Approach to Patients With Diabetes Mellitus

8/14/2019 Approach to Patients With Diabetes Mellitus

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Appr oac h toppr oac h toPatients wi thati ents wi thDiabetes Mel litusiabetes Mel litus


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Th e Pa ncreash e Pa ncreas Located in the upper abdomenLocated in the upper abdomen

Has two functions:Has two functions:

ExocrineExocrine

EndocrineEndocrine


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Exocrine PancreasExocrine Pancreas Secretion of digestive enzymes high inSecretion of digestive enzymes high in

protein and electrolyte-rich fluidprotein and electrolyte-rich fluid Alkaline in nature (sodium bicarbonate) toAlkaline in nature (sodium bicarbonate) to

neutralize gastric acid juice that enters theneutralize gastric acid juice that enters theduodenumduodenum Amylase aids digestion of carbohydratesAmylase aids digestion of carbohydrates Trypsin aids digestion of proteinsTrypsin aids digestion of proteins

Lipase adis digestion of fatsLipase adis digestion of fats

****** secretinsecretin is the stimulus for bicarbonateis the stimulus for bicarbonate

secretionsecretion****** CCK-PZCCK-PZ is the stimulus for digestive enzymeis the stimulus for digestive enzyme

secretionsecretion


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Endocrine PancreasEndocrine Pancreas

Islets of Langerhans are collections of cellsIslets of Langerhans are collections of cells

embedded in the pancreatic tissuesembedded in the pancreatic tissues Beta cells secretes insulin which in turn permitsBeta cells secretes insulin which in turn permits

the entry of glucose to cellsthe entry of glucose to cells

Alpha cells secretes glucagon which in turnAlpha cells secretes glucagon which in turn

raise the blood glucose by converting glycogen toraise the blood glucose by converting glycogen toglucoseglucose

Delta cells - secretes somatostatin which exertsDelta cells - secretes somatostatin which exerts

a hypoglycemic effect by interfering with releasea hypoglycemic effect by interfering with release

of glucagon from the pancreas.of glucagon from the pancreas.


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Cla ssific atio ns o f DMla ssific atio ns o f DM Type 1Type 1

- auto immune beta cell destruction- auto immune beta cell destruction

Type 2Type 2

Insulin resistanceInsulin resistance

Impaired insulin secretionImpaired insulin secretion

Increased glucose productionIncreased glucose production


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Cr ite ria fo r Dia gnosi sr ite ria fo r Dia gnosi s Two-hour plasma glucoseTwo-hour plasma glucose

>200mg/dL>200mg/dL

Random Blood SugarRandom Blood Sugar 200mg/dL plus symptoms of diabetes(3 Ps)200mg/dL plus symptoms of diabetes(3 Ps)

Fasting Plasma GlucoseFasting Plasma Glucose

Normal : 126mg/dL126mg/dL


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Risk Factors for Typ e2isk Factors for Typ e2DMM Family historyFamily history

Obesity: >20%DBWObesity: >20%DBW

Age >45yearsAge >45years

Previously identified IFGPreviously identified IFG

History of GDM or delivery of baby >9lbs.History of GDM or delivery of baby >9lbs.

Hypertension >140/90mmHgHypertension >140/90mmHg

HDL > 35mg/dL; triglyceride 250mg/dLHDL > 35mg/dL; triglyceride 250mg/dL


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Hist oryist ory Symptoms relate to the diagnosis of diabetes:Symptoms relate to the diagnosis of diabetes:

hyper/hypoglycemiahyper/hypoglycemia Results of blood glucose monitoringResults of blood glucose monitoring Status, symptoms and management ofStatus, symptoms and management of

complicationscomplications Compliance to dietary management,Compliance to dietary management,

prescribed exercise regimen, pharmacologicprescribed exercise regimen, pharmacologic

treatmenttreatment Lifestyle, cultural, psychosocial and economicLifestyle, cultural, psychosocial and economic

factorsfactors


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Lab e xamin atio nab e xamin atio n HgbAHgbA1c1c

Fasting lipid profileFasting lipid profile

Test for microalbuminuriaTest for microalbuminuria

Serum creatine levelSerum creatine level

UrinalysisUrinalysis ECGECG


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Co mpli cations of DMo mpli cations of DM ChronicChronic

MicrovascularMicrovascular

MacrovascularMacrovascular

AcuteAcute

DKADKA

NKHSNKHS


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Ac ute Co mplic ationsc ute Co mplic ations Diabetic Ketoacidosis seen primarily in type I DMDiabetic Ketoacidosis seen primarily in type I DM

Ketosis marked increase in fatty acid release fromKetosis marked increase in fatty acid release fromadipocytes with resulting shift toward ketone bodyadipocytes with resulting shift toward ketone body

synthesis in the liversynthesis in the liver Reduced insulin levels + elevated cathecolamines and growthReduced insulin levels + elevated cathecolamines and growth

hormone = increased lipolysis and free fatty acidshormone = increased lipolysis and free fatty acids

Symptoms:Symptoms: Nausea/vomitingNausea/vomiting

Thirst/polyuriaThirst/polyuria Abdominal painAbdominal pain

Altered mental functionAltered mental function

Shortness of breathShortness of breath


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Nonketotic Hyperosmolar State due toNonketotic Hyperosmolar State due toinadequate fluid intake and insulininadequate fluid intake and insulin

deficiencydeficiency Hyperglycemia induces osmotic diuresis thatHyperglycemia induces osmotic diuresis that

leads to profound intravascular depletionleads to profound intravascular depletionexacerbated by inadequate fluid intakeexacerbated by inadequate fluid intake

S/SxS/Sx PolyuriaPolyuria

Orthostatic hypotensionOrthostatic hypotension

Neurologic symptoms :altered mental statusNeurologic symptoms :altered mental statuslethargy seizurelethargy seizure

Absence of DKA symptomsAbsence of DKA symptoms


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Ch ronic Co mpli cationsh ronic Co mpli cationsVascular ComplicationsVascular Complications

MacrovascularMacrovascular

Coronary artery diseaseCoronary artery disease Peripheral vascular diseasePeripheral vascular disease

MicrovascularMicrovascular

RetinopathyRetinopathy

NeuropathyNeuropathy

nephropathynephropathy


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Nonvascular ComplicationsNonvascular Complications

GastroparesisGastroparesis Sexual dysfunctionSexual dysfunction

Skin problemsSkin problems

infectioninfection


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Me chanisms ofe chanisms ofComplicationsomplications

AGE theoryAGE theory

Increased intracellular glucose leads toIncreased intracellular glucose leads to

formation of advanced glycolysationformation of advanced glycolysationproducts (AGEs) abnormal proteinproducts (AGEs) abnormal protein

function altered cell functionfunction altered cell function

Increased AGEs renal, vascularIncreased AGEs renal, vascular

connective tissue effects + cytokines, growthconnective tissue effects + cytokines, growthfactorsfactors


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Sorbitol theorySorbitol theory

Hyperglycemia glucose metabolism byHyperglycemia glucose metabolism by

sorbitol pathway (glucose converted tosorbitol pathway (glucose converted tosorbitol through aldose reductase) sorbitol through aldose reductase)

alterations in osmolality and redox potentialalterations in osmolality and redox potential

altered cell function! altered cell function!


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Components ofomponents ofDia betic Ma nagementia betic Ma nagement NutritionalNutritional

ExerciseExercise

MonitoringMonitoring

PharmacologicPharmacologic

EducationEducation

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Approach to Patients With Diabetes Mellitus