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  • Diabetes Mellitis – inadequate production of insulin which is required to maintain nrmal blood glucose levels. Glucose is the only substance that brain cells can readily and efficiently use for energy source. Anabolism – constructive phase of metabolism, require energy to drive them, ex synthesis of glycogen from glucose. Catabolism – breakdown phase, release energy, ex breakdwn of glucose to CO2, water and ATP Insulin – primary hormone during high levels of glucose, enabling cells to use glucose directly and to store energy as glycogen, protein and fat. Glucagon – primary hormone during low periods of blood glucose stimulating catabolic metabolism to produce energy from bdy stores. Insulin binds to receptors on cells which change its membrane permeability for glucose. Under inadequate insulin levels, the body turns to fat as the primary energy source. In the liver, catabolism of the fatty acids produces acetoacetic acid, acetone. The buildup of these ketones in the blood is called ketosis thus diabetic ketoacidosis.
  • Kidneys – when blood glucose >180 mg/dL, glucose is lost in urine. This can lead to dehydration because of osmotic diuresis leading to polyuria and polydipsia (thirst) In addition, potassium follows resulting in hypokalemia and heart problems
  • Endocrinology

    1. 1. Endocrinology
    2. 2. Sections Anatomy and Physiology Endocrine Disorders and Emergencies
    3. 3. Anatomy & Physiology Endocrine Glands  Have systemic effects.  Act on specific target tissues in specific ways.  May have single or multiple targets. Disorders  Disorders result from over- or underproduction of hormone(s).
    4. 4. Hypothalmus Located deep within the cerebrum.  Some cells relay messages from the autonomic nervous system to the central nervous system.  Other cells respond as gland cells to release hormones.
    5. 5. Posterior Pituitary Diabetes Insipidus Oxytocin and Pregnancy
    6. 6. Anterior Pituitary
    7. 7. Thyroid Gland Hyperthyroidism & Hypothyroidism
    8. 8. Parathyroid Gland
    9. 9. Thymus Gland
    10. 10. Pancreas Combination Organ  Exocrine tissues called acini secrete digestive enzymes into the small intestine.  Endocrine tissues secrete hormones.  Glycogenolysis.  Gluconeogenesis.
    11. 11. Pancreas
    12. 12. Adrenal Gland Adrenal Medulla  Inner segment of adrenal gland.  Closely tied to autonomic nervous system. Adrenal Cortex  Outer layers of endocrine tissue, which secrete steroidal hormones.
    13. 13. Adrenal Gland
    14. 14. Gonads Female  Ovaries Male  Testes
    15. 15. Pineal Gland Located in the roof of the thalamus.  Related to the body’s “biological clock.”  Implicated in Seasonal Affective Disorder.
    16. 16. Other Organs with Endocrine Activity Placenta  Releases hCG throughout gestation Digestive Tract  Gastrin and secretin Heart  ANH Kidneys  Renin
    17. 17. Endocrine Disorders and Emergencies Disorders of the Pancreas Disorders of the Thyroid Gland Disorders of the Adrenal Glands
    18. 18. Disorders of the Pancreas Diabetes Mellitus  Glucose Metabolism  Metabolism • Anabolism & catabolism
    19. 19. 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
    20. 20. 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.
    21. 21. 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.
    22. 22. Diabetic Emergencies
    23. 23. Diabetic Emergencies
    24. 24. Blood Glucose Determination Choose a vein, and prep the site.
    25. 25. Blood Glucose Determination Perform the venipuncture.
    26. 26. Blood Glucose Determination Place a drop of blood on the reagent strip. Activate the timer.
    27. 27. Blood Glucose Determination Wait until the timer sounds.
    28. 28. Blood Glucose Determination Wipe the reagent strip.
    29. 29. Blood Glucose Determination Place the reagent strip in the glucometer.
    30. 30. Blood Glucose Determination Read the blood glucose level.
    31. 31. Blood Glucose Determination Administer 50% dextrose intravenously, if the blood glucose level is less than 80 mg.
    32. 32. Diabetic Emergencies Diabetic Ketoacidosis  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.
    33. 33. 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.
    34. 34. Diabetic Emergencies Hyperglycemic Hyperosmolar Nonketotic (HHNK) Coma  Pathophysiology  Found in Type II diabetics.  Results in blood glucose levels up to 1000mg/dL.  Insulin activity prevents buildup of ketones.  Sustained hyperglycemia results in marked dehydration. • Often related to dialysis, infection, and medications.  Very high mortality rate.
    35. 35. Diabetic Emergencies 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.
    36. 36. 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.
    37. 37. Diabetic Emergencies 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.
    38. 38. Diabetic Emergencies  Management • Maintain airway and support breathing as indicated. • Determine blood glucose level and obtain blood sample. • Establish IV access. • If blood glucose <60mg/dL or is unknown, administer 25– 50g of 50% Dextrose IV. • If IV cannot be established, administer 0.5–1.0mg glucagon intramuscularly. • Monitor cardiac rhythm and vital signs. • Expedite transport.
    39. 39. Disorders of the Thyroid Gland 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.
    40. 40. Disorders of the Thyroid Gland  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.
    41. 41. Disorders of the Thyroid Gland 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.
    42. 42. Disorders of the Thyroid Gland 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.
    43. 43. Disorders of the Thyroid Gland 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
    44. 44. Disorders of the Thyroid Gland Assessment and Management  Focus on maintaining ABCs.  Closely monitor cardiac and pulmonary status.  Establish IV access, but limit fluids.  Expedite transport.
    45. 45. Disorders of the Adrenal Gland 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
    46. 46. Disorders of the Thyroid Gland 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
    47. 47. Disorders of the Adrenal Gland  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.
    48. 48. Disorders of the Adrenal Gland  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
    49. 49. Disorders of the Adrenal Gland 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.
    50. 50. Summary Anatomy & Physiology Endocrine Disorders and Emergencies