Nrsg 407

PANCREAS  Exocrine Secretes digestive enzymes into the small intestines Breakdown of CHO, protein, and fats  Endocrine Produces hormones Insulin Glucagon

EXOCRINE FUNCTION  CCK: Cholecystokinin Stimulus for enzyme secretion  Secretin Secretion of bicarb and water  Lipase: Fats  Amylase: Carbohydrates  Trypsin: Proteins

EXOCRINE FUNCTION  90% of pancreatic digestive enzymes are proteolytic  Trypsin  Chymotrypsin splits proteins into peptones  Elastase Breakdown elastic tissue

EXOCRINE FUNCTION  Amylolytic Breakdown of carbohydrates Amylase  Lipolytic Breakdown of fats Lipase Phospholipase A

ENDOCRINE FUNCTION Islet of Langerhans  Alpha cells  Glucagon: ↑ blood glucose  Beta cells  Insulin: ↓ blood glucose  Delta cells  Somatostatin

PANCREATITIS  Inflammation of the pancreas  Autodigestion of the pancreas by pancreatic enzymes  Cellular destruction and organ damage

ACUTE PANCREATITS  Acute Mild or Non- hemorrhagic Severe or Hemorrhagic Fulminant

EPIDEMIOLOGY  185,000 cases each year  150,000 cholelithiasis or sustained alcohol abuse  African-Americans are at ↑ risk

CAUSES  Alcohol consumption  Gallstones  Pancreatic obstruction  Drugs and toxins  Hyperlipidemia  Family history  Trauma and iatrogenic factors

SIGNS and SYMPTOMS  Severe abdominal pain Epigastrium radiating to midback Not relieved by vomiting  Fever, malaise  Nausea, vomiting  Rigid and distended  Rebound tenderness  Absent or diminished bowel sounds

SIGNS and SYMPTOMS  Dyspnea and Tachypnea  Pulmonary infiltrates  Grey Turner’s sign  Large ecchymosis appearing in the flanks  Cullen’s sign  Ecchymosis in umbilical area  Hypovolemic Shock

DIAGNOSTIC FINDINGS  Serum Amylase Normal (23-85 u/L)  Serum Lipase Normal (0-160 u/L)  Serum trypsinogen: elevated  Urinary amylase: elevated

DIAGNOSTIC FINDINGS  Hematocrit: initially elevated then later decreased  WBC: elevated  C-reactive protein: elevated  Liver function tests: elevated

DIAGNOSTIC FINDINGS  Sodium and Potassium: decreased  Blood glucose: elevated  Serum Calcium: decreased  Albumin and Magnesium: decreased

DIAGNOSTIC FINDINGS  Abdominal and Chest X-ray  CT scan, Ultrasound, MRI  Endoscopic Retrograde Cholangiopancreatography (ERCP)  Aspiration biopsy  Stool studies: steatorrhea

COMPLICATIONS  Hypovolemic shock 3 rd spacing Hemorrhage Vomiting Decreased protein intake

COMPLICATIONS  Pulmonary complications Atelectasis Acute lung injury Pleural effusion ARDS

COMPLICATIONS  Cardiovascular Release of myocardial depressant factor  Pancreatic pseudocyst Cavity next to pancreas Filled with necrotic products

COMPLICATIONS  Pancreatic abscess 2-4 weeks after episode Necrosis of tissue Relocation of bacteria  Hypocalcaemia can occur with severe disease

COMPLICATIONS  Fluid and electrolytes Vomiting NG suction Redistribution of fluids

NURSING IMPLICATIONS  Vital signs Hypovolemic shock Sepsis  Laboratory values Amylase, Lipase BMP  Fluid and electrolytes NPO NGT Nutrition

NURSING IMPLICATIONS  Administer pain medication  Monitor blood glucose  Monitor intake and output  Daily weight

CHRONIC PANCREATITIS  Persistent inflammation of the pancreas  Scarring and calcification of the pancreatic ducts

CAUSES  70% is caused by alcohol abuse  20% is caused by obstruction, trauma, metabolic disturbances

SIGNS & SYMPTOMS  80% of pancreatic destruction causes Malabsorption resulting in nutritional deficits Diarrhea and steatorrhea Impaired glucose regulation

DIAGNOSTIC FINDINGS  LFT, CMP, CBC, ESR  Stool studies  Abdominal CT scan Images organ, detect inflammation  Abdominal US Detect inflammation and calcifications  ERCP looks for stones

Pancreas  Islets of Langerhans  Glucagon – alpha cells  Insulin – beta cells  Hormones secreted directly into blood capillaries  Readily available for use

Insulin – Hypoglycemic effect  Regulated by several chemical, hormonal, and neural factors  Blood glucose elevated  insulin leaves blood and enters cells  decrease blood glucose

Insulin  Affects CHO, lipid, and protein metabolism  Assists in glucose transport  Causes glucose to leave blood  Serum glucose will fall

Glucagon – Hyperglycemic effect  Glucose levels low, glucagon secreted  Opposite action of insulin

  Disorder of insulin action or secretion (usually both)  Results in high blood glucose  Two different types of diabetes:  Type I  Autoimmune disorder  Type II  Multifactorial disease DIABETES

Diabetes Mellitus  Disorder of CHO metabolism  Involves deficiency of insulin  OR resistance to insulin  OR both  End result: hyperglycemia

Diabetes Mellitus  Related to destruction of beta cells in pancreas  Insulin can neither be produced or secreted  Can also have insulin receptor defects  Will need mandatory dietary modifications

Type I DM  Considered juvenile – usually under 30 y/o  Sudden onset of symptoms  Usually not obese  Autoimmune response destroys beta cells

s/s Type I DM  Hyperglycemia – BS > 126 mg/dl on 2 separate occasions  Polyuria  Polyphagia  Polydipsia  Glucosuria  Weight loss  Fatigue

Type I DM – Insulin dependent  Insulin dependent  Usually not insulin resistant  Normal insulin receptors  Decreased plasma insulin  Most common complication – Diabetic ketoacidosis (DKA) [blood sugars >600 mg/dl

Untreated DM  Long-term damage to arteries  Heart disease  Stroke  Kidney disease  Blindness  Peripheral neuropathy

  Classic symptoms:  Increased urination, increased thirst, and unexplained weight loss plus random blood glucose ≥ 200mg/dL  OR Fasting (8 hours+) ≥126mg/dL  OR Blood glucose ≥200mg/dL two hours after a standard carbohydrate load  Oral Glucose tolerance (OGTT)  Any glucose ≥200mg/dL  Exception: someone receiving IV infusion of glucose Diagnosis

  Autoimmune destruction of beta cells causes a decrease in or absence of insulin production by islets of Langerhans  Islets are infiltrated by T lymphocytes  Has genetic component  Environmental factors also play a role Type I

  Mixture of genetic and environmental factors  Obesity is the underlying cause of most type II diabetes  Also lifestyle factors play an important role  Is characterized by:  Decreased sensitivity of peripheral cells to the effect of insulin (insulin resistance)  Beta-cell dysfunction that prevents adequate insulin response to decreased peripheral cell sensitivity and high blood glucose Type II

  Due to causes other than obesity  Pregnancy  Drug therapy (steroids, Cushing disease)  Diabetes usually will disappear when underlying condition is corrected Secondary Type II

  Excessive glucose binds to extracellular proteins to form abnormal glycoproteins that negatively impact vascular endothelium  Increases inflammation  Promotes thrombosis  Loosens endothelial cells  Stimulates proliferation of vascular smooth muscle cells (atherosclerosis)  Promotes vascular disease Diabetic Complications

  High intracellular glucose results in increased oxidative stress (diabetic neuropathy)  Also stimulates production of mediators that:  Stimulate growth of new blood vessels (diabetic retinal disease)  Promote thrombosis  Promotes vascular inflammation  Promotes vasoconstriction Complications cont’d

  Acidosis occurs due to absence of insulin because in the absence of glucose, body must burn fat for fuel  Fat is broken down into fatty acids-transported to liver and converted into ketones to be burned for fuel  Lowers blood pH  Present mainly with Type I diabetes Diabetic Ketoacidosis

  Usually seen years after onset of hyperglycemia  Infections: due to impaired neutrophil & macrophage function and impaired delivery of circulating cells and molecules necessary for host defense  Vascular disease relating complications:  Atherosclerosis (increases risk of MI, stroke, lower extremity gangrene)  Diabetic retinopathy  Diabetic nephropathy  Diabetic neuropathy Long-Term Complications of DM

  Lifestyle changes  Type I: insulin replacement  Type II: oral hypoglycemic drug to increase insulin secretion, insulin or both Treatment