Diabetes Mellitus

Diabetes Mellitus
Rainier Icamina
Diabetes Mellitus (DM)
Comprises a group of common

metabolic disorder that share the
phenotype of hyperglycemia
Caused by complex interaction of:

Genetics
Environmental factors
Life style choices

Factors contributing to hyperglycemia:

Reduced insulin secretion
Decreased glucose utilization
Increase glucose production
Classification
Based on pathogenic process that leads to
hypoglycemia
Type 1 DM
Type 2 DM
Classification
Type 1 DM
Type 1A DM
– autoimmune beta cell destruction which leads to
insulin deficiency
Type 1B DM
– lack immunologic markers indicative of an
autoimmune destructive process of the beta cells.
However, they develop insulin deficiency by
unknown mechanisms and are ketosis prone
Classification
Type 2 DM
– Heterogeneous group of disorder characterized by variable degrees of insulin
resistance, impaired insulin secretion and increase glucose production.
Other Types of DM
Maturity Onset Diabetes Of The Young (MODY)
– Subtype of DM characterized by autosomal dominant inheritance, early onset
of hyperglycemia and impairment of insulin secretion
Classification
Gestational Diabetes Mellitus (GDM)
Insulin resistance related to metabolic
changes of late pregnancy, increase insulin
requirements and may lead to IGT
Most women revert to normal glucose
tolerance post-partum but have a substantial
risk (30 – 60%) of developing DM later in life
Diabetes
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Epidemiology
Prevalence has risen the past two decades
Type 2 DM expected to rise more
Age
Prevalence increase with age
– 0.19% < 20 yo
– 8.60% > 20 yo
– 20.1% > 65 yo
Gender
Similar to men and women at all ages but slightly
greater in men > 60 yo
Epidemiology
Geographic Variation
Type 1 DM
– Scandanavia, Northern Europe, United States
Type 2 DM
– Certain Pacific Islands, India, United States
Diabetes Mellitus
Risk Factors
Family History of Diabetes
Obesity (BMI > 25 kg/m2)
Race/ethnicity
(African, American, Hispanic American, Native American, Asian
American, Pacific Islander)
Previously identified IFG or IGT
Diabetes Mellitus
Risk Factors
History of GDM or delivery of baby > 4kg (>9lbs)
Hypertension (140/90)
HDL < 35mg/dl (0.90mmol/L) and/or Triglyceride level > 250 mg/dl
(2.82 mmol/L)
Polycystic ovary syndrome or acanthosis nigricans
History of vascular disease
Insulin
Biosynthesis
Preproinsulin
Produced in beta
cells of pancreatic
islet
Proinsulin
Mature Insulin C peptide

Insulin
Action Insulin
Receptor
Stimulate Intrinsic
Tyrosine Kinase Activity
Widespread Metabolic
and Mitogenic Effects
Insulin
Action
Insulin
Action
Glucose uptake
Glycogen synthesis
Protein synthesis
Lipogenesis
Regulation of various genes in insulin – responsive cells
Insulin
Insulin
Secretion
Pathogenesis Type 1 DM
Genetic susceptible
individuals
Normal beta cells autoimmune beta cell mass frank diabetes

at birth destruction declines
nitric oxide metabolites
Honeymoon
HLA region apoptosis phase
Chromosome 6 CD8+Tcell cytotoxicity
complete
destruction
Diabetes Mellitus
Pathophysiology of Type 2 DM
Insulin resistance
Impaired insulin production
Increase hepatic glucose production
Diabetes Mellitus
Insulin resistance
Result from combination of genetic
susceptibility and obesity
– Adipocytes – secret biologic products that
modulate insulin secretion and action (leptin,
TNF-a, FFA, resin and adiponectin)
PI-3-kinase signaling defect

– Reduce translocation of GLUT4 to plasma
membrane
Diabetes Mellitus
Insulin resistance
Result from combination of genetic
susceptibility and obesity
– Adipocytes – secret biologic products that
modulate insulin secretion and action (leptin,
TNF-a, FFA, resin and adiponectin)
PI-3-kinase signaling defect

– Reduce translocation of GLUT4 to plasma
membrane
Diabetes Mellitus
Impaired insulin secretion
Second genetic defect superimposed by
insulin resistance leading to beta cell failure
Glucose toxicity
– Chronic hyperglycemia impairs islet function
Lipotoxicity
– Elevation of FFA and dietary fat worsens islet
function
Diabetes Mellitus
Increase hepatic glucose production
Insulin resistance in the liver reflects failure

of hyperinsulinemia to suppress
gluconeogenesis
– Result in fasting hyperglycemia and decrease
glycogen storage
Diabetes Mellitus
Clinical Symptoms
Polyuria
Polydipsia
polyphagia
Weight loss
Fatigue
Weakness
Blurring of vision
Frequent superficial infections
Slow healing of skin lesions
Diabetes Mellitus
Diagnosis
Diagnostic Criteria
Diabetes Mellitus
Glucose tolerance
Normal
FPG < 5.6 mmol/L (100mg/dl)
IFG
FPG > 5.6 - < 7.0 mmol/L (126mg/dL)
DM
FPG > 7.0 mmol/L
The Roles of A1C
Surrogate marker for risk of
diabetic complications
Useful assessment of glycemic
control during clinical
management
Proposed future measure for
screening or confirming the
diagnosis of diabetes
21
Diabetes Mellitus
Diabetes Mellitus
Acute Complications
Diabetic Ketoacidosis (DKA)
Result from relative or absolute insulin deficiency
Combined with counter regulatory hormone excess
Promote gluconeogenesis, glycogenolysis, lipolysis

– ketone body formation
–
Clinical Features of DKA
Nausea and Vomiting
Abdominal pain
Tachycardia
Hypotension
Kussmaul sign
Lethargy and CNS depression
Cerebral Edema
Clinical Features of DKA
Nausea and Vomiting
Abdominal pain
Tachycardia
Hypotension
Kussmaul sign
Lethargy and CNS depression
Cerebral Edema
Hyperglycemic Hyperosmolar State
Relative insulin deficiency and inadequate fluid intake
Absence of Ketosis
Relative insulin deficiency and inadequate fluid intake
Absence of Ketosis
Clinical features
Polyuria
Weight loss
Diminished oral intake
Mental confusion
Lethargy or Coma
PE
Profound dehydration
Hyperosmolality
Hypotension
Tachycardia
Laboratories
Management for DKA
Management for HHS
Fluid replacement
1 to 3 L 0.9% normal saline - initial
0.45% saline initially then 5% dextrose in D5W
Potassium repletion
Management for HHS
Fluid replacement
1 to 3 L 0.9% normal saline - initial
0.45% saline initially then 5% dextrose in D5W
Potassium repletion
Chronic Complications
Divided into 2
Vascular
– Microvascular
– Macrovascular
Non Vascular
Divided into 2
Vascular
– Microvascular
– Macrovascular
Non Vascular
Diabetes Mellitus
Mechanism is unknown
4 prominent theories
Formation of advanced glycosylation end products (AGEs)
Sorbitol pathway of glucose metabolism
Formation of protein kinase C (PKC)
Hexosamine pathway
Diabetes Mellitus
AGEs
Formed via non-enzymatic glycosylation of intra and
extracellular proteins
Cross-link protein, accelerate atherosclerosis,
promote glumerular dysfunction, reduce nitric oxide
synthesis, induce endothelial dysfunction, and alter
extracellular matrix composition and structure
Serum levels correlates with levels of glycemia
Diabetes Mellitus
Sorbitol Pathway
Intracellular glucose
predominantly metabolize by phosphorelation and glycolysis
converted to sorbitol by enzyme aldose reductase
Increased sorbitol concentration alters redox potential, increase
cellular osmolality, generates reactive oxygen species
Leads to other types of cellular dysfunction
Diabetes Mellitus
PKC
Hyperglycemia increase the formation of diglycerol
leading to activation of PKC
Alters transcription of genes for fibronectin type I, type IV

collagen, contractile proteins, and extracellular matrix
proteins in the endothelial cells and neurons
Diabetes Mellitus
Hexosamine Pathway
Hyperglycemia increases the flux through the hexosamine
pathway, which generates
fructose-6-phosphate
– Substrate for O-linked glycosilation and proteoglycan production
Alter function by glycosylation of proteins such as
endothelial nitric oxide synthase
Change in gene expression of transforming growth
factor B or plasminogen activator inhibitor - I
Diabetes Mellitus
Diabetes Mellitus
Complications
Ophthalmologic
DM is the leading cause of blindness between age 20 –
74 in the US
25 times more likely to become legally blind
Result from progressive diabetic retinopathy and

clinically significant macular edema
Complications
Ophthalmologic
Diabetic Retinopathy
2 stages
Nonproliferative
Prolifertive
Complications
Nonproliferative
– Appears late in the first decade or early in the second decade
– Characterize by : retinal vascular microaneurysm
blot hemorrhages
cotton wool spots
Pathologic mechanism
Retinal ischemia
– Loss of retinal pericytes
– Increase retinal vascular permiability
– Alterations in retinal blood flow
– Abnormal retinal microvasculature
Complications
Proliferative
Neovasccularization in response to retinal hypoxia
Newly formed vessels appears near the optic nerve and/or macula and rupture easily
Leads to vitreous hemorrhage
–
Fibrosis
–
Retinal detachment
–
Complications
Complications
Renal Complications
Diabetic Nephropathy
Leading cause of ESRD in US
Leading cause of DM related morbidity and mortality
Most patient have diabetic retinopathy
Mechanism:
Hemodynamic alterations in renal microcirculation
Structural changes in the glumerulus
Complications
sequence
1st yr 1 – 5 yrs 5 – 10 yrs
Glomerular Thickening of Excrete small
hyperperfusion glomerular basement amt of albumin
Renal Hypertrophy membrane in urine
GFR Glomerular hypertrohy 40%
Mesingial volume
expansion Progress to overt
GFR n proteinuria
50%
ESRD 7 – 10yrs
Complications
Type 2 DM nephropathy
Microalbuminuria or overt nephropathy may be present at time of
diagnosis
Hypertension
Microalbuminuria is less predictive of diabetic nephropathy and
progression of overt nephropathy
Complications
Treatment
Prevention is the optimal therapy
– detection of microalbuminemia at an early stage when effective
therapies can be instituted
Complications
Treatment
Prevention is the optimal therapy
detection of microalbuminemia at an early stage when effective therapies can be instituted
–
Complications
Treatment
Interventions effective in slowing progression:
Near normalization of glycemia
– Strict blood pressure control
– Administration of ACE inhibitors and ARBs
– Treatment of dyslipidemia
–
Complications
Treatment
Interventions effective in slowing progression:
Near normalization of glycemia
– Strict blood pressure control
– Administration of ACE inhibitors and ARBs
– Treatment of dyslipidemia
–
Complications
Treatment
ACE inhibitors and ARBs
Reduce progression of nephropathy
– Repeat measurement of proteinuria after 2 – 3 moths of therapy
–
Blood pressure control

1 DM – ACE inhibitors
– 2DM – ARBs
–
Complications
Complications
Neuropathy
Occurs 50% of individuals with long standing type 1 and type 2 DM
Manifest as:
Polyneuropathy
Mononeuropathy
Autonomic neuropathy
Complications
Neuropathy
Polyneuropathy
Clinical findings
Frequently present with distal sensory loss
–
Hyperesthesia, Paresthesia, dysesthesia
–
Pain typically involves the lower extremities, usually present at rest and worsen at night.
As it progress, the pain subsides and eventually disappears, but sensory deficit in lower extremities
persist
Complications
Neuropathy
Mononeuropathy
Dysfunction of isolated cranial or peripheral nerves
Presents with pain and motor weakness in the distribution of a single nerve
3rd cranial nerve most commonly affected
– Heralded by diplopia
Complications
Neuropathy
Autonomic neuropathy
Involves cholinergic, noradrenergic, and peptidergic
system
Clinical findings
– Tachycardia and orthostatic hypotension
– Gastroparesis
– Bladder emptying abnormalities
– Hyperhydrosis of upper extremities and anhidrosis of feet
Complications
Neuropathy
Treatment
Glycemic control
Avoidance of alcohol
Vitamin suppliments
Symptomatic treatment
Chronic painful diabetic neuropathy

– May respond to: tricyclic antidepressants, gabapentin,
NSIAD
Complications
Gastrointestinal / Genitourinary Dysfunction
GI
Symptoms
– Delayed gastric emptying
» anorexia
» nausea
» vomiting
» early satiety
» abdominal bloating
– Constipation and diarrhea
Complications
Genitourinary
Cystopathy
– Inability to sense a full bladder
– Failure to void completely
Erectile dysfunction
Female sexual dysfunction
Complications
Treatment for GI
Improved glycemic control
Small frequent meals
Low fat meal
Complications
Treatment for GI
Dopamine agonist
Bethanechol
Loperamide
Diabetic diarrhea
–
Complications
Treatment for Cystopathy
Timed voiding or self catheterization
Bethanechol
Sildenafil
Erectile dysfunction
–
Complications
Cardiovascular
Cardiovascular disease is increased in individuals with type 1 or 2 DM
Marked increased (5 fold):
Peripheral arterial disease
Congestive heart failure
– Coronary artery disease
– Myocardial infarction
– Sudden death
–
–
Three fold increase risk for CVD

Complications
Cardiovascular
Risk factors
Dyslipidemia
Hypertension
Obesity
Reduced physical activity
Smoking
Complications
Cardiovascular
Treatment
Glycemic control
Aggressive cardiovascular risk modificaton
Use of stents and GP IIb/IIIA platelet inhibitor has improved the outcome of diabetic patient
PCI
CABG
Complications
Cardiovascular
Treatment
Risk factors:
– Dyslipidemia
– Hypertension
Complications
LDL control Treatment target: LDL <100

mg/dL
Standard method HMG-CoA reductase

inhibitors (statins)
Individualized options Intestinal cholesterol

absorption inhibitors
Bile acid–binding resins
Nicotinic acid
Complications
Triglyceride control
Treatment target:
<150 mg/dL
ndard treatment Fibric acid derivative (fibrate)
ividualized option Nicotinic acid

Caution is needed with combinations
Combining statins with fibrates or nicotinic
acid can cause
rhabdomyolysis or myositis, especially in
elderly patients or those with renal
insufficiency
Complications
Blood Pressure Control
Treatment target: BP <130/80 mm Hg
Standard methods Angiotensin-converting
enzyme
(ACE) inhibitor
(1, 2, or 3 agents Angiotensin-receptor blocker
(ARB)
may be needed) Thiazide
β -Blocker
Individualized options α –Adrenergic blocker or

central adrenergic agent
Complications
Summary of Main Metabolic Targets in
Diabetes
Blood pressure <130/80 mm Hg
LDL cholesterol <100 mg/dL
A1C <7% (<6.5%)

Complications
Lower Extremity
Leading cause of nontraumatic lower extremity amputation
Foot ulcers and infections
Pathologic factors:
– Neuropathy
– Abnormal foot biomechanics
– Peripheral arterial disease
– Poor wound healing
Complications
Lower Extremity
Risk factors for foot ulcer or amputation:
Male
Diabetes > 10 years
Peripheral neuropathy
Abnormal structure of foot
Peripheral arterial disease
Smoking
Poor glycemic control
History of previous ulcer
or amputation
Complications
Lower Extremities
Treatment
Prevention through identification of high risk patient
Patient education:
– Careful selection of foot wear
– Daily inspection of feet
– Daily foot hygiene
– Avoidance of self-treatment of foot abnormalities and high risk behavior
– Prompt consultation
Complications
Lower Extremities
Treatment
Osteomyelitis
– Combination of prolonged antibiotics and possible debridement of infected bone
– Peripheral bypass – effective in promoting wound healing
Diabetic foot ulcers
– Off loading
– Debridement
– Wound dressing
– Antibiotics
– Revascularization
– Limited amputation
Complications
Lower Extremities
Treatment
Infection
– Mild or non limb threatening
» Oral anitbiotics
» Surgical debridement
» Local wound care
– Severe Infection
» Intravenous antibiotic (broad spectrum coverage)
» Bed rest
» Local wound care
» Urgent surgical debridment
Complications
Complications
Infections in DM
Pneumonia
Gram (-), S. Aureus, and M. tubeculosis
UTI
E. coli, Candida, and Torulopsis glabrata
Complications are:
emphysematous pyelonephritis
Emphysematous cystitis
Skin– and soft tisue
–
Skin folds and nares – S. aureus
Complications
Complications
Complications
Diabetes Mellitus
Approach to patient
History PE
Weight or BMI
Family history of DM
Retinal examination
Risk factors
involved Orthostatic blood
pressure
Symptoms of
Foot examination
hyperglycemia
Peripheral pulses
Insulin injection sites
Teeth and gums
Diabetes Mellitus
Approach to patient
Classify the patient
Type 1 DM Type 2 DM
Onset of DM prior age 30
Diabetes after age of 30
Lean body habitus
Usually obese
Requirement of insulin as
initial therapy May not require insulin
Propensity to develop therapy
ketoacidosis May have:
An increase risk of other – Insulin resistance
autoimmune disorder – HPN
– CVD
– Dyslipidemia
– PCOS
Diabetes Mellitus
Approach to patient
Laboratory Assessment
First asses the if patient meet the diagnostic criteria for DM
Asses degree of glycemic control – A1c
Screen patient for DM associated conditions

Diabetes Mellitus
Approach to patient

Diabetes Mellitus
Approach to patient

Diabetes Mellitus
Treatment
Overall principle:
Eliminate symptoms related to
hyperglycemia
Reduce or eliminate long term microvascular
and macrovascular complications
Allow patient to achieve normal lifestyle if
possible
Diabetes Mellitus
Treatment Type 1 DM
Establishment of a target level of
glycemic control
Diabetes Mellitus
Treatment
Nutrition
Goal is to coordinate and match caloric
intake, both temporally and quantitatively,
with the appropriate amount of insulin.
Diabetes Mellitus
Treatment
Nutrition
Goal is to coordinate and match caloric
intake, both temporally and quantitatively,
with the appropriate amount of insulin.
Diabetes Mellitus
Treatment
Exercise
Cardiovascular risk reduction
Reduce blood pressure
Reduction in body fat
Lowers plasma glucose

Increase insulin sensitivity
Diabetes Mellitus
Treatment
Intensive management
Goal is to achieve euglycemia or near-
normal glycemia
– Patient education
– Comprehensive recording of plasma glucose
measurement and nutritional intake
– Variable insulin regimen that matches glucose
intake and insulin dose
Diabetes Mellitus
Treatment
Intensive management
Goal is to achieve euglycemia or near-
normal glycemia
– Patient education
– Comprehensive recording of plasma glucose
measurement and nutritional intake
– Variable insulin regimen that matches glucose
intake and insulin dose
Diabetes Mellitus
Treatment
Insulin
Treatment
Insulin Preparations
Normal Daily Plasma Insulin
Profile
µ U/mL
100
B L D
80
60
40
20
0600 0800 1200 1800 2400 0600
Time of day
B=breakfast; L=lunch; D=dinner
Action Profiles of Insulin Analogues
Plas
ma
Aspart, lispro 4–6 hours
insul
in Regular 6–8 hours
level NPH 12–20 hours
s
Ultralente 18–24 hours
Glargine 24 hours
0 1 2 3 4 5 6 7 8 9 101112131415161718192021222324
Hours
Diabetes Mellitus
Treatment for Type 1 DM
One common use regimen consist of twice daily injection of (NPH or
lente) mixed with short acting insulin before morning and evening meal
Effective in avoiding severe hyperglycemia
It does not generate near normal glycemic control
Enforce rigid schedule for the patient
Diabetes Mellitus
One common use regimen consist of twice daily injection of (NPH
or lente) mixed with short acting insulin before morning and
evening meal
Effective in avoiding severe hyperglycemia
It does not generate near normal glycemic control
Split-Mixed Regimen
Human Insulins
NPH NPH
Regular Regular
µ U/mL
100
B L D
80
Normal pattern
60
40
20
0600 0800 1200 1800 2400 0600
Time of day
Diabetes Mellitus
Multiple-component insulin regimen
Combination of:
– Basal insulin
– Preprandial short acting insulin
Offer patient more flexibility in terms of lifestyle

Best chance of near normoglycemia
Diabetes Mellitus
Multiple-component insulin regimen
Combination of:
– Basal insulin
– Preprandial short acting insulin
Offer patient more flexibility in terms of lifestyle

Best chance of near normoglycemia
Normal Daily Plasma Insulin
Profile
µ U/mL
100
B L D
80
60
40
20
0600 0800 1200 1800 2400 0600
Time of day
Treatment
Management of type 2 DM
Goal is similar to type 1 DM
Glycemic control
Treatment of conditions associated with type 2
DM
Detection and management of DM complication
Treatment
Treatment
Glucose lowering agent
Increase insulin secretion
Reduce glucose production
Increase insulin sensitivity
Treatment
Treatment
Treatment
Management for Type 2 DM
Insulin
Initial therapy for DM
Single dose of intermediate or long-acting insulin (0.3 – 0.4

U/kg per day)
– Given either before breakfast (NPH, lente, ultralente) or before
bedtime (NPH, lente, ultralente, glargine)
Treatment
Choice of initial glucose-lowering-agent
Initial choice is influence by level of
hyperglycemia
FPG <200 – 250 mg/dL – often respond well to
single oral dose
FBG > 250 mg/ dL – may respond partially but
are unlikely to achieve normoglycemia
Treatment
Combination therapy
Common regimen used:
Insulin secretagogue + metformin or thiazolidinedione
Sulfonylurea + metformin or thiazolidinedione
Insulin + metformin or thiazolidinedione
Treatment
Treatment
Insulin Secretagogues
Sulfonylureas, Repaglinide, and Nateglinide
Mechanism of action Increase basal and/or postprandial

insulin secretion
Efficacy depends upon Functioning β -cells
Power Sulfonylureas, repaglinide:
decrease A1C 1%–2%
Nateglinide:
decreases A1C 0.5%–1%
Dosing Sulfonylureas: 1 or 2 times daily
Repaglinide, nateglinide:
3 or 4 times daily with meals
Side effects Weight gain, allergy (rare)
Main risk Hypoglycemia
Biguanides
Metformin
Primary mechanism Decreases hepatic glucose

of action production
Efficacy depends upon Presence of insulin
Power Decreases A1C 1%–2%
Dosing 2 or 3 times daily (metformin)
1 or 2 times daily (metformin XR)
Side effects Diarrhea, nausea
Main risk Lactic acidosis
α-Glucosidase Inhibitors
Acarbose and Miglitol
Mechanism of action Delay carbohydrate absorption

Efficacy depends upon Postprandial hyperglycemia
Power Decrease A1C 0.5%–1%
Dosing 3 times daily
Side effects Flatulence
Main risk Liver enzyme elevation
(rare)
PPAR Agents: Glitazones (TZDs)
Pioglitazone and Rosiglitazone
Mechanism of action Enhance tissue response to insulin

Efficacy depends upon Presence of insulin and resistance
to its action
Power Decrease A1C 0.9%–1.6%
Dosing Once daily
Side effects Edema, weight gain, anemia
Main risk Congestive heart failure
Diabetes Mellitus
END $

Diabetes Mellitus

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Diabetes Mellitus

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Diabetes Mellitus

Comprises a group of common

Caused by complex interaction of:

Comprises a group of common

Factors contributing to hyperglycemia:

Mature Insulin C peptide

Normal beta cells autoimmune beta cell mass frank diabetes

PI-3-kinase signaling defect

PI-3-kinase signaling defect

Insulin resistance in the liver reflects failure

Promote gluconeogenesis, glycogenolysis, lipolysis

Alters transcription of genes for fibronectin type I, type IV

Result from progressive diabetic retinopathy and

Blood pressure control

Chronic painful diabetic neuropathy

Three fold increase risk for CVD

LDL control Treatment target: LDL <100

Standard method HMG-CoA reductase

Individualized options Intestinal cholesterol

ividualized option Nicotinic acid

Individualized options α –Adrenergic blocker or

Summary of Main Metabolic Targets in

Blood pressure <130/80 mm Hg

LDL cholesterol <100 mg/dL

A1C <7% (<6.5%)

Asses degree of glycemic control – A1c

Screen patient for DM associated conditions

Asses degree of glycemic control – A1c

Screen patient for DM associated conditions

Asses degree of glycemic control – A1c

Screen patient for DM associated conditions

Lowers plasma glucose

0600 0800 1200 1800 2400 0600

0600 0800 1200 1800 2400 0600

Offer patient more flexibility in terms of lifestyle

Offer patient more flexibility in terms of lifestyle

0600 0800 1200 1800 2400 0600

Single dose of intermediate or long-acting insulin (0.3 – 0.4

Mechanism of action Increase basal and/or postprandial

Primary mechanism Decreases hepatic glucose

Mechanism of action Delay carbohydrate absorption

Mechanism of action Enhance tissue response to insulin

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