GOOD GOOD MORNINGMORNING

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

JamieJamie

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

ArthurArthur

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