The endocrine system consists of glands that secrete hormones directly into the bloodstream to regulate distant target organs and tissues. The pituitary gland is called the "master gland" as it controls other endocrine glands by producing hormones that stimulate or inhibit their secretions. Disorders of the endocrine system can result from too little or too much hormone production and can have wide-ranging effects on the body if left untreated.

1. The Endocrine SystemSURG LT CDR ASHVINI JAKHAR

2. Endocrine GlandsControls many body functionsexerts control by releasing special chemical substances into the blood called hormonesHormones affect other endocrine glands or body systemsDuctless glandsSecrete hormones directly into bloodstreamHormones are quickly distributed by bloodstream throughout the body

3. HormonesChemicals produced by endocrine glandsAct on target organs elsewhere in bodyControl/coordinate widespread processes:HomeostasisReproductionGrowth & DevelopmentMetabolismResponse to stressOverlaps with the Sympathetic Nervous System

4. HormonesHormones are classified as:ProteinsPolypeptides (amino acid derivatives)Lipids (fatty acid derivatives or steroids)

5. HormonesAmount of hormone reaching target tissue directly correlates with concentration of hormone in blood.Constant level hormonesThyroid hormonesVariable level hormonesEpinephrine (adrenaline) releaseCyclic level hormonesReproductive hormones

6. The Endocrine SystemConsists of several glands located in various parts of the bodySpecific GlandsHypothalamusPituitaryThyroidParathyroidAdrenalKidneysPancreatic IsletsOvariesTestes

7. Pituitary GlandSmall 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.

8. Pituitary GlandTwo areasAnterior PituitaryPosterior PituitaryStructurally, functionally different

9. Pituitary GlandAnterior PituitaryThyroid-Stimulating Hormone (TSH)stimulates release of hormones from Thyroidthyroxine (T4) and triiodothyronine (T3): stimulate metabolism of all cellscalcitonin: lowers the amount of calcium in the blood by inhibiting breakdown of bonereleased when stimulated by TSH or coldabnormal conditionshyperthyroidism: too much TSH releasehypothyroidism: too little TSH release

10. Pituitary GlandAnterior PituitaryGrowth Hormone (GH)stimulates growth of all organs and increases blood glucose concentrationdecreases glucose usageincreases consumption of fats as an energy sourceAdreno-Corticotrophic Hormone (ACTH)stimulates the release of adrenal cortex hormones

11. Pituitary GlandAnterior PituitaryFollicle Stimulating Hormone (FSH)females - stimulates maturation of ova; release of estrogenmales - stimulates testes to grow; produce spermLuteinizing Hormone (LH)females - stimulates ovulation; growth of corpus luteummales - stimulates testes to secrete testosterone

12. Pituitary GlandAnterior PituitaryProlactinstimulates breast development during pregnancy; milk production after deliveryMelanocyte Stimulating Hormone (MSH)stimulates synthesis, dispersion of melanin pigment in skin

13. Pituitary GlandPosterior PituitaryStores, releases two hormones produced in hypothalamusAntidiuretic hormone (ADH)Oxytocin

14. Pituitary GlandPosterior PituitaryAntidiuretic hormone (ADH)Stimulates water retention by kidneysreabsorb sodium and waterAbnormal conditionsUndersecretion: diabetes insipidus (“water diabetes”)Oversecretion: Syndrome of Inappropriate Antidiuretic Hormone (SIADH)OxytocinStimulates contraction of uterus at end of pregnancy (Pitocin®); release of milk from breast

15. HypothalamusProduces 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 pituitaryWhat are these two hormones?

16. HypothalamusAlso responsible for:Regulation of water balanceEsophageal swallowingBody temperature regulation (shivering)Food/water intake (appetite)Sleep-wake cycleAutonomic functions

17. Pineal GlandLocated within the DiencephalonMelatoninInhibits ovarian hormonesMay regulate the body’s internal clock

18. ThyroidLocated below larynx and low in neckNot over the thyroid cartilageThyroxine (T4) and Triiodothyronine (T3)Stimulate metabolism of all cellsCalcitoninDecreases blood calcium concentration by inhibiting breakdown of bone

19. ParathyroidsLocated on posterior surface of thyroidFrequently damaged during thyroid surgeryParathyroid hormone (PTH)Stimulates Ca2+ release from bonePromotes intestinal absorption and renal tubular reabsorption of calcium

20. ParathyroidsUnderactivityDecrease serum Ca2+Hypocalcemic tetanySeizures Laryngospasm

21. ParathyroidsOveractivityIncreased serum Ca2+Pathological fracturesHypertensionRenal stonesAltered mental status“Bones, stones, hypertones, abdominal moans”

22. Thymus GlandLocated in anterior chest Normally absent by ~ age 4Promotes development of immune-system cells (T-lymphocytes)

23. Adrenal GlandsSmall glands located near (ad) the kidneys (renals) Consists of:outer cortexinner medulla

24. Adrenal GlandsAdrenal Medullathe Adrenal Medulla secretes the catecholamine hormones norepinephrine and epinephrineEpinephrine and NorepinephrineProlong and intensify the sympathetic nervous system response during stress

25. Adrenal GlandsAdrenal CortexAldosterone (Mineralocorticoid)Regulates electrolyte (potassium, sodium) and fluid homeostasisCortisol (Glucocorticoids)Antiinflammatory, anti-immunity, and anti-allergy effects.Increases blood glucose concentrationsAndrogens (Sex Hormones)Stimulate sexual drive in females

26. Adrenal GlandsAdrenal CortexGlucocorticoidsaccounts for 95% of adrenal cortex hormone production the level of glucose in the bloodReleased in response to stress, injury, or serious infection - like the hormones from the adrenal medulla

27. Adrenal GlandsAdrenal CortexMineralcorticoidswork to regulate the concentration of potassium and sodium in the body

28. OvariesLocated in the abdominal cavity adjacent to the uterusUnder the control of LH and FSH from the anterior pituitaryProduce eggs for reproductionProduce hormonesestrogenprogesteroneFunctions include sexual development and preparation of the uterus for implantation of the egg

29. OvariesEstrogenDevelopment of female secondary sexual characteristicsDevelopment of endometriumProgesteronePromotes conditions required for pregnancyStabilization of endometrium

30. TestesLocated in the scrotumControlled by anterior pituitary hormones FSH and LHProduce sperm for reproductionProduce testosterone -promotes male growth and masculinizationpromotes development and maintenance of male sexual characteristics

31. PancreasLocated in retroperitoneal space between duodenum and spleenHas both endocrine and exocrine functionsExocrine PancreasSecretes key digestive enzymesEndocrine PancreasAlpha Cells - glucagon productionBeta Cells - insulin productionDelta Cells - somatostatin production

32. PancreasExocrine functionSecretesamylaselipase

33. PancreasAlpha Cells

34. Glucagon

35. Raises blood glucose levels

36. Beta Cells

37. Insulin

38. Lowers blood glucose levels

39. Delta Cells

40. Somatostatin

41. Suppresses release of growth hormoneDisorders of the Endocrine System

42. Abnormal Thyroid FunctionHypothyroidismToo little thyroid hormoneHyperthyroidism(Thyrotoxicosis / Thyroid Storm)Too much thyroid hormone

43. HypothyroidismThyroid hormone deficiency causing a decrease in the basal metabolic ratePerson is “slowed down”Causes of Hypothyroidism:Radioactive iodine ablationNon-compliance with levothyroxineHashimoto’s thyroiditis - autoimmune destruction

44. HypothyroidismConfusion, drowsiness, comaCold intolerantHypotension, BradycardiaMuscle weaknessDecreased respirationsWeight gain, ConstipationNon-pitting peripheral edemaDepressionFacial edema, loss of hairDry, coarse skinAppearance of Myxedema

45. HypothyroidismMyxedema Coma

46. Severe hypothyroidism that can be fatal

47. Management of Myxedema Coma

48. Control airway

49. Support oxygenation, ventilation

50. IV fluids

51. Later

52. Levothyroxine (Synthroid®)

53. HydrocortisoneHyperthyroidismExcessive levels of thyroid levels cause hypermetabolic statePerson is “sped up”.Causes of HyperthyroidismOvermedication with levothyroxine (Synthroid®) - Fad dietsGoiter (enlarged, hyperactive thyroid gland)Graves Disease

54. HyperthyroidismNervousness, irritable, tremors, paranoid

55. Warm, flushed skin

56. Heat intolerant

57. Tachycardia - High output CHF

58. Hypertension

59. Tachypnea

60. Diarrhea

61. Weight loss

62. Exophthalmos

63. GoiterHyperthyroidismTreatmentAirway/Ventilation/OxygenECG monitorIV access - Cautious IV fluidsAcetaminophen for feverBeta-blockersConsider benzodiazepines for anxietyPTU (propylthiouracil)Usually short-term use prior to more definitive treatmentSSKI® (potassium iodide)

64. Thyroid Storm/ThyrotoxicosisSevere form of hyperthyroidism that can be fatalAcute life-threatening hyperthyroidismCauseIncreased physiological stress in hyperthyroid patients

65. Thyroid Storm/ThyrotoxicosisSevere tachycardiaHeart FailureDysrhythmiasShockHyperthermiaAbdominal painRestlessness, Agitation, Delirium, Coma

66. Thyroid Storm/ThyrotoxicosisManagement

67. Airway/Ventilation/Oxygen

68. ECG monitor

69. IV access - cautious IV fluids

70. Control hyperthermia

71. Active cooling

72. Acetaminophen

73. Inderal (beta blockers)

74. Consider benzodiazepines for anxiety

75. Potassium iodide (SSKI®)

76. Propylthiouracil (PTU)Abnormal Adrenal Function HyperadrenalismExcess activity of the adrenal glandCushing’s Syndrome & DiseasePheochromocytomaHypoadrenalism (adrenal insufficiency)Inadequate activity of the adrenal glandAddison’s disease

77. HyperadrenalismPrimary Aldosteronism Excessive secretion of aldosterone by adrenal cortexIncreased Na+/H2OPresentationheadachenocturia, polyuriafatiguehypertension, hypervolemiapotassium depletion

78. HyperadrenalismAdrenogenital syndrome“Bearded Lady”Group of disorders caused by adrenocortical hyperplasia or malignant tumorsExcessive secretion of adrenocortical steroids especially those with androgenic or estrogenic effectsCharacterized bymasculinization of womenfeminization of menpremature sexual development of children

79. HyperadrenalismCushing’s SyndromeResults from increased adrenocortical secretion of cortisolCauses include:ACTH-secreting tumor of the pituitary (Cushing’s disease)excess secretion of ACTH by a neoplasm within the adrenal cortexexcess secretion of ACTH by a malignant growth outside the adrenal glandexcessive or prolonged administration of steroids

80. HyperadrenalismCushing’s SyndromeCharacterized by:truncal obesitymoon facebuffalo humpacne, hirsutismabdominal striaehypertensionpsychiatric disturbancesosteoporosisamenorrhea

81. HyperadrenalismCushing’s DiseaseToo much adrenal hormone productionadrenal hyperplasia caused by an ACTH secreting adenoma of the pituitary“Cushingoid features”striae on extremities or abdomenmoon facebuffalo humpweight gain with truncal obesitypersonality changes, irritable

82. HyperadrenalismCushing’s SyndromeManagementAirway/Ventilation/OxygenSupportive careAssess for cardiovascular event requiring treatmentsevere hypertensionmyocardial ischemia

83. HyperadrenalismPheochromocytomaCatecholamine secreting tumor of adrenal medullaPresentationAnxietyPallor, diaphoresisHypertensionTachycardia, PalpitationsDyspneaHyperglycemia

84. HyperadrenalismPheochromocytomaManagementSupportive care based upon presentationAirway/Ventilation/OxygenCalm/ReassureAssess blood glucose Consider beta blocking agent - LabetalolConsider benzodiazepines

85. HypoadrenalismAdrenal Insufficiencydecrease production of glucocorticoids, mineralcorticoids and androgensCausesPrimary adrenal failure (Addison’s Disease)Infection (TB, fungal, Meningococcal)AIDSProlonged steroid use

86. HypoadrenalismPresentationHypotension, ShockHyponatremia, HyperkalemiaProgressive Muscle weaknessProgressive weight loss and anorexiaSkin hyperpigmentationareas exposed to sun, pressure points, joints and creasesArrhythmiasHypoglycemiaN/V/D

87. HypoadrenalismManagementAirway/Ventilation/OxygenECG monitorIV fluidsAssess blood glucose - D50 if hypoglycemicSteroids hydrocortisone or dexamethasoneflorinef (mineralcorticoid)Vasopressors if unresponsive to IV fluids

88. Diabetes Mellitus

89. Diabetes MellitusChronic metabolic diseaseOne of the most common diseases in North AmericaAffects 5% of USA population (12 million people)Results in insulin secretion by the Beta () cells of the islets of Langerhans in the pancreas, AND/ORDefects in insulin receptors on cell membranes leading to cellular resistance to insulinLeads to an  risk for significant cardiovascular, renal and ophthalmic disease

90. Regulation of GlucoseDietary IntakeComponents of food:CarbohydratesFatsProteinsVitaminsMinerals

91. Regulation of GlucoseThe other 3 major food sources for glucose arecarbohydratesproteinsfatsMost sugars in the human diet are complex and must be broken down into simple sugars: glucose, galactose and fructose - before use

92. Regulation of Glucose CarbohydratesFound in sugary, starchy foodsReady source of near-instant energyIf 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

93. Regulation of GlucoseFatsBroken down into fatty acids and glycerol by enzymesExcess fat stored in liver or in fat cells (under the skin)

94. Regulation of GlucosePancreatic hormones are required to regulate blood glucose levelglucagon released by Alpha () cellsinsulin released by Beta Cells ()somatostatin released by Delta Cells ()

95. Regulation of GlucoseAlpha () cells release glucagon to control blood glucose levelWhen blood glucose levels fall,  cells  the amount of glucagon in the bloodThe 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)

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

97. Regulation of GlucoseDelta Cells () produce somatostatin, which inhibits both glucagon and insulininhibits insulin and glucagon secretion by the pancreasinhibits digestion by inhibiting secretion of digestive enzymesinhibits gastric motilityinhibits absorption of glucose in the intestine

98. Regulation of GlucoseBreakdown of sugars carried out by enzymes in the GI systemAs simple sugars, they are absorbed from the GI system into the bodyTo be converted into energy, glucose must first be transmitted through the cell membraneGlucose molecule is too large and does not readily diffuse

99. Regulation of GlucoseGlucose 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 levelsInsulin serves as the messenger - travels via blood to target tissuesCombines with specific insulin receptors on the surface of the cell membrane

100. Regulation of GlucoseBody strives to maintain blood glucose between 60 mg/dl and 120 mg/dl.Glucosebrain is the biggest user of glucose in the bodysole energy source for brainbrain does not require insulin to utilize glucose

101. Regulation of GlucoseInsulinGlucagonGlucagon and Insulin are opposites (antagonists) of each other.

102. Regulation of GlucoseGlucagonReleased in response to:Sympathetic stimulationDecreasing blood glucose concentrationActs primarily on liver to increase rate of glycogen breakdownIncreasing blood glucose levels have inhibitory effect on glucagon secretion

103. Regulation of GlucoseInsulinReleased in response to:Increasing blood glucose concentrationParasympathetic innervationActs on cell membranes to increase glucose uptake from blood streamPromotes facilitated diffusion of glucose into cells

104. Diabetes Mellitus2 Types historically based on age of onset (NOT insulin vs. non-insulin)Type Ijuvenile onsetinsulin dependentType IIhistorically adult onsetnow some morbidly obese children are developing Type II diabetesnon-insulin dependentmay progress to insulin dependency

105. Types of Diabetes MellitusType IType IISecondaryGestational

106. Pathophysiology of Type I Diabetes MellitusCharacterized by inadequate or absent production of insulin by pancreasUsually presents by age 25Strong genetic componentAutoimmune featuresbody destroys own insulin-producing cells in pancreasmay follow severe viral illness or injuryRequires lifelong treatment with insulin replacement

107. Pathophysiology of Type II Diabetes MellitusPancreas continues to produce some insulin however disease results from combination of:Relative insulin deficiency Decreased sensitivity of insulin receptorsOnset usually after age 25 in overweight adultsSome morbidly obese children develop Type II diabetesFamilial componentUsually controlled with diet, weight loss, oral hypoglycemic agentsInsulin may be needed at some point in life

108. Secondary Diabetes MellitusPre-existing condition affects pancreasPancreatitisTrauma

109. Gestational Diabetes MellitusOccurs during pregnancyUsually resolves after deliveryOccurs rarely in non-pregnant women on BCPsIncreased estrogen, progesterone antagonize insulin

110. Presentation of New Onset Diabetes Mellitus3 PsPolyuriaPolydipsiaPolyphagiaBlurred vision, dizziness, altered mental statusRapid weight lossWarm dry skin, Weakness, Tachycardia, Dehydration

111. Long Term Treatment of Diabetes MellitusDiet regulatione.g. 1400 calorie ADA dietExerciseincrease patient’s glucose metabolismOral hypoglycemic agentsSulfonylureasInsulinHistorically produced from pigs (porcine insulin)Currently genetic engineering has lead to human insulin (Humulin)

112. Long Term Treatment ofDiabetes MellitusInsulinAvailable in various forms distinguished on onset and duration of actionOnsetrapid (Regular, Semilente, Novolin 70/30)intermediate (Novolin N, Lente)slow (Ultralente)Durationshort, 5-7 hrs (Regular)intermediate, 18-24 hrs (Semilente, Novolin N, Lente, NPH)long-acting, 24 - 36+ hrs (Novolin 70/30, Ultralente)

113. Long Term Treatment ofDiabetes MellitusInsulinMust be given by injection as insulin is protein which would be digested if given orallyextremely compliant patients may use an insulin pump which provides a continuous dosecurrent research studying inhaled insulin form

114. Long Term Treatment of Diabetes MellitusOral Hypoglycemic AgentsStimulate 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]

115. Emergencies Associated Blood Glucose LevelHyperglycemiaDiabetic Ketoacidosis (DKA)Hyperglycemic Hyperosmolar Nonketotic Coma (HHNC)Hypoglycemia “Insulin Shock”

116. HyperglycemiaDefined as blood glucose > 200 mg/dl CausesFailure to take medication (insulin)Increased dietary intakeStress (surgery, MI, CVA, trauma)FeverInfectionPregnancy (gestational diabetes)

117. HyperglycemiaTwo hyperglycemic diabetic states may occurDiabetic Ketoacidosis (DKA)Hyperglycemic Hyperosmolar Non-ketotic Coma (HHNC)

118. Diabetic Ketoacidosis (DKA)Occurs in Type I diabetics (insulin dependency)Usually associated with blood glucose level in the range of 200 - 600 mg/dlNo insulin availability results in ketoacidosis

119. Diabetic Ketoacidosis (DKA)PathophysiologyResults from absence of insulinprevents glucose from entering the cellsleads to glucose accumulation in the bloodCells become starved for glucose and begin to use other energy sources (primarily fats)Fat metabolism generates fatty acidsFurther metabolized into ketoacids (ketone bodies)

120. Diabetic Ketoacidosis (DKA)Pathophysiology (cont)Blood sugar rises above renal threshold for reabsorption (blood glucose > 180 mg/dl)glucose “spills” into the urineLoss of glucose in urine causes osmotic diuresisResults indehydrationacidosiselectrolyte imbalances (especially K+)

121. Diabetic Ketoacidosis (DKA)PresentationGradual onset with progressionWarm, pink, dry skin Dry mucous membranes (dehydrated)Tachycardia, weak peripheral pulsesWeight lossPolyuria, polydipsiaAbdominal pain with nausea/vomitingAltered mental statusKussmaul respirations with acetone (fruity) odor

122. Volume DepletionPolydipsiaShockDiabetic KetoacidosisInadequate insulinIncreased Blood SugarCells Can’t Burn GlucoseCells Burn FatPolyphagiaOsmoticDiuresisKetone BodiesPolyuriaMetabolic AcidosisFruityBreathKussmaul Breathing

123. Management of DKAAirway/Ventilation/Oxygen NRB maskAssess blood glucose level & ECGIV access, large bore NSnormal saline bolus and reassessoften requires several litersAssess for underlying cause of DKATransportHow does fluid treat DKA?

124. Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC)Usually occurs in type II diabeticsTypically very high blood sugar (>600mg/dl)Some insulin availableHigher mortality than DKA

125. Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC)PathophysiologySome minimal insulin productionenough insulin available to allow glucose to enter the cells and prevent ketogenesisnot enough to decrease gluconeogenesis by liverno ketosisExtreme hyperglycemia produces hyperosmolar state causingdiuresissevere dehydrationelectrolyte disturbances

126. Volume DepletionPolydipsiaShockHyperosmolar Hyperglycemic Nonketotic Coma (HHNC)Inadequate insulinIncreased Blood SugarOsmoticDiuresisPolyuria

127. Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC)PresentationSame as DKA but with greater severityHigher blood glucose levelNon-insulin dependent diabetesGreater degree of dehydration

128. Management of HHNCSecure airway and assess ventilationConsider need to assist ventilationConsider need to intubateHigh concentration oxygenAssess blood glucose level & ECGIV access, large bore NSnormal saline bolus and reassessoften requires several litersAssess for underlying cause of HHNCTransport

129. Further Management of HyperglycemiaInsulin (regular)Correct hyperglycemiaCorrection of acid/base imbalancesBicarbonate (severe cases documented by ABG)Normalization of electrolyte balanceDKA may result in hyperkalemia 2o to acidosisH+ shifts intracellularly, K+ moves to extracellular spaceUrinary K+ losses may lead to hypokalemia once therapy is started

130. HypoglycemiaTrue hypoglycemia defined as blood sugar < 60 mg/dlALL hypoglycemia is NOT caused by diabetesCan occur in non-diabetic patientsthin young femalesalcoholics with liver diseasealcohol consumption on empty stomach will block glucose synthesis in liver (gluconeogenesis)Hypoglycemia causes impaired functioning of brain which relies on constant supply of glucose

131. HypoglycemiaCauses of hypoglycemia in diabeticsToo much insulinToo much oral hypoglycemic agentLong half-life requires hospitalizationDecreased dietary intake (took insulin and missed meal)Vigorous physical activityPathophysiologyInadequate blood glucose available to brain and other cells resulting from one of the above causes

132. HypoglycemiaPresentationHunger (initially), HeadacheWeakness, Incoordination (mimics a stroke)Confusion, Unusual behaviormay appear intoxicatedSeizuresComaWeak, rapid pulseCold, clammy skinNervousness, trembling, irritability

133. Hypoglycemia: PathophysiologyBlood Glucose FallsBrain Lacks GlucoseSNSResponseAltered LOCSeizuresHeadacheDizzinessBizarre BehaviorWeaknessAnxietyPallorTachycardiaDiaphoresisNauseaDilated Pupils

134. HypoglycemiaBeta Blockers may mask symptoms by inhibiting sympathetic response

135. Management of Hypoglycemia Secure airway manually suction prnVentilate prnHigh concentration oxygenVascular accessLarge bore IV catheterSaline lock, D5W or NSLarge proximal vein preferredAssess blood glucose level

136. Management of HypoglycemiaOral glucoseONLY if intact gag reflex, awake & able to sit up15gm-30gm of packaged glucose, orMay use sugar-containing drink or foodOral route often slowerIntravenous glucoseAdult: Dextrose 50% (D50) 25gms IV in patent, free-flowing vein, may repeatChildren: 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]

137. Management of HypoglycemiaGlucagonUsed if unable to obtain IV access1 mg IMRequires glycogen storesslower onset of action than IV routeWhat persons are likely to have inadequate glycogen stores?

138. Management of Hypoglycemia Have patient eat high-carbohydrate mealTransport?Patient Refusal PolicyContact medical controlLeave only with responsible family/friend for 6 hoursMust educate family/friend to hypoglycemic signs/symptomsAdvise to contact personal physicianTransportHypoglycemic patients on oral agents (long half life)Unknown, atypical or untreated cause of hypoglycemia

139. Long-term Complications of Diabetes MellitusBlindnessRetinal hemorrhagesRenal DiseasePeripheral NeuropathyNumbness in “stocking glove” distribution (hands and feet)Heart Disease and StrokeChronic state of Hyperglycemia leads to early atherosclerosisComplications in Pregnancy

140. Long-term Complications of Diabetes MellitusDiffuse AtheroscleroisAMICVAPVDHypertensionRenal failureDiabetic retinopathy/blindnessGangrene

141. Long-term Complications of Diabetes MellitusDiabetics 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-diabetic10% of all diabetics develop renal disease usually resulting in dialysis

142. Long-term Complications of Diabetes MellitusPeripheral NeuropathySilent MIVague, poorly-defined symptom complexWeaknessDizzinessMalaiseConfusionSuspect MI in any diabetic with MI signs/symptoms with or without CP

143. Diabetes in PregnancyEarly pregnancy (<24 weeks)Rapid embryo growthDecrease in maternal blood glucoseEpisodes of hypoglycemia

144. Diabetes in PregnancyLate pregnancy (>24 weeks)Increased resistance to insulin effectsIncreased blood glucoseKetoacidosis

145. Diabetes in PregnancyIncreased maternal risk for:Pregnancy-induced hypertensionInfections VaginalUrinary tract

146. Diabetes in PregnancyIncreased fetal risk for:High birth weightHypoglycemiaLiver dysfunction-hyperbilirubinemiaHypocalcemia

147. Assessment of the Diabetic PatientMaintain high-degree of suspicionAssess blood glucose level in all patients withseizure, neurologic S/S, altered mental statusvague history or chief complaintBlood glucose assessment IS NOT necessary in all patients with diabetes mellitus!!

148. Assessment of the Diabetic PatientHistory and Physical Exam includesLook 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 infectionFoot cellulitis / ulcersRecent illness or physiologic stressors

149. Blood Glucose AssessmentCapillary vs. venous blood sampleDepends on glucometer modelUsually capillary preferredDextrostick vs GlucometerDextrostick - colorimetric assessment of blood provides glucose estimateGlucometer - quantitative glucose measurementNeonatal bloodMany glucometers are not accurate for neonates