Approach To Patients With Diabetes Mellitus

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