METABOLIC & ENDOCRINE FUNCTION

A. Assessment and Management of Patients with Hepatic Disorders

Liver 

Largest gland of the body. Contains Kupffer s cells, which remove bacteria in the portal venous blood. glucose and protein metabolism.  

Regulates

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Manufactures & secretes biles, has a major role for digestion & absorption of fats in the GI tract. Aids in the digestion of fats, and carbohydrates. Stores and filters blood ( 200200400ml of blood stored) Stores Vitamin A, D, and B12 and Iron

- Removes waste products from the bloodstream & secretes into the bile. Located @ the upper Right portion of Abdominal Cavity Weight ( 1500g) and is divided to four lobes - - .

Is a by product of the use of amino acids from protein for gluconeogenesis.glucose is taken up from the portal venous blood by the liver converted to glycogen stored in hepatocytes. Ammonia Conversion . Glucose Metabolism . . 2.Functions of the Liver 1.

alpha and beta globulins. 3.Conversion of Ammonia Urea: Role of the liver. blood clotting factors. specific transport proteins and most of the plasma lipoproteins.. Protein Metabolism . .It synthesizes albumin.

fatty acids can be broken down for the production of energy and ketone bodies ( acetoacetic acid. and acetone). .this only occurs when availability of glucose for metabolism is limited during starvation or in uncontrolled diabetes.Fat Metabolism . betabetahydroxybuteric acid.4. .

5. B. Iron Copper . Vitamin and Iron Storage - Vitamin A.complex Bvitamins are stored in large amounts in the liver. and B.

6.pass effect that their use is essentially limited. amphetamines Note: Some medication have a large firstfirst. . Drug Metabolism Following Medications that the liver metabolizes: 1. Anesthetics 5. sedative agents 4. barbiturates 2. opioids 3.

.7. Bile salts together with cholesterol and licithin. Bile Formation - - - Bile is formed by the hepatocytes and collected in the caniculi and bile ducts. are required for emulcification of fats in the intestine necessary for efficient digestion & absorption. Collected and stored in the gallbladder and emptied into the intestine when needed for digestion.

8. . Increase: indicates presence of liver disease when the flow of bile is impeded or with excessive destruction of RBC. Bilirubin Excretion - - Bilirubin is a pigment derived fro the breakdown of hemoglobin by cells of the reticuloendothelial system. including Kupffer cells of the liver.

ASSESSMENT Symptoms that suggests liver disease: Jaundice Malaise Weakness Fatigue Pruritus Abdominal Pain .

Fever Anorexia Weight Edema Gain abdominal girth Hematemesis Melena Hematochezia Easy bruising Decrease libido Changes in mental acuity Increase .

Lifestyle behavior: sexual practices behavior: . and valproic acid) or other OTC drugs or dietary supplements. and travel hx) History of alcohol and drug use (acetaminophen. ketoconazole. agents: recreational. Or infectious agents: ( occupational.Health history - - - Exposure to hepatotoxic subs.

Wilson s disease) .- Current and Past Medical historyhistoryfamilial liver disorders ( gallstone disease.

lactic dehydrogenase .bilirubin .serum aminotransferases*** .Serum Enzyme Activity: Alkaline phosphatase .clotting factors and lipids.Serum concentrations of protein albumin and globulins) . - .ammonia .

and liver cancer ALT ( Alanine aminotransferase) / SGPT ( serum glutamic.hepatitis. 3. 4. Aminotranferasescirrhosis.pyruvic transaminase) glutamicAST ( aspartate aminotranferase)/ SGOT ( serum glutamic.Most Frequently used to test for Liver damage 1. Serum Aminotranferases.oxaloacetic glutamictransaminase) GGT ( gamma glutamyl tranferase)tranferase)cholestasis . 2.

16 seconds Time.10 LDH.10-48 IU/L GGT.( 4.5 g/dl) Albumin.Liver Function Studies: protein.3.1.( 7-7.12 AST ( SGOT) 10-40 units 10 ALT ( SGPT).5.7 Prothrombin Time.5 g/dl)  Albumin.35 units SGPT) GGT.7protein.7.3 g/dl) globulin.5.12.100 Serum .100-200 units LDH.( 1.4 Serum globulin.

250 mg/dl 150Cholesterol 1. LDL. Serum Ammonia.2-120 Ammoniamicrogram/dl/ 150. HDL.< 130 microgram/dl LDL-  .male: 35-70mg/dl female: HDL353535-85 mg/dl 2.

Procedure: Liver Biopsy Description: A needle is inserted through the abdominal wall to the liver to obtain a tissue sample for biopsy and microscopic examination. .

d. c. partial thromboplastin time. b. Obtained informed consent Assess results of coagulation tests ( prothrombin time.Pre procedure: a. platelet count) Administer a sedative as prescribed Position: Supine or left lateral .

d. Assess vital signs Assess biopsy site for bleeding Monitor peritonitis Maintain bedrest for several hours Position: Right side with pillow under the coastal margin to decrease hemorrhage . b. e.Post procedure: a. c.

f. Other Dx Tests: Ultrasonography. . Instruct to avoid coughing and straining. computed tomography. MRI. g. Laparoscopy. Instruct to avoid heavy lifting and strenuous exercise x 1 week.

Significant Symptoms of Liver Disease 1.5mg/dl . Jaundice .sclerae and skin yellow tinged/ greenish yellow. elevationBilirubin level elevation2.2.

Decrease conjugation of bilirubin 4. Impaired uptake of bilirubin by the liver cells 3.4 Major Causes of Jaundice: 1. Excessive destruction of RBC. Obstruction of bile flow in the canaliculi . 2.

. with hemolytic transfusion reactions and other hemolytic disorders.is encountered in pt. .increase destruction of RBC increase bilirubin concentration in the blood.Types of jaundice: Hemolytic Jaundice . 1.

viral infection ( hepa A. yellow fiver virus. Hepatocellular Jaundice . medication or chemical toxicity ( phosphorus) or from alcohol intake.2. Epstein Barr virus.C or E). . B. .inability of damaged liver cells to clear normal amounts of bilirubin from the blood.

Liver Cirrhosis is a form of hepatocellular disease. . . elevate. .serum bilirubin and urine urobilinogen elevate..AST & ALT levels increased: increased: indicate cellular necrosis.

Obstructive Jaundice . tumor or pressure.caused by intrahepatic obstruction .stool: light/ clay colored . an inflammatory process.skin: itchy .Dyspepsia .occlusion of the bile duct by a gallstone. .3 .

normal liver histology and liver function test results.. . Hereditary Hyperbilirubinemia . .Increase serum bilirubin levels resulting from inherited disorders which produce jaundice.bilirubin and alkaline phosphatase level s are elevated. 4.

( prehepatic.Portal Hypertension .portal vein pressure: 12 mm Hg .is characterized by increase resistance to flow in the portal venous system.PVP normal: 5-10 mm Hg 5- . posthepatic and intrahepatic obstruction to the liver lobules). .

caused by portal vein thrombosis and compression by cancer or enlarged lymph nodes. Prehepatic . Posthepatic . Budd. 2.Chiari Syndrome Budd- .is located at the between the junction of the left and right hepatic duct to the point where duct opens into the intestine.1. Eg.

Intrahepatic .3. Major cause of Portal Hypertension: Alcoholic cirrhosis .obstruction occur within the Liver.

Ascites Several factors that contribute to fluid accumulation are:  Increase capillary pressure caused by portal hypertension  Obstruction of the venous flow through the liver  Salt & water retention by the kidney  Decrease colloidal osmotic pressure. .

3.Clinical Manifestations: 1. 4. Fluid & Electrolyte imbalances are common. . 2. Increased abdominal girth Rapid weight gain*** Striae and distended veins in the abdominal wall.

Diagnostic Findings: .body weight measurement*** .Percussion of the abdomen . .Abdominal girth measurement .Assessing for abdominal fluid wave.

 Dietary Modification: Modification: Strict sodium restriction  Table salts  Salty foods  Salted butter and margarine  Canned and frozen foods  Commercial salt substitutes should be approved: contains ammonia which precipitate to hepatic coma.Medical Management: 1. . coma.

2.hyponatremia lasix)Ammonium chloride and acetazolamide ( Diamox) are contraindicated: hepatic coma . Diuretics     Spironolactone ( Aldactone).prevents Aldactone)potassium loss Aldosterone Furosemide ( lasix).

hyponatremia. . hypokalemia. Complications of diuretic therapy:  Fluid & Electrolyte disturbances: hypovolemia. encephalopathy.

. Paracentesis .3. Bedrest 4.is the removal of fluid from the peritoneal cavity through a small surgical incision or puncture made through the abdominal wall under sterile conditions.

This is in combination with IV infusion of salt poor albumin or other colloid..In Paracentesis. use a large volume ( 5-6 liters) is safe to treat with 5severe ascites. .

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. C .D . bacteria. E. or exposure to medications or hepatotoxins.Inflammation of the liver caused by a virus. G. B.HEPATITIS . Types : Hepa A.

Medical & Nursing Management: HEPA A 1. 3. Abstain alcohol intake.( small frequent meals) 2. Environmental Sanitation and hygiene measures ( hand washing). . Bed rest during acute stage and diet.

administered by injection. . . anorexia. Late side effects: bone marrow effects: suppression. Side effects: effects: fever. and bacterial infection. chills. Alpha interferon. nausea. myalgias and fatigue.5 million uinterferonu10million u 3x weekly for 4-6 4months. alopecia. thyroid dysfunction.Medical & Nursing Management: HEPA B 1.

2. Lamivudine ( Epvir) Adefovir ( Hepseral) Bedrest Avoid protein intake .2 antiviral agents: 1.

.due to chronic alcoholism. . 3 Types of Cirrhosis: Alcoholic cirrhosis.most common type of cirrhosis.HEPATIC CIRRHOSIS 1. .scar tissue cirrhosissurrounds the portal areas.

3.scarring around cirrhosisthe bile ducts. Post necrotic cirrhosis.2.result from chronic biliary obstruction & infection.broad cirrhosisbands of scar tissue cause by acute viral hepatitis. Biliary cirrhosis. . .

 Hepatomegaly  Fetor hepaticus  Asterixis ( liver flap)  Spider .Clinical Manifestations:  Emaciation  Ascites angiomas: nose. cheeks. and shoulder. upper thorax.

 Peritonitis  Gastrointestinal  Edema  Vitamin varices deficiency and anemia  Mental deterioration .

decrease  Serum globulin.prolong time Liver biopsy.gives confirmation of biopsydiagnosis. GGT. AST.elevate test Prothrombin time.  Serum .Diagnostic Findings: AlbuminAlbumin.increase GGT Bilirubin test.increase globulin AST.

 Restrict Sodium & fluid intake  Administer Diuretics as prescribed.C.  Provide supplemental vitamins ( B complex.Nursing Management for cirrhosis: cirrhosis: the head of the bed to minimize SOB. folic acid and thiamine) as prescribed.  Elevate . and K. Vitamin A.

 Monitor LOC. assess for precoma state ( tremors.  Weight and measure abdominal girth daily. delirium)  Monitor for asterixis . Monitor I & O and electrolyte balance.

administer Vit K if prescribed . Maintain gastric intubation to assess bleeding and esophagogastric balloon tamponade to control bleeding varices.  Administer blood products  Monitor coagulation lab. results.

. Administer Lactulose ( Chronulac). which decreases the pH of the bowel. decreases production of ammonia by bacteria in the bowel.  Administer neomycin ( mycifradin) to inhibit protein synthesis in bacteria and decrease the production of ammonia. and facilitates the excretion of ammonia.

. sedatives and barbiturates and any hepatotoxic medications. Avoid medications: narcotics.  Instruct about the restriction of alcohol intake  Prepare for paracentesis and surgical shunting procedures.

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50 ml of bile. 30- .a pear shaped.Anatomy of Gallbladder Gallbladder .5.10 cm long.7. .lies in the shallow depression on the inferior surface of the liver.stores 30. .5. 7. hollow saclike organ.

PZ)stimulus for digestive enzyme secretion.pancreozymin ( CCK.hormone.Function:   Storage and concentrate bile.PZ). stimulates contraction of the gallbladder. major CCK. CholecystokininCholecystokinin. .

 Bile is composed of: Sodium Potassium Calcium Chloride and bicarbonate Lecithin. cholesterol. bile salts . bilirubin. fatty acids. bilirubin. cholesterol.

Exocrine Pancreas.aids in digestion of proteins   .the secretion Pancreasinfluences by the vagus nerve -digestive enzyme that secrete: amylaseamylase.aids in digestion of carbohydrates TrypsinTrypsin.Functions of Pancreas: 1.

digestion of fats SecretinSecretin.PZ. major stimulus for digestive enzyme secretion is the hormone CCKCCK.  LipaseLipase.major stimulus for increase bicarbonate secretion from the pancreas. .

Glucagon DeltaDelta.composed of Langerhansalpha.Insulin AlphaAlpha.2.Somatostatin . beta & delta cells. Endocrine pancreas Islets of Langerhans. BetaBeta.

. Insulin ( Beta cells) .lower blood glucose by permitting entry of glucose into the cell of the liver.promotes storage of fat in adipose tissue and synthesis of proteins. . muscle & other tissues as glycogen and used for energy.A.

.fats & proteins are used for energy instead of glucose.Note ***If absent: .glucose can t enter into the cells and excreted in the urine ( DM) .

B. Glucagon ( alpha cells) .is secreted by the pancreas in response to decrease in level of blood glucose.used to raise blood glucose by converting glycogen to glucose in the liver. . .

Somatostatin .C. .exerts a hypoglycemic effect.

.bacterial invasion 1.acute inflammation is associated with gallstones.Disorders of the Gallbladder: Cholecystitis . CalculusCalculus. (Chronic) .cause gallbladder contraction due to inefficient emptying of bile.

4 hrs.  Right Upper Quadrant Pain .Clinical Manifestations:  Nausea & Vomiting  Indigestion  Belching  Flatulence  Epigastric Pain radiates to scapulascapula2.

rigidity. Guarding. and rebound tenderness  Mass @ RUQ  Murphy s sign  Tachycardia .

mainly cholesterol and bilirubin.2. Cholelitiasis. or gallstone.is caused by precipitation of substances contained in bile. . gallstone. .

Clinical Manifestations: Indigestion and biliary colic Jaundice Steatorrhea & Clay colored stool Dark orange and foamy urine Jaundice Vitamin deficiency Pruritus .

4. 6. 2. 3. Abdominal X ray Ultrasonography Radionuclide imaging Cholecystography Endoscopic Retrograde cholangiopancreotography ( ERCP) Percutaneous Transhepatic Cholangiography .Diagnostic Findings: 1. 5.

Maintain NPO status during nausea & vomiting.Nursing Management: 1. Note: Morphine & codeine should not be given. Administer analgesic and antibiotic agents. . 3. Maintain nasogastric decompression/ suctioning for severe vomiting or anti emetics. 2.

4. Administer antispasmodic agents. 5. Avoid fatty foods ( cream, pork, fried foods), egg, gas forming vegetables and alcohol.

6. Ursodeoxycholic ( UDCA) & chenodeoxycholic acid ( CDCA) - dissolve small, radiolucent gallstones composed of cholesterol. Not applicable: - cystic duct occlusion, pigment stones.

Non surgical implementation:
1.  

Dissolution therapy remove cholesterol stones Direct contact with repeated injections and aspirations of dissolution agent via percutaneous catheter

2. Extracorporeal shock wave lithotripsy  Shock waves are administered that disintegrate stones in the biliary system  Oral dissolution follows

Surgical Implementation:
1. 2.

CholecystectomyCholecystectomy- removal of the gallbladder CholedochotomyCholedochotomy- incision into the common bile duct to remove the stone

Post operative Implementation: 
Monitor

for respiratory complications secondary to pain at the incision site  Encourage deep breathing & coughing  Encourage early ambulation  Encourage splinting during coughing

 Administer anti emetic. analgesic as prescribed  Maintain NPO status and NG tube suction  Advance from clear liquids to solids  Maintain and monitor drainage from the T tube .

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Pancreas lies transversely in the posterior part of the upper abdomen.  head part is @ the right of the abdomen  Body lies beneath the stomach  .

2 Types of Pancreatic Disease: 1. Acute Pancreatitis 2. Chronic Pancreatitis .

life-threatening disorder lifeassociated with escape of activated pacreatic enzymes into the pancreas and surrounding tissues.Acute Pancreatitis  severe. .

Clinical Manifestations of Acute Pancreatitis: Initial sign: severe midepigastric or periumbilical pain radiates to the back Ominous sign: rigid board like abdomen Severe pancreatitis: Ecchymosis Common: Abdominal distention Tachycardia. fever. . hypotension. cool & clammy skin.

 Turner s sign or cullen s sign  Common:Nausea . Hypocalcemia & vomiting  Shock in severe episodes. with respiratory distress and acute renal failure.

16. 48 Serum lipase.Diagnostic Findings: Serum amylase level.200 mg/dl glucose .14 days.48 hrs lipase24to 5.000 cells/ micro increaseliters  Elevated Blood glucose. 5 WBC increase.increase for 24.increase for levelthe 24 hrs to 48.72 hrs.

Na.lactate dehydrogenase. Magnesium and K is low because of dehydration and vomiting  Serum . Ca.more dehydrogenase350 IU/L  AST ( increase 250 IU/L)  Serum albumin.

 CT is most definitive in determining pancreatic changes . Abdominal X ray detect pancreatic calcifications or gallstones suggest an alcohol or biliary obstruction.

b.Nursing Interventions: Oral foods and fluids are withheld  Rest the GI tract a. Gastric suctioning is instituted to treat distention of the bowel and prevent further stimulation of the pancreatic enzymes. Withhold oral feedings to decrease pancreatic secretions.  .

fluids & electrolytes are administered for shock & hypotension.  Anticholinergic drugs to provide smooth muscle relaxation  IV .  relief such as Meperidine rather than Morphine.

Maintenance of alkaline gastric pH with H2 receptor antagonists and antacids  Antibiotic therapy for infection or sepsis  Maintenance of adequate oxygenation 

Surgical Interventions: 
Incision

& drainage of infection & pseudocysts.  Debridement or pancreatectomy to remove necrotic pancreatic tissue.  Cholecystectomy for gallstone pancreatitis.

Complications:
1. 2. 3. 4. 5.

Pancreatic ascites, abscess, or pseudocyst Acute respiratory distress syndrome Hemorrhage with hypovolemic shock Acute renal failure Sepsis and multiple organ dysfunction syndrome

Nursing Diagnosis:  Acute Pain r/t disease process Fluid Volume r/t vomiting. fever and fluid shifts  Deficient  Ineffective Breathing Pattern r/t severe pain and pulmonary complication .

.Chronic Pancreatitis . .persistence of pancreatic cellular damage after acute inflammation and decreased pancreatic endocrine and exocrine function.progressive destruction of the pancreas.

nausea & vomiting.Clinical Manifestations:  Pain located in the epigastrium or left upper quadrant radiating to the back more constantly and occurring at unpredictable intervals. anorexia  Malabsorption and steatorrhea  Diabetes Mellitus .  Weight loss.

Diagnostic Findings: Serum amylase & lipase.normal to lipaselow  Fecal fat analysis determines need for pancreatic  Bilirubin & alkaline phosphatasephosphataseelevated  .

abnormal test Plain abdominal X ray  CT scan  ERCP  .Secretin and cholecystokinin stimulatory test.

Nursing Management: Pain management  Correction of nutritional deficiencies.  Pancreatic enzyme replacement  Treatment of DM  Endoscopic placement of pancreatic stent allowing free flow of pancreatic juices through distorted and irregular/ narrowed pancreatic duct.  .

Surgical Interventions: Pancreaticojejunostomy  Sphincteroplasty  Drain pancreatic pseudocyst into external drain  Whipple procedure  Autotransplantation of islet cells  .

Complications:  Pancreatic pseudocyst  Pancreatic ascites and pleural effusions  GI hemorrhage  Biliary Tract obstruction  Pancreatic fistula .

Nursing Diagnosis: Acute and chronic Pain r/t chronic and unrelenting insult to pancreas  Imbalanced Nutrition: Less than Body Requirements r/t glucose intolerance  Anxiety r/t surgical intervention  .

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.Diabetes Mellitus  Metabolic disorder characterized by increase glucose level in the blood ( hyperglycemia) resulting from defects in insulin secretion.

 .Function of Insulin: hormone produced by the pancreas  Controls the glucose level in the blood thru regulating the production and storage of glucose.

Risk factors: Family history  Obesity  Race/ ethnicity  Age  Hypertension 140/ 90 mmHg  HDL cholesterol < 35 mg/dl  History of gestational diabetes  .

Types of Diabetes Mellitus:
1. Type I DM Insulin- dependent Insulin-

2. Type II- Non- insulin II- Nondependent DM

Criteria for diagnosis of DM:
1. Symptoms of diabetes plus casual

plasma glucose concentration > 200mg/dl. 2. Fasting Plasma glucose > 126 mg/dl. 3. 2-h postload glucose > 200mg/dl 2during oral glucose tolerance test ( OGTT)

Diabetes Management:
Nutritional Objective: - to control total caloric intake to attain or maintain a reasonable body weight and control blood glucose levels.
1.

 Incorporate diet into individuals client needs. lifestyle and cultural and socio economic patterns. .

30% fats 10%10%.20% protein .According to ADA ( American diet Association) recommend all levels of caloric intake: 50%50%.60% carbohydrates 20%20%.

counting grams of carbohydrates Eg. Carbohydrate counting. . 1.a tool for countingblood glucose management.should be eaten in moderation to prevent postprandial blood glucose levels. A.Carbohydrates . 15 g of carbo.1 serving of apple 2 carboinches or 1 slice bread.

.encourage the use of legumes & whole grains to help reduce saturated fats and cholesterol. .B. Fats 10% saturated fats .less than 300mg/day dietary cholesterol.

Fiber soluble: soluble: legumes. . Insoluble: Insoluble: whole grain breads and cereals and some vegetables. oats and some fruits helps blood glucose.3.

Food classification Systems: 1. Exchange Lists Food guide Pyramid 2. .

S/E: facial flushing. Esp. thirsty. warmth. sweating.Other dietary concerns:  Alcohol IntakeIntake.main danger is Hypoglycemia. . .when taking diabinese is disulfiram ( atabuse) type reaction. taking insulin. n/v.headache.

Exercise benefits: lower blood glucose level Reduces cardiovascular risks Improves circulation and muscle tone Decreases total cholesterol and triglycerides levels Encourage weight loss  .2.

 Instruct the pt. who requires insulin should be instructed to eat 15g carbohydrate snack ( a fruit exchange) or snack of complex carbo. to check blood glucose level before. . and after exercise  Initially. With protein before exercise to prevent hypoglycemia. pt. during.

 If the blood glucose level is greater than 250 mg/dl and urinary ketones are present. the pt. is instructed not to exercise until blood glucose is nearly normal and urinary ketones are negative. .

.Self Monitoring of blood glucose:  Provide the client with the current blood glucose level and information to maintain good glycemic control.  A cornerstone of insulin therapy.

.Stress the importance of following the manufacturer s instruction . .caution with clients with retinopathy & neuropathy.- it requires a finger prick to obtain a drop of bood for testing.

. the meter automatically displays the blood glucose level less than 1 minute..the strip is place in the meter first before the blood is applied.Stress the importance of Handwashing . Once the blood is placed on the strip.

used to hemoglobindescribe hgb into which glucose has been incorporated.6. A1C .12 weeks 6.an index of blood glucose level over 6.3 months.Glycosylated hemoglobin. 2- .0 % normal .is a blood test that reflects average blood glucose levels over a period of 2.

-teach the client that the second voided urine specimen is most accurate. .a less reliable indicator for blood glucose monitoring. Urine Testing .

. .presence of ketones may indicate ketoacidosis..urine ketone testing should be performed during illness and whenever the client with DM type I has glycosuria greater than 240 mg/dl for 2 consecutive testing periods. ketoacidosis.

 Insulin Slight  Insulin  administration of purer insulin prep. tenderness and induration 1-2 h after injection. 1dimpling or pitting of subcutaneous fat.Complication of Insulin therapy:  Local  Allergic Reactions Lipodystrophy Resistance redness.  prednisone is prescribed . swelling.

cause blood glucose to rise @ 3 am. . Dawn Phenomenon  release of growth hormone. administration of intermediate acting insulin @ 10 pm.

 develop at peak insulin times and during night . Somogyi s phenomenon  a rebound phenomenon that occurs during the initial period of blood glucose control.

elevated at bedtime. decrease at 2 am to 3 am. increasing the bedtime snack.  .  Treatment include decreasing evening dose of intermediate acting insulin.

. Glucose from bedtime to morning. Insulin Waning  A progressive rise of bld.  treatment is increasing the evening dose of intermediate or long acting insulin.

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Endocrine System:  1. 3. electrolyte and acid. Functions: Maintenance and regulation of vital functions Response to stress and injury Growth & development Energy metabolism Reproduction Fluid. 2. 5. 6.base balance acid- . 4.

Pituitary .Endocrine System A. .located @ the base of the brain .controls sexual development & function .commonly referred as master gland .influences water absorption by the kidney.controlled by the hypothalamus .

.synthesized in the hypothalamus for storage. . secreted by the posterior lobe of the pituitary gland. Posterior Pituitary  Vasopressin ( ADH & Oxytocin) .A.important hormones.

. .controls the excretion of water by the kidney.secretion is stimulated by an increase osmolality of the blood or by decrease in BP..

 Oxytocin . .facilitates milk ejection during lactation.increases the force of uterine contraction during labor & delivery .

Anterior Pituitary A. E. B. C.B. D. Major Hormone: FSH ( Follicle Stimulating Hormone) LH ( Luteinizing Hormone) Prolactin ACTH TSH Growth Hormone . F.

Disorders of Pituitary Gland A.results in failure of tubular reabsorption of water in the kidneys. .hyposecretion of ADH and deficiency of vasopressin. Diabetes Insipidus . .

24 L). polydipsia. hypercalcemia  Decrease urine specific gravitygravity1.001.Clinical Manifestations: like urine with no albumin & glucose  Classic signs: Hypernatremia. 4dehydration  WaterWater- . hypokalemia.005  Polyuria( 4.1.0011.

dry mucous membranes  Postural hypotension  Tachycardia . Fatigue  Decrease skin turgor.

withholding fluids for 8-12 hours 8.weighing frequently .Diagnostic Findings:  Fluid deprivation test . .plasma and urine osmolality studies are performed @ beginning and end of the test.

indicates bright MRIspot  . plasma and urine osmolality. desmopressin therapy and IV of hypotonic saline solution  skull x ray & MRI.24 hour urine output  plasma level of ADH.

2. 3. To replace ADH To ensure adequate fluid replacement To identify and correct the underlying intracranial pathology .Medical Management: 1.

2 administration every 1212.Pharmacologic Therapy 1.24 hours . administered intranasally . Desmopressin acetate ( DDAVP) .a synthetic vasopressin.1.

every 12.IM.given @ night.2. Vasopressin tannate ( Pitressin Tannate) 12.96 hours .S/E: abdominal cramps . rotation of injection site .

increases Na diureticsexcretion .Other drugs: Clofibrate chlorpropamide ( Diabinese)Diabinese)hypoglycemia Thiazide diuretics.

. 3. specific gravity of urine 5.Nursing Interventions: 1. Provide a safe environment esp. in pt with change of LOC. Monitor I & O. Monitor electrolyte values and signs of dehydration 4. 2. Monitor VS and neurologic and cardiovascular status. Maintain adequate fluid intake. weights.

.Excessive ADH secretion . Syndrome of Inappropriate Anti diuretic Hormone Secretion ( SIADH) .Occurred in severe pneumonia.Retain fluids & develop a sodium deficiency known as dilutional hyponatremia .Cannot excrete a dilute urine .B. pneumothorax and other disorder of the lungs.

Hypertension 5. Dilutional hyponatremia 7. Weight gain 4. Anorexia. Tachycardia 6. 3. 2. nausea & vomiting . Change in LOC and mental status changes. Fluid volume overload.Clinical Manifestations: 1.

Monitor fluid and electrolyte balance. Administer demeclocycline (Declomycin) . Daily weight Urine & blood chemistries. 5. 2. Close monitoring of fluid intake & output.Nursing Management: 1. 3. 4.

hyposecretion of growth hormone by the anterior pituitary.C. . Hypopituitarism Description: .

Retarded physical growth Premature aging Low intellectual development Poor development of secondary sex characterisitcs . 2.Clinical Manifestations: 1. 4. 3.

Encourage client to express feelings related to altered body image Prepare to administer human growth hormone ( hGH) . 3.Nursing Interventions: 1. Provide emotional support. 2.

D. Hyperpitiutarism  Hypersecretion of GH which results in gigantism and acromegaly .

6. 2. 4. 7. rough skin Organomegaly Hypertension Deepening of the voice .1. 8. Clinical Manifestations: Large hands and feet Arthritic changes Visual disturbances Diaphoresis Oily. 3. 5.

Complications: increased intracranial pressure ( ICP). .removal of the pituitary gland. bleeding & meningitis. Prepare the client for hypophysectomy.Nursing interventions: 1. HypophysectomyHypophysectomy.

controls the rate of body metabolism and growth.Thyroid gland - butterflybutterfly.shaped organ located in the lower neck anterior to the trachea.about 5x the blood flow to the liver . . .

Iodine Role of Iodine: . Triiodothyronine ( T3) 3. Thyroxine ( T4) 2.essential to the thyroid gland for synthesis of its hormones.Hormones: 1. Thyrocalcitonin 4. .

Hypothyroidism  Hyposecretion of thyroid hormone  Characterized by decrease rate of body metabolism  Subclinical form: myxedema  Most common cause: autoimmune thyroiditis ( Hashimoto s disease) .A.

muscle aches. 4. paresthesia Weight gain Dry skin and hair Loss of body hair . 2. 3.Clinical Manifestations: 1. 6. 7. 5. Fatigue Intolerance to cold Weakness.

Cardiac disorders . Menstrual disturbances 13.8. Generalized puffiness and edema around the eyes and face 11. Forgetfulness & loss of memory 12. Constipation 10. Bradycardia 9.

goiter. Synthetic levothyroxine ( Synthroid or Levothroid) .used in treating hypothyroidism and suppressing nontoxic goiter.hormone replacement is given depends on TSH concentration .Pharmacologic therapy 1.

Levothyroxine sodium ( Synthroid) commonly prescribed. Instruct about thyroid replacement therapy Low calorie. 2. cholesterol and low saturated fat diet . 4.Nursing interventions: 1. 3. Monitor VS. HR and rhythm Administer thyroid replacement.

Assess for constipation. . Provide warmth environment 7. provide roughage and fluids 6. nervousness and insomnia 9. Report for chest pain immediately.5. Monitor for overdose of thyroid medication: tachycardia. Avoid sedatives and narcotics 8. restlessness.

Hyperthyroidism Hypersecretion of thyroid hormone  Increase rate of body metabolism  Grave s disease: most common disease: type of hyperthyroidism  Most common cause: thyroiditis.B. cause: excessive ingestion of thyroid hormone  .

such as tachycardia and palpitations 3.Thyrotoxicosis: nervousness 2.Clinical Manifestations: 1. Cardiac dysrhytmias. Protruding eyeballs ( exophthalmos) 4. irritable . Diarrhea 6. Weight loss 5.

Increase appetite 11. Osteoporosis & fracture . moist & soft 10. Flushed skin.7. Heat intolerance 9. Pulse rapid 8.

. Provide high calorie diet. Obtain daily weights. 4. 2.Nursing Interventions: 1. 5. Provide cool and quiet environment 3. Provide adequate rest. Administer iodine preparation that inhibit the release of thyroid hormone.

Use of radioisotope 123 I or 131 I. Administer Propanolol ( Inderal) for tachycardia . and levothyroxine 7. anti thyroid hormone.6.

Controls Ca and phosphorus metabolism Produces parathyroid hormone ( PTH) - - .Parathyroid gland - Located near the thyroid.

Hypoparathyroidism caused by parathyroid hormone deficiency  Precipitating factors: thyroidectomy.A. parathyroidectomy. radical neck dissection  .

3. 2. irritability and depression . 4.Clinical Manifestations: 1. Hypocalcemia and Hyperphosphatemia Numbness and tingling in the face + Trousseau s sign & Chvostek s sign Hypotension Anxiety. 5.

cardiac dysryhthmias. photophobia.6. laryngospasm. Signs of overt tetany. seizures . carpopedal spasm. such as bronchospasm. dysphagia.

2.Nursing Interventions: 1. 4. Monitor VS Monitor signs of tetany and hypocalcemia Initiate seizure precautions Place tracheostomy set. oxygen and suction at bedside . 3.

Prepare to administer Ca gluconate IV or Ca chloride 6. Instruct client in the administration of Vit D supplements it enhances Ca absorption from the GI tract . Provide high Ca and low phophorus diet 7.5.

Administer phosphate binders to enhance excretion of phosphate through the GI tract .8.

Hyperparathyroidism  Hypersecretion of theparathyroid hormone  characterized by bone decalcification and development of renal calculi ( Kidney stone) .B.

Clinical Manifestations: 1. 4. 3. 2. Hypercalcemia and hypophosphatemia Fatifue and muscle weakness Skeletal pain and tenderness Bone deformities Anorexia. epigastric pain Weight loss . 6. N/V. 5.

Renal stone . Constipation 8. Hypertension 9.7. Cardiac dysrhythmias 10.

Nursing Interventions: 1. 4. esp BP Monitor for dysrhyhmias Monitor I & O and for signs of renal stones Encourage fluids Administer Lasix to lower Ca absorption . 5. Monitor VS. 3. 2.

Monitor Ca & phosphorus level. Administer Ca chelators 10.6. Administer IV normal saline sol n 7. Administer phosphate 8. Administer calcitonin ( Calcimar) to decrease skeletal Ca release and increase renal clearance of Ca 9. .

Prepare patient for parathyroidectomy .11. Assess for tingling and numbness in the muscles and signs of hypocalcemia 12.

. and protein metabolism . fat.influences the development of sexual characteristics.regulates sodium and electrolyte balance .Adrenal gland .Affects carbohydrate.rest upon each kidney .

works as part of SNS. inner core and medulla. . synthesizes glucocorticoids and mineralocorticoids and secretes small amounts of sex hormones ( androgens & estrogens) 2. produces epinephrine & norepinephrine.- 2 parts: 1. outer shell. adrenal cortex. adrenal medulla.

Addison s Disease idiopathic atrophy of the adrenal gland  Adrenal cortex is inadequate due to surgical removal of both adrenal gland  Caused by infection: TB & histoplasmosis  Inadequate ACTH secretion  .

Clinical Manifestations: 1. 3. Emaciation 4. weakness and dehydration 2. Decrease blood glucose. Major problem: fatigue. apathy . Addisonian crisis: hypotension. dehydration and cyanosis 5. sodium and increase in potassium.

Diarrhea and restlessness . rapid respiration. Nausea 10. rapid weak pulse. decrease BP 8. Abdominal pain 11.6. Confusion 7. Circulatory shock: pallor. Headache 9.

Medical Management: 1.hypotension Aminespersists Glucocorticoids taken 2/3 @ 8am remaining is 4pm . 4. 3. 2. Administering fluids and corticosteroids Hydrocotisone IV 5%normal salinesalinegives 170 calories Vasopressor Amines.

3. trauma and surgery . BP. infection. weight and I & O Monitor blood glucose and potassium levels Administer mineralocorticoids and glucocorticoids medications Observe for addisonian crisis secondary to stress.Nursing Interventions: 1. 4. Monitor VS. 2.

Cushing s Syndrome  Caused by excessive corticoid production secondary to hyperplasia or malignant adrenal tumor  Benign  Ectopic production of ACTH by malignancy .

3. 2. Truncal obesity with thin extremities Moonface Classic picture: buffalo hump neck and supraclavicular areas  Heavy trunk  Thin extremities  .Clinical Manifestations: 1.

WBC and decrease Potassium and Ca 5. hyperglycemia. Reddish purple striae on the abdomen and upper thighs 7. Increase Na retention & water. Ecchymoses ( bruises) 6. Hirsutism .4.

Hypertension 9. Increased susceptibility to infection .8.

screening test for testdiagnosis of cushing s syndrome .Diagnostic Findings:  Overnight dexamethasone suppression test.

3. Values: glucose. cytadren. sodium.Nursing Interventions: 1. an adrenal enzyme inhibitor . weight Monitor lab. 4. WBC. Monitor BP Monitor I & O. 2. K and Ca Provide good skin care Administer aminoglutethimide ( Elipten. 5.

and adrenalectomy .6. Prepare client for Transpphenoidal hypophysectomy treatment of choice .

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