A ppr oac h to

Pati ents wi th
Di abetes Mel litus
Th e Pa ncreas

 Located in the upper abdomen

 Has two functions:
 Exocrine
 Endocrine
 Exocrine Pancreas
 Secretion of digestive enzymes high in
protein and electrolyte-rich fluid
 Alkaline in nature (sodium bicarbonate) to
neutralize gastric acid juice that enters the
duodenum
 Amylase – aids digestion of carbohydrates
 Trypsin – aids digestion of proteins
 Lipase adis digestion of fats
*** secretin is the stimulus for bicarbonate
secretion
*** CCK-PZ is the stimulus for digestive enzyme
secretion
 Endocrine Pancreas
 Islets of Langerhans are collections of cells
embedded in the pancreatic tissues
 Beta cells – secretes insulin which in turn permits
the entry of glucose to cells
 Alpha cells – secretes glucagon which in turn
raise the blood glucose by converting glycogen to
glucose
 Delta cells - secretes somatostatin which exerts
a hypoglycemic effect by interfering with release
of glucagon from the pancreas.
Cla ssific atio ns o f DM

 Type 1
- auto immune beta cell destruction
 Type 2
 Insulin resistance
 Impaired insulin secretion
 Increased glucose production
Cr ite ria fo r Dia gnosi s
 Two-hour plasma glucose
 >200mg/dL
 Random Blood Sugar
 200mg/dL plus symptoms of diabetes(3 P’s)
 Fasting Plasma Glucose
 Normal : <110mg/dL
 IFG: >110 but <126mg/dL
 DM: > 126mg/dL
Risk Factors for Typ e2
DM
 Family history
 Obesity: >20%DBW
 Age >45years
 Previously identified IFG
 History of GDM or delivery of baby >9lbs.
 Hypertension >140/90mmHg
 HDL > 35mg/dL; triglyceride 250mg/dL
Hist ory
 Symptoms relate to the diagnosis of diabetes:
hyper/hypoglycemia
 Results of blood glucose monitoring
 Status, symptoms and management of
complications
 Compliance to dietary management,
prescribed exercise regimen, pharmacologic
treatment
 Lifestyle, cultural, psychosocial and economic
factors
Ph ysic al Examination

 Blood pressure (sitting and standing)

 BMI
 Fundoscopic examinaton
 Foot examination
 Skin examination
 Neurologic examination
 Oral examination
Lab e xamin atio n

 HgbA1c
 Fasting lipid profile
 Test for microalbuminuria
 Serum creatine level
 Urinalysis
 ECG
Co mpli cations of DM

 Chronic
 Microvascular
 Macrovascular
 Acute
 DKA
 NKHS
Ac ute Co mplic ations
 Diabetic Ketoacidosis – seen primarily in type I DM
 Ketosis – marked increase in fatty acid release from
adipocytes with resulting shift toward ketone body
synthesis in the liver
 Reduced insulin levels + elevated cathecolamines and growth
hormone = increased lipolysis and free fatty acids
 Symptoms:
 Nausea/vomiting
 Thirst/polyuria
 Abdominal pain
 Altered mental function
 Shortness of breath
 Physical Findings
 Tachycardia
 Dry mucous membrane/reduced skin turgor
 Dehydration/hypotension
 Tachypnea/ Kussmaul’s respiration
 Fever, lethargy
 Precipitating event
 Inadequate insulin administration
 Infection (pneumonia/UTI/sepsis)
 Infarction
 Drugs (coccaine)
 Nonketotic Hyperosmolar State – due to
inadequate fluid intake and insulin
deficiency
 Hyperglycemia induces osmotic diuresis that
leads to profound intravascular depletion
exacerbated by inadequate fluid intake
 S/Sx
 Polyuria
 Orthostatic hypotension
 Neurologic symptoms :altered mental status
lethargy seizure
 Absence of DKA symptoms
Ch ronic Co mpli cations

Vascular Complications
 Macrovascular
 Coronary artery disease
 Peripheral vascular disease
 Microvascular
 Retinopathy
 Neuropathy
 nephropathy
 Nonvascular Complications
 Gastroparesis
 Sexual dysfunction
 Skin problems
 infection
Me chanisms of
Co mpli cations
AGE theory
 Increased intracellular glucose leads to
formation of advanced glycolysation
products (AGE’s) – abnormal protein
function – altered cell function
 Increased AGEs – renal, vascular
connective tissue effects + cytokines, growth
factors
 Sorbitol theory
 Hyperglycemia – glucose metabolism by
sorbitol pathway (glucose converted to
sorbitol through aldose reductase) –
alterations in osmolality and redox potential
– altered cell function!
 Diacylglycerol (DAGs)
 Hyperglycemia – formation of DAGs –
activation of protein kinase (PKC) – altered
enzyme function,altered gene expression &
growth factors
Co mponents of
Dia betic Ma nagement
 Nutritional
 Exercise
 Monitoring
 Pharmacologic
 Education