Endocrine SystemEndocrine System
Regulates body systems Regulates body systems Hormones secreted into the blood streamHormones secreted into the blood stream Each hormone has 1 or more target organs Each hormone has 1 or more target organs
(receptor sites)(receptor sites) Rhythmic pattern of release Rhythmic pattern of release Problems arise from either production or Problems arise from either production or
receptor sitesreceptor sites Most problems are chronic requiring self-Most problems are chronic requiring self-
managementmanagement
HormonesHormones
Responsible for regulating:Responsible for regulating:– ReproductionReproduction– Growth & DevelopmentGrowth & Development– Energy production & useEnergy production & use– Maintenance of internal environmentMaintenance of internal environment
CatecholaminesCatecholamines
Amino Acid derivativesAmino Acid derivatives– EpinephrineEpinephrine– NorepinephrineNorepinephrine– ThyroxinThyroxin
Easily replacedEasily replaced Many can be oralMany can be oral
Proteins & PeptidesProteins & Peptides
Chains of Amino AcidsChains of Amino Acids Difficult to isolate & engineerDifficult to isolate & engineer None survive the GI systemNone survive the GI system Proteins:Proteins:
– Larger moleculesLarger molecules– Insulin, Calcitonin, Growth Hormone, FSHInsulin, Calcitonin, Growth Hormone, FSH
Peptides:Peptides:– Releasing Factors in Hypothalamus & Releasing Factors in Hypothalamus &
Posterior Pituitary (Neurohypophysis)Posterior Pituitary (Neurohypophysis)– Oxytocin, Vasopressin Oxytocin, Vasopressin
SteroidsSteroids
Formed from cholesterolFormed from cholesterol Easily produced for replacementEasily produced for replacement Most can be oralMost can be oral Include Adrenal and Sex Glands:Include Adrenal and Sex Glands:
– AldosteroneAldosterone– CortisolCortisol– EstrogenEstrogen– TestosteroneTestosterone
Pharmacologic UsesPharmacologic Uses
DiagnosticDiagnostic– ACTH to stimulate the AdrenalsACTH to stimulate the Adrenals– Thyroglobin to check thyroid responseThyroglobin to check thyroid response
ReplacementReplacement– InsulinInsulin– EstrogenEstrogen– ThyroidThyroid
Pharmacologic EffectsPharmacologic Effects– Steroids to decrease inflammationSteroids to decrease inflammation
FeedbackFeedback
Secreted when the body identifies a needSecreted when the body identifies a need
Changes in the blood level or other Changes in the blood level or other hormones may cause an increase or hormones may cause an increase or decrease in secretiondecrease in secretion
Negative Feedback:Negative Feedback:– Hormone produces an effect, when it is Hormone produces an effect, when it is
strong enough, further hormone secretion strong enough, further hormone secretion is inhibited, decreasing physiologic effect.is inhibited, decreasing physiologic effect.
Feedback LoopsFeedback Loops
Hypothalamus
Releasing Factor
Pituitary
Hormone A
Target Organ
Hormone B
Biologic Effect
__
__
Negative Feedback Loop
Physiologic Changes Physiologic Changes with Agingwith Aging
Reduction in hormone productionReduction in hormone production Changes in hormone clearanceChanges in hormone clearance Decreased cellular responsivenessDecreased cellular responsiveness Changes in;Changes in;
– Physical activity levelPhysical activity level– Nutritional statusNutritional status– Body compositionBody composition
Causes of DiseaseCauses of Disease
Over or Under Production Over or Under Production Transport abnormalitiesTransport abnormalities Inability of target tissues to respondInability of target tissues to respond Problems with the feedback Problems with the feedback
mechanismmechanism PrimaryPrimary SecondarySecondary
PituitaryPituitary
Anterior PituitaryAnterior Pituitary– Hypothalamic releasing factors Hypothalamic releasing factors
stimulate the release or inhibit the stimulate the release or inhibit the release of hormonesrelease of hormones
Posterior PituitaryPosterior Pituitary– Hormones produced in the Hormones produced in the
hypothalamus are stored in the hypothalamus are stored in the posterior lobe until stimulated by the posterior lobe until stimulated by the hypothalamus via nerve impulseshypothalamus via nerve impulses
Hypothalamus
Neuro - Secretory Cells
Hormone Producing Cells
Releasing Factor Producing Cells
PosteriorAnterior
Portal Vessel
Anterior PituitaryAnterior Pituitary
Growth Hormone (GH)Growth Hormone (GH) GonadotropicGonadotropic
– Lutenizing Hormone (LH)Lutenizing Hormone (LH)– Follicle Stimulating Hormone (FSH)Follicle Stimulating Hormone (FSH)
Adrenocorticotropic Hormone (ACTH)Adrenocorticotropic Hormone (ACTH) Thyroid Stimulating Hormone (TSH)Thyroid Stimulating Hormone (TSH) Prolactin (PRL)Prolactin (PRL) Melanocyte-stimulating Hormone Melanocyte-stimulating Hormone
(MSH)(MSH)
Anterior PituitaryAnterior PituitaryGrowth Hormone Growth Hormone (Somatotropin) (Somatotropin)
Growth Hormone increases bone growth Growth Hormone increases bone growth and tissue cell size by changing and tissue cell size by changing metabolism, antagonizing the action of metabolism, antagonizing the action of insulin, and increasing fat mobilization for insulin, and increasing fat mobilization for energy use. energy use.
Deficiency - Dwarfism = delay in all body Deficiency - Dwarfism = delay in all body parts with no mental impairment. parts with no mental impairment.
Excess - Gigantism in childhood, Excess - Gigantism in childhood, acromeglia in adults. acromeglia in adults.
AcromegalyAcromegaly Acromegaly is the Greek word for "extremities" and Acromegaly is the Greek word for "extremities" and
"enlargement”"enlargement”
Signs and symptoms vary, dependent upon how long Signs and symptoms vary, dependent upon how long the patient has had the disease, but may include…the patient has had the disease, but may include…
– Swelling of the hands and feet Swelling of the hands and feet – Facial features become coarse as bones grow Facial features become coarse as bones grow – Body hair becomes coarse as the skin thickens and/or Body hair becomes coarse as the skin thickens and/or
darkens darkens – Increased perspiration accompanied with body odor Increased perspiration accompanied with body odor – Protruding jaw Protruding jaw – Voice deepening Voice deepening
Anterior PituitaryAnterior PituitaryGonadotropic Hormone Gonadotropic Hormone
Gonadotropin-releasing hormone Gonadotropin-releasing hormone (Gn-RH)(Gn-RH)
– Produced and released from the Produced and released from the hypothalamus. Stimulates the hypothalamus. Stimulates the secretion of secretion of follicle stimulating follicle stimulating hormone (FSH)hormone (FSH) and and lutenizing hormone lutenizing hormone (LH)(LH), from the anterior pituitary. , from the anterior pituitary.
Anterior PituitaryAnterior PituitaryAdrenocorticotropic Adrenocorticotropic Hormone (ACTH)Hormone (ACTH)
Stimulates the Stimulates the adrenal cortex adrenal cortex to synthesize to synthesize and release and release cortisols in cortisols in response to response to stress.stress.
Anterior PituitaryAnterior PituitaryThyroid Stimulating Thyroid Stimulating Hormone (TSH) Hormone (TSH)
Hypothalamus releases TRHHypothalamus releases TRH
Stimulates the anterior pituitary to Stimulates the anterior pituitary to produce TSHproduce TSH
Regulates the amount of thyroid Regulates the amount of thyroid hormone produced and released into hormone produced and released into the bloodstream by the thyroid glandthe bloodstream by the thyroid gland
Posterior PituitaryPosterior Pituitary
OxytocinOxytocin– Uterine contractionUterine contraction– Milk let downMilk let down
ADH (Vasopressin)ADH (Vasopressin)– Renal conservation of waterRenal conservation of water– VasoconstrictionVasoconstriction– Increase GI motilityIncrease GI motility– Released in response to plasma Released in response to plasma
osmolarityosmolarity
SIADH - Syndrome of SIADH - Syndrome of Inappropriate ADHInappropriate ADH ADH releaseADH release Water Reabsorption into circulation Water Reabsorption into circulation
-Renal Tubules-Renal Tubules Extravascular FluidExtravascular Fluid Plasma OsmolalityPlasma Osmolality Glomerular Filtration RateGlomerular Filtration Rate Serum Sodium Levels Serum Sodium Levels
CEREBRAL EDEMACEREBRAL EDEMA
Diabetes InsipidusDiabetes Insipidus
ADH DeficiencyADH Deficiency Water excretion and blood Water excretion and blood
concentrationconcentration ADH is a peptide and can not be taken ADH is a peptide and can not be taken
orallyorally Treatment:Treatment:
– Vasopressin (Pitressin) - short acting Vasopressin (Pitressin) - short acting injectioninjection
– Lypressin and Desmopressin - nasal sprayLypressin and Desmopressin - nasal spray
Adrenal CortexAdrenal Cortex
Glucocorticoids (Cortisol)Glucocorticoids (Cortisol)– Release is under ACTH controlRelease is under ACTH control
Mineral-corticoids (Aldosterone)Mineral-corticoids (Aldosterone)– Renin-Angiotensin system and KRenin-Angiotensin system and K++ levels levels– Stimulated by NaCl depletionStimulated by NaCl depletion
AndrogensAndrogens– Growth of hair folliclesGrowth of hair follicles
Stress increases cortisol and aldosterone to Stress increases cortisol and aldosterone to maintain CV tone.maintain CV tone.
Impairment of release leads to adrenal crisisImpairment of release leads to adrenal crisis
Cushing SyndromeCushing Syndrome
Excess of corticosteroids secreted Excess of corticosteroids secreted by the adrenal cortexby the adrenal cortex
Iatrogenic - prolonged use Iatrogenic - prolonged use Lab - 24Lab - 2400 urine for cortisol urine for cortisol Tx - Surgery, Radiation, Suppress Tx - Surgery, Radiation, Suppress
synthesis using drug therapysynthesis using drug therapy Prolonged steroid use - TAPER dosesProlonged steroid use - TAPER doses Post-op carePost-op care
Addison'sAddison's
Adrenocorticol insufficiencyAdrenocorticol insufficiency AutoimmuneAutoimmune Sxs - weight loss, anorexia, weakness, Sxs - weight loss, anorexia, weakness,
low BP, low sodium, high potassium, low BP, low sodium, high potassium, nausea & vomiting, diarrheanausea & vomiting, diarrhea
Tx - GlucocorticoidsTx - Glucocorticoids– MineralcorticoidsMineralcorticoids
Adrenal CrisisAdrenal Crisis
Adrenal MedullaAdrenal Medulla
PheochromocytomaPheochromocytoma– Neoplasm increasing catecholaminesNeoplasm increasing catecholamines– Surgical removalSurgical removal
Sxs - episodic HTN, increased Sxs - episodic HTN, increased metabolism, hyperglycemiametabolism, hyperglycemia
Lab - urine metanephrinesLab - urine metanephrines Monitor wide BP fluctuationsMonitor wide BP fluctuations
The Thyroid GlandThe Thyroid Gland
Normal thyroid levels are essential to Normal thyroid levels are essential to regulate cellular metabolism, and for regulate cellular metabolism, and for normal growth and development.normal growth and development.
Production of thyroid hormone is Production of thyroid hormone is caused by release of TSH (stimulated caused by release of TSH (stimulated by TRH)by TRH)– Thyroxin - TThyroxin - T44
– Triiodothyronine - TTriiodothyronine - T33
ThyroidThyroid
Essential to regulate metabolismEssential to regulate metabolism Caused by release of TSH:Caused by release of TSH:
– Thyroxin - TThyroxin - T44
– Triiodothyronine - TTriiodothyronine - T33
Stimulated by increased CaStimulated by increased Ca++++ in blood in blood– Calcitonin - lowers blood levels by inhibiting Calcitonin - lowers blood levels by inhibiting
bone re-absorptionbone re-absorption Low calcium levels suppress the release of Low calcium levels suppress the release of
calcitonincalcitonin Elevated levels increase it’s secretionElevated levels increase it’s secretion
Prevalence of Thyroid Prevalence of Thyroid DisordersDisorders
In the United States, approximately In the United States, approximately 7.5 percent of the population (about 7.5 percent of the population (about 1 in every 13 individuals) have been 1 in every 13 individuals) have been diagnosed with thyroid disorders, diagnosed with thyroid disorders, and nearly another 1 percent are and nearly another 1 percent are estimated to have undiagnosed estimated to have undiagnosed thyroid maladies. thyroid maladies.
HyperthyroidHyperthyroid
Graves DiseaseGraves Disease Multinodular GoiterMultinodular Goiter Symptoms:Symptoms:
– Increased metabolism Increased metabolism – Increase stimulation of sympathetic nervous systemIncrease stimulation of sympathetic nervous system– ExopthalmosExopthalmos
Thyroid Storm – Thyrotoxicosis----Severe Thyroid Storm – Thyrotoxicosis----Severe and life and life threateningthreatening
Treatment - Propylthiouracil, Inderol, Iodine, Radiation, Treatment - Propylthiouracil, Inderol, Iodine, Radiation, Surgery Surgery
HypothyroidHypothyroid
Infants - long gestation, failure to thriveInfants - long gestation, failure to thrive Childhood - AutoimmuneChildhood - Autoimmune Adult - Atrophy or Decreased TSHAdult - Atrophy or Decreased TSH
– Myxedema - interstitial edema, fatigue, Myxedema - interstitial edema, fatigue, lethargy, impaired memory leading to coma lethargy, impaired memory leading to coma high mortality rate.high mortality rate.
– Long term - Sxs related to increased protein Long term - Sxs related to increased protein turnoverturnover
– Cardiovascular, GI, and reproductiveCardiovascular, GI, and reproductive Replacement TherapyReplacement Therapy
ParathyroidParathyroid
Maintains extracellular CaMaintains extracellular Ca++++ levels levels Parathormone - Calcitonin antagonistParathormone - Calcitonin antagonist
– Release stimulated by low blood levels Release stimulated by low blood levels of Caof Ca++++ or high levels of phosphates or high levels of phosphates
– Increases CaIncreases Ca++++ blood levels blood levels– Reabsorption of CaReabsorption of Ca++++ and Phos. from and Phos. from
bonesbones– Increase GI absorptionIncrease GI absorption– Increase reabsorption in kidneysIncrease reabsorption in kidneys
HyperparathyroidHyperparathyroid
Primary - Parathyroid tumor or hyperplasiaPrimary - Parathyroid tumor or hyperplasia Secondary - Response to Low CaSecondary - Response to Low Ca++++ levels levels
– ESRD - Response to phosphate ESRD - Response to phosphate excretion problems excretion problems
– Nursing - increase fluids, low calcium Nursing - increase fluids, low calcium diet, avoid immobilitydiet, avoid immobility
Mithramycin - antihypercalcemic agentMithramycin - antihypercalcemic agent Post-op removal - observe for tetany, fluid Post-op removal - observe for tetany, fluid
and electrolyte problemsand electrolyte problems
HypoparathyroidHypoparathyroid
Accidental removal or vascular Accidental removal or vascular damage during surgerydamage during surgery
Sxs - Tetany, Chvostek’s signSxs - Tetany, Chvostek’s sign Lab- low calcium, low PTH, and Lab- low calcium, low PTH, and
high Phos.high Phos. Tx - Vitamin D, Calcium Tx - Vitamin D, Calcium
supplements, and Phosphate supplements, and Phosphate bindersbinders
PancreasPancreas
InsulinInsulin– BetaBeta cells of Langerhans cells of Langerhans– Stored in Beta Cells as ProinsulinStored in Beta Cells as Proinsulin– Catalyst to cellular metabolismCatalyst to cellular metabolism– Promotes storage of CHO in liver, muscle cells, and fat Promotes storage of CHO in liver, muscle cells, and fat
depositsdeposits GlucagonGlucagon
– Opposes the action of InsulinOpposes the action of Insulin– AlphaAlpha cells produce cells produce– Acts to mobilize liver glycogen and convert to glucose Acts to mobilize liver glycogen and convert to glucose
Diabetes MellitusDiabetes Mellitus
Chronic hyperglycemia---main feature in Chronic hyperglycemia---main feature in all types of diabetes mellitus. Resulting all types of diabetes mellitus. Resulting from:from:– Insulin secretionInsulin secretion– Insulin actionInsulin action– Or bothOr both
Disease classifiedDisease classified– Age of onsetAge of onset– Problem causing the lack of insulinProblem causing the lack of insulin– Severity of the deficiencySeverity of the deficiency
Cost of Diabetes in the Cost of Diabetes in the United States, 2002United States, 2002
Total (direct and indirect):Total (direct and indirect): $132 $132 billionbillion
Direct medical costs:Direct medical costs: $92 billion $92 billion Indirect costs:Indirect costs: $40 billion $40 billion
(disability, work loss, premature (disability, work loss, premature mortality)mortality)
Blood Glucose ValuesBlood Glucose Values
Normal Normal – Fasting blood glucose – Fasting blood glucose levels of <110 mg/dLlevels of <110 mg/dL
Significant abnormal resultsSignificant abnormal results – – Levels>126mg/dL obtained on at Levels>126mg/dL obtained on at least two occasions are diagnostic least two occasions are diagnostic of diabetes, even in older adults.of diabetes, even in older adults.
Diabetes CausesDiabetes Causes
Inability to use CHOInability to use CHO
Insulin action ineffective at tissue Insulin action ineffective at tissue site site oror not enough Insulin not enough Insulin availableavailable
Diabetes CausesDiabetes Causes
Glycogen fails to store in liverGlycogen fails to store in liver– Conversion of glycogen to glucose Conversion of glycogen to glucose
NOTNOT affected affected
Increased metabolism of proteins Increased metabolism of proteins and fats and fats – Leads to Ketone productionLeads to Ketone production
InsulinInsulin
Glucose transport across cell membraneGlucose transport across cell membrane Storage of glucose as glycogenStorage of glucose as glycogen Increased fat depositsIncreased fat deposits Decreased protein breakdownDecreased protein breakdown Increased transport of amino acids into the Increased transport of amino acids into the
cell for protein synthesiscell for protein synthesis Absence = Increased osmotic pressureAbsence = Increased osmotic pressure 3 Poly’s3 Poly’s
Type IType I
Beta cell destructionBeta cell destruction
Rapid onsetRapid onset
Must be given InsulinMust be given Insulin
Ketoacidosis proneKetoacidosis prone
Type IIType II
Enough Insulin to prevent DKAEnough Insulin to prevent DKA May have increased May have increased oror decreased Insulin decreased Insulin
productionproduction Decreased tissue response to InsulinDecreased tissue response to Insulin Abnormal liver glucose regulation Abnormal liver glucose regulation Oral Agent:Oral Agent:
– Increase Insulin productionIncrease Insulin production– Improve cell receptor bindingImprove cell receptor binding– Regulate liver glucose productionRegulate liver glucose production
Impaired Glucose Impaired Glucose ToleranceTolerance ““Borderline Diabetes”Borderline Diabetes” Blood Glucose levels above Blood Glucose levels above
normal, but below levels to Dx normal, but below levels to Dx DiabetesDiabetes
May progress to DiabetesMay progress to Diabetes Need close monitoringNeed close monitoring Diet and ExerciseDiet and Exercise
GestationalGestational
Intolerance of glucose during pregnancyIntolerance of glucose during pregnancy Insulin resistance to increase glucose Insulin resistance to increase glucose
available to the babyavailable to the baby Paced with placental hormonesPaced with placental hormones GTT returns to normal in 3-5 weeks after GTT returns to normal in 3-5 weeks after
deliverydelivery Approximately 30% develop Diabetes Approximately 30% develop Diabetes
within the next 5-10 yearswithin the next 5-10 years Glucose Tolerance TestGlucose Tolerance Test
Baby EffectsBaby Effects
Increase amounts of amniotic fluidIncrease amounts of amniotic fluid
Large fetusLarge fetus
Hypoglycemic reactions after birthHypoglycemic reactions after birth
Respiratory Distress SyndromeRespiratory Distress Syndrome
TestsTests
Blood SugarBlood Sugar Glycosylated Hemoglobin (HbA1c)Glycosylated Hemoglobin (HbA1c)
– The higher the number the poorer The higher the number the poorer the control. the control.
GTT - Glucose Tolerance TestGTT - Glucose Tolerance Test Capillary Blood Glucose (CBG)Capillary Blood Glucose (CBG)
TreatmentTreatment
DietDiet– ADA Exchange listADA Exchange list– Individually prescribedIndividually prescribed
ExerciseExercise– Type I - IDDMType I - IDDM
Increases Insulin sensitivity of cellsIncreases Insulin sensitivity of cells Reduce Insulin dose or snack before exerciseReduce Insulin dose or snack before exercise
– Type II - NIDDMType II - NIDDM Increases Insulin binding at receptorsIncreases Insulin binding at receptors May initially elevate blood sugarsMay initially elevate blood sugars
Insulin TreatmentInsulin Treatment
Goal: Match Normal Secretion Goal: Match Normal Secretion Patterns of the BodyPatterns of the Body
Multiple types of InsulinMultiple types of Insulin Administration techniquesAdministration techniques Site RotationsSite Rotations PumpsPumps New TechnologyNew Technology
Somogyi EffectSomogyi Effect
Wide difference in CBG’sWide difference in CBG’s– Low in early AMLow in early AM– High after breakfastHigh after breakfast
Counter regulatory to Counter regulatory to hypoglycemia during the nighthypoglycemia during the night
Treatment - lower Insulin dose in Treatment - lower Insulin dose in the evening or increase food the evening or increase food intake before bedintake before bed
Dawn PhenomenonDawn Phenomenon
High CBG’s and possibly Ketones High CBG’s and possibly Ketones in the morningin the morning
Dawn release of Growth Hormone Dawn release of Growth Hormone or Cortisolor Cortisol
Treatment - Change Insulin times Treatment - Change Insulin times and/or increase Insulin doseand/or increase Insulin dose
Look at client’s entire Look at client’s entire management programmanagement program
SulfonylureasSulfonylureas
Must be producing some InsulinMust be producing some Insulin Action:Action:
– Stimulate Beta cell release of InsulinStimulate Beta cell release of Insulin– Increase Insulin receptor sensitivityIncrease Insulin receptor sensitivity– May decrease liver glucose May decrease liver glucose
productionproduction Do Not Take Extra if Overeats!Do Not Take Extra if Overeats! Hypoglycemia may be prolongedHypoglycemia may be prolonged
HypoglycemicsHypoglycemics
Alpha-Glycosidase InhibitorsAlpha-Glycosidase Inhibitors– Delay digestion and absorption of CHODelay digestion and absorption of CHO
BiguanidesBiguanides– Decrease glucose absorption, decrease glucose Decrease glucose absorption, decrease glucose
production in liver, and improves insulin sensitivity in production in liver, and improves insulin sensitivity in tissuestissues
MeglitinidesMeglitinides– Stimulates Beta cells and improves insulin response Stimulates Beta cells and improves insulin response
to glucoseto glucose ThiazolidinedionesThiazolidinediones
– Lowers insulin resistance by re-sensitizing the body Lowers insulin resistance by re-sensitizing the body to its own insulinto its own insulin
HypoglycemiaHypoglycemia
Too much Insulin or not enough foodToo much Insulin or not enough food Symptoms due to rapid drop in Blood Symptoms due to rapid drop in Blood
SugarSugar Adrenergic (Fight or Flight) SymptomsAdrenergic (Fight or Flight) Symptoms Glyconeurogenic (Brain) SymptomsGlyconeurogenic (Brain) Symptoms Beta Blockers mask the symptomsBeta Blockers mask the symptoms Elderly often present with Elderly often present with BrainBrain
symptoms symptoms FIRSTFIRST
DKA - Diabetic DKA - Diabetic KetoacidosisKetoacidosis
No Insulin leads to:No Insulin leads to:
– Use of glucoseUse of glucose
– Breakdown of fats to fatty acids to KetonesBreakdown of fats to fatty acids to Ketones
– Acidosis causes KAcidosis causes K++ to leave cells and water to leave cells and water
lossloss
– Severe dehydration with high Severe dehydration with high serumserum K K++
levelslevels
HHNK - HHNK - Hyperglycemic Hyperosmolar NonKetosisHyperglycemic Hyperosmolar NonKetosis
Enough Insulin to Avoid DKAEnough Insulin to Avoid DKA High Blood Glucose Levels lead to High Blood Glucose Levels lead to
Osmotic DiuresisOsmotic Diuresis HypovolemiaHypovolemia Treatment = Insulin and Rapid IV Fluid Treatment = Insulin and Rapid IV Fluid
ReplacementReplacement Prevent by Pushing Fluids When Serum Prevent by Pushing Fluids When Serum
Osmolarity Nears 320Osmolarity Nears 320 2(Na+K) +2(Na+K) + BS BS + + BUN BUN
18 2.818 2.8
Chronic ComplicationsChronic Complications
80% of Medical Spending80% of Medical Spending Increasing as Population AgesIncreasing as Population Ages MicrovascularMicrovascular MacrovascularMacrovascular PATIENT EDUCATIONPATIENT EDUCATION
Pattern Management Pattern Management RuleRule
Target Glucose GoalsTarget Glucose Goals Regular CBG’sRegular CBG’s Record CBG’s & eventsRecord CBG’s & events Study a 3 day patternStudy a 3 day pattern Determine Insulin responsible for problemsDetermine Insulin responsible for problems Insulin by 1 or 2 UnitsInsulin by 1 or 2 Units One change at a timeOne change at a time Treat low CBG’s Treat low CBG’s FIRSTFIRST 3 days before another change3 days before another change
Client #1Client #1
A.M. NOON P.M. H.S.
2/1 84 191 114 97
2/2 78 222 104 135
2/3 90 201 117 103
2/4 86 186 129 132
Client #2Client #2
A.M. NOON P.M. H.S.
2/1 64 191 114 67
2/1 68 262 204 135
2/3 50 201 47 103
2/4 86 66 129 132
Client #3Client #3
A.M. NOON P.M. H.S.
2/1 254 271 314 397
2/2 278 282 304 335
2/3 264 261 387 403
2/4 286 286 329 332
Home CausesHome Causes
Oral Medication ErrorsOral Medication Errors– Dose, Timing, Double MedicationDose, Timing, Double Medication– Bring Bring ALLALL Meds from home Meds from home
Insulin ErrorsInsulin Errors– Technique ProblemsTechnique Problems– Observe technique ASAPObserve technique ASAP– Check dose and timing at homeCheck dose and timing at home
Diet Misinformation / ChangesDiet Misinformation / Changes