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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