1. Endocrine Emergencies

2.  Endocrine System  Physiology/Patho  Function  Disorders of the Pancreas  Disorders of the Thyroid Gland  Disorders of the Adrenal Glands  Endocrine System  Physiology/Patho  Function  Disorders of the Pancreas  Disorders of the Thyroid Gland  Disorders of the Adrenal Glands Endocrine Disorders and Emergencies

3. Endocrine System  Consists of glands that secrete hormones  Maintains homeostasis with the use of hormonal chemical messengers…tend to be widespread in effect  Consists of glands that secrete hormones  Maintains homeostasis with the use of hormonal chemical messengers…tend to be widespread in effect

4. Hormones  Are released as changes in the internal environment occur  Transported by the blood throughout the body  One may control the secretion of another  Hormonal action controlled by negative feedback  Are released as changes in the internal environment occur  Transported by the blood throughout the body  One may control the secretion of another  Hormonal action controlled by negative feedback

5. They are located throughout the body.  Hypothalamus  Pituitary  Thyroid  Parathyroid  Thymus  Hypothalamus  Pituitary  Thyroid  Parathyroid  Thymus There are eight major glands in the endocrine system:  Pancreas  Adrenals  Gonads  Pineal The Endocrine System

6. The Major Glands of the Endocrine System

7. Disorders of the Pancreas  Beta Cells secrete insulin to decrease blood sugar  Alpha Cells secrete glucagon to increase blood sugar  Delta cells secrete somatostatin suppresses secretion of glucagon and insulin  Beta Cells secrete insulin to decrease blood sugar  Alpha Cells secrete glucagon to increase blood sugar  Delta cells secrete somatostatin suppresses secretion of glucagon and insulin

8. Disorders of the Pancreas  Glucose Metabolism  anabolism & catabolism  Glucose Metabolism  anabolism & catabolism

9. Disorders of the Pancreas Insulin is required for glucose metabolism  Presence of enough insulin to meet cellular needs.  Ability to bind in a manner to stimulate the cells adequately.  When unable to obtain energy from glucose, the body begins to use fatty stores. Ketones and ketosis.  Regulation of Blood Glucose  Hypoglycemia and hyperglycemia  Role of pancreas, liver, and kidneys  Osmotic diuresis and glycosuria Insulin is required for glucose metabolism  Presence of enough insulin to meet cellular needs.  Ability to bind in a manner to stimulate the cells adequately.  When unable to obtain energy from glucose, the body begins to use fatty stores. Ketones and ketosis.  Regulation of Blood Glucose  Hypoglycemia and hyperglycemia  Role of pancreas, liver, and kidneys  Osmotic diuresis and glycosuria

10. Insulin Regulated by glucose in the body  After a meal >>>hyperglycemia  pancreas stimulates insulin via the islet cells [beta cells]  Secretion is halted when the blood glucose is low >>>hypoglycemia [Negative Feedback] Regulated by glucose in the body  After a meal >>>hyperglycemia  pancreas stimulates insulin via the islet cells [beta cells]  Secretion is halted when the blood glucose is low >>>hypoglycemia [Negative Feedback]

11. Glucagon  Insulin antagonist – actions are opposite  Secreted during low levels of glucose >>>hypoglycemia  Causes glucose to move from cells, specifically the liver

12. Regulation of Insulin Secretion glucagon somatostatin insulin GLUCOSE Glut-2 Increased secretion of Insulin Decreases blood glucose Liver Releases glucose and ketones Endocrine Pancreas

13. Pathogenesis of Diabetes Impaired Transport of Glucose into Cells HYPERGLYCEMIA CELL ENERGY breakdown of fat and protein ketogenesis blood osmolality cells shrink glycosuria dehydration thirst HR warm,dry Fruity Kussmaul Coma breath resp

14. Diabetes Mellitus  Type I Diabetes Mellitus  Also called juvenile or insulin-dependent diabetes mellitus (IDDM).  Characterized by low production of insulin.  Closely related to heredity.  Results in pronounced hyperglycemia.  Symptoms of untreated Type I DM include polydipsia, polyuria, polyphagia, weight loss, and weakness.  Untreated or noncompliant patients may progress to ketosis and diabetic ketoacidosis.  Type I Diabetes Mellitus  Also called juvenile or insulin-dependent diabetes mellitus (IDDM).  Characterized by low production of insulin.  Closely related to heredity.  Results in pronounced hyperglycemia.  Symptoms of untreated Type I DM include polydipsia, polyuria, polyphagia, weight loss, and weakness.  Untreated or noncompliant patients may progress to ketosis and diabetic ketoacidosis.

15. Diabetes Mellitus  Type II Diabetes Mellitus  Also called adult-onset or non-insulin-dependent diabetes mellitus (NIDDM).  Results from decreased binding of insulin to cells.  Related to heredity and obesity.  Accounts for 90% of all diagnosed diabetes patients.  Less risk of fat-based metabolism.  Results in less-pronounced hyperglycemia.  Hyperglycemic hyperosmolar nonketotic acidosis.  Managed with dietary changes and oral drugs to stimulate insulin production and increase receptor effectiveness.  Type II Diabetes Mellitus  Also called adult-onset or non-insulin-dependent diabetes mellitus (NIDDM).  Results from decreased binding of insulin to cells.  Related to heredity and obesity.  Accounts for 90% of all diagnosed diabetes patients.  Less risk of fat-based metabolism.  Results in less-pronounced hyperglycemia.  Hyperglycemic hyperosmolar nonketotic acidosis.  Managed with dietary changes and oral drugs to stimulate insulin production and increase receptor effectiveness.

16. Diabetic Emergencies

18.  Diabetic Ketoacidosis - Hyperglycemia  Pathophysiology  Results from the body’s change to fat metabolism.  Continuous buildup of ketones produces significant acidosis.  Signs and Symptoms  Extended period of onset (12–24 hours).  Sweet, fruity breath odor.  Potassium-related cardiac dysrhythmias.  Kussmaul’s respiration.  Decline in mental status and coma.  Diabetic Ketoacidosis - Hyperglycemia  Pathophysiology  Results from the body’s change to fat metabolism.  Continuous buildup of ketones produces significant acidosis.  Signs and Symptoms  Extended period of onset (12–24 hours).  Sweet, fruity breath odor.  Potassium-related cardiac dysrhythmias.  Kussmaul’s respiration.  Decline in mental status and coma.

19. Diabetic Emergencies Assessment and Management  Focused History & Physical Exam Obtain SAMPLE and OPQRST histories. Look for medical identification.  Management Maintain airway and support breathing as indicated. Determine blood glucose level and obtain blood sample. If blood glucose unknown, administer 25g 50% dextrose. Establish IV and administer normal saline per local protocol. Monitor cardiac rhythm and vital signs. Expedite transport.  Focused History & Physical Exam Obtain SAMPLE and OPQRST histories. Look for medical identification.  Management Maintain airway and support breathing as indicated. Determine blood glucose level and obtain blood sample. If blood glucose unknown, administer 25g 50% dextrose. Establish IV and administer normal saline per local protocol. Monitor cardiac rhythm and vital signs. Expedite transport.

20. The future 1 - Continuous glucose sensor monitors blood sugar level 2 - Data transmitted for the computer program to work out insulin dose 3 - Insulin pump delivers the dose 1 - Continuous glucose sensor monitors blood sugar level 2 - Data transmitted for the computer program to work out insulin dose 3 - Insulin pump delivers the dose

21. Diabetic Emergencies  Hyperglycemic Hyperosmolar Nonketotic (HHNK) Coma  Pathophysiology  Found in Type II diabetics.  Results in blood glucose levels far above the norm  Insulin activity prevents buildup of ketones.  Sustained hyperglycemia results in marked dehydration. Often related to dialysis, infection, and medications.  Very high mortality rate.  Hyperglycemic Hyperosmolar Nonketotic (HHNK) Coma  Pathophysiology  Found in Type II diabetics.  Results in blood glucose levels far above the norm  Insulin activity prevents buildup of ketones.  Sustained hyperglycemia results in marked dehydration. Often related to dialysis, infection, and medications.  Very high mortality rate.

22. Hyperglycemic Hyperosmolar Nonketotic (HHNK) Coma  Signs & Symptoms  Gradual onset over days.  Increased urination and thirst, orthostatic hypotension, and altered mental status.  Assessment & Management  Difficult to distinguish from diabetic ketoacidosis in the prehospital setting.  Treatment is identical to diabetic ketoacidosis.  Signs & Symptoms  Gradual onset over days.  Increased urination and thirst, orthostatic hypotension, and altered mental status.  Assessment & Management  Difficult to distinguish from diabetic ketoacidosis in the prehospital setting.  Treatment is identical to diabetic ketoacidosis.

23. Diabetic Emergencies  Hypoglycemia  Pathophysiology  True medical emergency resulting from low blood glucose levels; rarely seen outside diabetics.  By the time signs and symptoms develop, most of the body’s stores have been used.  Diabetics with kidney failure are predisposed to hypoglycemia.  Hypoglycemia  Pathophysiology  True medical emergency resulting from low blood glucose levels; rarely seen outside diabetics.  By the time signs and symptoms develop, most of the body’s stores have been used.  Diabetics with kidney failure are predisposed to hypoglycemia.

24. Hypoglycemia  Signs & Symptoms  Altered mental status with rapid onset  Frequently involves combativeness.  Diaphoresis and tachycardia  Hypoglycemic seizure and coma  Assessment and Management  Focused History & Physical Exam  Obtain SAMPLE and OPQRST histories.  Look for medical identification.  Signs & Symptoms  Altered mental status with rapid onset  Frequently involves combativeness.  Diaphoresis and tachycardia  Hypoglycemic seizure and coma  Assessment and Management  Focused History & Physical Exam  Obtain SAMPLE and OPQRST histories.  Look for medical identification.

25. Management Diabetic Emergencies Maintain airway and support breathing as indicated. Determine blood glucose level and obtain blood sample. Establish IV access. If blood glucose <4.0 mmol/L or is unknown, administer 50 ml of 50% Dextrose IV. If IV cannot be established, administer 0.5–1.0mg glucagon intramuscularly. Monitor cardiac rhythm and vital signs. Expedite transport. Maintain airway and support breathing as indicated. Determine blood glucose level and obtain blood sample. Establish IV access. If blood glucose <4.0 mmol/L or is unknown, administer 50 ml of 50% Dextrose IV. If IV cannot be established, administer 0.5–1.0mg glucagon intramuscularly. Monitor cardiac rhythm and vital signs. Expedite transport.

26. The Canadian Diabetes Association 2003 Clinical Practice Guidelines recently lowered the blood glucose (sugar) target levels. Canadians with type 2 diabetes need to understand what those new levels are, and how meeting these new targets can help them stay healthy and live well with diabetes. Recommended Targets for People With Diabetes* AIC A1C Fasting blood glucose / blood glucose before meals (mmol/L ) Blood glucose two hours after eating (mmol/L) Blood Pressure Cholesterol Target for most patients with diabetes =7.0 % 4.0 to 7.0 5.0 to 10.0 130 / 80 LDL: below 2.5 Total Cholesterol to HDL ratio: below 4 Normal range =6.0% 4.0 to 6.0 5.0 to 8.0

27. Onsetany ageadults Weightunderweightobese Immune-mediatedYESNO Ketoacidosis YES NO Insulin secretion NO YES Beta cell function NO YES Genetic predisposition Moderate Very Strong Onsetany ageadults Weightunderweightobese Immune-mediatedYESNO Ketoacidosis YES NO Insulin secretion NO YES Beta cell function NO YES Genetic predisposition Moderate Very Strong Type 1 Compare Type 1 and Type 2 Type 2

28. HIGH Blood Sugar HIGH Blood Sugar LOW Blood Sugar LOW Blood Sugar Increased thirst and urination hunger ketones in urine aching, weak heavy breathing nausea,vomiting Fatigue seizure Increased thirst and urination hunger ketones in urine aching, weak heavy breathing nausea,vomiting Fatigue seizure cold sweats headache trembling pounding heart sleepiness personality change hunger cold sweats headache trembling pounding heart sleepiness personality change hunger KNOW THE DIFFERENCE

29. Diabetes Now that you mastered Diabetes Mellitus There is More!!!!! What is Diabetes Insipidus? Now that you mastered Diabetes Mellitus There is More!!!!! What is Diabetes Insipidus?

30.  Grave’s Disease  Pathophysiology  Probably hereditary in nature.  Autoantibodies are generated that stimulate thyroid tissue to produce excessive hormone.  Signs & Symptoms  Agitation, emotional changeability, insomnia, poor heat tolerance, weight loss, weakness, dyspnea.  Tachycardia and new-onset atrial fibrillation.  Protrusion of the eyeballs or goiters.  Grave’s Disease  Pathophysiology  Probably hereditary in nature.  Autoantibodies are generated that stimulate thyroid tissue to produce excessive hormone.  Signs & Symptoms  Agitation, emotional changeability, insomnia, poor heat tolerance, weight loss, weakness, dyspnea.  Tachycardia and new-onset atrial fibrillation.  Protrusion of the eyeballs or goiters. Disorders of the Thyroid Gland

31.  Assessment & Management  Usually arise from cardiovascular signs/symptoms. Manage signs and symptoms.  Thyrotoxic Crisis (Thyroid Storm)  Pathophysiology  Life-threatening emergency, usually associated with severe physiologic stress or overdose of thyroid hormone.  Results when thyroid hormone moves from bound state to free state within the blood.  Assessment & Management  Usually arise from cardiovascular signs/symptoms. Manage signs and symptoms.  Thyrotoxic Crisis (Thyroid Storm)  Pathophysiology  Life-threatening emergency, usually associated with severe physiologic stress or overdose of thyroid hormone.  Results when thyroid hormone moves from bound state to free state within the blood. Disorders of the Thyroid Gland

32.  Signs & Symptoms  High fever (106º F or higher)  Reflected in increased activity of sympathetic nervous system. Irritability, delirium or coma Tachycardia and hypotension Vomiting and diarrhea  Assessment and Management  Support airway, breathing, and circulation.  Monitor closely and expedite transport.  Signs & Symptoms  High fever (106º F or higher)  Reflected in increased activity of sympathetic nervous system. Irritability, delirium or coma Tachycardia and hypotension Vomiting and diarrhea  Assessment and Management  Support airway, breathing, and circulation.  Monitor closely and expedite transport. Disorders of the Thyroid Gland

33.  Hypothyroidism and Myxedema  Pathophysiology  Can be inherited or acquired.  Chronic untreated hypothyroidism creates myxedema. Thickening of connective tissue in skin and other tissues. Infection, trauma, CNS depressents, or a cold environment can trigger progression to a myxedemic coma.  Hypothyroidism and Myxedema  Pathophysiology  Can be inherited or acquired.  Chronic untreated hypothyroidism creates myxedema. Thickening of connective tissue in skin and other tissues. Infection, trauma, CNS depressents, or a cold environment can trigger progression to a myxedemic coma. Disorders of the Thyroid Gland

34.  Signs & Symptoms  Fatigue, slowed mental function  Cold intolerance, constipation, lethargy  Absence of emotion, thinning hair, enlarged tongue  Cool, pale doughlike skin  Coma, hypothermia, and bradycardia  Signs & Symptoms  Fatigue, slowed mental function  Cold intolerance, constipation, lethargy  Absence of emotion, thinning hair, enlarged tongue  Cool, pale doughlike skin  Coma, hypothermia, and bradycardia Disorders of the Thyroid Gland

35.  Assessment and Management  Focus on maintaining ABCs.  Closely monitor cardiac and pulmonary status.  Establish IV access, but limit fluids.  Expedite transport.  Assessment and Management  Focus on maintaining ABCs.  Closely monitor cardiac and pulmonary status.  Establish IV access, but limit fluids.  Expedite transport. Disorders of the Thyroid Gland

36.  Signs & Symptoms  Weight gain  “Moon-faced” appearance  Fat accumulation on the upper back  Skin changes and delayed healing of wounds  Mood swings  Impaired memory or concentration  Signs & Symptoms  Weight gain  “Moon-faced” appearance  Fat accumulation on the upper back  Skin changes and delayed healing of wounds  Mood swings  Impaired memory or concentration Disorders of the Thyroid Gland

37.  Hyperadrenalism (Cushing’s Syndrome)  Pathophysiology  Often due to abnormalities in the anterior pituitary or adrenal cortex.  May also be due to steroid therapy for nonendocrine conditions such as COPD or asthma.  Long-term cortisol elevation causes many changes. Atherosclerosis, diabetes, hypertension Increased response to catecholamines Hypokalemia and susceptibility to infection  Hyperadrenalism (Cushing’s Syndrome)  Pathophysiology  Often due to abnormalities in the anterior pituitary or adrenal cortex.  May also be due to steroid therapy for nonendocrine conditions such as COPD or asthma.  Long-term cortisol elevation causes many changes. Atherosclerosis, diabetes, hypertension Increased response to catecholamines Hypokalemia and susceptibility to infection Disorders of the Adrenal Gland

38.  Assessment & Management  Support ABCs.  Use caution when establishing IV access.  Report any observations indicative of Cushing’s Syndrome to the receiving facility.  Adrenal Insufficiency (Addison’s Disease)  Pathophysiology  Due to destruction of the adrenal cortex.  Often related to heredity.  Stress may trigger Addisonian crisis.  Assessment & Management  Support ABCs.  Use caution when establishing IV access.  Report any observations indicative of Cushing’s Syndrome to the receiving facility.  Adrenal Insufficiency (Addison’s Disease)  Pathophysiology  Due to destruction of the adrenal cortex.  Often related to heredity.  Stress may trigger Addisonian crisis. Disorders of the Adrenal Gland

39.  May be related to steroid therapy. Sudden withdrawal can trigger Addisonian crisis.  Signs & Symptoms  Progressive weakness, fatigue, decreased appetite, and weight loss  Hyperpigmentation of skin and mucous membranes  Vomiting or diarrhea  Hypokalemia and other electrolyte disturbances  Unexplained cardiovascular collapse  May be related to steroid therapy. Sudden withdrawal can trigger Addisonian crisis.  Signs & Symptoms  Progressive weakness, fatigue, decreased appetite, and weight loss  Hyperpigmentation of skin and mucous membranes  Vomiting or diarrhea  Hypokalemia and other electrolyte disturbances  Unexplained cardiovascular collapse Disorders of the Adrenal Gland

40.  Assessment and Management  Maintain ABCs.  Closely monitor cardiac and pulmonary status.  Obtain blood glucose level and treat for hypoglycemia if present.  Establish IV and provide aggressive fluid resuscitation.  Expedite transport.  Assessment and Management  Maintain ABCs.  Closely monitor cardiac and pulmonary status.  Obtain blood glucose level and treat for hypoglycemia if present.  Establish IV and provide aggressive fluid resuscitation.  Expedite transport. Disorders of the Adrenal Gland

41. Summary  Endocrine Disorders and Emergencies