complications:
the pancreas 1. Alkaline pH causes trypsin production to activate other proteolytic
- Hemorrhagic: enzymatic digestion of the gland is more enzymes in the pancreas
widespread and damage extend into the retroperitoneal tissues 2. Blockage of ducts by edema or stones causes increase pressure
• Chronic pancreatitis: chronic calcifying pancreatitis within d/t changes in F/E; fat is trapped
3. The duct ruptures, releasing enzymes
CAUSES OF PANCREATITIS 4. Phospo lipase A and elastase digest pancreatic and surrounding
• Alcoholism and biliary tract disease tissues/membranes
• Post-surgical and blunt abdominal trauma 5. Edema, interstitial hemorrhage, vascular damage and necrosis
6. Release histamine and bradykinin which increases vascular
• Infection – mumps, mycoplasma, coxsackie virus B
permeability and vasodilation and causes circulating shock
• Connective tissue disease/SLE
• Diuretics, antimicrobials, corticosteroids, estrogen, opiates Chronic pancreatitis: Pathophysiology
• Pregnancy, hyperlipidemia, hypercalcemia 1. Pancreatic juices contain increased protein and decreased
• Heredity: idiopathic, pancreatic cancer bicarbonate so that it allows protein and calcium precipitates within
the pancreatic duct
Chronic pancreatitis may also be due to: 2. Result to the formation of plugs leading to dilation and atrophy of
• Chronic obstruction of the common bile duct acinar tissue which is replaced by fibrotic tissue and stenosis (lesser
• Cystic fibrosis opening)
• Severe protein calorie malnutrition 3. Obstruction and backflow of pancreatic secretions
4. Necrosis of the pancreas and development of a pseudocyst (an
THEORIES OF ENZYME ACTIVATION encapsulated collection of fluid, pancreatic juice, enzymes, debris
and blood outside the normal duct system
• Bile reflux theory 5. Continuing auto-digestion forms wall around pseudocyst and
- Obstruction of the common channel (bile duct) causes reflux necrosis
into the pancreatic tissues and enzyme activation causing 6. Abscesses develop
autodigestion
- N: trypsinogen: inactive proteolytic enzyme activated by Clinical manifestations of Pancreatitis
trypsin come up with enterokinase goes to intestine. • Pain – mild to severe, constant and incapacitating in the epigastrium
- A: Reflux trypsinogen activated in liver and other parts of the abdomen, radiating to the back, flanks and
trypsinogen contain proteolytic ability goes back to pancreas substernal area, exacerbated by eating and trunk extension.
digestion of pancreas • Grey Turner’s sign – purplish discoloration of the flank caused by
hemorrhagic necrosis of the pancreas
• Hypersecretion-obstruction theory • Cullen’s sign – purplish discoloration on the peri-umbilical area
- Rupture of pancreatic duct occurs with disruption or tearing caused by hemorrhagic necrosis of the pancreas
of cell membranes • Rigid, boardlike abdomen – grave sign of peritoneal irritation
 •Abdominal guarding
•Nausea, vomiting
•Fever
• Loose, bulky, foul smelling stool due to lack of lipase (not able to
digest the fats)
• Hyperglycemia – due to islet cell damage, patients reaction to
stress
• Hypovolemia – due to loss of large amounts of protein rich fluid into
the tissues and periotoneal cavity
• Hypocalcemia – calcium soaps form with fatty acids released by
lysocytes with destruction of abdominal and retroperitoneal fat
• Jaundice – common bile duct obstruction by pancreatic edema
Diagnostic Test for pancreatitis:
• Serum amylase - >25-125 U/L but stats to fall after 2 days
• Elevated urine amylase after serum amylase falls
• Elevated serum lipase - >10-140 U/L
• Elevated ALT (Alanine amino transferase) may suggest gallstones
• Increased serum bilirubin – due to obstruction of bile flow
• CT scan – enlarged pancreas
• ERCP – endoscopic cannulation of the ampulla of Vater and
retrograde injection of radiographic dye into the bile ducts with the
help of a duodenoscope.
Major complications:
• Cardiovascular – hypotension d/t decrease fluid and increase portal
pressure
• Hematologic – Leukocytosis, anemia, DIC
• Respiratory – atelectasis, pleural effusion, ARDS
• GI Hemorrhage
• Pancreas and liver – hemorrhage, ascites, abscesses
• Renal – oliguria and increased BUN (severe bleeding)
• Metabolic – increased blood glucose, decreased calcium, increased
triglycerides
• Neurologic - encephalopathy
Medical and Nursing Management:
• Maintain circulating volume and replace F/E loss-IV fluids, colloids
• Alleviate pain
• Reduce pancreatic stimulus – lavage, suctioning, withhold all oral
intake
• Prevent or treat infection
• Prevent hyperglycemia
• Advise patient not to take anything by mouth
• Watch for diarrhea and steatorrhea
• Take frequent small meals
Medications:
1. Antacids – to neutralize gastric secretions
2. Barbiturates and tranquilizers – to reduce emotional tension
3. Narcotics – to control pain (Meperidine [Demerol]) is used if a
narcotic analgesic is required – causes less spasm in the ducts
4. Cardiotonics – to lessen strain on the heart
5. Anticholinergics – to suppress vagal stimulation
6. Antibiotics
7. Pancreatic enzymes – give in chronic because patient may still eat
• For patients with chronic pancreatitis enzyme replacement
(pancreatin, pancrealipase)
8. Surgical Management:
• Whipple’s procedure – radical pancreas resection with
pancreatojejunostomy
• Peustow procedure – anastomosis of the pancreatic duct
with a loop of intestine.

Nursing Diagnosis:
• Pain
• Altered nutrition
• Fluid volume deficit
• Ineffective breathing pattern
• Impaired health maintenance

Note: Insulin-mediator of activity

 • Infection – may predispose a person to stone formation

Pathophysiology of Cholecystitis
1. Begins with gallstone formation
2. Stones block the drainage of bile
3. Bile acts as an irritant causing cellular infiltration
4. Gallbladder becomes inflamed, edematous and distended
CHOLECYSTITIS/CHOLELITHIASIS 5. Venus congestion and occlusion
6. Gallbladder becomes necrotic
7. Bacterial growth secondary to ischemia
• Cholecystitis – an acute (common in middle aged persons) or
chronic (common in elderly) inflammation of the gallbladder. Clinical Manifestation
• Cholelithiasis – the formation or presence of stones or calculi in the • Ingestion after eating foods high in fat
gallbladder • Pain and tenderness in the right subcostal region or the epigastric
- Basically, cholelithiasis develops when the balance that keeps region, radiating to the scapula and shoulder
cholesterol, bile salts, and calcium in solution is altered so that • Anorexia, N/V, flatulence, bloating, belching dyspepsia
precipitation of these substances occur • Positive murphy’s sign (inspiratory arrest upon pressure to RUQ)
• Choledocholelithiasis – the presence of stones or calculi in the • Diaphoresis, increased HR and RR
common bile duct • Low grade fever and chills
• Palpable gallbladder
Note: common stone - cholesterol • Leukocytpsos (manifestations of inflammation)
• Mild jaundice if with stones
• Occurs more commonly in women, obese, pregnant, DM, • Grayish, white stool, dark yellow or dark amber colored urine
multiparous, use of birth control pills.
• Caused by an alteration in lipid metabolism Therapeutic management
• May be due to bacteria • Supportive management like bed rest, NPO with NGT drain
• Other causes: chemical irritants, kink in the neck of the gallbladder, • IVF, antimetics
mucous obstruction, fasting and trauma • Narcotic – analgesics and antispasmodics
• Antibiotics
Types of gallstones: • Dissolution therapy: Chenodeoxycholic acid and Ursodiol
1. Cholesterol stones • Extracorporeal shock wave lithotripsy – with a lithotripter and water
- 70% cholesterol (yellowish, brownish) bag for amplification
- Results from cholesterol supersaturated bile, nucleation and
precipitation of cholesterol monohydrate crystals Surgical management
- More prevalent • Laparoscopic laser cholecystectomy
2. Pigment stones - involving only 3 small puncture to the abdomen, laser and
- With high concentration of unconjugated bilirubin – carbon dioxide
polymerized bilirubin or calcium bilirubin (associated with • Abdominal cholecystectomy
infections) - removal of the gallbladder, cystic duct, vein and artery are
- They are colored black or brown and are radiopaque ligated
3. Mixed stones
- Combination Care of Patient with a T-tube

Theories of Gallstone formation Purposes:

• Bile – may undergo a change in composition 1. Promotes drainage of bile while the common bile duct is healing after
• Gallbladder stasis – may lead to bile statsis it has been dilated or explored
 2. Provides a means for snaring and removing of additional tests after a - Reaches its intensity in 2 weeks and lasts from 4-6 weeks
cholecystectomy - S/S: jaundice, increased ALT, AST, decreased serum albumin
3. Maintains patency of the remaining ducts levels
4. Prevents bile leakage into the peritoneal cavity 3. Posticeteric phase
5. Assess the amount, color, consistency and odor of drainage every 4- - Begins with the disappearance of jaundice and normally lasts for
8 hours several weeks and may take as long as 4 months.
6. Report sudden increase in bile output after decreasing pattern is
established Categories of Hepatitis
- Inspect site for bile leakage and inflammation 1. Hep A (HAV)
- Semi-fowler’s keep drainage system below gallbladder - Oral-fecal contamination
- Never manipulate the tube without the doctors orders - Abrupt onset
- Observe stools for brown color 7-10 days post op - No chronic carriers
- Mortality infrequent
2. Hep B (HBV)
DISTURBANCES IN HEPATIC - Percutaneous or permucosal routes
- Onset is insidious
FUNCTION - Can become chronic carriers
3. Hep C (HCV)
- Thru infected blood transfusion and parenteral drug abuse
Hepatitis – an inflammation of the liver resulting from viral agents, bacterial - Onset is insidious
agents, or exposure to hepatotoxins or drugs such as carbon tetrachloride or - No vaccine available
acetaminophen 4. Hep D (HDV)
- Same transmission of as Hep B
Note: ALL blood pass to the liver before returning to the vena cava. - Occurs as coinfection with HBV or superinfection in HBV carrier
5. Hep E (HEV)
Pathophysiology - Oral-fecal contamination courses similar to Hep A
6. Hep F (HFV)
Diffuse inflammatory infiltration of hepatic tissues with mononuclear cells - Infection routes similar to Hep A and E
7. Hep G (HGV)
Swelling of liver cells - Coinfection with Hep C

Degeneration and regeneration occurs simultaneously Manifestations

- Jaundice, clay-colored stools, increase bilirubin, darkened urine
Distortion of normal lobular pattern - Pruritus
- Abdominal pain
Pressure within and around the portal vein areas - Fever, fatigue, weakness
- Anorexia, nausea, vomiting
Obstruction of bile channels - Bleeding tendencies, anemia (not able to produce clotting factors)

Treatment
Phases of Viral Hepatitis - F/E replacement
1. Preiceteric (Prodromal phase) - Vitamin K replacement
- lasts for 1 week - Antihistamines
- S/S: increased temperature, chills, nausea, vomiting, weakness, - Antiemetics
general malaise, loss of weight. - Rest
2. Iceteric phase - Diet
 DIARRHEA
CONSTIPATION
Normal adult: <200mg/day
- Inability to evacuate stool
2 Types:
Causes: 1. Small volume
- Antacids with Aluminum Chloride - Volume of feces not increase d/t intestinal motility
- Muscle weakness, pain by abdominal surgery 2. Large volume
- Decrease fluid intake - Caused by underlying condition
- Neurogenic
- Depression
- Decrease motility Different mechanism:
- Low residue diet
- Lesion of anus 1. Osmotic
- Drawing of water to the lumen by osmosis
5 signs: 2. Secretory
- Straining - Excessive mucosal secretion
- Lumpy/hard stool - Inhibition of sodium reabsorption because of chloride and
- Blockage of anurectal bicarbonate rich fluid
- Incompletely evacuation of stool 3. Motility
- <3 bowel movement/wk.

Diagnosis:
- Digital exam
- Proctosigmoidoscopy (direct visualization)
- Barium enema

Management:
- Increase fluid intake
- Increase fiber diet
- Bowel retraining
- Bulk supplement (Metamucil)
- Enema (help trained bowel)