The Endocrine System :The Endocrine System EMS Professions Temple College


Endocrine Glands :Endocrine Glands Controls many body functions exerts control by releasing special chemical substances into the blood called hormones Hormones affect other endocrine glands or body systems Ductless glands Secrete hormones directly into bloodstream Hormones are quickly distributed by bloodstream throughout the body


Hormones :Hormones Chemicals produced by endocrine glands Act on target organs elsewhere in body Control/coordinate widespread processes: Homeostasis Reproduction Growth & Development Metabolism Response to stress Overlaps with the Sympathetic Nervous System


Hormones :Hormones Hormones are classified as: Proteins Polypeptides (amino acid derivatives) Lipids (fatty acid derivatives or steroids)


Hormones :Hormones Amount of hormone reaching target tissue directly correlates with concentration of hormone in blood. Constant level hormones Thyroid hormones Variable level hormones Epinephrine (adrenaline) release Cyclic level hormones Reproductive hormones


The Endocrine System :The Endocrine System Consists of several glands located in various parts of the body Specific Glands Hypothalamus Pituitary Thyroid Parathyroid Adrenal Kidneys Pancreatic Islets Ovaries Testes


Pituitary Gland :Pituitary Gland Small gland located on stalk hanging from base of brain - AKA “The Master Gland” Primary function is to control other glands. Produces many hormones. Secretion is controlled by hypothalamus in base of brain.


Pituitary Gland :Pituitary Gland Two areas Anterior Pituitary Posterior Pituitary Structurally, functionally different


Pituitary Gland :Pituitary Gland Anterior Pituitary Thyroid-Stimulating Hormone (TSH) stimulates release of hormones from Thyroid thyroxine (T4) and triiodothyronine (T3): stimulate metabolism of all cells calcitonin: lowers the amount of calcium in the blood by inhibiting breakdown of bone released when stimulated by TSH or cold abnormal conditions hyperthyroidism: too much TSH release hypothyroidism: too little TSH release


Pituitary Gland :Pituitary Gland Anterior Pituitary Growth Hormone (GH) stimulates growth of all organs and increases blood glucose concentration decreases glucose usage increases consumption of fats as an energy source Adreno-Corticotrophic Hormone (ACTH) stimulates the release of adrenal cortex hormones


Pituitary Gland :Pituitary Gland Anterior Pituitary Follicle Stimulating Hormone (FSH) females - stimulates maturation of ova; release of estrogen males - stimulates testes to grow; produce sperm Luteinizing Hormone (LH) females - stimulates ovulation; growth of corpus luteum males - stimulates testes to secrete testosterone


Pituitary Gland :Pituitary Gland Anterior Pituitary Prolactin stimulates breast development during pregnancy; milk production after delivery Melanocyte Stimulating Hormone (MSH) stimulates synthesis, dispersion of melanin pigment in skin


Pituitary Gland :Pituitary Gland Posterior Pituitary Stores, releases two hormones produced in hypothalamus Antidiuretic hormone (ADH) Oxytocin


Pituitary Gland :Pituitary Gland Posterior Pituitary Antidiuretic hormone (ADH) Stimulates water retention by kidneys reabsorb sodium and water Abnormal conditions Undersecretion: diabetes insipidus (“water diabetes”) Oversecretion: Syndrome of Inappropriate Antidiuretic Hormone (SIADH) Oxytocin Stimulates contraction of uterus at end of pregnancy (Pitocin®); release of milk from breast


Hypothalamus :Hypothalamus Produces several releasing and inhibiting factors that stimulate or inhibit anterior pituitary’s secretion of hormones. Produces hormones that are stored in and released from posterior pituitary What are these two hormones?


Hypothalamus :Hypothalamus Also responsible for: Regulation of water balance Esophageal swallowing Body temperature regulation (shivering) Food/water intake (appetite) Sleep-wake cycle Autonomic functions


Pineal Gland :Pineal Gland Located within the Diencephalon Melatonin Inhibits ovarian hormones May regulate the body’s internal clock


Thyroid :Thyroid Located below larynx and low in neck Not over the thyroid cartilage Thyroxine (T4) and Triiodothyronine (T3) Stimulate metabolism of all cells Calcitonin Decreases blood calcium concentration by inhibiting breakdown of bone


Parathyroids :Parathyroids Located on posterior surface of thyroid Frequently damaged during thyroid surgery Parathyroid hormone (PTH) Stimulates Ca2+ release from bone Promotes intestinal absorption and renal tubular reabsorption of calcium


Parathyroids :Parathyroids Underactivity Decrease serum Ca2+ Hypocalcemic tetany Seizures Laryngospasm


Parathyroids :Parathyroids Overactivity Increased serum Ca2+ Pathological fractures Hypertension Renal stones Altered mental status “Bones, stones, hypertones, abdominal moans”


Thymus Gland :Thymus Gland Located in anterior chest Normally absent by ~ age 4 Promotes development of immune-system cells (T-lymphocytes)


Adrenal Glands :Adrenal Glands Small glands located near (ad) the kidneys (renals) Consists of: outer cortex inner medulla


Adrenal Glands :Adrenal Glands Adrenal Medulla the Adrenal Medulla secretes the catecholamine hormones norepinephrine and epinephrine Epinephrine and Norepinephrine Prolong and intensify the sympathetic nervous system response during stress


Adrenal Glands :Adrenal Glands Adrenal Cortex Aldosterone (Mineralocorticoid) Regulates electrolyte (potassium, sodium) and fluid homeostasis Cortisol (Glucocorticoids) Antiinflammatory, anti-immunity, and anti-allergy effects. Increases blood glucose concentrations Androgens (Sex Hormones) Stimulate sexual drive in females


Adrenal Glands :Adrenal Glands Adrenal Cortex Glucocorticoids accounts for 95% of adrenal cortex hormone production  the level of glucose in the blood Released in response to stress, injury, or serious infection - like the hormones from the adrenal medulla


Adrenal Glands :Adrenal Glands Adrenal Cortex Mineralcorticoids work to regulate the concentration of potassium and sodium in the body


Ovaries :Ovaries Located in the abdominal cavity adjacent to the uterus Under the control of LH and FSH from the anterior pituitary Produce eggs for reproduction Produce hormones estrogen progesterone Functions include sexual development and preparation of the uterus for implantation of the egg


Ovaries :Ovaries Estrogen Development of female secondary sexual characteristics Development of endometrium Progesterone Promotes conditions required for pregnancy Stabilization of endometrium


Testes :Testes Located in the scrotum Controlled by anterior pituitary hormones FSH and LH Produce sperm for reproduction Produce testosterone - promotes male growth and masculinization promotes development and maintenance of male sexual characteristics


Pancreas :Pancreas Located in retroperitoneal space between duodenum and spleen Has both endocrine and exocrine functions Exocrine Pancreas Secretes key digestive enzymes Endocrine Pancreas Alpha Cells - glucagon production Beta Cells - insulin production Delta Cells - somatostatin production


Pancreas :Pancreas Exocrine function Secretes amylase lipase


Pancreas :Pancreas Alpha Cells Glucagon Raises blood glucose levels Beta Cells Insulin Lowers blood glucose levels Delta Cells Somatostatin Suppresses release of growth hormone


Disorders of the Endocrine System :Disorders of the Endocrine System


Abnormal Thyroid Function :Abnormal Thyroid Function Hypothyroidism Too little thyroid hormone Hyperthyroidism(Thyrotoxicosis / Thyroid Storm) Too much thyroid hormone


Hypothyroidism :Hypothyroidism Thyroid hormone deficiency causing a decrease in the basal metabolic rate Person is “slowed down” Causes of Hypothyroidism: Radioactive iodine ablation Non-compliance with levothyroxine Hashimoto’s thyroiditis - autoimmune destruction


Hypothyroidism :Hypothyroidism Confusion, drowsiness, coma Cold intolerant Hypotension, Bradycardia Muscle weakness Decreased respirations Weight gain, Constipation Non-pitting peripheral edema Depression Facial edema, loss of hair Dry, coarse skin Appearance of Myxedema


Hypothyroidism :Hypothyroidism Myxedema Coma Severe hypothyroidism that can be fatal Management of Myxedema Coma Control airway Support oxygenation, ventilation IV fluids Later Levothyroxine (Synthroid®) Hydrocortisone


Hyperthyroidism :Hyperthyroidism Excessive levels of thyroid levels cause hypermetabolic state Person is “sped up”. Causes of Hyperthyroidism Overmedication with levothyroxine (Synthroid®) - Fad diets Goiter (enlarged, hyperactive thyroid gland) Graves Disease


Hyperthyroidism :Hyperthyroidism Nervousness, irritable, tremors, paranoid Warm, flushed skin Heat intolerant Tachycardia - High output CHF Hypertension Tachypnea Diarrhea Weight loss Exophthalmos Goiter


Hyperthyroidism :Hyperthyroidism Treatment Airway/Ventilation/Oxygen ECG monitor IV access - Cautious IV fluids Acetaminophen for fever Beta-blockers Consider benzodiazepines for anxiety PTU (propylthiouracil) Usually short-term use prior to more definitive treatment SSKI® (potassium iodide)


Thyroid Storm/Thyrotoxicosis :Thyroid Storm/Thyrotoxicosis Severe form of hyperthyroidism that can be fatal Acute life-threatening hyperthyroidism Cause Increased physiological stress in hyperthyroid patients


Thyroid Storm/Thyrotoxicosis :Thyroid Storm/Thyrotoxicosis Severe tachycardia Heart Failure Dysrhythmias Shock Hyperthermia Abdominal pain Restlessness, Agitation, Delirium, Coma


Thyroid Storm/Thyrotoxicosis :Thyroid Storm/Thyrotoxicosis Management Airway/Ventilation/Oxygen ECG monitor IV access - cautious IV fluids Control hyperthermia Active cooling Acetaminophen Inderal (beta blockers) Consider benzodiazepines for anxiety Potassium iodide (SSKI®) Propylthiouracil (PTU)


Abnormal Adrenal Function :Abnormal Adrenal Function Hyperadrenalism Excess activity of the adrenal gland Cushing’s Syndrome & Disease Pheochromocytoma Hypoadrenalism (adrenal insufficiency) Inadequate activity of the adrenal gland Addison’s disease


Hyperadrenalism :Hyperadrenalism Primary Aldosteronism Excessive secretion of aldosterone by adrenal cortex Increased Na+/H2O Presentation headache nocturia, polyuria fatigue hypertension, hypervolemia potassium depletion


Hyperadrenalism :Hyperadrenalism Adrenogenital syndrome “Bearded Lady” Group of disorders caused by adrenocortical hyperplasia or malignant tumors Excessive secretion of adrenocortical steroids especially those with androgenic or estrogenic effects Characterized by masculinization of women feminization of men premature sexual development of children


Hyperadrenalism :Hyperadrenalism Cushing’s Syndrome Results from increased adrenocortical secretion of cortisol Causes include: ACTH-secreting tumor of the pituitary (Cushing’s disease) excess secretion of ACTH by a neoplasm within the adrenal cortex excess secretion of ACTH by a malignant growth outside the adrenal gland excessive or prolonged administration of steroids


Hyperadrenalism :Hyperadrenalism Cushing’s Syndrome Characterized by: truncal obesity moon face buffalo hump acne, hirsutism abdominal striae hypertension psychiatric disturbances osteoporosis amenorrhea


Hyperadrenalism :Hyperadrenalism Cushing’s Disease Too much adrenal hormone production adrenal hyperplasia caused by an ACTH secreting adenoma of the pituitary “Cushingoid features” striae on extremities or abdomen moon face buffalo hump weight gain with truncal obesity personality changes, irritable


Hyperadrenalism :Hyperadrenalism Cushing’s Syndrome Management Airway/Ventilation/Oxygen Supportive care Assess for cardiovascular event requiring treatment severe hypertension myocardial ischemia


Hyperadrenalism :Hyperadrenalism Pheochromocytoma Catecholamine secreting tumor of adrenal medulla Presentation Anxiety Pallor, diaphoresis Hypertension Tachycardia, Palpitations Dyspnea Hyperglycemia


Hyperadrenalism :Hyperadrenalism Pheochromocytoma Management Supportive care based upon presentation Airway/Ventilation/Oxygen Calm/Reassure Assess blood glucose Consider beta blocking agent - Labetalol Consider benzodiazepines


Hypoadrenalism :Hypoadrenalism Adrenal Insufficiency decrease production of glucocorticoids, mineralcorticoids and androgens Causes Primary adrenal failure (Addison’s Disease) Infection (TB, fungal, Meningococcal) AIDS Prolonged steroid use


Hypoadrenalism :Hypoadrenalism Presentation Hypotension, Shock Hyponatremia, Hyperkalemia Progressive Muscle weakness Progressive weight loss and anorexia Skin hyperpigmentation areas exposed to sun, pressure points, joints and creases Arrhythmias Hypoglycemia N/V/D


Hypoadrenalism :Hypoadrenalism Management Airway/Ventilation/Oxygen ECG monitor IV fluids Assess blood glucose - D50 if hypoglycemic Steroids hydrocortisone or dexamethasone florinef (mineralcorticoid) Vasopressors if unresponsive to IV fluids


Diabetes Mellitus :Diabetes Mellitus


Diabetes Mellitus :Diabetes Mellitus Chronic metabolic disease One of the most common diseases in North America Affects 5% of USA population (12 million people) Results in  insulin secretion by the Beta () cells of the islets of Langerhans in the pancreas, AND/OR Defects in insulin receptors on cell membranes leading to cellular resistance to insulin Leads to an  risk for significant cardiovascular, renal and ophthalmic disease


Regulation of Glucose :Regulation of Glucose Dietary Intake Components of food: Carbohydrates Fats Proteins Vitamins Minerals


Regulation of Glucose :Regulation of Glucose The other 3 major food sources for glucose are carbohydrates proteins fats Most sugars in the human diet are complex and must be broken down into simple sugars: glucose, galactose and fructose - before use


Regulation of Glucose :Regulation of Glucose Carbohydrates Found in sugary, starchy foods Ready source of near-instant energy If not “burned” immediately by body, stored in liver and skeletal muscle as glycogen (short-term energy) or as fat (long-term energy needs) After normal meal, approximately 60% of the glucose is stored in liver as glycogen


Regulation of Glucose :Regulation of Glucose Fats Broken down into fatty acids and glycerol by enzymes Excess fat stored in liver or in fat cells (under the skin)


Regulation of Glucose :Regulation of Glucose Pancreatic hormones are required to regulate blood glucose level glucagon released by Alpha () cells insulin released by Beta Cells () somatostatin released by Delta Cells ()


Regulation of Glucose :Regulation of Glucose Alpha () cells release glucagon to control blood glucose level When blood glucose levels fall,  cells  the amount of glucagon in the blood The surge of glucagon stimulates liver to release glucose stores by the breakdown of glycogen into glucose (glycogenolysis) Also, glucagon stimulates the liver to produce glucose (gluconeogenesis)


Regulation of Glucose :Regulation of Glucose Beta Cells () release insulin (antagonistic to glucagon) to control blood glucose level Insulin  the rate at which various body cells take up glucose  insulin lowers the blood glucose level Promotes glycogenesis - storage of glycogen in the liver Insulin is rapidly broken down by the liver and must be secreted constantly


Regulation of Glucose :Regulation of Glucose Delta Cells () produce somatostatin, which inhibits both glucagon and insulin inhibits insulin and glucagon secretion by the pancreas inhibits digestion by inhibiting secretion of digestive enzymes inhibits gastric motility inhibits absorption of glucose in the intestine


Regulation of Glucose :Regulation of Glucose Breakdown of sugars carried out by enzymes in the GI system As simple sugars, they are absorbed from the GI system into the body To be converted into energy, glucose must first be transmitted through the cell membrane Glucose molecule is too large and does not readily diffuse


Regulation of Glucose :Regulation of Glucose Glucose must pass into the cell by binding to a special carrier protein on the cell’s surface. Facilitated diffusion - carrier protein binds with the glucose and carries it into the cell. The rate at which glucose can enter the cell is dependent upon insulin levels Insulin serves as the messenger - travels via blood to target tissues Combines with specific insulin receptors on the surface of the cell membrane


Regulation of Glucose :Regulation of Glucose Body strives to maintain blood glucose between 60 mg/dl and 120 mg/dl. Glucose brain is the biggest user of glucose in the body sole energy source for brain brain does not require insulin to utilize glucose


Regulation of Glucose :Regulation of Glucose Insulin Glucagon Glucagon and Insulin are opposites (antagonists) of each other.


Regulation of Glucose :Regulation of Glucose Glucagon Released in response to: Sympathetic stimulation Decreasing blood glucose concentration Acts primarily on liver to increase rate of glycogen breakdown Increasing blood glucose levels have inhibitory effect on glucagon secretion


Regulation of Glucose :Regulation of Glucose Insulin Released in response to: Increasing blood glucose concentration Parasympathetic innervation Acts on cell membranes to increase glucose uptake from blood stream Promotes facilitated diffusion of glucose into cells


Diabetes Mellitus :Diabetes Mellitus 2 Types historically based on age of onset (NOT insulin vs. non-insulin) Type I juvenile onset insulin dependent Type II historically adult onset now some morbidly obese children are developing Type II diabetes non-insulin dependent may progress to insulin dependency


Types of Diabetes Mellitus :Types of Diabetes Mellitus Type I Type II Secondary Gestational


Pathophysiology of Type I Diabetes Mellitus :Pathophysiology of Type I Diabetes Mellitus Characterized by inadequate or absent production of insulin by pancreas Usually presents by age 25 Strong genetic component Autoimmune features body destroys own insulin-producing cells in pancreas may follow severe viral illness or injury Requires lifelong treatment with insulin replacement


Pathophysiology of Type II Diabetes Mellitus :Pathophysiology of Type II Diabetes Mellitus Pancreas continues to produce some insulin however disease results from combination of: Relative insulin deficiency Decreased sensitivity of insulin receptors Onset usually after age 25 in overweight adults Some morbidly obese children develop Type II diabetes Familial component Usually controlled with diet, weight loss, oral hypoglycemic agents Insulin may be needed at some point in life


Secondary Diabetes Mellitus :Secondary Diabetes Mellitus Pre-existing condition affects pancreas Pancreatitis Trauma


Gestational Diabetes Mellitus :Gestational Diabetes Mellitus Occurs during pregnancy Usually resolves after delivery Occurs rarely in non-pregnant women on BCPs Increased estrogen, progesterone antagonize insulin


Presentation of New Onset Diabetes Mellitus :Presentation of New Onset Diabetes Mellitus 3 Ps Polyuria Polydipsia Polyphagia Blurred vision, dizziness, altered mental status Rapid weight loss Warm dry skin, Weakness, Tachycardia, Dehydration


Long Term Treatment of Diabetes Mellitus :Long Term Treatment of Diabetes Mellitus Diet regulation e.g. 1400 calorie ADA diet Exercise increase patient’s glucose metabolism Oral hypoglycemic agents Sulfonylureas Insulin Historically produced from pigs (porcine insulin) Currently genetic engineering has lead to human insulin (Humulin)


Long Term Treatment ofDiabetes Mellitus :Long Term Treatment ofDiabetes Mellitus Insulin Available in various forms distinguished on onset and duration of action Onset rapid (Regular, Semilente, Novolin 70/30) intermediate (Novolin N, Lente) slow (Ultralente) Duration short, 5-7 hrs (Regular) intermediate, 18-24 hrs (Semilente, Novolin N, Lente, NPH) long-acting, 24 - 36+ hrs (Novolin 70/30, Ultralente)


Long Term Treatment ofDiabetes Mellitus :Long Term Treatment ofDiabetes Mellitus Insulin Must be given by injection as insulin is protein which would be digested if given orally extremely compliant patients may use an insulin pump which provides a continuous dose current research studying inhaled insulin form


Long Term Treatment of Diabetes Mellitus :Long Term Treatment of Diabetes Mellitus Oral Hypoglycemic Agents Stimulate the release of insulin from the pancreas, thus patient must still have intact beta cells in the pancreas. Common agents include: Glucotrol® (glipizide) Micronase® or Diabeta® (glyburide) Glucophage® (metformin) [Not a sulfonylurea]


Emergencies Associated Blood Glucose Level :Emergencies Associated Blood Glucose Level Hyperglycemia Diabetic Ketoacidosis (DKA) Hyperglycemic Hyperosmolar Nonketotic Coma (HHNC) Hypoglycemia “Insulin Shock”


Hyperglycemia :Hyperglycemia Defined as blood glucose > 200 mg/dl Causes Failure to take medication (insulin) Increased dietary intake Stress (surgery, MI, CVA, trauma) Fever Infection Pregnancy (gestational diabetes)


Hyperglycemia :Hyperglycemia Two hyperglycemic diabetic states may occur Diabetic Ketoacidosis (DKA) Hyperglycemic Hyperosmolar Non-ketotic Coma (HHNC)


Diabetic Ketoacidosis (DKA) :Diabetic Ketoacidosis (DKA) Occurs in Type I diabetics (insulin dependency) Usually associated with blood glucose level in the range of 200 - 600 mg/dl No insulin availability results in ketoacidosis


Diabetic Ketoacidosis (DKA) :Diabetic Ketoacidosis (DKA) Pathophysiology Results from absence of insulin prevents glucose from entering the cells leads to glucose accumulation in the blood Cells become starved for glucose and begin to use other energy sources (primarily fats) Fat metabolism generates fatty acids Further metabolized into ketoacids (ketone bodies)


Diabetic Ketoacidosis (DKA) :Diabetic Ketoacidosis (DKA) Pathophysiology (cont) Blood sugar rises above renal threshold for reabsorption (blood glucose > 180 mg/dl) glucose “spills” into the urine Loss of glucose in urine causes osmotic diuresis Results in dehydration acidosis electrolyte imbalances (especially K+)


Diabetic Ketoacidosis (DKA) :Diabetic Ketoacidosis (DKA) Presentation Gradual onset with progression Warm, pink, dry skin Dry mucous membranes (dehydrated) Tachycardia, weak peripheral pulses Weight loss Polyuria, polydipsia Abdominal pain with nausea/vomiting Altered mental status Kussmaul respirations with acetone (fruity) odor


Diabetic Ketoacidosis :Diabetic Ketoacidosis Increased Blood Sugar Osmotic Diuresis Polyuria Cells Can’t Burn Glucose Cells Burn Fat Polyphagia Ketone Bodies Metabolic Acidosis Fruity Breath Kussmaul Breathing Inadequate insulin


Management of DKA :Management of DKA Airway/Ventilation/Oxygen NRB mask Assess blood glucose level & ECG IV access, large bore NS normal saline bolus and reassess often requires several liters Assess for underlying cause of DKA Transport How does fluid treat DKA?


Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC) :Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC) Usually occurs in type II diabetics Typically very high blood sugar (>600mg/dl) Some insulin available Higher mortality than DKA


Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC) :Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC) Pathophysiology Some minimal insulin production enough insulin available to allow glucose to enter the cells and prevent ketogenesis not enough to decrease gluconeogenesis by liver no ketosis Extreme hyperglycemia produces hyperosmolar state causing diuresis severe dehydration electrolyte disturbances


Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC) :Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC) Increased Blood Sugar Osmotic Diuresis Polyuria Inadequate insulin


Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC) :Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC) Presentation Same as DKA but with greater severity Higher blood glucose level Non-insulin dependent diabetes Greater degree of dehydration


Management of HHNC :Management of HHNC Secure airway and assess ventilation Consider need to assist ventilation Consider need to intubate High concentration oxygen Assess blood glucose level & ECG IV access, large bore NS normal saline bolus and reassess often requires several liters Assess for underlying cause of HHNC Transport


Further Management of Hyperglycemia :Further Management of Hyperglycemia Insulin (regular) Correct hyperglycemia Correction of acid/base imbalances Bicarbonate (severe cases documented by ABG) Normalization of electrolyte balance DKA may result in hyperkalemia 2o to acidosis H+ shifts intracellularly, K+ moves to extracellular space Urinary K+ losses may lead to hypokalemia once therapy is started


Hypoglycemia :Hypoglycemia True hypoglycemia defined as blood sugar < 60 mg/dl ALL hypoglycemia is NOT caused by diabetes Can occur in non-diabetic patients thin young females alcoholics with liver disease alcohol consumption on empty stomach will block glucose synthesis in liver (gluconeogenesis) Hypoglycemia causes impaired functioning of brain which relies on constant supply of glucose


Hypoglycemia :Hypoglycemia Causes of hypoglycemia in diabetics Too much insulin Too much oral hypoglycemic agent Long half-life requires hospitalization Decreased dietary intake (took insulin and missed meal) Vigorous physical activity Pathophysiology Inadequate blood glucose available to brain and other cells resulting from one of the above causes


Hypoglycemia :Hypoglycemia Presentation Hunger (initially), Headache Weakness, Incoordination (mimics a stroke) Confusion, Unusual behavior may appear intoxicated Seizures Coma Weak, rapid pulse Cold, clammy skin Nervousness, trembling, irritability


Hypoglycemia: Pathophysiology :Hypoglycemia: Pathophysiology Blood Glucose Falls Brain Lacks Glucose SNS Response Altered LOC Seizures Headache Dizziness Bizarre Behavior Weakness Anxiety Pallor Tachycardia Diaphoresis Nausea Dilated Pupils


Hypoglycemia :Hypoglycemia Beta Blockers may mask symptoms by inhibiting sympathetic response


Management of Hypoglycemia :Management of Hypoglycemia Secure airway manually suction prn Ventilate prn High concentration oxygen Vascular access Large bore IV catheter Saline lock, D5W or NS Large proximal vein preferred Assess blood glucose level


Management of Hypoglycemia :Management of Hypoglycemia Oral glucose ONLY if intact gag reflex, awake & able to sit up 15gm-30gm of packaged glucose, or May use sugar-containing drink or food Oral route often slower Intravenous glucose Adult: Dextrose 50% (D50) 25gms IV in patent, free-flowing vein, may repeat Children: Dextrose 25% (D25) @ 2 - 4 cc/kg (0.5 - 1 gm/kg) [Infants - may choose Dextrose 10% @ 0.5 - 1 gm/kg or 5 - 10 cc/kg]


Management of Hypoglycemia :Management of Hypoglycemia Glucagon Used if unable to obtain IV access 1 mg IM Requires glycogen stores slower onset of action than IV route What persons are likely to have inadequate glycogen stores?


Management of Hypoglycemia :Management of Hypoglycemia Have patient eat high-carbohydrate meal Transport? Patient Refusal Policy Contact medical control Leave only with responsible family/friend for 6 hours Must educate family/friend to hypoglycemic signs/symptoms Advise to contact personal physician Transport Hypoglycemic patients on oral agents (long half life) Unknown, atypical or untreated cause of hypoglycemia


Long-term Complications of Diabetes Mellitus :Long-term Complications of Diabetes Mellitus Blindness Retinal hemorrhages Renal Disease Peripheral Neuropathy Numbness in “stocking glove” distribution (hands and feet) Heart Disease and Stroke Chronic state of Hyperglycemia leads to early atherosclerosis Complications in Pregnancy


Long-term Complications of Diabetes Mellitus :Long-term Complications of Diabetes Mellitus Diffuse Atherosclerois AMI CVA PVD Hypertension Renal failure Diabetic retinopathy/blindness Gangrene


Long-term Complications of Diabetes Mellitus :10% of all diabetics develop renal disease usually resulting in dialysis Diabetics are up to 4 times more likely to have heart disease and up to 6 times more likely to have a stroke than a non-diabetic Long-term Complications of Diabetes Mellitus


Long-term Complications of Diabetes Mellitus :Long-term Complications of Diabetes Mellitus Peripheral Neuropathy Silent MI Vague, poorly-defined symptom complex Weakness Dizziness Malaise Confusion Suspect MI in any diabetic with MI signs/symptoms with or without CP


Diabetes in Pregnancy :Diabetes in Pregnancy Early pregnancy (<24 weeks) Rapid embryo growth Decrease in maternal blood glucose Episodes of hypoglycemia


Diabetes in Pregnancy :Diabetes in Pregnancy Late pregnancy (>24 weeks) Increased resistance to insulin effects Increased blood glucose Ketoacidosis


Diabetes in Pregnancy :Diabetes in Pregnancy Increased maternal risk for: Pregnancy-induced hypertension Infections Vaginal Urinary tract


Diabetes in Pregnancy :Diabetes in Pregnancy Increased fetal risk for: High birth weight Hypoglycemia Liver dysfunction-hyperbilirubinemia Hypocalcemia


Assessment of the Diabetic Patient :Assessment of the Diabetic Patient Maintain high-degree of suspicion Assess blood glucose level in all patients with seizure, neurologic S/S, altered mental status vague history or chief complaint Blood glucose assessment IS NOT necessary in all patients with diabetes mellitus!!


Assessment of the Diabetic Patient :Assessment of the Diabetic Patient History and Physical Exam includes Look for insulin syringes, medical alert tag, glucometer, or insulin (usually kept in refrigerator) Last meal and last insulin dose Missed med or missed meal? Signs of infection Foot cellulitis / ulcers Recent illness or physiologic stressors


Blood Glucose Assessment :Blood Glucose Assessment Capillary vs. venous blood sample Depends on glucometer model Usually capillary preferred Dextrostick vs Glucometer Dextrostick - colorimetric assessment of blood provides glucose estimate Glucometer - quantitative glucose measurement Neonatal blood Many glucometers are not accurate for neonates


Case Study #1 :Case Study #1 You are dispatched to a college residence hall to see a 20-year-old female complaining of fever and a fluttering in her chest. You find her awake but she appears very anxious. Airway - Open without assistance Breathing - Slightly increased ventilatory rate; No obvious abnormal sounds of breathing Circulation - Rapid, strong, regular radial pulse; Skin warm and pink


Case Study #1 :Case Study #1 You direct your partner to assess vital signs while you place the patient on Oxygen 15 lpm by NRB mask. Your physical exam findings are: trembling, nervous warm, flushed skin clear and equal lung sounds Your partner relays the following vital signs to you: Pulse - 120, regular, strong BP - 144/88 Ventilatory rate - 20, regular with adequate TV Glucose - 110 mg/dl ECG - Sinus tachycardia with occasional PACs What additional information regarding her history would you like to know?


Case Study #1 :Case Study #1 The patient states this has occurred before but never lasted this long. She has not been ill lately other than some recurrent diarrhea and weight loss. She has attributed these to worrying about finals. She has no significant medical history and takes no meds. She denies use of any drugs. She has no family history of pulmonary disease, diabetes or heart disease. Her mother, however, does have a problem with something in her neck for which she takes medication. What are the two most probable diagnosis for this patient?


Case Study #2 :Case Study #2 You are dispatched to a residence to see a 44-year-old man who has fainted. You arrive to find him semi-reclined in bed. He is awake and very wide-eyed but appears very tired. Airway - Maintained without assistance Breathing - No obvious distress; No obvious, unusual sounds Circulation - Rapid, weak, irregular radial pulse


Case Study #2 :Case Study #2 Your partner assesses vital signs while you obtain the following history: Hx of Present Illness: For the past month, he has felt very weak and dizzy; He has not felt like eating and has been losing weight. He has also experienced N/V/D on a few days this month. Past Medical Hx: Has been fairly healthy all of his life; Three months ago he became ill with bacterial meningitis for which he was successfully treated.


Case Study #2 :Case Study #2 Vital signs are: Pulse: 110-126, irregular BP: 92/62 Ventilatory rate: 20, regular Skin: cool, clammy ECG: Atrial fibrillation Blood glucose: 74 mg/dl What should you include in your differential diagnosis?


Case Study #2 :Case Study #2 Your partner is a brand new, naïve paramedic. He comments to the patient, “That is a great tan you have. Have you been on a tropical vacation lately?” Now, what do you believe is the most likely diagnosis for this patient? What is your treatment plan for this patient?


Case Study #3 :Case Study #3 Your last call (you hope) of the shift is to a manufacturing plant for a possible drug overdose. Your patient is a 24-year-old female. The patient’s supervisor states the woman seems very jittery and “out of it”. You find the patient to be a very thin female who is acting unusual. Airway - Maintained without assistance Breathing - No distress or unusual sounds Circulation - Rapid, strong, regular radial pulse with clammy skin Disability - Confused and answers questions slowly


Case Study #3 :Case Study #3 Your partner quickly assesses the patient’s vital signs and relays the following: Pulse - 110, regular, strong BP - 108/76 Ventilatory rate - 16 with clear and equal lung sounds Skin - pale, cool, clammy Pupils - dilated, equal and reactive to light ECG - Sinus tachycardia without ectopy History No significant medical history; No recent illness; No meds What would you like to include in your differential diagnosis for this patient?


Case Study #3 :Case Study #3 A coworker now tells you that the patient is going through a difficult divorce and has not been eating well lately Your partner now tells you the patient’s blood glucose is 40 mg/dl Would this patient be a good candidate for Glucagon therapy if an IV can not be established quickly? What is your specific diagnosis now?