Interventions for Clients with Problems of the Biliary System and Pancreas

 The Gallbladder and pancreas

 The gallbladder

 The gallbladder, a pear-shaped, hollow, saclike organ, 7.5 to 10 cm (3 to 4 in)

long, lies in a shallow depression on the inferior surface of the liver, to which
it is attached by loose connective tissue.

 The capacity of the gallbladder is 30 to 50 mL of bile.

 Its wall is composed largely of smooth muscle.

 The gallbladder is connected to the common bile duct by the cystic duct

 Function of the gallbladder

 storage depot for bile

 gallbladder bile is five to ten times more concentrated than that

originally secreted by the liver.

 The pancreas

 A fish shaped gland

 Location: lies retroperitoneally in the upper abdominal cavity behind the

stomach and extends horizontally from the duodenal C-loop to the spleen.

 Divided into portions:

 Head

 Body

 Tail

 Function of the pancreas

 Two major cellular bodies with separate functions:

 Ascinar Cells - Exocrine (80%)

 secretes enzymes for digestion (trypsin, chymotrypsin,

carboxypeptidase, amylase, and lipase)

 Islet of Langerhans – Endocrine

 Alpha cells – glucagon

 Beta cells – insulin

The hormones produced are essential in the regulation of metabolism

 Acute Cholecystitis

 Acute cholecystitis is the inflammation of the gallbladder.

 Cholelithiasis (gallstones) usually accompanies cholecystitis.

 Acalculous cholecystitis inflammation can occur in the absence of gallstones.

 Calculous cholecystitis is the obstruction of the cystic duct by a stone, which

creates an inflammatory response.

 Chronic Cholecystitis

 Repeated episodes of cystic duct obstruction result in chronic inflammation

 Etiology and genetic risks:

 Excessive dietary cholesterol intake

 DM type I

 Rapid weight loss

 Alcohol intake

 Crohn’s disease

 Pancreatitis, cholangitis (complications)

 Jaundice

 Icterus

 Obstructive jaundice

 Pruritus

 Clinical Manifestations

 Flatulence, dyspepsia, eructation, anorexia, nausea and vomiting, abdominal

pain

 Biliary colic (severe pain due to obstruction)

 Murphy’s sign (pain increases with deep inspiration)

 Blumberg’s sign

 Rebound tenderness

 Steatorrhea (fatty stools)

 Fever (37 t0 39 degrees Celcius)

 Diagnostic assessment

 ALKALINE PHOSPHATASE

 AST

 LACTATE DEHYDROGENASE (LDH)

 SERUM BILIRUBIN

 CBC
  UTZ

 HEPATOBILIARY SCAN

 Nonsurgical Management

 Diet therapy: low-fat diet, fat-soluble vitamins, bile salts

 Drug therapy: opioid analgesia with meperidine hydrochloride(Demerol),

antispasmodic or anticholinergic drugs(Atropine and dicyclomine : Bentyl,
Lomine) antiemetic

 Percutaneous transhepatic biliary catheter insertion – decompress

extrahepatic ducts

 Surgical Management

 Laparoscopic cholecystectomy – minimal envasive surgery

 Standard preoperative care – NPO prior to surgey

 Operative procedure

 Postoperative care

 Free air pain result of carbon dioxide retention in the abdomen

 Ambulation

 Return to activities in 1 to 3 weeks

 Traditional Cholecystectomy

 Standard preoperative care

 Operative procedure

 Postoperative care

 Meperidine hydrochloride via patient-controlled analgesia pump

 Antiemetics

 Wound care

(Continued)

 Traditional Cholecystectomy (Continued)

 Care of the T-tube

 Nothing by mouth

 Diet therapy

 Early post-op when bile flow is reduced :low-fat diet

 No special diet required

 Avoid excessive intake of fat

 Cancer of the Gallbladder

 Anorexia, weight loss, nausea, vomiting, general malaise, jaundice,

hepatosplenomegaly, chronic, progressively severe epigastric or right upper
quadrant pain

 Poor prognosis

 Surgery, radiation, chemotherapy

 Acute Pancreatitis

 Serious and possibly life-threatening inflammatory process of the pancreas

 Necrotizing hemorrhagic pancreatitis

 Lipolysis – Hallmark of pancreatic necrosis

 Proteolysis – autodigestion; Trypsin

 Necrosis of blood vessels – Elastase – elastic fiberss of the blood vessels to

dissolve.

 Inflammation

 Theories of enzyme activation

 The bile reflux (“common channel”) - obstruction

 Hypersecretion-obstruction theory- disruption or tearing

 Alcohol Induced – metabolic effect

 Complications of Acute Pancreatitis

 Hypovolemia

 Hemorrhage

 Acute renal failure

 Paralytic ileus

 Hypovolemic or septic shock

 Pleural effusion, respiratory distress syndrome, pneumonia

 Multisystem organ failure

 Disseminated intravascular coagulation

 Diabetes mellitus

 etiology

 Unknown

 Excessive alcohol ingestion

 Biliary diseases, gallstones (obstruction)

 Iaotrogenic – trauma from surgical manipulation

 Pancreatic obstruction

 Metabolic disturbances: hyperlipidemia, hyperparathyroidism, or

hypercalcemia

 Renal disturbances; failure or transplantation

 Familial; inherited pancreatitis

 Penetrating gastric or duodenal ulcers, resulting in peritonitis

 Viral infections

 Toxicities of drugs

 Clinical Manifestations

 Generalized jaundice

 Cullen’s sign – gray-blue discoloration of the abdomen and periumbilical area

 Turner’s sign – gray-blue discoloration of the flanks

 Bowel sounds – paralytic (adynamic) ileus

 Abdominal tenderness, rigidity, guarding

 Pancreatic ascites

 Significant changes in vital signs

 Diagnostic assessment

 Serum Amylase and Lipase

 Trypsin testing

 CBC

 Serum Calcium

 ALT

 X-ray

 CT-scans

 MRI

 Acute Pain

 Interventions include:

 Comfort measures to reduce pain including fasting and drug therapy

 Endoscopic retrograde cholangiopancreatography

 Surgical Management
Endoscopic Retrograde Cholangiopancreatography (ERCP)

Laproscopic Cholecystectomy

 Preoperative care: NG tube may be inserted

 Operative procedures

 Postoperative care

 Monitor drainage tubes and record output from drain.

 Provide meticulous skin care and dressing changes.

 Maintain skin integrity.

 Pharmacolic management

 Anticholinergics: Atropine (Urised),

 Glucagons

 calcitonin (Calcimar)

 histamine receptor antagonists (e.g. ranitidine (zantac))

 Protease inhibitors

 Antibiotic therapy: cefuroxime (zinacef), ceftazidime (Ceptaz), and imipenem

cilastin (Primiaxin)

 Imbalanced Nutrition; Less Than Body Requirements

 Interventions include:

 Nothing by mouth in early stages

 Antiemetics for nausea and vomiting

 Total parenteral nutrition

 Small, frequent, moderate to high-carbohydrate, high-protein, low-fat

meals

 Avoidance of foods that cause gastrointestinal stimulation

 Chronic Pancreatitis

 Progressive destructive disease of the pancreas, characterized by remissions

and exacerbations

 Chronic calcifying (CCP) – protein plugging

 Chronic obstructive – inflammation, spasm & obstruction

 Nonsurgical management includes:

 Drug therapy

 Analgesic administration
  Enzyme replacement

 Insulin therapy

 Diet therapy

 Pancreatic Abscess

 Most serious complication of pancreatitis; always fatal if untreated

 High fever

 Blood cultures

 Drainage via the percutaneous method or laparoscopy

 Antibiotic treatment alone does not resolve abscess

 Pancreatic Pseudocyst

 Complications: hemorrhage, infection, bowel obstruction, abscess, fistula

formation, pancreatic ascites

 May spontaneously resolve

 Surgical intervention after 6 weeks

 Pancreatic Carcinoma

 Nonsurgical management

 Drug therapy

 Radiation therapy

 Biliary stent insertion

 Surgical Management

 Preoperative care

 NG tube may be inserted

 TPN typically begun

 Operative procedure may include Whipple procedure

 Postoperative care

 Observe for complications

 Gastrointestinal drainage monitoring

 Positioning

 Fluid and electrolyte assessment

 Glucose monitoring

 Interventions for Clients with Diabetes Mellitus

 Types of Diabetes

 Type I

 Type 2

 Gestational

 Other types include:

◦ Genetic defect beta cell or insulin

◦ Disease of exocrine pancreas

◦ Drug or chemical induced

◦ Infections

◦ Others

 Absence of Insulin

 Hyperglycemia

 Polyuria

 Polydipsia

 Polyphagia

 Hemoconcentration, hypervolemia, hyperviscosity, hypoperfusion, and

hypoxia

 Acidosis, Kussmaul respiration

 Hypokalemia, hyperkalemia, or normal serum potassium levels

 Acute Complications of Diabetes

 Diabetic ketoacidosis

 Hyperglycemic-hyperosmolar-nonketotic syndrome

 Hypoglycemia from too much insulin or too little glucose

 Chronic Complications of Diabetes

 Cardiovascular disease

 Cerebrovascular disease

 Retinopathy (vision) problems

 Diabetic neuropathy

 Diabetic nephropathy

 Male erectile dysfunction

 Assessment
 History

 Blood tests

◦ Fasting blood glucose test: two tests > 126 mg/dL

◦ Oral glucose tolerance test: blood glucose > 200 mg/dL at 120 minutes

◦ Glycosylated hemoglobin assays

◦ Glucosylated serum proteins and albumin

 Urine Tests

 Urine testing for ketones

 Urine testing for renal function

 Urine testing for glucose

 Risk for Injury Related to Hyperglycemia

 Interventions include:

◦ Dietary interventions, blood glucose monitoring, medications

◦ Oral therapy

 Sulfonylurea agents

 Meglitinide analogues

 Biguanides

 Alpha-glucosidase inhibitors

 Thiazolinedione antidiabetic agents

 Drug Therapy

 Drug administration

 Drug selection

 Insulin therapy:

◦ Insulin analogue

◦ Short-acting insulin

◦ Concentrated insulin

◦ Intermediate

◦ Fixed-combination

◦ Long-acting

◦ Buffered insulins

 Insulin Regimens
 Single daily injection protocol

 Two-dose protocol

 Three-dose protocol

 Four-dose protocol

 Combination therapy

 Intensified therapy regimens

 Pharmacokinetics of Insulin

 Injection site

 Absorption rate

 Injection depth

 Time of injection

 Mixing insulins

 Complications of Insulin Therapy

 Hypoglycemia

 Lipoatrophy

 Dawn phenomenon

 Somagyi's phenomenon

 Alternative Methods of Insulin Administration

 Continuous subcutaneous infusion of insulin

 Implanted insulin pumps

 Injection devices

 New technology includes:

◦ Inhaled insulin

◦ Transdermal patch (being tested)

 Client Education

 Storage and dose preparation

 Syringes

 Blood glucose monitoring

 Interpretation of results

 Frequency of testing
 Blood glucose therapy goals

 Diet Therapy

 Goals of diet therapy

 Principles of nutrition in diabetes

◦ Protein, fats and carbohydrates, fiber, sweeteners, fat replacers

◦ Alcohol

◦ Food labeling

◦ Exchange system, carbohydrate counting

◦ Special considerations for type 1 and type 2 diabetes

 Exercise Therapy

 Benefits of exercise

 Risks related to exercise

 Screening before starting exercise program

 Guidelines for exercise

 Exercise promotion

 Whole-Pancreas Transplantation

 Operative procedure

 Rejection management

 Long-term effects

 Complications

 Islet cell transplantation hindered by limited supply of beta cells and

problems caused by antirejection drugs

 Risk for Delayed Surgical Recovery

 Interventions include:

◦ Preoperative care

◦ Intraoperative care

◦ Postoperative care and monitoring includes care of:

 Cardiovascular

 Renal

 Nutritional

 Risk for Injury Related to Sensory Alterations

 Interventions and foot care practices:

◦ Cleanse and inspect the feet daily.

◦ Wear properly fitting shoes.

◦ Avoid walking barefoot.

◦ Trim toenails properly.

◦ Report nonhealing breaks in the skin.

 Wound Care

 Wound environment

 Debridement

 Elimination of pressure on infected area

 Growth factors applied to wounds

 Chronic Pain

 Interventions include:

◦ Maintenance of normal blood glucose levels

◦ Anticonvulsants

◦ Antidepressants

◦ Capsaicin cream

 Risk for Injury Related to Disturbed Sensory Perception: Visual

 Interventions include:

◦ Blood glucose control

◦ Environmental management

 Incandescent lamp

 Coding objects

 Syringes with magnifiers

 Use of adaptive devices

 Ineffective Tissue Perfusion: Renal

 Interventions include:

◦ Control of blood glucose levels

◦ Yearly evaluation of kidney function

◦ Control of blood pressure levels

◦ Prompt treatment of UTIs

 ◦ Avoidance of nephrotoxic drugs

◦ Diet therapy

◦ Fluid and electrolyte management

 Potential for Hypoglycemia

 Blood glucose level < 70 mg/dL

 Diet therapy: carbohydrate replacement

 Drug therapy: glucagon, 50% dextrose, diazoxide, octreotide

 Prevention strategies for:

◦ Insulin excess

◦ Deficient food intake

◦ Exercise

◦ Alcohol

 Potential for Diabetic Ketoacidosis

 Interventions include:

◦ Monitoring for manifestations

◦ Assessment of airway, level of consciousness, hydration status, blood

glucose level

◦ Management of fluid and electrolytes

◦ Drug therapy goal: to lower serum glucose by 75 to 150 mg/dL/hr

◦ Management of acidosis

◦ Client education and prevention

 Potential for Hyperglycemic-Hyperosmolar Nonketotic Syndrome and Coma

 Interventions include:

◦ Monitoring

◦ Fluid therapy: to rehydrate the client and restore normal blood glucose
levels within 36 to 72 hr

◦ Continuing therapy with IV regular insulin at 10 units/hr often needed

to reduce blood glucose levels

 Health Teaching

 Assessing learning needs

 Assessing physical, cognitive, and emotional limitations

 Explaining survival skills

 Counseling

 Psychosocial preparation

 Home care management

 Health care resources