1. Inflammatory Bowel Disease:
A. Risk factor
a. Autoimmune disease
1. Environmental or bacterial causes an overactive, inappropriate, sustained
immune response in genetically susceptible person
2. Inflammation causes widespread tissue destruction
b. Environmental factors
1. Diet, smoking, and stress alter microbial flora
2. High intake of: refined sugar, fat, polyunsaturated fatty acid, omega-6 fatty
acid;
3. Low intake of raw fruit, vegetables, omega 3-rich foods, dietary fiber
c. Drug associations
1. NSAIDS, antibiotics, oral contraceptives
2. Genetic link: 200 genes associated with IBD
B. Treatment
a. A Dietary modifications: increased calories, protein, and fluids. Encourage client to
eat small servings several times a day.
b. B Medications for Crohn’s disease.
c. 1. Anti-inflammatory: aminosalicylates (sulfasalazine; see Appendix 7-2)
d. and corticosteroids (see Appendix 7-2).
e. 2. Antimicrobials: prevent or treat infection.
f. 3. Immunosuppressants to decrease or suppress the immune response
g. 4. Biologic and targeted medications: infliximab (Remicade), adalimumab (Humira),
and certolizumab pegol (Cimzia)
h. 5. Antidiarrheals.
i. C Medications for ulcerative colitis: aminosalicylates and corticosteroids to
decrease inflammation.
j. D Surgical intervention may be necessary if client fails to respond to medical
management and if fistulas, perforation, bleeding, or intestinal obstruction occur.
1. 1. Total removal of colon, rectum, and anus with formation of permanent
ileostomy (see Appendix 18-8).
2. 2. Total removal of colon, rectum, and anus with formation of continent
ileostomy (Kock’s pouch).
3. 3. Total removal of colon with formation of an ileoanal reservoir (J pouch).
4. 4. Minimally invasive surgery (MIS) involves a laparoscopy to remove small
areas of diseased tissue in the ileum and ileocecal areas.
C. Manifestation
a. A Risk factors/etiology.
b. 1. Familial tendency.
c. 2. Commonly occur in the teenage years, with a second peak in occurrence in
clients 60 years old and older.
d. 3. Altered inflammatory response.
e. B Clinical manifestations—Crohn’s disease.
f. 1. Steatorrhea, multiple diarrhea stools per day.
g. 2. Weight loss; nutritional deficiencies; impaired absorption of vitamin B12
(cobalamin).
h. 3. Intermittent fever.
i. 4. Entire thickness of bowel wall is involved; fistulas are not uncommon.
j. 5. Nausea, cramping, flatulence.
D.
E.
F.
G.
H.
k. C Clinical manifestations—ulcerative colitis.
l. 1. Rectal bleeding.
m. 2. Diarrhea, one to two diarrhea stools per day; may contain small amounts of
blood.
n. 3. Number of stools increases with exacerbation of condition; 10 to 20 stools per
day in acute exacerbation.
o. 4. Increased in systemic symptoms (fever, malaise, anorexia) with exacerbation.
p. 5. Tenesmus (uncontrollable straining).
q. 6. Minimal small bowel involvement.
Postoperative Nursing Implications—Initial Care
a. • Evaluate stoma every 8 hours after surgery. It should remain pink and moist; dark
blue stoma indicates ischemia.
b. • Measure the stoma and select an appropriately sized appliance. Mild to moderate
swelling is common for the first 2 to 3 weeks after surgery, which necessitates
changes in size of the appliance.
c. • Appliance should fit easily around the stoma and cover all healthy skin.
d. • Keep the skin around the stoma clean, dry, and free of stool and intestinal
secretions. Prevent contamination of the abdominal incision.
e. • Change the skin appliance only when it begins to leak or becomes dislodged.
Ostomy teaching
Ostomy assessment
Ostomy care & management
1. Ostomy bags should be changed when about one-third full to avoid weight of
bag dislodging skin barrier.
Complication
a. A Crohn’s disease.
1. 1. Perirectal and intraabdominal fistulas; fissures and rectal abscesses. 2.
Perforation and peritonitis.
2. 3. Nutritional deficiencies, especially of fat-soluble vitamins.
b. B Ulcerative colitis.
1. 1. Perforation and peritonitis with toxic megacolon.
2. 2. Increased risk for cancer after 10 years.
1. Interstitial Obstruction
A. LBO vs SBO manifestations
a. Onset - Prox SBO; Rapid, Distal SBO; Rapid Large Bowel; Gradual
b. Pain - Prox SBO; Colicky, cramping, occurs at frequent intervals Distal SBO; Colicky, occurs more intermittently
Large Bowel; Persistent, cramping
c. Bowel movement - Prox SBO; Feces for a short time, Distal SBO; Gradual constipationLarge Bowel;
Obstipation
d. Abdominal distention - Prox SBO; Minimal Distal SBO; Increased, Large Bowel; Increased
B. Treatment
a. A Mechanical and vascular intestinal obstructions are generally treated surgically;
ileostomy or colostomy may be necessary.
b. B Conservative treatment includes nasogastric suctioning and decompression
c. C Fluid and electrolyte replacement; antibiotic therapy.
d. D. Intussusception: pneumoenema (air enema) with or without water- soluble
contrast or ultrasound guided hydrostatic (saline) reduction.
e. 1. Risk of intestinal perforation exists with hydrostatic reduction.
f. 2. Emergency surgical repair if hydrostatic reduction is not successful.
1. Pancreatitis: - due to trauma, the use of alcohol, biliary tract disease, viral or bacterial
disease, hyperlipidemia, hypercalcemia, cholelithiasis, hyperparathyroidism, ischemic
vascular disease, and peptic ulcer disease.
A. Acute Manifestation
a. • Abdominal pain predominant
b. • Left upper quadrant or mid-epigastric
c. • Radiates to back
d. • Sudden onset
e. • Deep, piercing, continuous, or steady
f. • Eating fatty food worsens pain
g. • Starts when recumbent
h. • Not relieved with vomiting
i. Flushing • Cyanosis • Dyspnea • Nausea/vomiting • Low-grade fever • Leukocytosis
• Hypotension, tachycardia • Jaundice
j. • Abdominal tenderness with muscle guarding • Decreased or absent bowel sounds
• Crackles in lungs • Abdominal skin discoloration
k. • Grey Turner’s spots or sign • Cullen’s sign • Shock
B. Chronic Manifestation
a. Abdominal pain and tenderness
b. b. Left upper quadrant mass
c. c. Steatorrhea and foul-smelling stools that may increase in volume as pancreatic
insufficiency increases
d. d. Weight loss
e. e. Muscle wasting
f. f. Jaundice
g. g. Signs and symptoms of diabetes mellitus
C. Interpersonal care (management)
a. Acute
1. • Relief of pain
2. • Prevention or alleviation of shock
3. • Decreased pancreatic secretions
4. • Correction of fluid/electrolyte imbalances • Prevention/treatment of infections
5. • Removal of precipitating cause
6. Conservative therapy
A. Shock - Plasma or plasma volume expanders (dextran or albumin)
B. Fluid/electrolyte problems
C. • Lactated Ringer’s solution
D. • Central venous pressure reading
E. • Ongoing hypotension
F. • Vasoactive drugs: dopamine • Prevent infection
G. • Enteral nutrition
H. • Antibiotics
I. • Endoscopically or CT-guided percutaneous aspiration
J. Supportive care
a. • Aggressive hydration
b. • Pain management
1. • IV opioid analgesics, antispasmodic agent •
2. Management of metabolic complications
3. • Oxygen, glucose levels
c. • Minimizing pancreatic stimulation
1. • NPO status, NG suction, decreased acid secretion, enteral
nutrition if needed
d. Surgical therapy
1. • For gallstones
A. • ERCP plus endoscopic sphincterotomy
B. • Laparoscopic cholecystectomy
e. Uncertain diagnosis •
f. Not responding to conservative therapy • Drainage of necrotic fluid
collections
K. Drug therapy
a. • IV morphine
b. • Antispasmodics
c. • Carbonic anhydrase inhibitors
d. • Antacids
e. • Proton pump inhibitors
L. Nutritional therapy
a. • NPO status initially
b. • Enteral versus parenteral nutrition
c. • Monitor triglycerides if IV lipids given
d. • Small, frequent feedings when able
e. • High-carbohydrate • No alcohol • Supplemental fat-soluble vitamins
f.
b. Chronic
1. • Analgesics for pain relief (morphine or fentanyl patch [Duragesic])
2. • Diet - Bland, low-fat • Small, frequent meals
3. • No smoking, No alcohol or caffeine
4. Pancreatic enzyme replacement
5. • Contain amylase, lipase, trypsin Bile salts Insulin or oral hypoglycemic agents
Acid-neutralizing and acid-inhibiting drugs Antidepressants
6. • Surgery
A. • Indicated when biliary disease is present or if obstruction or pseudocyst
develops
B. • Diverts bile flow or relieves ductal obstruction
C. • Choledochojejunostomy • Roux-en-Y pancreatojejunostomy
D. Endoscopic procedures
a. • Pancreatic drainage
b. • ERCP with sphincterotomy and/or stent placement
A. Treatment (CONTROL PAIN)
a. Decrease stimulus
1. NPO status; IV Fluids, Suctions, Bed rest
b. Surgery interventions to eliminate precipitation factors
c. Drug Therapy
d. • Pain medication (e.g., morphine)
e. • PPI (e.g., omeprazole [Prilosec])
f. • Antibiotics (if necrotizing pancreatitis)
1. Pancreatic cancer
A. Pre op
a. A Maintain nasogastric suctioning; assess for adequate hydration. B Control
hyperglycemia.
b. C Assess cardiac and respiratory stability.
c. D Assess for development of thrombophlebitis.
B. post op
a. A Extensive surgical resection of the pancreas and surrounding tissue.
b. B Evaluate for hypercoagulable state, as well as bleeding tendencies.
c. C Monitor for fluctuation in serum glucose levels.
d. D Maintain NPO status and nasogastric suction until peristalsis returns.
e. E Encourage adequate nutrition when appropriate.
f. 1. Decrease fats and increase carbohydrates. 2. Small, frequent feedings.
g. F Closely observe for development of problems from thromboemboli to coagulation
problems; surgery and immobility.
C. Risk factor
a. Chronic pancreatitis
b. Diabetes type 2
c. Age (between 60 – 80 yo)
d. Smoking
e. Family history of pancreatic cancer
f. High fat diet
g. African American have a higher incidence of pancreatic cancer than whites
1. Cirrhosis:
A. Risk factors
a. 1. Excessive, prolonged alcohol consumption.
b. 2. Nutritional deficiencies.
c. 3. Frequently, a combination of alcoholism and nutritional deficiency.
d. 4. Predisposing chronic hepatic and biliary infections.
B. Manifestation
a. 1. GI disturbances: anorexia, indigestion, change in bowel habits, weight loss.
b. 2. Changes in the skin.
1. a. Jaundice (hepatocellular and biliary), pruritus.
2. b. Spider angiomas on the face, neck, and shoulders.
3. c. Palmar erythema: reddened areas on the palms that blanch with pressure.
c. 3. Blood disorders: anemia.
d. 4. Coagulation disorders: spontaneous bruising from thrombocytopenia.
e. 5. Changes in sexual characteristics: gynecomastia, impotence in males;
amenorrhea, vaginal bleeding in females.
f. 6. Peripheral neuropathy: probably caused by inadequate intake of vitamin B
complex.
g. 7. Hepatomegaly, splenomegaly.
h. 8. Portal hypertension.
1. a. Esophageal varices that bleed easily.
2. b. Hemorrhoids.
3. c. Collateral veins visible on abdominal wall.
4. d. Development of edema and ascites.
5. e. Edema generally occurs in feet, ankles, and presacral area.
6. f. Severe abdominal distention and weight gain with ascites.
7. g. Presence of fluid waves in the abdomen.
i. 9. Portal-systemic encephalopathy
1. a. Changes in mental responsiveness.
2. b. Level of concentration: ask client to repeat a series of numbers; if client has
encephalopathy, he or she will be unable to repeat a 4- to 6-digit sequence.
3. c. Memory: determine client’s ability to recall recent events (yesterday or past
week) and remote events (last year).
4. d. Apraxia: deterioration in writing and drawing; inability to construct or draw a
figure.
5. e. Asterixis (flapping tremors): clients with asterixis are unable to hold their
hands out in front of them when asked; a flapping of the hands will occur.
6. f. Fetor hepaticus: musty, sweet odor to breath due to inability of liver to
degrade digestive products.
C. Diagnostic studies (labs, procedures ect..)
a. Biopsy - gold standard
b. Enzyme levels, including alkaline phosphatase, AST, ALT, and γ-glutamyl
transpeptidase (GGT),
c. total protein and albumin
d. Serum bilirubin, globulin lvls
e. Cholesterol LVL
f. PT time
g. US Elastography (Fibroscan)
h. Liver Biopsy
D. Complications
a. 1. Portal hypertension: A persistent increase in pressure in the portal vein that
develops as a result of obstruction to flow.
b. 2. Ascites
c. a. Accumulation of fluid in the peritoneal cavity that results from venous congestion
of the hepatic capillaries
d. b. Capillary congestion leads to plasma leaking directly from the liver surface and
portal vein.
e. 3. Bleeding esophageal varices: Fragile, thin-walled, distended esophageal veins
that become irritated and rupture
f. 4. Coagulation defects
g. a. Decreased synthesis of bile fats in the liver prevents the absorption of fat-soluble
vitamins.
h. b. Without vitamin K and clotting factors II, VII, IX, and X, the client is prone to
bleeding.
i. 5. Jaundice: Occurs because the liver is unable to metabolize bilirubin and because
the edema, fibrosis, and scarring of the hepatic bile ducts interfere with normal bile
and bilirubin secretion
j. 6. Portal systemic encephalopathy: End-stage hepatic failure characterized by
altered level of consciousness, neurological symptoms, impaired thinking, and
neuromuscular disturbances; caused by failure of the diseased liver to detoxify
neurotoxic agents such as ammonia
k. 7. Hepatorenal syndrome
l. a. Progressive renal failure associated with hepatic failure
m. b. Characterized by a sudden decrease in urinary output, elevated blood urea
nitrogen and creatinine levels, decreased urine sodium excretion, and increased
urine osmolarity
E. Management of complications
a. 1. Rest.
b. 2. Dietary modification: increase calories and carbohydrates; protein and fat may be
consumed as tolerated.
c. To assess for and prevent complications of hepatic encephalopathy.
d. A Frequent assessment of responsiveness.
e. B Assess for changes in level of orientation and motor abnormalities (asterixis).
f. C Decrease production of ammonia.
g. 1. Increase carbohydrates and fluids.
h. 2. Decrease activity, because ammonia is a by-product of metabolism.
i. 3. GI bleeding will increase ammonia levels as a result of the breakdown of red
blood cells.
j. 4. Lactulose to promote excretion of ammonia in the stool; diarrhea may occur.
k. 5. Nonabsorbable intestinal antibiotics (see Appendix 7-2) will decrease protein
breakdown.
l. D Prompt treatment of hypokalemia.
1. Liver Cancer:
A. Risk factor
a. Cirrhosis of the liver
1. Accounts for 80% of primary liver cancers
b. ! Hepatitis C
1. ! Accounts for 50%-60% of all liver cancers
c. ! Hepatitis B
1. ! Accounts for 20% of all liver cancers
d. ! Obesity
e. ! Comorbidity
f. Excessive alcohol use
g. ! Smoking
h. ! Age
1. ! Not common in persons under 40 years of age
i. ! Family history
j. ! Race/Ethnicity
1. ! More prevalent in African Americans and Asian Americans
1. Appendicitis
A. Treatment
B. Diagnostic Studies and Interprofessional Care
a. • H & P; WBC, UA • CT scan; US or MRI
b. • Surgery: appendectomy
1. • Immediate to avoid rupture; peritonitis
2. • IV fluid and antibiotics
C. Nursing Management
a. • Preoperative:
1. • Administer IV fluid and analgesia
2. • Prevent complications
3. • Keep NPO • Monitor VS • Antiemetics
b. • Postoperative:
1. • General postop care (laparotomy)
2. • Early ambulation; advance diet as tolerated
3. • IV antibiotics if ruptured
D. Manifestations
a. • Initially dull periumbilical pain; anorexia, nausea, vomiting
b. • Persistent pain RLQ at McBurney’s point
c. • Fever, localized tenderness, rigidity, rebound tenderness, muscle guarding
d. • pain with cough, sneeze, deep breath
e. • Lie still with right leg flexed
f. • Older adult: less pain, slight fever, right iliac fossa discomfort
1. Peritonitis
A. Manifestation
a. Presence of precipitating cause.
1. Sharp or knifelike pain and/or dull and deep-seated pain over involved area;
rebound tenderness; pain may radiate to back, shoulder, or scapula.
2. Sudden, excruciating pain suggests the possibility of rupture.
3. Abdominal mass or distention: note color and contour of abdomen.
4. Abdominal muscle rigidity (“board-like” abdomen), guarding.
5. Unexplained persistent or labile fever.
6. Anorexia, nausea, vomiting.
7. Tachycardia, hypotension, shallow respirations: signs of impending or actual
shock.
8. Decreased or absent bowel sounds.
9. Hypovolemia, dehydration.
10. Shallow respirations in attempt to avoid pain.
B. Management - To maintain fluid and electrolyte balances and reduce gastric
distention. To provide pain control, wound care, prevent complications of
immobility, and monitor postoperative progress
a. Preoperative or Nonoperative
1. • NPO status
2. • IV fluid replacement - normal saline or lactated Ringer’s solution to maintain
hydration and urine output of 30 mL/hr; assess urine specific gravity.
3. • NG to low-intermittent suction
4. • O2 PRN
5. • Parenteral nutrition as needed
b. Drug Therapy
1. • Antibiotic therapy
2. • Analgesics (e.g., morphine)
3. • Antiemetics as needed
c. Postoperative
1. • NPO status
2. • NG to low-intermittent suction
3. • Semi-Fowler’s position
4. • IV fluids with electrolyte replacement
5. • PN as needed
6. • Blood transfusions as needed
d. Drug Therapy
1. • Antibiotic therapy
2. • Sedatives and opioids
3. • Antiemetics as needed
1. Viral Hepatitis (A, B, C, D, E):
A. Mode of Transmission
a. Hepatitis A/E- Formerly known as infectious hepatitis. VACCINE HEP A; Two
doses are needed at least 6 months apart for lasting protection.
1. Crowded conditions (day care, nursing home)
2. Exposure to poor sanitation
b. Transmission A/E
1. Fecal-oral route
2. Person-to-person contact
3. Parenteral
4. Contaminated fruits or vegetables, or uncooked shellfish
5. Contaminated water or milk
6. Poorly washed utensils
c. Hepatitis B/C/D
1. Blood or body fluid contact
2. Infected blood products
3. Infected saliva or semen
4. Contaminated needles
5. Sexual contact
6. Parenteral
7. Perinatal period
8. Blood or body fluid contact at birth
B. Manifestation pathology
a. Clinical manifestations: all clients experience inflammation of the liveR tissue and
exhibit similar symptoms.
1. Anicteric phase.
A. a. Anorexia, nausea, malaise, headache. b. Upper right quadrant
discomfort.
B. c. Low-grade fever, hepatomegaly.
C. 2. Icteric phase (jaundiced).
2. a. Dark urine caused by increased excretion of bilirubin.
A. b. Pruritus due to accumulation of bile salts beneath the skin.
B. c. Stools light and clay colored.
C. d. Liver remains enlarged and tender.
3. Posticteric phase (after jaundice).
A. a. Malaise, easily fatigued.
B. b. Hepatomegaly remains for several weeks.
4. 4. Anicteric hepatitis (absence of jaundice).
A. a. Frequently occurs in children.
B. b. Many clients with hepatitis A and hepatitis C (non-A, non-B) may not
show clinical jaundice.
C. c. Unexplained fever, general GI disturbances.
D. d. Anorexia and malaise.
C. Diagnostic studies
D. Labs
a. Liver and pancreas laboratory studies
b. 1. Liver enzyme levels (alkaline phosphatase [ALP], aspartate aminotransferase
[AST], and alanine aminotransferase [ALT]) are elevated with liver damage or bilary
obstruction. Normal reference intervals: ALP, 38-126 U/L (0.65-2.14 µkat/L); AST, 0
to 35 U/L (0 to 35 U/L); ALT, 4 to 36 U/L (4 to 36 U/L).
c. 2. Prothrombin time is prolonged with liver damage. Normal reference interval: 11 to
12.5 seconds.
d. 3. The serum ammonia level assesses the ability of the liver to deaminate protein
byproducts. Normal reference interval: 10 to 80 mcg/dL (6 to 47 mcmol/L).
e. 4. An increase in cholesterol level indicates pancreatitis or biliary obstruction.
Normal reference interval: less than 200 mg/dL (less than 5.0 mmol/L).
f. 5. An increase in bilirubin level indicates liver damage or biliary obstruction. Normal
reference intervals: total, 0.3 to 1.0 mg/dL (5.1 to 17 mcmol/L); indirect, 0.2 to 0.8
mg/dL (3.4 to 12 mcmol/L); direct, 0.1 to 0.3 mg/dL (1.7 to 5.1 mcmol/L).
g. 6. Increased values for amylase and lipase levels indicate pancreatitis. Normal
reference intervals: amylase, 60 to 120 Somogyi units/dL (100 to 300 U/L); lipase, 0
to 160 U/L (0 to 160 U/L)
1. Gallbladder Disease:
A. Etiology - Unknown cause.
a. Cholecystitis
1. Inflammation of the gallbladder that may occur as an acute or chronic process
2. Acute inflammation is associated with gallstones (cholelithiasis).
3. Chronic cholecystitis results when inefficient bile emptying and gallbladder
muscle wall disease cause a fibrotic and contracted gallbladder.
4. Acalculous cholecystitis occurs in the absence of gallstones and is caused by
bacterial invasion via the lymphatic or vascular system.
B. Risk factor - 4 F's are seen
a. Fatty
b. Fertile
c. Female
d. Forty or Fifty
C. Teaching
a. Postoperative teaching should include:
1. 1. Remove the bandages on the puncture sites the day after surgery and you
can shower.
2. 2. Notify your HCP if any of the following signs and symptoms occurs:
A. Redness, swelling, bile-colored drainage or pus from any incision
B. Severe abdominal pain, nausea, vomiting, fever, chills
3. You can gradually resume normal activities.
4. Return to work within 1 wk of surgery.
5. You can resume your usual diet, but a low-fat diet is usually better tolerated for
several weeks after surgery
1. Diverticular Disease:
A. Nutritional Therapy
a. Provide bed rest during the acute phase.
‣ Maintain NPO status or provide clear liquids during the acute phase as prescribed.
‣ Introduce a fiber-containing diet gradually, when the inflammation has resolved.
‣ Instruct the client to increase fluid intake to 2500 to 3000 mL daily, unless
contraindicated.
‣ Instruct the client to eat soft high-fiber foods, such as whole grains; the client should
avoid high-fiber foods when inflammation occurs, because these foods will irritate the
mucosa further.
‣ Instruct the client to avoid gas-forming foods or foods containing indigestible
roughage, seeds, nuts, or popcorn, because these food substances become trapped
in diverticula and cause inflammation.
‣ Instruct the client to consume a small amount of bran daily and to take bulk-forming
laxatives as prescribed to increase stool mass
1. Function:
A. Gallbladder
a. The primary function of the gallbladder is concentration and storage of bile.
b. The presence of fatty materials in the duodenum stimulates the liberation of
cholecystokinin, which causes contraction of the gallbladder and relaxation of the
sphincter of Oddi.
B. Liver
a. Synthesis of absorbed nutrients.
b. Removes excess glucose and amino acids from the portal blood
c. Synthesis of prothrombin for normal clotting mechanisms. Vitamin K 1342 is
necessary for adequate prothrombin production.
d. Vitamin and mineral storage.
1. Produces and stores vitamins A and D.
2. Vitamin B12 and iron are stored in the liver.
3. Drug metabolism: barbiturates, amphetamines, and alcohol are metabolized by
the liver.
4. Production of bile and bile salts.
e. Stores and filters blood (200 to 400 mL of blood stored)
f. The liver secretes bile to emulsify fats (500 to 1000 mL of bile/day).
C. Spleen
a. produces lymphocytes and plasma cells and filters the blood.
b. The spleen removes and breaks down the hemoglobin in worn-out red blood cells.
This results in the production of bilirubin.
c. Bilirubin is carried from the spleen to the liver for excretion.
D. Pancreas
a. produces the enzymes trypsin, amylase, and lipase, which are secreted into the
duodenum and are necessary for the digestion and absorption of nutrients.
b. Influences carbohydrate metabolism, indirectly influences fat and protein
metabolism, and produces insulin and glucagon
c. Exocrine gland
1. Secretes sodium bicarbonate to neutralize the acidity of the stomach contents
that enter the duodenum
2. Pancreatic juices contain enzymes for digesting carbohydrates, fats, and
proteins.
d. Endocrine gland
1. Secretes glucagon to raise blood glucose levels and secretes somatostatin to
exert a hypoglycemic effect
2. The islets of Langerhans secrete insulin.
3. Insulin is secreted into the bloodstream and is important for carbohydrate
metabolism.