2. • GM, 54y/o male with a chief complaint of
right gluteal swelling accompanied by weight
loss, polyuria, polydipsia
• 2015: diabetes – Metformin 500mg BID
• PSH: non smoker, non alcoholic
• (+) use of reading glasses, bilateral arcus
senilis
3. Definition
• Diabetes Mellitus - refers to a group of
common metabolic disorders that share the
phenotype of hyperglycemia
• Hyperglycemia
– Reduced insulin secretion
– Decreased glucose utilization
– Increased glucose production
4. Epidemiology
• Prevalence- 30 million cases in 1985 to 285
million in 2010
• US- 0.2% in individuals aged <20 years and
11.3% in individuals aged >20 years, 26.9% in
individuals >65 years
• prevalence of type 2 DM is rising more
rapidly, due to increase in obesity and
reduced activity levels as countries become
more industrialized,
5. Classification
• Type 1 – due to B-cell destruction, usually leading to
absolute insulin deficiency
• Type 2 – due to a progressive insulin secretory defect
on the background of insulin resistance
• Gestational diabetes mellitus (GDM) – diabetes
diagnosed in the second or third trimester of
pregnancy that is not clearly overt diabetes
• Specific types of diabetes due to other causes,
– e.g., monogenic diabetes syndromes (such as neonatal
diabetes and maturity-onset diabetes of the young
[MODY]), diseases of the exocrine pancreas (such as cystic
fibrosis), and drug- or chemical-induced diabetes (such as
in the treatment of HIV/AIDS or after organ
transplantation)
19. Foundations of care:
• All individuals should limit their sedentary time
by breaking up extended amounts of time (>90
mins) sitting time
• Weight loss of 2-8kg may provide clinical benefit
in type 2 DM
• E cigarettes are not alternative to smoking or
facilitate smoking cessation
• All >=65 (w/ or w/o DM) should receive the
pneumococcal conjugate vaccine 13 PCV13
followed by PPSV23 6 to 12 mos later if they have
never received these vaccines before
20. Glycemic targets
• Pre meal glucose of 80-130mg/dl (previous
70-130)
– To better reflect new data comparing actual
average glucose levels with A1c targets
21. Approaches to glycemic treatment
• Pharma therapy for type 1 DM
(recommendations):
– Use MDI injections (3-4 injections/day of basal and
prandial insulin) or CSII therapy
– Match prandial insulin to carb intake, premeal blood
glucose and anticipated physical activity
– For most patients (elevated risk for hyperglycemia)
use insulin analogs
– For patients with frequent nocturnal hypoglycemia/or
hypoglycemia unawareness, a sensor augmented low
glucose threshold suspend pump may be considered
22. • Pharma therapy for type 2 DM
– Metformin is not contraindicated, and if tolerated,
is preferred
– Newly diagnosed type 2 DM and markedly
symptomatic &/or elevated A1C, consider insulin
therapy (w/ or w/o additional agents)
–
23. Cardiovascular disease and risk
management
• Recommended goal for diastolic BP 90mmHg
(from 80mmHg)
• Treatment initiation (and initial statin dose) is
now driven primarily by risk status rather than
LDL cholesterol level
• Lipid monitoring
– Diabetes diagnosis
– Initial medical evaluation
– Age 40
24. Microvascular complications of the
foot
• To target those with high risk for foot
complication: must be examined
– Insensate feet
– Foot deformities
– History of foot ulcers
28. Type 1 DM
• Insulin
– Recomibant DNA technology
– Insulin analogues
– Short acting: lispro
– Long acting: glargine
– Regimen:
• Long acting- supply basal insulin; given 35-45min prior to meal
• Short acting- prandial insulin; before or just after a meal (<20
minutes)
• Intermediate acting- 2/3 in AM and 1/3 in PM
– Preprandial insulin dose
• Insulin-to-carbohydrate ratio1-1.5units/10g carbohydrates
• 1 unit of insulin for every 2.7mmol/L over preprandial glucose target
• Insulin requirement 0.5-1U/kg per day
29. • Three major components of Exogenous
Insulin Therapy
– Basal insulin- regulate metabolic process even in
the absence of meals
– Bolus or nutritional- cover glycemic excursions
following meal or other nutritional supplements
– Correction dose- supplemental dose of short or
rapid acting insulin given to correct elevations in
glucose despite use of basal and bolus insulin
30. Type 2 DM
• 20-50% have DM complications
• Cardiovascular risk is the leading
cause of mortality
• Initial pharmacologic therapy:
metformin
• Insulin therapy
• Lean individuals, weight loss
• Renal and hepatic disease
• Hospitalized, acutely ill
• Single dose long acting insulin 0.3-
0.4 U/kg day given either before
breakfast and in the evening or just
before bedtime
31. • Insulin therapy
– Basal bolus
• Insulin requirements= 0.3-0.5U/kg per day
– 50% pre meal divided in doses prior to meal
– 50% basal (2/3 pre breakfast, 1/3 pre dinner)
32. Monitoring of glycemic control
• SMBG
– Self monitoring blood glucose
– Patients routinely measure their plasma glucose 3 or more times per
day to select mealtime bolus of short acting insulin and to modify
long acting insulin doses
– Assess efficacy of medication and impact on diet
• Long term glycemic control
– HbA1c
• Glycemic control over 2-3 months
• Measurement at least twice per year
– Fructosamine
• Glycated albumin, glycemic control over 2 weeks
34. Prevention
• Patient education
– Self monitoring
– Insulin administration
– Prevention and management of hyperglycemia
– Foot and skin care
– risk factor- modifying activities
• Nutrition
– Medical nutrition therapy
• Delay onset of type 2 DM in high risk individuals through weight reduction
• Improve glycemic control
• Manage diabetes related complications
• Exercise
– Cardiovascular risk reduction, dec BP, maintain muscle mass, reduce fat and
weight loss
– 150 min/ week distributed over at least 3 days of moderate aerobic physical
activity
factors contributing to hyperglycemia include reduced insulin
secretion, decreased glucose utilization, and increased glucose production.
Individuals with a genetic susceptibility
have normal beta cell mass at birth
but begin to lose beta cells secondary
to autoimmune destruction that occurs
over months to years. This autoimmune
process is thought to be triggered by an
infectious or environmental stimulus and
to be sustained by a beta cell–specific
molecule. In the majority, immunologic
markers appear after the triggering event
but before diabetes becomes clinically overt. Beta cell mass then
begins to decrease, and insulin secretion progressively declines,
although normal glucose tolerance is maintained. The rate of
decline in beta cell mass varies widely among individuals, with
some patients progressing rapidly to clinical diabetes and others
evolving more slowly. Features of diabetes do not become evident
until a majority of beta cells are destroyed (70–80%). At this point,
residual functional beta cells exist but are insufficient in number to
maintain glucose tolerance.
After the initial clinical presentation of type 1 DM, a
“honeymoon” phase may ensue during which time glycemic control
is achieved with modest doses of insulin or, rarely, insulin is
not needed. However, this fleeting phase of endogenous insulin
production from residual beta cells disappears as the autoimmune
process destroys remaining beta cells, and the individual becomes
insulin deficient. Some individuals with long-standing type 1 diabetes
produce a small amount of insulin (as reflected by C-peptide
production) and some individuals have insulin-positive cells in the
pancreas at autopsy.
Insulin secretion and insulin sensitivity are related,
and as an individual becomes more insulin resistant (by moving from point A
to point B), insulin secretion increases. A failure to compensate by increasing
the insulin secretion results initially in impaired glucose tolerance (IGT;
point C) and ultimately in type 2 DM (point D). (
