Endocrine System Mr. Homood Alharbi

1. 1 Endocrine System Mr. Homood Alharbi

2. 2 Assessment&Management ?Anatomic & physiologic overview Has far-reaching effect because it link to nervous & immunity system Regulation of internal environment affect every aspect of life

3. 3 Glands of the Endocrine System The endocrine system include Pituitary Thyroid Parathyroid Adrenal Pancreatic islets Ovaries &Testes Exocrine glands such as sweet glands

4. 4 Function & regulation of Hormones Classification & Action of Hormones Peptide &Protein Hormones (Insulin) interact with receptor site on the cell surface (acts within seconds & minuets ) Amine Hormones (epinephrine ) similar to protein & peptide ) Steroid Hormones (Hydrocortisone ) need several hours to act.

5. 5 Assessment Health History Changes in energy level & fatigue Changes in ability to carry out daily activities Changes in heat & cold tolerance Recent change in weight Changes in sexual function Changes in memory,mood,&ability to concern Altered sleep pattern

6. 6 Assessment Physical Assessment Assess for change in appearance such as :- changes in skin texture hypo&hyper thyroidism , facial hair in women , moon face , obesity of trunk , thinness of extremities …… etc V\S measured & compare with previous readings hypertensions ? hyper function of adrenal gland hypotension ? hypo function of adrenal gland

7. 7 Assessment Diagnostic Evaluation Blood Test : to determine hormone level in blood Urine Test : end product excreted by kidney (24 urine collection) Hormone Stimulation & Suppression Test

8. 8 The pancreas Exocrine : secretion collected in the pancreatic duct which join the bile duct Amylase ---- aid in digestion of carbohydrate Trypsin ---- aid in digestion of proteins Lipase ---- aid in digestion of fat Endocrine secreted from Islet of Langerhans Insulin ---- secreted by Beta cells Glucagon (convert glycogen to glucose) ---- secreted by Alpha cells Somatostin (hypoglycemic effect) ---- secreted by Delta cells

9. 9 Pancreatitis Inflammation of the pancreas Clinical Manifestations Severe Abd pain is the major symptom of pancreatitis Pain occurs in the epigastric area 24-48 hrs after heavy meal or alcohole Accompanied by Abd distension & decrease peristalsis Doesn't relieved by antacids or vomiting Radiating to back Tenderness

10. 10 Pancreatitis Clinical Manifestations 2. Ill appearance , reged Abd ,nausea & vomiting 3. Ecchymosis around the umbilicus 4. Hypotension , hypovolemia, &shock 5. Fever , Jaundice , mental confusion ,& agitation 6. Cyanosis ,cold clammy skin 7. Renal failure 8. Respiratory distress ,hypoxia, dyspnea, & tackypnea

11. 11 Pancreatitis Medical Management Pain Management “morphine” Intensive care (correction of fluid & blood loss homodynamic monitoring , Insulin & Antibiotics ) Respiratory Care “humi O2 , intubation ,& MV Surgery “ lapartomy for diagnosis, debride or resection of necrotic tissue Surgery is risky & need multiple drainage

12. 12 Diabetes Mellitus (DM) It is a group of metabolic diseases ch.ch. By hyperglycemia resulting from defect in insulin secretion ,insulin action or both A chronic disease involving the inability to synthesize insulin Etiology is unclear Involves genetics, auto-immune response, virus, obesity, infection.

13. Normal Blood Sugar level (BS) RBS < 180- 200 mg/dl (9.9-11.1 mmol/L) FBS< 126 mg/dl (7.0 mmol/L) Hypoglycemia BS < 60 mg/dl (3.5 mmol/L) Plasma glucose level is 10-15 % higher than finger stick BS. Test for BS should be done before tha meal & 2 hours after the meal. 13

14. 14 DM Types Type 1 - Insulin-dependent, pancreas does not produce sufficient insulin. Requires injections. Common in children. Type 2 - Non-insulin dependent, insufficient insulin used or cells are not sensitive to insulin. Increase among adolescents. Treated with tablets early, then insulin later on Diabetes Mellitus associated with other conditions & syndrome Gestational - diabetes developed during pregnancy

15. 15 DM Functions of Insulin:- Transports & Metabolizes glucose for energy Stimulates storage of glucose in the liver & muscles “as glycogen Enhances storage of dietary fat in adipose tissues Accelerates transport of aminoacids into cells Assessment & Diagnostic Findings “ see your text book” The presence of abnormally high blood glucose levels is the criterion on which diagnosis of Diabetes is based

16. 16 DM Clinical Manifestations :- Includes three Ps Polyurea Polydipsia Polyphagia Other symptoms includes Fatigue ,weakness &dry skin Sudden vision changes Numbness in hands & feet Recurrent infection with slow healed sores The onset of type 1 may associated with nausea ,vomiting ,or Abd pain

17. 17 DM Management The therapeutic goal is to achieve euglycemia without hypoglycemia & without seriously disrupting usual lifestyle and activity. There are Five Components of Management Nutrition Management Exercise Monitoring Glucose & Ketones Pharmacological Therapy Education

18. 18 Diabetes Diet & meal planning : meet nutritional and energy needs maintain ideal & reasonable weight reduce blood lipid levels maintain normal blood glucose levels High protein, high fiber (useful for cholesterol absorption & lowering cholesterol in blood) to assist in glucose absorption 10-20% protein, 30% or less fat, 50-60% carbohydrate

19. 19 Diabetes 2. Exercise Exercise reduces blood glucose, which may reduce need for insulin. Used with diet to achieve lower glucose. Pt with blood glucose more than 250 mg/dl should not begin exercise until keton test is negative. Regular daily slow gradual exercise is encouraged , walking is a safe form of exercise

20. 20 Diabetes 3. Monitoring Glucose & Ketones Allows detection & prevention of Hypo&Hyper glycemia Plays a crucial role in normalizing blood glucose level which may reduce the risk for long term complication Done by : Self Monitoring of Blood Glucose Lab Urine Testing for Glucose & Ketones

21. 21 Diabetes 4. Pharmacological Therapy A. Insulin For type 1 diabetes & may be used for type 2 for long term basis if oral hypoglycemic agents failed. Types of insulin “ short, intermediate, long” . Complications: (Systemic) Insulin reaction. Hypoglycemia may developed in : usually before meals but can be at any time. Glucose below 50 or 60 mg. From increased exercise, increased insulin, or lack of food.

22. 22 Diabetes S&S: weakness, headache, sweating, tremor, palpitations, mental changes. Will lead to coma. Give juice with sugar Memory aid: Symptom Implication Cold and clammy… give hard candy Hot and dry... glucose is high Other complications include ( local complications): Local allergic reaction , redness,swelling,&tenderness Lipoatrophy &Lipohyperatrophy

23. 23 Diabetes B. oral Antidiabetic Agents : affective for type 2 diabetic pt who can't controlled by diet & exercise Sulfonylureas “chlorpromide” : act by stimulate the pancreas to secrete insulin & improve Insulin action at the cellular level & decrease liver glucose Biguarides “glucophage” : facilitating insulin action in peripheral receptor sites --- gives in combination with Sulfonylureas Oral Alpha Glucosidase Inhibitors : delaying the absorption of glucose in the intestine

24. 24 Diabetes Acute Complication of Diabetes: Hypoglycemia : a decrease in blood glucose level to less than 50-60 caused by too much insulin or oral agents , too little food ,or excessive activity S&S : Sweating ,tremor, tachycardia, nervousness & hunger. In mild : confusion ,headache numbness of lips & tongue , & drowsiness. In severe : seizures , difficulty arousing from sleep & loss of consciousness.

25. 25 Diabetes Management : Immediate Treatment must be given 10-15 mg of a fast acting carbohydrates, repeated every 15 min if no response For unconscious Pt Glucagon 1mg S/C or IM , or IV dose mainly in hospital

26. 26 Diabetes 2. Diabetic Ketoacidosis : When the availabe glucose is not enough, the liver convert Fatty into Ketone bodies which is acids. Thus, acids accumulated in the circulation lead to metabolic Ketoacidosis S&S “see the Textbook” The main cause of DKA : Missed dose of insulin Illness or infection Undiagnosed & untreated diabetes Management : Rehydration & Replace of Electrolytes Correction of Acidosis Insulin & IV Dextrose

27. 27 Long Term Complications of DM Usually not occur within first 5-10yrs 1. Macro vascular Complications Blood vessels walls thicken and occluded (sclerosis developed, Coronary Artery Diseases , Cerebro vascular Diseases & peripheral vascular Diseases) 2. Micro vascular Complications (Retinopathy) 3. Nephropathy 4. Diabetic Nephropathies

28. 28 Function of the liver Glucose Metabolism : Glucose taken up from portal venous by liver & converted into glycogen which stored in the hepatocyts Gluconeogenesis Ammonia Conversion : protein in stomach is converted to amino acid, which enter bolood inform of ammonia, liver convert it to urea.

29. 29 liver functions cont. 3. Protein Metabolism : (albumin, oncotic pressure, clotting factors) 4. Fat Metabolism 5. Vit & Iron storage 6. Drug Metabolism 7. Bilirubin excretion (end products of died RBC, Jundice).

30. 30 liver functions cont. 8. Bile Formation : Bile formed in hepatocytes composed of water ,electrolytes ,fatty acids , billirubin ,cholesterol ,& bile salt Bile stored in Gallbladder empted in intestine as needed for fat emulsification Function of Gallbladder Storage of bile 5-10 times concentrated Bile secretion in intestine by contraction

31. 31 Liver Diagnostic Evaluation : 1. Liver Function Test : Serum Aminotransferase (transaminase) injury of liver & acute liver disease such as Hepatitis Alanine Aminotrasferase (ALT ) SGPT Aspartate Aminotransferase (AST) SGOT Gamma Glutamyl Transferase (GGT) 2. Percutaneous Needle Biopsy : useful when other lab tests not diagnostic 3. Other Diagnostic Tests : liver U/S , liver CT scanning ,MRI , & laparoscopy

32. 32 Hepatic Dysfunction Result from damage of the liver cells Causes: Infectious agents (bacterial &viral) Metabolic Disorders Toxins &Medications Nutritional Deficiency Anoxia & Hypersensitivity

33. 33 Hepatic Dysfunction Clinical Manifestations 1. Jaundice :resulting from increased bilirubin concentration in the blood, due to hepatic, gallbladder dysfunction or hematological problem 2. Nutritional deficiency Which result from the inability of the damaged liver cells to metabolize certain vitamins: Vit A night blindness Vit K bleeding tendency Vit C hemorrhage lesions

34. 34 Hepatic Dysfunction 3.Hepatic Encephalopathy :Reflecting accumulation of ammonia in the serum due to impaired protein metabolism by the diseased liver which lead to brain dysfunction & damage. Lactulose is the management. 4. Portal hypertension & acites Formation of esophageal ,gastric, &hemorrhoidal varices Accumulation of fluid in Abd cavity “acites”

35. 35  Hepatic Disorders Hepatitis A Virus (HAV) Accounts 20-25% of hepatic infection caused by RNA virus of the Enterovirus Family Mode of Transmission :fecal –oral rout ,through ingestion of infected food or liquids Child & adults acquire the infection through contact Incubation period : 15-50 days (average of 30 days) Course of illness : lasting 4-8 weeks Recovery is the rule ,rarely complicated ,Immunity Mortality rate is approximately 0.5%

36. 36 Hepatitis A Virus (HAV) Clinical Manifestations Many Pts symptomless & anictric Mild flu like upper respiratory tract infection with low grade fever Anorexia is an early symptom & is often severe Later jaundice & dark urine may became apparent Indigestion ,vague epigastric distress ,nausea ,heart burn & flatulence

37. 37 Hepatitis A Virus (HAV) Prevention Vaccination Precautions Medical Management Bed rest in acute stage & appropriate diet Stimulate appetite to control weight loss Gradual but progressive ambulation Provide rest after activity

38. 38 Hepatitis B virus (HBV) Transmitted: through blood Found in : blood, saliva, semen, &vaginal secretion Incubation period 1-6 months Recovery : most adults recover within 6 months Mortality : about 10%

39. 39 Hepatitis B virus (HBV) Clinical Manifestations Arthralgia & rashes Loss of appetite ,dyspnea , Abd pain itching ,generalize malaise & weakness If jaundice developed light stool & dark urine Tender liver & enlarged to 12-14 cm vertically Fever & respiratory symptoms are rare

40. 40 Hepatitis B virus (HBV) Prevention : The Goals of prevention is to : Interrupt the chain of transmission Protect people of high risk by immunization To use passive immunization for unprotected people

41. 41 Hepatitis B virus (HBV) Medical Management The goals of management are to : Minimize infectivity Normalize liver inflammation Decrease symptoms Bed rest may be recommended Maintain adequate nutrition Proteins are restricted when ability of liver to metabolize proteins is impaired

42. 42 Hepatitis B virus (HBV) Nursing Management Convalescence may be prolonged so during this period nurse make gradual resumption of physical activity Psychological consideration Decrease fear & anxiety of family & patient

43. 43 Hepatitis C Virus non A non B hepatitis Incubation period 15-160 days Transmitted by blood transfusion & sexual contact No benefit from rest ,diet ,or vit supplement Combination of Interferon & Ribovirin. Can cause liver cirhosis, which required liver transplant.

44. Hepatitis D Virus (HDV) Requires Hep.B for replication. Common in IV injection, sexual. The incubation period: 21-140 days. Symptoms are similar to Hep.B 44

45. Hepatitis E Virus (HEV) Transmitted by fecal, oral, contaminated water. The incubation period: 15-65 days. Resemble to Hep.A Chronic forms don’t developed. 45

46. 46 Fulminant Hepatic Failure It is the clinical syndrome of sudden & severely impaired liver function in a previously healthy person Pattern of progression from jaundice to encephalopathy identified by time but agreement one specific classification not yet However three categories cited Hyperacute : duration of jaundice 0-7 days Acute : 8-28 days Subacute : 28-72 days

47. 47 Fulminant Hepatic Failure Cause : viral hepatitis , toxic medication & chemicals , metabolic disturbances& structural changes Prognosis much worse than chronic liver failure but the hepatic lesion is potentially reversible rate 50-85. S&S : Jaundice & profound anorexia Accompanied with : coagulation defect ,renal failure, electrolytes disturbances, hypoglycemia, & encephalopathy. Management Plasma exchange Monitor &manage complication “cerebral edema” Liver transplantation

48. 48  Hepatic Cirrhosis It is a chronic disease ch.ch. By replacement of normal liver tissue with diffuse fibrosis that disrupts the structure & function of the liver Types of cirrhosis Alcoholic cirrhosis : most common Post necrotic cirrhosis Billiary Cirrhosis

49. 49  Hepatic Cirrhosis Clinical Manifestations : “see your textbook” Medical Management Based in presenting symptoms e.g. antacid , vit K sparing diuretics for ascitis if present Adequate Balanced diet & avoidance of alcohol Colchicine (anti-inflammatory) which increase survival of mild &moderate cirrhosis

50. 50 Hepatic & Billiary Disorders Hepatic Cirrhosis Nursing Management : Providing Rest Improving Nutritional Status Providing Nursing Care & reducing risk for injury Monitoring & Managing potential complication

51. 51 Cholecystitis Acute infection of the gallbladder. causes pain ,tenderness , & rigidity of the upper right Abdomen & associated with nausea ,vomiting ,& the usual signs of acute inflammation. A calculus Cholecystitis : describes acute gallbladder inflammation in the absence of obstruction by stone Calculus cholecystitis : a gallbladder stones obstruct bile out flow , occur in 90% of Pt with acute cholecystitis

52. 52 Cholecystitis Clinical Manifestations May be silent & produce mild GI symptoms Pain & Billiary Colic Jaundice Changes in stool & urine color Vitamin Deficiency

53. 53 Cholecystitis Diagnostic Evaluation Abdominal X- ray U/S. Endoscopic Retrograde Cholengiopancreatiography (ERCP) Percutaneous Transhepatic Cholengiography

54. 54 Cholecystitis Medical Management: Nutritional & supportive Therapy 1. Diet limited to low fat liquid after episode. 2. Powdered supplement high in protein & carbohydrates ,then as tolerated cooked fruit ,rice ,lean meat ,non gas forming vegetables , bread , coffee & tea. 3. Avoid egg , creama , cheese , & alcohol

55. 55 Cholecystitis Pharmacologic Therapy Ursodexycholic Acid & Chendeoxycholic Acid used to disolved small gallstones composed of cholesterol Not indicated for patients with pigment stone

56. 56 Cholecystitis Non Surgical Removal of Gallstone Dissolving gallstone by infusion of a solvent into gallbladder through ERCP Extracorporeal Shock- Wave Lithotripsy (ESWL). Surgical Management Laparoscopic Cholecystictomy Open Cholecystictomy

57. 57 Pituitary Gland 1.27 cm in diameter Called master gland Divided into three lobes Controlled by hypothalamus pituitary Hormones controlled by releasing factors (RF) , secreted by hypothalamus which reach the pituitary by portal blood system

58. 58 Pituitary Gland Posterior Pituitary “the important hormones” Vasopressin “ADH” Oxytocin ejection of milk , uterine contraction The two hormones synthesized in hypothalamus & storage in pituitary Anterior pituitary “the important hormones”: Follicle Stimulating Hormones (FSH) Luitinizing Hormone (LH) Adrenocorticotropic Hormone (ACTH) Thyroid Stimulating Hormone (TSH) Growth Hormone (GH)

59. 59 Pituitary Gland Abnormal pituitary function : over secretion or under secretion of of any of the hormones Hypopituitararism Disease of pituitary it self or of hypothalamus May result from destruction of the anterior lobe Pan hypothyroidism Simond’s disease total absence of all P . Secretions. Postpartum Pituitary Necrosis Shaheen’s Syndrome failure of A . pituitary

60. 60 Diabetes Insipidus It is a disorder of the posterior lobe of the pituitary gland due to deficiency of Vasopressin “ADH” It ch.ch. By polydipsia & large volume of diluted urine It may Secondary to brain tumor ,brain trauma or infection of nervous system, failure of the renal tubules to respond to ADH due to hypokalemia ,hypercalcemia or medication. Assessment & Diagnostic evaluation Fluid Deprivation Test Plasma level of vasopressin Assessment of cause of disease if not obvious

61. 61 Diabetes Insipidus Clinical Manifestations Diluted water like urine . Pt tend to drink 4 liter of fluids daily Abrupt or insidious onset in adult If fluid restricted pt experience an insatiable craving for fluid and develop hypernatremia or dehydration

62. 62 Diabetes Insipidus Medical Management 1. Vasopressin Replacement Desmopressin : administered intranasaly2-4 times /day Lypressin “Diapid” short acting 2.Phamacotherapy to conserve fluids : “clofibrate & hypolipidemic agent & diabenase” 3. Treatment of nephrogenic causes

63. 63 Thyroid Gland It is a butterfly shaped organ located in the lower neck anterior to the trachea It is about 5cm long & 3cm wide , 30mg weight It produces 3 hormones -Thyroxin T4 -Triiodothyronin T3 -Calcitonin Regulation of thyroid function -Thyrotropin “TSH”

64. 64 Thyroid Gland Examination of Thyroid Gland Inspection & Palpation Thyroid Stimulating Hormone level Serum T3 & T4 Radioactive Iodine Uptake Fine-Needle Aspiration Biopsy Thyroid Scan & MRI

65. 65 Thyroid Gland Abnormalities of Thyroid Function Hypothyroidism Decrease in hormones secretion result from sub optimal levels of thyroid hormones Causes : - -Autoimmune Thyroditis “Hashomotus”.

66. 66 Thyroid Gland Types of Hypothyroidism. Thyroidal hypothyroidism (primary) :- dysfunction of the thyroid gland it self Central Hypothyroidism :- dysfunction of thyroid caused by failure of the pituitary gland , hypothalamus , or both.

67. 67 Thyroid Gland Clinical Manifestation Early symptoms :- Hair loss , Brittle nails , dry skin Numbness , tingling of fingers , horsiness Menstrual Disturbances Sever hypothyroidism Subnormal Temperature & Heart rate Weight Gain ,Thickened Skin ,feeling of cold Mask & Expressionless Face Irritability , Epethatic ,Mental Dullness

68. 68 Thyroid Gland Slow speech , tongue enlargement Increase size of hands & face Constipation 3. In advanced cases Dementia , sleep apnea Plural effusion ,respiratory muscle weakness 4. Severe cases associated with:- Elevated serum cholesterol level Atherosclerosis Coronary artery disease Poor left ventricle function

69. 69 Thyroid Gland Medical Management Thyroid Hormones Replacement Supportive Therapy Prevention of cardiac dysfunction Nursing Management Modifying activity Promoting physical comfort “don’t use heat pad or heat blanket Providing emotional support

70. 70 Thyroid Gland Hyperthyroidism It is the second most common endocrine disorder after Diabetes Mellitus. Result from excessive output of thyroid hormones. Affect women eight times more frequently than men

71. 71 Thyroid Gland Clinical Manifestations Nervousness ,irritability, fine tremor of hands Flushed ,warm , soft & moist skin Poor Heat toleration Increase appetite & dietary intake & weight loss Fatigue & change in bowel function Increase systolic blood pressure ,palpitation ,atrial fibrillation & cardiac failure Osteoporosis & bone fracture .

72. 72 Thyroid Gland Management Radioactive Iodine Therapy: destroy the over active thyroid cells Pharmacologic Therapy : inhibit stages of hormone synthesis “Tapazole , Propacil” Adjunctive Therapy :Iodide compound to decrease production of hormones & to reduce vascularity of thyroid gland “K iodide” ,which make surgery saver Surgical Management Subtotal Thyroidectomy.

73. 73 Parathyroid Glands Parathormone :- regulate calcium & phosphorus metabolism Parathormone calcium absorption from kidney ,the intestine & bones ( increase blood level of Ca) Parathormone lower phosphorous level Calcium phosphate may precipitate in various organ& cause tissue calcification Parathormone regulated by the serum level of ionized Ca Ca Parathormone secretion

74. 74 Parathyroid Glands Abnormalities Hyperparathyroidism hypoparathyroidism

75. 75 The Adrenal Gland Each Adrenal Gland is ,in reality ,two endocrine gland with separate ,& independent function Adrenal Medulla Epinephrine Nor epinephrine Adrenal Cortex Glucocorticoids (Hydrocortisone) Miniralocorticoid (Aldesterone) Androgens (Male Sex Hormone)

76. 76 The Adrenal Gland Addison’s Disease: (Adrenocortical Insufficiency) Decreased cortical activity from atrophy, TB, or virus (histoplasmosis) Clinical Manifestations weakness, fatigue, emaciation, dark pigmentation, Gastrointestinal disturbances low BP, low glucose and sodium, high potassium reduced BMR,, dehydration Mental status changes (depression ,apathy &confusion)

77. 77 The Adrenal Gland Management Correct electrolyte imbalance Hydrocortisone “solu-cortef” Vasopressor for hypotesion Antibiotic for infection if it the cause Oral intake may initiated as soon as tolerated

78. 78 The Adrenal Gland Addisonian Crisis A status progressed disease with acute hypotension ch.ch. Cyanosis ,fever & classic signs of shock Nursing Management Assessing Patient Monitoring for Addisonian Crisis Restoring fluid balance Improving Activity tolerance

79. 79 The Adrenal Gland Cushing’s Syndrom From excessive ACTH or cortisone, hyperplasia of cortex or pituitary tumor. Clinical Manifestations: hypotension, decrease inflammatory response, decrease wound healing. Assessment & Diagnostic Evaluation Increase blood glucose level &Na Decrease in K & WBCs count Plasma ACTH 24 hr urinary free cortison

80. 80 The Adrenal Gland Medical Management Treatment of cause Bilateral Adrenoectomy for adrenal hypertrophy Replacement therapy with Hydrocortison Adrenal enzyme inhibitors “Ketoconazole”

81. 81 Conclusion Any question?