DIABETES MELLITUS

NURE SHUKARE (MD)

2013 G.C
MWU

12/3/2012 1
 Diabetes Mellitus
Introduction

 A group of common metabolic disorders that share the

phenotype of hyperglycemia.
 Several distinct types of DM are caused by a complex
interaction of genetics & environmental factors.
 Depending on the etiology of the DM, factors contributing to
hyperglycemia include reduced insulin secretion, decreased
glucose utilization, & increased glucose production.
 Metabolic dysregulation associated with DM causes
secondary pathophysiologic changes in multiple organ
systems that impose a burden on the individual with
diabetes & on the health care system.

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 Classification

 Classified on the basis of the pathogenic process that leads to

hyperglycemia, as opposed to earlier criteria such as age of onset
or type of therapy.
 Two broad categories of DM are designated type 1 & 2.
 Type 1 DM is the result of complete or near-total insulin
deficiency.
 Type 2 DM is a heterogeneous group of disorders Xzed by variable
degrees of insulin resistance, impaired insulin secretion, &
increased glucose production.
 Distinct genetic & metabolic defects in insulin action &/or
secretion give rise to the common phenotype of hyperglycemia in
type 2 DM.

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 Other Types of DM

 Other etiologies for DM include:

 Specific genetic defects in insulin secretion or action,
 Metabolic abnormalities that impair insulin secretion,
 Mitochondrial abnormalities, &
 A host of conditions that impair glucose tolerance.
 Maturity-onset diabetes of the young (MODY) is a subtype of DM Xzed
by :
 Autosomal dominant inheritance,
 Early onset of hyperglycemia (usually <25 years), &
 Impairment in insulin secretion.
 Mutations in the insulin receptor cause a group of rare disorders Xzed
by severe insulin resistance.

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 Con…
 DM can result from pancreatic exocrine disease when the
majority of pancreatic islets are destroyed.
 Cystic fibrosis-related DM is an important consideration in
this pt population.
 Hormones that antagonize insulin action can also lead to
DM.
 Viral infections have been implicated in pancreatic islet
destruction but are an extremely rare cause of DM.
 A form of acute onset of type 1 diabetes, termed fulminant
diabetes, has been noted in Japan & may be related to viral
infection of islets.

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 Gestational Diabetes Mellitus (GDM)

 Glucose intolerance developing during pregnancy is classified as

gestational diabetes.
 Insulin resistance is related to the metabolic changes of late
pregnancy, & the increased insulin requirements may lead to IGT or
diabetes.
 GDM occurs in 7% (range 2–10%) of pregnancies in the U.S; most
women revert to normal glucose tolerance postpartum but have a
substantial risk (35–60%) of developing DM in the next 10–20 years.
 The International Diabetes & Pregnancy Study Groups now
recommends that diabetes diagnosed at the initial prenatal visit
should be classified as "overt" diabetes rather than gestational
diabetes

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 Etiologic Classification of DM

I. Type 1 diabetes (beta cell destruction, usually

leading to absolute insulin deficiency)
A. Immune-mediated
B. Idiopathic
 Formerly known as insulin-dependent DM.
 Usually occurs in childhood or early adulthood
(age less than 30).
 Patients are usually thin.
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 Con…
 They require insulin for survival & develop
ketoacidosis when pts are not on adequate insulin
therapy.
 This accounts for 10% of cases of DM.
 Oral hypoglycemic agents will not be effective to lower
the blood glucose level.
 Due to β-cell destruction, with absolute deficiency of
insulin, w/h is of multifactorial causes such as genetic
predisposition, viral & autoimmune attacks on the
beta islet cells.
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 Con…
II. Type 2 diabetes (may range from predominantly insulin resistance with
relative insulin deficiency to a predominantly insulin secretory defect with
insulin resistance)
 Formerly non insulin-dependent DM.
 Usually occurs in people >40 years of age.
 Most (about 60%) of the pts are obese.
 Occurs with intact β-cell function but there is peripheral tissue resistance to
insulin.
 There may be some decrease in insulin production or a hyperinsulin state.
 Pts are not prone to develop ketoacidosis but may develop it under
conditions of stress.
 Pts do not require insulin for survival at least in the earlier phase of ds.
 Blood sugar level can be corrected by oral hypoglycemic agents.

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 Con…
. Other specific types of diabetes
III

 A. Genetic defects of beta cell function Xzed by mutations in:

     1. Hepatocyte nuclear transcription factor (HNF4-α) 4 α (MODY 1)
        2. Glucokinase (MODY 2)
        3. HNF-1 (MODY 3)
        4. Insulin promoter factor-1 (IPF-1; MODY 4)
        5. HNF-1β(MODY 5)
        6. NeuroD1 (MODY 6)
        7. Mitochondrial DNA
        8. Subunits of ATP-sensitive potassium channel
        9. Proinsulin or insulin

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 Con…
  B. Genetic defects in insulin action Fibrocalculous pancreatopathy,
        1. Type A insulin resistance Mutations in carboxyl ester lipase
        2. Leprechaunism     D. Endocrinopathies—:
        3. Rabson-Mendenhall Sxx Acromegaly,
        4. Lipodystrophy Sxx Cushing's syndrome,
C. Diseases of the exocrine  Glucagonoma,
pancreas: Pheochromocytoma,
Pancreatitis, Hyperthyroidism,
Pancreatectomy, Somatostatinoma,
Neoplasia,  Aldosteronoma
Cystic fibrosis,    
Hemochromatosis,

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 Con…
 E. Drug- or chemical-induced :  Alpha-interferon,
 Glucocorticoids,  Protease inhibitors,
 Vacor (a rodenticide),  Antipsychotics (atypicals &
 Pentamidine, others),
 Nicotinic acid,  Epinephrine
 Diazoxide,     F. Infections:
 β-adrenergic agonists,  Congenital rubella,
 Thiazides,  Cytomegalovirus,
 Hydantoins,  Coxsackievirus
 Asparaginase,   

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 Con…
 G. Uncommon forms of  Turner's syndrome,
immune-mediated diabetes:  Friedreich's ataxia,
 "stiff-person" Sxx,  Huntington's chorea,
 anti-insulin receptor  Laurence-Moon-Biedl
antibodies syndrome,
 H. Other genetic syndromes  myotonic dystrophy,
sometimes associated with  porphyria,
diabetes:
 Prader-Willi syndrome
 Wolfram's syndrome,
IV. Gestational DM (GDM)
 Down's syndrome,
 Klinefelter's syndrome,

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 Epidemiology

 Worldwide prevalence of DM has risen dramatically over the past two

decades, from an estimated 30 million cases in 1985 to 285 million in
2010.
 Based on current trends 438 million individuals will have DM by the
year 2030.
 Although the prevalence of both type 1 & type 2 DM is increasing
worldwide, the prevalence of type 2 DM is rising much more rapidly,
b/c of increasing obesity, reduced activity as countries become more
industrialized, & the aging of the population.
 In 2010, the prevalence of DM ranged from 11.6 to 30.9% in the 10
countries with the highest prevalence (Naurua, UAE, Saudi Arabia,
Mauritius, Bahrain, Reunion, Kuwait, Oman, Tonga, Malaysia—in
descending prevalence).

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 Con….
 In U.S (2010) 25.8 million persons, or 8.3% of the population,
had diabetes.
 DM increases with aging.
 Prevalence of DM in the U.S was estimated to be 0.2% in
individuals aged <20 yrs & 11.3% in individuals aged >20 yrs.
 In individuals aged >65 yrs, the prevalence of DM was 26.9%.
 The prevalence is similar in men & women throughout most
age ranges (11.8% & 10.8%, respectively, in individuals aged
>20 years).
 In 2030 the greatest number of individuals with diabetes will
be aged 45–64 years.

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 Con…
 There is geographic variation in the incidence of both type 1 & 2 DM.
 Scandinavia has the highest incidence of type 1 DM (e.g., in Finland,
the incidence is 57.4/100,000/yr).
 The Pacific Rim has a much lower rate of type 1 DM (in Japan &
China, the incidence is 0.6–2.4/100,000/yr);
 Northern Europe & U.S have intermediate rate (8–20/100,000/yr).
 Much of the increased risk of type 1 DM is believed to reflect the
frequency of high-risk human leukocyte antigen (HLA) alleles among
ethnic groups in d/t geographic locations.
 The prevalence of type 2 DM is highest in certain Pacific islands & the
Middle East & intermediate in countries such as India & the U.S.
 This variability is likely due to genetic, behavioral, & env’tal factors.

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 Con…
 DM prevalence also varies among d/t ethnic populations within a given
country.
 E.g,prevalence of DM in the U.S (age > 20 yrs) was 7.1% in non-Hispanic
whites, 7.5% in Asian Americans, 11.8% in Hispanics, & 12.6% in non-
Hispanic blacks.
 Onset of type 2 DM occurs at an earlier age in ethnic groups other than
non-Hispanic whites.
 In Asia, the prevalence of DM is increasing rapidly & the diabetes
phenotype appears to be d/t from that in the U.S & Europe—onset at a
lower BMI & younger age, greater visceral adiposity, & reduced insulin
secretory capacity.
 In U.S, DM was listed as the 7th leading cause of death.
 DM was the 5th leading cause of death worldwide.

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 Con…
 Africa is not free from this disease w/h traditionally is considered
the disease of the affluent societies of the first world.
 In Tunisia the prevalence of DM is 4%, in South Africa 5%, in
Tanzania 0.9%.
 In Ethiopia one community based study showed that the
prevalence of DM in Gondar area of northern Ethiopia was found
to be about 0.5%, & about 4.7% among older than 40 years.
 Emigrants from Ethiopia to Israel have shown a higher prevalence
of 8.9%.
 These findings imply that the incidence of disease increases with
increasing age, as well as either the dietary habit or sedentary &
stressful life style of the developed countries.

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 Diagnosis

 Glucose tolerance is classified into three broad categories:

 Normal glucose homeostasis,
 Impaired glucose homeostasis &
 Diabetes mellitus,
 Glucose tolerance can be assessed using :
 Fasting plasma glucose (FPG),
 Response to oral glucose challenge(OGTT), or
 Hemoglobin A1C (A1C).
 FPG <5.6 mmol/L (100 mg/dL), a plasma glucose <140 mg/dL
(11.1 mmol/L) following an oral glucose challenge, & A1C <5.6%
are considered to define normal glucose tolerance.

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 Criteria for the Diagnosis of DM

 Sxs of diabetes plus

 RBG ≥200 mg/dLor 
 FBG ≥126 mg/dLor 
 A1C ≥ 6.5%or 
   2-h plasma glucose ≥200 mg/dL during an
OGTT.
 

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 Con…

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 Con…
 The current criteria for the diagnosis of DM emphasize that the
A1C or the FPG as the most reliable & convenient tests for
identifying DM in asymptomatic individuals.
 OGTT although still a valid means for diagnosing DM, is not often
used in routine clinical care.
 Abnormalities on screening tests for DM should be repeated
before making a definitive diagnosis of DM, unless acute
metabolic derangements or a markedly elevated plasma glucose
are present.
 These criteria also allow for the diagnosis of DM to be withdrawn
in situations when the glucose intolerance reverts to normal.

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 Screening

 Use of the FPG or the A1C as a screening test for type 2 DM

is recommended b/c :
1. Large number of individuals who meet the current criteria
for DM are asxtic & unaware that they have the disorder,
2. Epidemiologic studies suggest that type 2 DM may be
present for up to a decade before diagnosis,
3. Some individuals with type 2 DM have one or more
diabetes-specific Cxs at the time of their Dx, &
4. Teatment of type 2 DM may favorably alter the natural
history of DM.

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 Con…
 The ADA recommends screening all individuals >45 yrs
every 3 yrs & screening individuals at an earlier age if they
are overweight (BMI) >25 kg/m2 & have one additional
risk factor for diabetes.
 In contrast to type 2 DM, a long asymptomatic period of
hyperglycemia is rare prior to the DX of type 1 DM.
 A number of immunologic markers for type 1 DM are
becoming available, but their routine use is discouraged
pending the identification of clinically beneficial
interventions for individuals at high risk for developing
type 1 DM.

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 Risk Factors for Type 2 DM
 Family Hx of diabetes (i.e., parent or sibling with type 2 diabetes)
 Obesity (BMI ≥25 kg/m2)
 Physical inactivity
 Race/ethnicity (e.g., African American, Latino, Native American,
Asian American, Pacific Islander)
 Previously identified with IFG, IGT, or an A1C of 5.7–6.4%
 HX of GDM or delivery of baby >4 kg (9 lb)
 HTN (BP≥140/90 mmHg)
 HDL cholesterol level <35 mg/dL (0.90 mmol/L) &/or a triglyceride
level >250 mg/dL (2.82 mmol/L)
 Polycystic ovary syndrome or acanthosis nigricans
 HX of cardiovascular disease

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 Type 1 Diabetes Mellitus
Definition
 A group of common metabolic disorders that
share the phenotype of hyperglycemia.
 Caused by a complex interaction of genetics,
environmental factors, & lifestyle choices.
 Classified on the basis of a pathogenic process
leading to hyperglycemia

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 Con…
 Results from pancreatic beta-cell destruction,
usually leading to absolute insulin deficiency
 Type 1A DM results from autoimmune beta-cell
destruction, which leads to insulin deficiency.
 Type 1B DM lacks immunologic markers
indicative of an autoimmune destructive process
of beta cells, but like type IA DM, it is a ketosis-
prone insulin deficiency that develops by
unknown mechanisms.
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 Etiology

Type 1A DM
 Results from synergistic effects of genetic,
environmental, & immunologic factors that
ultimately destroy pancreatic beta cells
 Genetic susceptibility
 Environmental triggers
 Putative triggers: viruses (esp. coxsackie & rubella),
bovine milk proteins, nitrosourea compounds
 Event may precede onset of DM by several years.
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 Con…
 Immunologic factors
 Abnormalities in the humoral & cellular arms of the immune
system that have been identified include:
– Islet-cell autoantibodies,
– Activated lymphocytes in the islets, peripancreatic lymph nodes, &
systemic circulation,
– T lymphocytes that proliferate when stimulated with islet proteins,
– Release of cytokines within the islets.
 Precise mechanisms of beta-cell death are not known but may
involve formation of nitric oxide metabolites, apoptosis, &
direct CD8+ T-cell cytotoxicity.

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 Con…
 Temporal development of type 1A DM
 Persons with genetic susceptibility have normal β-cell mass at birth but
begin to lose through autoimmune destruction over months to yrs.
 This autoimmune process is thought to be triggered by infectious or
env’tal stimulus & sustained by β-cell–specific antigens.
 The rate of decrease in β-cell mass varies widely, with some pts
progressing rapidly to clinical diabetes & others evolving more slowly.
 DM become evident once the majority (~80%) of β-cells are lost.
 Transition from glucose intolerance to frank DM is triggered by events
associated with ↑ed insulin requirements (e.g., infections or puberty).
 Type 1B DM __Etiology unknown

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 Associated Conditions

 Celiac sprue  Down’s syndrome

 Autoimmune disorders  Klinefelter’s syndrome
 Autoimmune thyroid  Turner’s syndrome
disease  Wolfram syndrome
 Adrenal insufficiency  Friedreich’s ataxia
 Pernicious anemia  Huntington’s chorea
 Vitiligo  Laurence-Moon-Biedl
 Genetic syndromes syndrome
 Myotonic dystrophy
sometimes associated
 Porphyria
with DM
 Prader-Willi syndrome

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 Con…
 Periodontal disease
 Psychiatric conditions (occur more frequently
in DM than the general population)
 Depression
 Eating disorders
– Binge-eating disorders
– Bulimia
– Anorexia nervosa

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 Natural history of type 1 diabetes

 The disease is progressive going through:

 Phases of antibody production,
 Phase of impaired GTT,
 Phase of abnormal FBS, &
 Phase of abnormal FBS with Ketonemia.

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 Honeymoon period
 In young people who are diagnosed for the first time to have
overt DM, the DM may have been precipitated by acute
metabolic stressful conditions (such as infection or
pregnancy).
 In such circumstances, the increased metabolic demand for
insulin, may lead to a relative insulin deficiency, & pts
become symptomatic, & may need exogenous insulin to
control their symptoms.
 With the return to baseline metabolic demands, when the
stressful event abates, the pancreatic reserve may be
adequate to maintain normal or near-normal blood glucose.

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 Con……
 Such pts may undergo a period of transient “cure”
during w/h time they may not require exogenous
Insulin to control their blood glucose level.
 Such pts are said to be in a “HONEYMOON”
period.
 This is unfortunately is transient & the pts will be
needing insulin again when the progressive
destruction of β-cells leads to absolute insulin
deficiency.

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 Symptoms & Signs

 DM & its Cxs produce a wide range of sxs & signs.

 Symptoms secondary to acute hyperglycemia
• May occur at any stage of the disease
 Symptoms related to chronic Cxs
• Begin to appear during second decade of hyperglycemia
 The most common presentation in nonobese young
persons is acute hyperglycemia.
 Older pts may present with more insidious onset of
sxs, or rarely, may be identified by laboratory testing.

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 Hyperglycemia
Symptoms Signs
 Polyuria  Frequent superficial
 Polydipsia infections (vaginitis,
 Weight loss fungal skin
infections)
 Fatigue
 Slow healing of skin
 Weakness
lesions after minor
 Blurry vision trauma

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 Historical features to assess

In persons with newly diagnosed DM

Complete medical Hx, with emphasis on DM-relevant aspects
Weight
Family Hx of DM & its Cxs
Risk factors for CVD
Exercise
Smoking
Ethanol use
Assess for sxs or signs of acute hyperglycemia.
Screen for:
Chronic Cxs & conditions associated with DM
DM-related comorbid conditions (CVD, HTN, dyslipidemia)

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 Con…
 In persons with previously diagnosed DM
 All of the above plus
 Assessment of prior diabetes care
 Type of therapy
 Prior hemoglobin A1C levels
 Results of self-monitoring of blood glucose (SMBG)
 Frequency of hypoglycemia
 Presence of DM-specific Cxs
 Assessment of pt’s knowledge about diabetes
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 Complete physical examination

Pay particular attention to:
Wt or BMI
Funduscopic examination
BP
BP >130/80 mmHg considered
HTN in DM
Examination of lower extremities
to seek evidence of:
Sites of skin ulceration
Peripheral neuropathy
•Vibratory sensation (128-MHz
tuning fork at base of great toe)
12/3/2012
• Ability to sense touch with
monofilament (5.07, 10-g )
Calluses
Superficial fungal infections
Nail disease
Foot deformities (e.g., hammer or
claw toes & Charcot foot)
Peripheral pulses
Insulin injection sites
Teeth & gums
Periodontal disease is more
frequent in DM.
40
 Diagnostic Approach
Diagnostic criteria for diabetes
 Sxs of diabetes plus
1. RBG concentration ≥11.1 mmol/L (200 mg/dL)
 Random: without regard to time since last meal
2. FPG ≥7.0 mmol/L (126 mg/dL)
 Fasting: no caloric intake for at least 8 hours
3. 2-hr plasma glucose ≥11.1 mmol/L (200 mg/dL) during OGTT.
 Test should be performed by using a glucose load containing
the equivalent of 75 g of anhydrous glucose dissolved in water.
 Not recommended for routine clinical use

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 Con….
 In the absence of unequivocal hyperglycemia &
acute metabolic decompensation, criteria should
be confirmed by repeated testing on a d/t day.
IFG
 Glucose level >5.6 mmol/ L (100 mg/dL) but <7.0
mmol/L (126 mg/dL)
 IGT
 Glucose level 7.8–11.1 mmol/L (140–200 mg/dL)
2 hours after a 75-g oral glucose load
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 Laboratory & additional assessments

 Assess diagnostic criteria for DM.

 Assess degree of glycemic control by measuring
hemoglobin A1C.
 Screen for DM-associated conditions (e.g.,
microalbuminuria, dyslipidemia, thyroid
dysfunction).
 Perform cardiac stress testing to screen for
asymptomatic coronary artery disease if the pt is
at high risk for cardiovascular disease.
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 Hemoglobin A1C
 Standard method for assessing long-term glycemic control.
 Should be measured in all persons with DM during the initial
evaluation & as part of comprehensive diabetes care
 Notes on use
 Hemoglobin A1C measurement is not currently recommended
for diagnosis.
 In standardized assays, the hemoglobin A1C value approximates
the following mean plasma glucose values.
 6% = Glucose 7.5 mmol/L (135 mg/dL)
 7% = Glucose 9.5 mmol/L (170 mg/dL)
 8% = Glucose 11.5 mmol/L (205 mg/dL)

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 Con…
 A 1% increase in the hemoglobin A1C level
translates into a 2.0-mmol/L (35-mg/dL)
increase in the mean glucose level.
 Significant interassay variations exist.
 Assay methods must be similar in order to
compare with prior measurements.
 Hemoglobinopathies, anemias, & uremia may
interfere with hemoglobin A1C results.

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 Immunologic markers
 Primarily used in initial evaluation for possible type 1 DM
 Islet-cell autoantibodies.
 Composite of several d/t antibodies directed at pancreatic islet molecules
(e.g., GAD, insulin, IA-2/ICA-512, & an islet ganglioside)
 Marker of autoimmune process of type 1A DM
 Present in:
• >75% of pts with new-onset type 1A DM
• 3–4% of first-degree relatives of persons with type 1A DM
 Presence predicts risk for type 1A DM.
• Persons with impaired insulin secretion after IV glucose tolerance testing:
>50% 5-year risk
• Without impaired insulin secretion: <25% 5-year risk
 Assays for autoantibodies to GAD-65 are commercially available & can be
helpful in confirming a diagnosis of type 1A DM.
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 Other laboratory tests

 C-peptide measurement
 Low level confirms need for insulin.
 May help distinguish type 1 DM from type 2
DM in some circumstances.

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Screening laboratory tests for DM-associated conditions

 Microalbuminuria
 Spot urine microalbumin/creatinine ratio (beginning
5 years after onset of type 1 DM)
 Microalbuminuria is defined by a
microalbumin/creatinine ratio >30 mg/g.
 Dyslipidemia
 Fasting lipid profile (annual)
 Thyroid dysfunction
 Serum thyroid-stimulating hormone
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 Treatment Approach

 Goals of therapy
 Eliminate symptoms related to
hyperglycemia.
 Achieve sustained euglycemia.
 Avoid hypoglycemia.
 Reduce or eliminate long-term microvascular
& macrovascular Cxs.
 Allow the pt to maintain normal lifestyle.
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Factors to consider in developing goals of therapy

 Age
 Ability to understand & implement complex Rx regimen
 Presence & severity of Cxs
 Ability to recognize hypoglycemic sxs
 Presence of other medical conditions or treatments that might
alter response to therapy
 Lifestyle & occupation (e.g., possible consequences of
experiencing hypoglycemia on the job)
 Level of support available from family & friends
 Life expectancy at time of Dx
 Presence of microvascular Cxs

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 Steps needed to reach goals

 Identify target level of glycemic control for each pt.

 Ideal goals for glycemic control
 Preprandial plasma glucose level: 5.0–7.2 mmol/L (90–
130 mg/dL)
 Peak postprandial plasma glucose level: <10 mmol/L
(<180 mg/dL)
 Hemoglobin A1C level: <7.0%
 Provide pt with educational & pharmacologic resources
necessary to reach goal.
 Monitor/treat DM-related Cxs.
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 Comprehensive care

Best accomplished by a multidisciplinary team approach.

 Primary care provider &/or endocrinologist or diabetologist.
 Certified diabetes educator.
 Nutritionist.
 Subspecialists with experience in treating DM-related Cxs
 Neurologist
 Nephrologist
 Vascular surgeon
 Cardiologist
 Ophthalmologist
 Podiatrist

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 Patient education

 Diabetes educator:
 A health care professional (nurse, dietician, or pharmacist) with specialized pt
education skills.
 Certified in diabetes education (e.g., American Association of Diabetes
Educators)
 Topics important for optimal care
 Nutrition, SMBG &Urine ketone monitoring
 Insulin administration
 Guidelines for diabetes management during illnesses
 Management of hypoglycemia
 Foot & skin care
 Diabetes management before, during, & after exercise
 Risk factor–modifying activities

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 Other steps

 Insulin replacement
 Treatment of cardiovascular risk factors

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 Specific Treatments
NutritionaL therapy

Nutritional recommendations for all persons with DM.

 Protein
 ~15–20% of kcal/d
 ~10% in pts with nephropathy
 Saturated fat
 <10% of kcal/d
 <7% in pts with elevated low-density lipoprotein cholesterol level
 Polyunsaturated fat
 ~10% of kcal/d
 Avoid trans-unsaturated fatty acids.

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 Con…
 60–70% of calories divided b/n carbohydrate &
monounsaturated fat
 Based on medical needs & personal tolerance
 Glycemic index of food is not as important.
 Use of caloric sweeteners, including sucrose, is acceptable.
 Fiber : 20–35 g/d
 Sodium: ≤3,000 mg/d
 Cholesterol: ≤300 mg/d
 Alcohol
 Same precautions as in general population
 May increase risk for hypoglycemia & should be taken with food

12/3/2012 56
 Exercise
Avoid exercise-related hyper- or hypoglycemia.
 Monitor blood glucose before, during, & after exercise.
 Delay exercise if blood glucose level is >250 mg/dL or <100
mg/dL, or if ketones are present.
 Monitor glucose level during exercise & ingest carbohydrate to
prevent hypoglycemia.
 Decrease insulin doses (based on previous experience) before
exercise & inject insulin into nonexercising area.
 Learn individual glucose responses to d/t types of exercise &
increase food intake for up to 24 hrs after exercise, depending
on intensity & duration of exercise.

12/3/2012 57
 Con….
 Relative contraindication: untreated proliferative
retinopathy
 May lead to vitreous hemorrhage or retinal detachment
 Consider formal exercise tolerance testing for:
 Age >35 years
 DM duration >15 years
 Microvascular complications
 Peripheral arterial disease
 Other risk factors for coronary artery disease
 Autonomic neuropathy

12/3/2012 58
 Insulin preparations

 Current insulin preparations  Insulin aspart

 Generated by recombinant • Onset: <0.25 hour
DNA technology • Peak: 0.5–1.5 hours
• Beef or pork insulins are no • Effective duration: 3–4 hrs
longer used.  Regular
 Short-acting • Onset: 0.5–1 hour
 Lispro • Peak: 2–3 hours
• Onset: <0.25 hour • Effective duration: 3–6 hrs
• Peak: 0.5–1.5 hours
• Effective duration: 3–4 hrs

12/3/2012 59
 con…
 Intermediate-acting
 NPH
– Onset: 2–4 hours
– Peak: 6–10 hours
– Effective duration: 10–16 hours
 Lente
– Onset: 3–4 hours
– Peak: 6–12 hours
– Effective duration: 12–18 hours
12/3/2012 60
 Con…
 Long-acting
 Ultralente
– Onset: 6–10 hours
– Peak: 10–16 hours
– Effective duration: 18–20 hours
 Glargine
– Onset: 4 hours
– Peak: minimal
– Effective duration: 24 hours
12/3/2012 61
 • Combinations

 75/25 (75% protamine lispro, 25% lispro)

– Onset: 0.5–1 hour
– Peak: dual
– Effective duration: 10–14 hours
 70/30 (70% NPH, 30% regular)
– Onset: 0.5–1 hour
– Peak: dual
– Effective duration: 10–16 hours
 50/50 (50% NPH, 50% regular)
– Onset: 0.5–1 hour
– Peak: dual
– Effective duration: 10–16 hours

12/3/2012 62
 Insulin regimens
General

 Goal: insulin regimens that mimic physiologic insulin

secretion (basal requirements & postprandial spikes)
 Basal requirements: intermediate- or long-acting insulins
 Prandial insulin: short-acting
• Lispro & insulin aspart: Inject just before or just after a meal.
• Regular insulin: Inject 30–45 minutes before a meal.
 The most physiologic regimens entail:
 More frequent insulin injections
 Greater reliance on short-acting insulin
 More frequent capillary plasma glucose measurements

12/3/2012 63
 Con…
 Daily insulin requirements
 Pts with type 1 DM require 0.5–1.0 U/kg per
day of insulin, divided into multiple doses.
 ~40–50% should be given as basal insulin.

12/3/2012 64
 Intermediate-acting insulin mixed with short-acting insulin

 Intermediate-acting insulin (NPH or lente) mixed with a short-

acting insulin before morning & evening meal
 2/3rd s of total daily insulin dose in morning
• 2/3rd s given as intermediate-acting insulin
• 1/3rd as short-acting
 1/3rd before evening meal
• ½ as intermediate-acting insulin
• ½ as short-acting
 Moving intermediate insulin from before the evening meal to
bedtime may:
• Avoid nocturnal hypoglycemia
• Provide more insulin as glucose levels increase in early morning
(dawn phenomenon)
12/3/2012 65
Continuous subcutaneous insulin infusion (CSII)

 Also referred to as insulin pump

 Sophisticated insulin infusion devices that can
accurately deliver small doses of insulin (microliters
per hour)
 Lispro or insulin aspart is most often used in CSII.
 Multiple basal infusion rates can be programmed to:
 Accommodate nocturnal versus daytime basal insulin
requirement
 Alter infusion rate during exercise
 Select different waveforms of insulin infusion

12/3/2012 66
 Con…
 Preprandial insulin ("bolus") is delivered on the basis of
instructions from the pt, who follows individualized algorithms
that account for the preprandial plasma glucose level,
anticipated carbohydrate intake.
 Requires a health professional with considerable experience
with insulin infusion devices & frequent pt interactions with
diabetes management team.
 Unique complications of CSII
 Infection at infusion site
 Unexplained hyperglycemia due to obstruction of infusion set
 Diabetic ketoacidosis if pump becomes disconnected

12/3/2012 67
 Intensive management

 Requires multiple resources, including:

 Thorough & continuing pt education.
Comprehensive recording of plasma glucose
measurements & nutrition intake by the pt.
 Variable insulin regimen that matches glucose intake &
insulin dose
• Insulin regimens usually include multiple-
component insulin regimens, multiple daily
injections, or insulin infusion devices
 Goal: achieve euglycemia or near-normal glycemia
12/3/2012 68
 Indications

Otherwise healthy adults with type 1 DM (selected adolescents &

older children).
 Purposeful, therapeutic attempt to avoid/lessen microvascular
Cxs.
 All pregnant women with DM.
 All women with DM who are planning pregnancy.
 Management of labile DM.
Availability of health care professionals with appropriate expertise.
 Pts who have had kidney transplantation for diabetic
nephropathy.
 Strongly encouraged in pts with newly diagnosed type 1 DM.

12/3/2012 69
 Benefits

 Reduction in microvascular complications.

 Possible delay or reduction in macrovascular Cxs.
 The pt experiences greater control over his or her DM.
 Improved sense of well-being, greater flexibility in
timing & content of meals, & capability to alter insulin
dosing with exercise.
 In pregnancy, reduces risk of fetal malformations &
morbidity
 Not associated with greater degree of side effects, such
as hypoglycemia or weight gain.
12/3/2012 70
 Complications
 Increased economic costs
 Greater demands on pt

12/3/2012 71
 Emerging therapies

 Whole-pancreas transplantation
 Conventionally performed concomitantly with renal
transplantation
 May normalize glucose tolerance in type 1 DM
 ~80% of simultaneous pancreas & kidney transplants remain
functioning at 1 year.
 Major disadvantage is immunosuppression.
 Pancreatic islet beta-cell transplantation
 Less invasive alternative to whole-pancreas transplantation.
 Current barriers to more widespread use of this approach
include poor islet beta-cell yield & tissue availability.

12/3/2012 72
 Con…
 Inhaled insulin & additional insulin analogues
are in advanced stages of clinical trials.
 Aminoguanidine, an inhibitor of formation of
advanced glycosylation end products, &
inhibitors of protein kinase C may reduce DM
Cxs.
 Closed-loop pumps that infuse appropriate
amount of insulin in response to changing
glucose levels are potentially feasible.
12/3/2012 73
 Perioperative management

 Assessment
 Measure hemoglobin A1C, to assess glycemic
control; optimize before surgery, if possible.
 Monitor electrolytes, renal function, &
intravascular volume.
 Consider preoperative cardiovascular evaluation,
even in asymptomatic persons.

12/3/2012 74
 Treatment regimens

Insulin infusion
 Preferred method for managing type 1 DM in the
perioperative period, especially if pt is receiving nil by po.
 Initial infusion rate: 0.5–5 U/h; dependent on degree of
insulin resistance & clinical situation.
 Adjustment of infusion rate by staff, based on algorithm or in
consultation with physician.
 Rate adjusted to maintain plasma glucose within optimal
range; based on hourly capillary glucose measurements.
 Can be temporarily discontinued if hypoglycemic; can resume
at lower infusion rate once plasma glucose level exceeds 5.6
mmol/L (100 mg/dL).

12/3/2012 75
 Con…
 Subcutaneous insulin regimens
 Reduced dose of subcutaneous, long-acting insulin may
suffice if:
– Brief diagnostic or surgical procedure
– Local or regional anesthesia
 Dose of long-acting insulin should be reduced by 30–
40%.
 Short-acting insulin is either held or reduced by 30–
40%.
 Glucose may be infused to prevent hypoglycemia.
12/3/2012 76
 Total parenteral nutrition (TPN)

 Greatly increases insulin requirements

 IV insulin infusion (rather than subcutaneous) is the
preferred mode of insulin administration.
• Use separate insulin infusion for rapid titration to
required dose.
• After determination of the total insulin dose, continue
to administer insulin as a separate infusion (preferred)
or add insulin directly to TPN solution.
 Subcutaneous insulin regimens
• Doses must be adjusted b/c TPN or enteral nutrition
is most often given continuously.
12/3/2012 77
 Monitoring
Guidelines for ongoing medical care

Monitor the level of glycemic control

with:
 SMBG (individualized frequency)
 Hemoglobin A1C testing (2–4x yearly)
 Pt education in diabetes management
(annual)
 Medical nutrition therapy & education
(annual)
12/3/2012 78
 Con…..

Surveillance for Cxs
1. Retinopathy :- Eye examination (annual)
The American Diabetes Association (ADA) recommends
the ff ophthalmologic examination schedule.
Onset of DM at ≤29 yrs: initial examination within 3–5
yrs of dx.
Onset of DM at ≥30 yrs: initial examination at time of
diabetes dx.
Women with DM contemplating pregnancy:
examination before conception & during first trimester
12/3/2012 79
 Con…
2. Neuropathy
 Foot examination (1–2 times yrly by physician; daily by pt.
 The ADA advises visual foot inspection for potential problems
at each outpatient visit.
3. Nephropathy (annually)
 If no protein on routine urinalysis: Measure microalbuminuria
with microalbumin/creatinine ratio in spot urine.
 If proteinuria on urinalysis: Quantify amount of protein by
standard urine protein measurements.
 Screening should commence 5 yrs after onset of type 1 DM.

12/3/2012 80
 Con…
4. BP measurement (quarterly)
5. Lipid profile (annually)
6. Influenza vaccine (annually)
7. Pneumococcal & tetanus immunizations (at recommended intervals)
8. Surveillance for comorbid conditions
 Periodic screening for thyroid disease, depression, & sexual dysfunction
 Consider antiplatelet therapy (aspirin, 75–162 mg/d) for the following.
 Secondary prevention of macrovascular disease in pts with diabetes with
a Hx of myocardial infarction, vascular bypass, CVD, peripheral vascular
disease, claudication, or angina
 Primary prevention of macrovascular disease in pts with diabetes & an
additional cardiovascular risk factor (age >40 years, smoking, HTN, obesity,
hyperlipidemia, albuminuria, or family Hx of coronary artery disease)

12/3/2012 81
 Con…
 Screening cardiac stress test should be
performed in the following situations.
 Symptoms of cardiac disease
 History of peripheral or cerebrovascular disease
 Sedentary lifestyle
 Age >35 years
 Plans to begin a vigorous exercise program
 Abnormal resting electrocardiogram

12/3/2012 82
 Complications

Acute complications
1. Hypoglycemia
2. Diabetic ketoacidosis
3. Hyperglycemic hyperosmolar state
 Primarily seen in patients with type 2 DM.

12/3/2012 83
 Chronic complications

 Responsible for majority of morbidity &

mortality associated with DM
 Leading cause of adult blindness,
nontraumatic lower-extremity amputation, &
end-stage renal disease in the U.S.
 Risk increases with duration of hyperglycemia.
 Usually becomes apparent in second decade of
hyperglycemia

12/3/2012 84
 Microvascular
 Eye disease
Retinopathy (nonproliferative or proliferative)
 Macular edema
 Other nonvascular eye disease (cataracts, glaucoma)
 Neuropathy
Sensory & motor(mononeuropathy &
polyneuropathy)
 Autonomic
 Nephropathy
12/3/2012 85
 Macrovascular

 Coronary artery disease

 Peripheral vascular disease
 Cerebrovascular disease
GI
 Gastroparesis
 Diarrhea
Genitourinary

12/3/2012 86
 Lower extremity
Amputation
DM is the leading cause of nontraumatic lower-
extremity amputation in the U.S.
Foot ulcers & infections
The interaction of several pathogenic factors
promote its development.
Approx. 15% of pts with DM develop a foot ulcer.
A significant subset undergo amputation; risk is 14–
24% with that ulcer or subsequent ulcers.

12/3/2012 87
 Con….
Risk factors for foot ulcers or amputations
 Male sex
 DM >10 years
 Peripheral neuropathy
Disordered proprioception
Poor wound healing
Abnormal structure of foot (bony abnormalities, callus, thickened
nails)
Peripheral arterial disease
Smoking
Hx of previous ulcer or amputation
Poor glycemic control

12/3/2012 88
 Infectious
 Persons with diabetes have a greater frequency & severity
of infection.
 Osteomyelitis
 Pneumonia
 UTI
 Skin & soft-tissue infections
 Several rare infections occur almost exclusively in DM.
 Rhinocerebral mucormycosis
 Emphysematous infections of gall bladder & urinary tract
 "Malignant" or invasive otitis externa
 Necrotizing fasciitis.

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 Dermatologic
 Common features
 Protracted wound healing
 Skin ulcerations
 Xerosis & pruritus
 Diabetic dermopathy (pigmented pretibial papules or
"diabetic skin spots")
 Bullous diseases (shallow pretibial ulcerations or erosions)
 Lipoatrophy & lipohypertrophy
 Can occur at insulin injection sites

12/3/2012 90
 Prognosis

 Prognosis is variable.
 Overall, the risk for death among diabetic persons is ~2X that of
people without diabetes.
 Heart disease: leading cause of death.
 Death rates due to heart disease are 2–4X higher in adults with
diabetes than adults without diabetes.
 Prognosis if coronary artery disease or myocardial infarction is
present is worse than for nondiabetic persons.
 Coronary artery disease is more likely to involve multiple vessels.
 After controlling for all known cardiovascular risk factors, type 2 DM
increases the cardiovascular death rate 2-fold in men & 4-fold in
women.

12/3/2012 91
 Con…
 Stroke
 Risk of stroke is 2–4x higher in adults with diabetes
than adults without diabetes.
 Approx. 65% of deaths in diabetic persons are due to
heart disease & stroke (macrovascular Cxs).
 Retinopathy: Diabetic persons are 25x more likely to
become legally blind than are persons without DM.
 Diabetic nephropathy is the leading cause of DM-
related morbidity & mortality.

12/3/2012 92
 Prevention

 No known prevention of type 1A DM in humans.

 Diabetes Prevention Trial—Type 1 concluded that
administering insulin to high-risk persons did not
prevent type 1A DM.
 Screening
 A number of immunologic markers for type 1 DM are
becoming available.
 Their routine use is discouraged pending identification
of clinically beneficial interventions for persons at high
risk for type 1 DM.

12/3/2012 93
 Type 2 Diabetes Mellitus
 A heterogeneous group of disorders Xzed by
variable degrees of insulin resistance,
impaired insulin secretion, & increased
glucose production
 Preceded by a period of abnormal glucose
homeostasis, classified as impaired fasting
glucose (IFG) or impaired glucose tolerance
(IGT)

12/3/2012 94
 Epidemiology
Type 2 DM
 Incidence/prevalence varies by geography
(likely owing to genetic, behavioral, and
environmental factors).
 Highest: certain Pacific islands
 Intermediate: India and U.S.
 Relatively low: Russia and China

12/3/2012 95
 Con…
 Prevalence is expected to increase more rapidly than type
1 DM b/c of increasing obesity & reduced activity levels
 Age of onset
 Can develop at any age
 Typically develops with increasing age, >30 years of age
 Age of diagnosis is decreasing in some ethnic groups.
 Eg., Occurs at an earlier age in ethnic groups other than
non- Hispanic whites
 Marked increase among overweight children &
adolescents

12/3/2012 96
 Risk Factors

 Family history of type 2 DM (i.e., parent or sibling)

 Obesity (body mass index >25 kg/m ) 2

 Particularly visceral or central (hip/waist ratio)

 Habitual physical inactivity
 Race/ethnicity
 African American
 Hispanic American
 Native American
 Asian American
 Pacific Islander

12/3/2012 97
 Con…
 Previously identified IFG or IGT
 40% risk of developing type 2 DM over the next 5 years
 Hx of gestational diabetes or delivery of baby >4 kg.
 HTN (BP >140/90 mmHg)
 HDL cholesterol level < 35 mg/dL (0.90 mmol/L)
&/or triglycerides >250 mg/dL (2.82 mmol/L)
 Polycystic ovary syndrome (PCOS)
 History of vascular disease

12/3/2012 98
 Etiology

 Type 2 DM is caused by a complex interaction of

genetics, environmental factors, & lifestyle choices.
 Insulin resistance & abnormal insulin secretion are
central to the development of type 2 DM.
 Controversy remains regarding the primary defect;
most studies support the view that:
 Insulin resistance precedes insulin secretory
defects.
 Diabetes develops when insulin secretion becomes
inadequate to compensate for insulin resistance
12/3/2012 99
 Con…
 Genetic considerations
 Major genes that predispose have yet to be identified; it is
clear that the disease is polygenic.
 Susceptibility genes or polymorphisms that have been
identified that may contribute to the risk of type 2 DM
include:
 Calpain 10,
 Pro12Ala (common) variant of peroxisome proliferator-
activated receptor γ,
 Glu23Lys variant of the ATP–sensitive potassium channel
Kir6.2.

12/3/2012 100
 Con….
 Concordance in identical twins: 70–90%.
 Concordance among fraternal twins is 20%.
 Familial aggregation Hx is common & up to 50% of
siblings & 33% of children of diabetics develop diabetes.
 One parent with disease: increased risk.
 Both parents with disease: risk approaches 40%
 A genetic defect may not manifest itself unless an
environmental event or another genetic defect, such as
obesity, is superimposed.

12/3/2012 101
 Con…
 Env’tal factors & lifestyle choices modulate
phenotypic expression.
 Nutrition
 Physical activity
 Pathophysiologic abnormalities
 Peripheral insulin resistance (especially muscle &
liver).
 Excessive hepatic glucose production.
 Impaired insulin secretion.
12/3/2012 102
 Associated Conditions

 Insulin resistance syndromes

 Metabolic syndrome
 Also referred to as insulin resistance syndrome or syndrome X.
 Spectrum of disorders with hyperglycemia as prominent feature
 Constellation of metabolic derangements includes:
• Insulin resistance
• Hypertension
• Dyslipidemia (low HDL cholesterol level & elevated triglyceride level)
• Central or visceral obesity
• Type 2 DM or IGT/IFG
• Accelerated cardiovascular disease
• Predisposition to fatty liver
 Very common; ~20% of U.S. adults

12/3/2012 103
 Con…
 PCOS
 Common disorder in premenopausal women
that is Xzed by chronic anovulation &
hyperandrogenism
 Insulin resistance (independent of obesity) is
present in the majority of pts.
 Associated with a substantially increased risk
for type 2 DM

12/3/2012 104
 Natural history of type 2 diabetes

Stage 1: Insulin resistance: increased glucose &

Non Esterified Fatty Acids (NEFA)
Stage 2: Increased insulin secretion:
compensatory hyperinsulinemia
Stage 3: Impaired glucose tolerance
Stage 4: Overt type 2 diabetes

12/3/2012 105
 Symptoms & Signs

 DM & its Cxs produce a wide range of Sxs & signs.

 Those secondary to acute hyperglycemia
• May occur at any stage of the disease.
 Those related to chronic complications
• Begin to appear during second decade of
hyperglycemia.
 A long asymptomatic period of hyperglycemia is
common in type 2 DM.

12/3/2012 106
 Symptoms of hyperglycemia
 Polyuria
 Polydipsia
 Weight loss
 Fatigue
 Weakness
 Blurry vision
 Results from changes in water content of lens
 Frequent superficial infections (vaginitis, fungal skin
infections)
 Slow healing of skin lesions after minor trauma.
12/3/2012 107
 Historical features to assess
In persons with newly diagnosed DM
 Complete medical history with emphasis on DM-relevant aspects
 Weight
 Family history of DM & its Cxs
 Risk factors for cardiovascular disease
 Exercise
 Smoking & Ethanol use
 Assess for Sxxs or signs of acute hyperglycemia.
 Screen for Chronic Cxs & conditions associated with DM.
 DM-related comorbidities (CVD, HTN, renal disease, retinopathy,
dyslipidemia).

12/3/2012 108
 Con…
In persons with previously diagnosed DM
 All of the above plus
 Assessment of prior diabetes care (in established DM)
 Type of therapy
 Prior hemoglobin A1C levels
 Results of self-monitoring of blood glucose (SMBG)
 Frequency of hypoglycemia
 Presence of DM-specific Cxs
 Assessment of pt’s knowledge about diabetes

12/3/2012 109
 Complete physical examination

Weight or body mass index

Retinal examination
BP:- BP > 130/80 mmHg considered HTN in DM
Careful examination of lower extremities to seek evidence of:
• Sites of potential skin ulceration
•Peripheral neuropathy
•Calluses , Superficial fungal infections , Nail disease
•Foot deformities (e.g., hammer or claw toes & Charcot foot)
Peripheral pulses
Insulin injection sites
Teeth & gums
• Periodontal disease more frequent in DM

12/3/2012 110
 DIAGNOSIS
Diagnostic criteria for diabetes

 Symptoms of diabetes plus

1. RBG concentration >11.1 mmol/L (200 mg/dL) or
 Random: without regard to time since last meal
 FPG level >7.0 mmol/L (126 mg/dL) or
 2-hour plasma glucose level >200 mg/dL during OGTT.
 Test should be performed by using a glucose
load containing equivalent of 75 g of anhydrous
glucose dissolved in water.
 Not recommended for routine clinical use.

12/3/2012 111
 Laboratory and additional assessments

 Assess diagnostic criteria for DM.

 Assess degree of glycemic control by
measuring hemoglobin A1C.
 Screen for DM-associated conditions (e.g.,
microalbuminuria, dyslipidemia).
 Perform cardiac stress testing to screen for
asxtic coronary artery disease if the pt is at
high risk for cardiovascular disease.

12/3/2012 112
 Hemoglobin A1C
Standard method for assessing long-term glycemic control
Should be measured in all pts with DM during the initial evaluation & as part of
comprehensive diabetes care
Notes on use
Hemoglobin A1C is not currently recommended for diagnosis.
In standardized assays, the hemoglobin A 1C value approximates the following
mean plasma glucose values.
–6%: 7.5 mmol/L (135 mg/dL)
–7%: 9.5 mmol/L (170 mg/dL)
–8%: 11.5 mmol/L (205 mg/dL)
–A 1% increase in the hemoglobin A 1C level translates into a 2.0-mmol/L (35 mg/dL)
increase in mean glucose level.
Hemoglobinopathies, anemias, & uremia may interfere with hemoglobin A 1C
results.

12/3/2012 113
 Other laboratory tests
C-peptide measurement
A low level confirms need for insulin.
May help distinguish type 1 DM from type 2 DM in some circumstances
Screening laboratory tests for DM-associated conditions
Microalbuminuria
–Spot urine microalbumin/creatinine ratio (at the time of initial
diagnosis of type 2 DM)
–Microalbuminuria is defined by a microalbumin/creatinine ratio >30
mg/g creatinine.
Dyslipidemia
–Fasting lipid profile (annual)

12/3/2012 114
 Treatment Approach
Goals of therapy
 Eliminate symptoms related to hyperglycemia.
 Achieve sustained euglycemia.
 Avoid hypoglycemia.
 Reduce or eliminate long-term microvascular &
macrovascular Cxs.
 Allow the pt to maintain as normal lifestyle as
possible.
12/3/2012 115
 Steps needed to reach goals
 Identify target level of glycemic control for each pt.
 Ideal goals for glycemic control
– Preprandial plasma glucose level: 5.0–7.2 mmol/L (90–
130 mg/dL)
– Peak postprandial plasma glucose level: <10 mmol/L
(<180 mg/dL)
– Hemoglobin A1C level: <7.0%
 Provide pt with educational & pharmacologic
resources necessary to reach goal.
 Monitor/treat DM-related complications.
12/3/2012 116
 Comprehensive care
 Best accomplished by a multidisciplinary team approach:
 Primary care provider &/or endocrinologist or diabetologist
 Certified diabetes educator
 Nutritionist
 Subspecialists with experience in DM-related Cxs
– Neurologist
– Nephrologist
– Vascular surgeon
– Cardiologist
– Ophthalmologist
– Podiatrist

12/3/2012 117
 Patient education
Diabetes educator
A health care professional (nurse, dietician, or pharmacist) with specialized pt
education skills
Certified in diabetes education (e.g., American Association of Diabetes Educators)
Topics important for optimal care
Nutrition
SMBG
Insulin administration (if needed)
Guidelines for diabetes management during illnesses
Management of hypoglycemia
Foot & skin care
DM Rx before, during, & after exercise (if taking insulin)
Risk factor–modifying activities

12/3/2012 118
 Treatment approach in a newly diagnosed
patient
 Diabetes management should begin with medical
nutrition therapy in most persons with mild
hyperglycemia (hemoglobin A1C level < ~9%).
 After medical nutrition therapy & increased
physical activity have been instituted, glycemic
control should be reassesed.
 If the pt’s glycemic target is not achieved after 4
wks of medical nutrition therapy, pharmacologic
therapy is indicated.
12/3/2012 119
 Pharmacologic management
 Oral glucose-lowering agents
 Usually are preferred by patients
 Should not be used in severely ill persons

12/3/2012 120
 Insulin therapy
 Insulin, alone or in combination with oral
agents, often becomes necessary as type 2
DM progresses.
 Insulin is sometimes used as the initial
glucose-lowering agent in pts with moderate
to severe hyperglycemia.

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 The use of Insulin in type 2 DM
 Insulin is usually added to an oral agent when glycemic control is
suboptimal at maximal doses of oral medications.
 An intermediate-acting agent is used starting with a low dose &
increasing as needed for glycemic control (such as 5 to 10 U of NPH
increasing as needed).
 Adding NPH at bedtime is generally more efficacious than using it
during the day.
 If using only insulin, start with an AM (morning) injection.
 The dose can be increased by 5 U every 3 to 7 days until adequate
control is achieved.
 If early morning hyperglycemia is a problem, intermediate-acting
insulin can be given twice daily as a split dose.

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 Specific Treatments
Medical nutrition therapy
 Nutritional recommendations for all persons with DM
Protein
– ~15–20% of kcal/d
– ~10% in patients with nephropathy
Saturated fat
– <10% of kcal/d
– <7% in patients with elevated low-density lipoprotein
cholesterol level
Polyunsaturated fat
– ~10% of kcal/d
– Avoid trans-unsaturated fatty acids.

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 Con…
 60–70% of calories divided b/n carbohydrate &
monounsaturated fat
– Based on medical needs & personal tolerance
 Use of caloric sweeteners, including sucrose, is acceptable.
 Fiber :- 20–35 g/d
– Increased consumption of soluble dietary fiber may
improve glycemic control.
 Sodium: <3,000 mg/d
 Cholesterol: <300 mg/d
 Alcohol :- Same precautions as in general population
– May ↑ risk for hypoglycemia & should be taken wz food
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 Exercise
 A regular physical activity program, adapted to the
presence of Cxs, is recommended for all pts with DM
who are capable of participating.
 Regular exercise provides the ff benefits in type 2 DM.
 Improves blood glucose control
 Reduces cardiovascular risk factors
 Contributes to weight loss & weight loss maintenance
 Increases insulin sensitivity
 Improves well-being

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 Con…
 Exercise-related hypoglycemia occurs less frequently in pts
with type 2 DM than in those with type 1 DM, but may
develop in those who are treated with insulin or sulfonylureas.
 Strategies to avoid exercise-related hypoglycemia (mainly for
persons requiring insulin therapy)
 Monitor blood glucose before, during, & after exercise as
needed.
 Ingest carbohydrate if needed to prevent hypoglycemia.
 Learn individual glucose responses to d/t types of exercise &
alter insulin doses in advance of anticipated exercise, if needed
(depending on intensity & duration).

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 Con…
 Relative contraindication: untreated proliferative
retinopathy
 May lead to vitreous hemorrhage or retinal detachment
 Consider formal exercise tolerance testing for:
 Age >35 years
 DM duration >15 years
 Microvascular complications
 Peripheral arterial disease
 Other risk factors of coronary artery disease
 Autonomic neuropathy

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 Oral glucose-lowering agents
 Indicated if the pt’s glyemic target is not achieved after 3–
4 weeks therapy with nutrition & exercise
 Insulin secretagogues
1. Sulfonylureas
– Mechanism of action: enhance insulin secretion
– Eg: chlorpropamide, tolazamide, tolbutamide, glimepiride,
glipizide, glyburide
– Anticipated reduction in hemoglobin A1C level: 1–2%
– Advantages: decreases FBS level, well tolerated
– Disadvantages: hypoglycemia, weight gain, hyperinsulinemia
– Contraindications: renal/liver disease

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 2. Meglitinides
Mechanism of action: enhance insulin secretion
 Examples: repaglinide, nateglinide
 Anticipated reduction in hemoglobin A1C value:
1–2%
 Advantages: short onset of action, lower
postprandial glucose level
 Disadvantage: hypoglycemia (lower risk than
observed with sulfonylureas)
 Contraindications: renal/liver disease
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 Biguanides
 Mechanism of action: reduce hepatic glucose production, Wt
loss, increase glucose utilization, decrease insulin resistance
 Examples: metformin
 Anticipated reduction in hemoglobin A1C level: 1–2%
 Advantages: Weight loss, improvement in lipid profile, no
hypoglycemia
 Disadvantages: diarrhea, nausea, risk of lactic acidosis
 Contraindications: serum Cr level >1.5 mg/dL (men) or >1.4
mg/dL (women); avoid use at time of radiographic contrast
studies, in seriously ill pts, in pts at risk for acidosis

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  α-Glucosidase inhibitors
 Mechanism of action: reduce glucose absorption by
inhibiting the enzyme that cleaves oligosaccharides into
simple sugars in the intestinal lumen.
 Examples: acarbose, miglitol
 Anticipated reduction in hemoglobin A1C level: 0.5–
1.0%
 Advantage: no risk of hypoglycemia
 Disadvantages: GI flatulence, small risk of increased
liver function values
 Contraindications: renal/liver disease
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  Thiazolidinediones
 Mechanism of action: decrease insulin resistance,
increase glucose utilization
 Examples: rosiglitazone, pioglitazone
 Anticipated reduction in hemoglobin A1C level: 1–2%
 Advantages: decrease insulin & sulfonylurea
requirements, decrease triglyceride level
 Disadvantage: weight gain, delayed response, need for
frequent hepatic monitoring for idiosyncratic
hepatocellular injury, financial cost
 Contraindications: liver disease, CHF (class III or IV)

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 Insulin secretagogues
 Most effective in pts with:
 Disease of relatively recent onset (<5 years)
 Tendency to obesity
 Residual endogenous insulin production
Sulfonylureas
 Should be initiated at low doses and increased at 1- to 2-week intervals on the
basis of SMBG results
 Should be taken shortly before a meal
 First-generation sulfonylureas
 At maximum doses, first-generation sulfonylureas similar in potency to second
generation sulfonylureas but have
– Longer half-life
– Greater incidence of hypoglycemia
– More frequent drug interactions

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 Con…
Chlorpropamide
• Approved daily dosage range: 100–500 mg
• Duration of action: >48 hours
• Clearance: renal

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 Con…
Tolazamide
• Approved daily dosage range: 100–1,000 mg
• Duration of action: 12–24 hours
• Clearance: hepatic, renal
Tolbutamide
• Approved daily dosage range: 500–3,000 mg
• Duration of action: 6–12 hours
• Clearance: hepatic
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 Con….
Second-generation sulfonylureas
 o Generally preferred over first generation drugs
Glimepiride
– Approved daily dosage range: 1–8 mg
– Duration of action: 24 hours
– Clearance: hepatic, renal
Glipizide
– Approved daily dosage range: 2.5–40 mg
– Duration of action: 12–18 hours
– Clearance: hepatic
Glipizide (extended release)
– Approved daily dosage range: 5–10 mg
– Duration of action: 24 hours
– Clearance: hepatic

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 Con…
Glyburide
– Approved daily dosage range: 1.25–20 mg
– Duration of action: 12–24 hours
– Clearance: hepatic, renal
Glyburide (micronized)
– Approved daily dosage range: 0.75–12 mg
– Duration of action: 12–24 hours
– Clearance: hepatic, renal

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 Con….
Meglitinides
 Given with each meal or immediately before to reduce
meal-related glucose excursions
Repaglinide
– Approved daily dosage range: 0.5–16 mg
– Duration of action: 2–6 hours
– Clearance: hepatic
Nateglinide
– Approved daily dosage range: 180–360 mg
– Duration of action: 2–4 hours
– Clearance: renal

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 Acute complications of DM

1. Hypoglycemia
2. Diabetic Ketoacidosis
3. Hyperosmolar Coma

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 1.Hypoglycemia
Definition: plasma glucose <70mg/dl.
 A complication of treatment!
 40mg/dl is the minimum for brain function.
 <40mg/dl = Risk for diabetic coma, seizures.
 Hypoglycemia in the diabetic pt is caused by:
 Overdose of insulin or hypoglycemic agents.
 Missing of meal
 Strenuous exercise
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 Clinical manifestations
 Early: secondary to the effect of hypoglycemia
effects of sympathetic on the brain(Neurogenic
stimulation such as: manifestations) such as
 Cold sweat,  Dizziness,
 Tremor,  Blurring,
 Hunger or  Headache,
 Palpitations.  Nightmares, &
 Late: If early sxs are  Coma may occur.
neglected then sxs of the

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 Management

 Any pt with diabetes losing consciousness

should always be considered hypoglycemic
until proven otherwise by blood sugar
determination & should be managed by rapid
IV administration of glucose or PO/ NG tube
administration of any concentrated sugar
solution.
 Prolonged unconsciousness requires
continuous 10% IV glucose administration.
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 Con…
 Mild
– carbohydrate 10-15 gram
 Moderate
– 20-30 gram of carbs
– Glucagon, 1 mg SC or IM
 Severe
– 50% dextrose 25 g IV
– Glucagon 1 mg IM or IV

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 Con…
 Glucose
– 15 grams of simple carbohydrates
• 8oz. fruit juice
• Half can regular soda
• 3 glucose tabs
• 1 tablespoon honey
 Glucagon injection
– Stimulates glycogen breakdown

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 2. Diabetic Ketoacidosis
Definition: is an acute metabolic crisis in pts with DM Xzed
by:
 Hyperglycemia (blood glucose level may range from 250-
600 mg /dl )
 Metabolic acidosis (ketosis)
 Hypotension & features of dehydration
 DKA was formerly considered as a hall mark of type 1 DM.
 However, currently it is known that some type 2 DM pts
who are being treated by oral hypoglycemic agent may
also develop DKA.

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 Precipitating factors
 DKA may occur after several days of worsening diabetic
control, or may appear suddenly within few hours.
 Some of the precipitating factors are:
 Intercurrent infection
 Poor compliance with insulin or discontinuation of insulin
 Dehydration
 Stressful conditions such as, trauma, surgery or of
emotional crisis
 Excessive alcohol ingestion

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 PATHOGENESIS
 Any event that ↓ insulin availability or cause stress that ↑ the
insulin demand, lead to insulin deficiency & the effect of counter
regulatory hormones such as glucagon, cortisol, epinephrine &
growth hormone becomes overwhelming.
 This biochemical changes bring about:
 ↑ed production of glucose by the liver & ↑ed glycogen
degradation to glucose
 ↓ed glucose uptake & utilization by muscles
 Lipolysis: enhanced break down of FFA & subsequent ketogenesis.
 This ↑s ketone bodies such as acetoacetic acid, β-hydroxybutyric
acid, & acetone, resulting in metabolic acidosis.

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 Pathogenesis

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 Signs & symptoms
 Volume depletion : DHN- dry tongue & bucal mucosa , poor skin
turgor & hypotension.
 Kussmaul respiration : deep & fast breathing resulting from
metabolic acidosis.
 Acetone ("fruity") odour of breath: due to acetone.
 Nausea & vomiting & frequent complaint of abdominal pain.
 Mental status changes : lethargy & confusion w/h may evolve
into coma with sever DKA.
 Cerebral edema: is seen most frequently in children.
 Signs of infection ,w/h may be precipitating DKA.
 A history of diabetes (unless first presentation).

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 Diagnostic Criteria for DKA and HHS
Mild DKA Moderate DKA Severe DKA HHS
Plasma glucose > 250 > 250 > 250 > 600
(mg/dL)
Arterial pH 7.25-7.30 7.00-7.24 < 7.00 > 7.30
Sodium Bicarbonate 15 – 18 10 - 15 < 10 > 15
(mEq/L)
Urine Ketones Positive Positive Positive Small
Serum Ketones Positive Positive Positive Small
Serum Osmolality Variable Variable Variable > 320
(mOsm/kg)
Anion Gap > 10 > 12 > 12 variable
Mental Status Alert Alert/Drowsy Stupor/Coma Stupor/Coma

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 Laboratory Diagnosis
1. RBS: hyperglycaemia.
 Blood glucose level is usually high (averaging 500 mg
/dl)
2. Urine dipstick for ketones:
 ketosis can be determined with bedside reagents.
 This test is 97% sensitive.
3. Arterial blood gas analysis :
 Can diagnose metabolic acidosis w/h is indicated by:
o Low serum bicarbonate level (below 10 mEq / L ) &
o Low blood PH ( < 7.35 )
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 4. Additional laboratory evaluation

a) Electrolytes:
 Serum K+ level: look for hyperkalemia or hypokalemia.
 Serum Na+: tends to be low b/c of dilution as the
osmotic effect of hypergycemia increases ECF volume.
 Serum osmolality is high
b) BUN & creatinine,
c) CXR,
d) Urine culture & sensitivity,
e) Blood cultures should also be done to identify an
infectious process.
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 Treatment of DKA
Acute management
1. Supportive therapy:
 ABC of life.
2. Fluid replacement:
 Fluid deficit in pts with DKA averages 3-5 L.
 Hence give 5- 6 L of fluid in the 1st 24 hours.
 Initially 1 L of NS (0.9 % NaCl) is given over ½ an hr.
 Continue with 1 L of NS/hr for the first 2-3 hrs.
 Then ½ NS (0.45 % NaCl) at slower rate till the pt is well
hydrated.
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 Con…
3. Insulin:
 Insulin is administered :
 To increase glucose use in the tissues,
 To inhibit ketogenesis, &
 To counter balance the effect of counter regulatory hormones.
Dosage & administration:
 20 Units of regular insulin, 10 U IV & 10 U IM is given with the
initial fluid resuscitation.
 Then 5-10 U/hr of regular insulin is given per hour till the
blood glucose level drops to 250-300mg/dl

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 Con…
 Blood glucose determination is done every hour.
 The expected rate of fall in serum glucose is 75-100 mg/dl/hr.
 When blood glucose reaches a range of 250 to 300 mg/dl, 5 -10 %
glucose solution should be infused to prevent hypoglycaemia.
 Insulin infusion should not be stopped until the Ketonemia clears.
 It is preferable to give 5% or 10% DW with insulin injection, rather
than stop the insulin, b/c insulin is still required to clear the
acidosis & ketotic state.
 Shift to sliding scale when ketone clears, until precipitating cause
is well controlled.
 Shift to intermediate insulin when pt’s blood sugar & precipitating
factor is under complete control.

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 Con…
4. Potassium replacement:
 Serum K+ level may be increased initially b/c of K+ ion movement
from ICF to ECF in metabolic acidosis.
 Later, the serum K+ becomes low b/c of both renal loss of K+ &
the movement of K+ ions back to ICF as the acidosis is corrected.
 Pts with DKA are expected to have a K+ deficit of 300-400 mEq,
w/h should promptly be replaced.
 Start replacing potassium as soon as the pt has adequate UOP.
 KCl is infused at a rate of 20 -40 mEq/hr.
 Monitor serum K+ level closely.
 Oral potassium can be given if IV potassium is not available.
 Encourage pts to eat potassium rich fruits such us banana.
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 Con…
 Phosphate is depleted as well.
 Phosphate may be added as KPO4 especially if serum
chloride becomes elevated
 “Pseudohyponatremia” is often present.
– Expect that the Na+ level will rise during treatment.
– Corrected Na+ = Measured Na+ + 0.016(measured glucose
- 100)
– If Na+ does not rise, true hyponatremia may be present
(possibly increasing cerebral edema risk) & should be
treated.

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 Con….
 BICARBONATE IS ALMOST NEVER ADMINISTERED
 Bicarbonate administration leads to increased
cerebral acidosis.
 HCO3- combines with H+ & dissociated to CO2 & H2O.
 Whereas bicarbonate passes the blood-brain barrier
slowly, CO2 diffuses freely, thereby exacerbating
cerebral acidosis & cerebral depression

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 Con…
 Indications for bicarbonate administration
include severe acidosis leading to
cardiorespiratory compromise.
 Increasing evidence suggests that subclinical
cerebral edema occurs in the majority of pts
treated with fluids & insulin for DKA.
 Cerebral edema is the major life-threatening
Cx seen in the treatment of children with DKA.

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 Con…
Clinically apparent cerebral edema occurs in ~1% of DKA.
Mortality is 40 - 90%.
Cerebral edema is responsible for 50 - 60% of DM deaths in children.
Cerebral edema usually develops several hrs after the institution of
therapy.
Manifestations include:
Headache,
Alteration in level of consciousness,
Bradycardia,
Emesis,
Diminished responsiveness to painful stimuli, &
Unequal or fixed & dilated pupils.

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 Con…
 Excessive use of fluids, large doses of insulin, & especially
the use of bicarbonate have been linked to the increased
formation of cerebral edema.
 Therapy of cerebral edema may include:
 Mannitol,
 Hypertonic saline &
 Hyperventilation

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 Con…
5. Close follow-up of pts
 Monitor serum glucose & K+ as well as urine output hrly.
 Maintenance fluids should consist of 0.45% (½ strength) saline
with additives as indicated; 150 to 200 ml/hr adjusted according
to urine output.
 Evaluate for potential precipitating factors, including infection,
pregnancy, Myocardial infarction, inappropriate use of insulin.
 Diet. Oral intake may resume when mental status of the pt
improves & nausea & vomiting are controlled.
 Initial diet should consist of fluids.
 Solid diet is may not be resumed until ketoacidosis is corrected.

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 3. Hyperglycemic Hyperosmolar State ( Non-
Ketotic Hyperosmolar Coma )
 Usually occurs in elderly type 2 DM pts.
 It is often precipitated by serious intercurrent
illnesses such as:
 myocardial infarction,
 stroke,
 pneumonia,
 sepsis etc.

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 Con…
Symptoms:
 Such pts present with several weeks Hx of polyuria, weight
loss, & diminished oral fluid intake that is followed by mental
confusion, lethargy or comma.
Physical examination:
 Pts have extreme DHN, hypotension, tachycardia & altered
state of consciousness or coma.
 The DHN is caused by a hyperglycemia induced osmotic
diuresis, when it is not matched by adequate fluid intake.
Laboratory: Very high serum blood glucose level (may range
from 600- 1200mg/dl)

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 Con…
Treatment involves
 Fluid replacement :administration of IV fluids
&
 Bringing down the blood sugar rapidly by
using rapidly acting insulin preparations.
 Identifying & treating the precipitating factor.

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 Chronic Complications of DM

 The chronic Cxs of DM affect many organ systems &

are responsible for majority of morbidity & mortality
associated with the diseases.
 Prevention of chronic Cx is one of the major goals of
care of the diabetic pts.
 This is attempted by achieving as near normal blood
glucose level as possible.
 Several studies have shown that with tight blood
glucose control, the occurrence of chronic Cxs can be
delayed by several years.
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 1. Retinopathy
 Is one of the commonest chronic CXs & one of
the leading causes of blindness in developed
countries.
 Symptoms may include :
 Difficulty of reading ,
 Blurring of vision,
 Shadowing w/h may later on progress to total
blindness.
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 Classification of Diabetic retinopathy

a) Background retinopathy: early changes w/h is

often asymptomatic
 Microaneurysm: occlusion of capillaries gives
rise to distention & eventual rupture of vessels.
 Dot hemorrhages:-increased permeability of
capillaries & from ruptured aneurysms.
 Hard exudates: proteins & lipids leak due to
increased permeability of capillaries.

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 Con….
b) Maculopathy: w/h manifests with central vision loss.
c) Proliferative retinopathy: aSxtic unless complicated by
hemorrhage
 Xzed by new vessels formation w/h is stimulated by ischemia.
d) Advanced diabetic disease: may cause severe vision loss to
the extent of complete blindness.
 Extensive fibrovascular proliferation develops following
ischemia & necrosis.
 Retinal detachment results from the deformity created by
extensive fibrosis.
 Vitreous hemorrhage refers to blood in the vitreous fluid.

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 Management

 Laser therapy
 ASA 100 mg /day may prevents further
occlusion of small capillarie.
 Surgery : Viterotomy removes blood clots &
fibrosis that obstruct vision.

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 2. Neuropathy

Symptoms include:
 Burning sensation, numbness
 Constipation or nocturnal diarrhea
 Impotence
 Foot ulcer

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 Classification of Diabetic Neuropathy

a) Polyneuropathy:
 Is the commonest neuropathy, Xzed by distal symmetrical,
predominantly sensory impairment w/h manifests with
tingling sensation, numbness, burning sensation etc.
 It is often progressive & may lead to total loss of sensation
& absence of deep tendon reflexes.
b) Radiculopathy: Xzed by neurogenic pain.
 It is often self limiting.
c) Amyotropy: atrophy of proximal muscles mainly around
the hip girdle.

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 Con…
d) Autonomic Neuropathy: may manifest with:-
 Postural hypotension.
 GI manifestations: gustatory sweating,
gastroparesis, nocturnal diarrhea.
 Genitourinary manifestations: neuropathic
bladder, erectile dysfunction (impotence)
e) Mononeuropathy: paralysis of a specific nerve or
nerves.
E.g. diplopia due to third & sixth nerves palsies.
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 Neuropathy management

 Symptomatic treatment :
 Pain control
 Diarrhea control
 Treatment of impotence

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 3. Nephropathy
Clincal fetures
 Periorbital edema (eye or facial puffiness),pedal edema ,
anasarca.
 Anemia, Uremia & osteodystrophy in pts with ESRD.
Lab: Progression from microalbuminuria to
Macroalbuminuria.
Management
 Tight BP control.
 ACEI: decreases progression of renal diseases.
 Renal transplantation or Dialysis in ESRD.
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 4. Diabetic Foot Ulcer

 The ff are underlying mechanism for diabetic foot ulcers

 Neuropathy
 Loss of pain sensation exposes to injury.
 Loss of sweating results dry skin that is susceptible to injury
 Vascular: poor blood supply to the foot causes decreased
healing of wound poor recovery from secondary infections.
 Abnormal Pressure loading: due to neuropathy (Charcot’s
joints) or anatomical deformity of the feet.
 Since the foot is not in a normal anatomic position it is
exposed to abnormal load & pressure sores develop.

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 Sxs & signs of foot ulcer
Numbness & burning, aching pain, swelling, darkening,
abscess & cold extremity.
Foot care: should be essential part of diabetes care.
 Put on comfortable shoe.
 Examine the foot daily to detect problems earlier.
 Wash dry and oil the feet.
 Take caution during nail cutting.
 Treat athletes’ foot or any other foot infection as early as
possible.
 Do not use hot water to wash the feet.
 Stop smoking.

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 THE END!!!

Thank you

12/3/2012 178