Diabetes Mellitus

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 Introduction
• Diabetes mellitus is a chronic disorder characterized
by the impaired metabolism of glucose & other
energy-yielding fuels as well as by the late
development of vascular and neuropathic
complications
• Diabetes comprises a group of disorders involving
distinct pathogenic mechanisms, for which
hyperglycemia is the common denominator
• Regardless of its cause, the disease is associated with
insulin deficiency, which may be absolute or relative
in the context of coexisting insulin resistance
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 CLASSIFICATION OF DIABETES MELLITUS
• Classified on the basis of the pathogenic process that
leads to hyperglycemia
1. Type 1 diabetes
– Autoimmune pancreatic β-cell destruction &
characterized by absolute insulin deficiency
2. Type 2 diabetes
– Characterized by variable degrees of insulin
resistance, impaired insulin secretion, &
increased glucose production

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 CLASSIFICATION (Cont’d)
3. Other specific types
– Genetic defects of β-cell function
– Genetic defects in insulin action
– Disease of the exocrine pancreas
• e.g., pancreatitis, trauma, pancreatectomy, neoplasia,
cystic fibrosis, hemochromatosis
– Endocrinopathies
• e.g., acromegaly, Cushing's syndrome, hyperthyroidism,
pheochromocytoma, glucagonoma, somatostatinoma,
– Drug or chemical induced
• e.g., pentamidine, nicotinic acid, glucocorticoids,
thyroid hormone, diazoxide, β-adrenergic agonists,
thiazides, phenytoin, interferon alfa
4. Gestational diabetes mellitus
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 Epidemiology
• Type 2 DM far more prevalent than Type 1 DM
• Worldwide prevalence of DM risen dramatically over the
past two decades,
– From an estimated 30 million cases in 1985 to 177 million
in 2000
– Prevalence of type 2 DM is rising much more rapidly
because of increasing obesity and reduced activity levels
• Prevalence & incidence of DM in Ethiopia clearly
on the rise in the past few decades
– Between 1975 & 1979 prevalence was reported to be
1.2% (1.4% in males & 0.3% in females )
– A study showed incidence of 8.9% of DM & another
8.9% of IGT among recently migrated Ethiopian Jews

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Criteria for the Diagnosis of Diabetes Mellitus
• At least one of the following
– Symptoms of diabetes plus Random Blood Glucose(RBS)
concentration 200 mg/dL or
– Fasting plasma glucose(FBS) 126 mg/dL or
– Two-hour plasma glucose 200 mg/dL during an oral
glucose tolerance test
• In absence of unequivocal hyperglycemia and acute metabolic
decompensation, these criteria should be confirmed by
repeat testing on a different day.

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 Pathobiology
• Insulin Secretion and Action
– Insulin is synthesized in pancreatic β cells
– Glucose concentration is the key regulator of insulin
secretion
– Insulin acts on its target tissues (liver, muscle, and fat,
primarily) through a specific insulin receptor
• Facilitates glucose uptake into cells
• Promotes the storage of carbohydrate and fat and
protein synthesis
– Counter-regulatory hormones oppose the metabolic
actions of insulin
• Include glucagon, growth hormone, cortisol, and
catecholamines
• Tend to increase glucose concentration in the blood
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Metabolic Effects of Insulin
• Glucose homeostasis reflects a balance between hepatic
glucose production and peripheral glucose uptake and
utilization
• In the fasted state, low basal insulin levels result in
diminished glucose uptake in peripheral insulin-sensitive
tissues (e.g., muscle and fat)
– Maintenance of stable blood glucose levels is achieved through
the release of glucose by the liver (to a small extent kidney) by
glycogenolysis and gluconeogenesis
– stimulated by Glucagon
• Fed State – Insulin released
– Stimulation of hepatic glucose uptake
– Acceleration of glucose uptake by peripheral tissues
– promotes the storage of carbohydrate and fat and protein
synthesis
Prevents large excursion of blood glucose level
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 Metabolic Defects in Diabetes
Fasting Hyperglycemia
• Results from an inappropriate increase in hepatic glucose
production due to accelerated gluconeogenesis
– Insulin deficiency and unopposed effect of counter-
regulatory hormones
– Fasting free fatty acid levels are also elevated in diabetes
because of accelerated mobilization of fat stores
Postprandial Hyperglycemia
• Impaired suppression of hepatic glucose production and the
liver's ability to store glucose as glycogen
• Reduces the capacity of myocytes to extract and store
ingested carbohydrate c and the excess glucose released from
the liver.
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Effects of severe insulin deficiency on body fuel
metabolism Lack of insulin leads to
• Mobilization of substrates
for gluconeogenesis and
ketogenesis from muscle
and adipose tissue,
• Accelerated production of
glucose and ketones by the
liver, and
• Impaired removal of
endogenous and exogenous
fuels by insulin-responsive
tissues.
The net results are severe
hyperglycemia and
hyperketonemia that
overwhelm renal removal
mechanisms
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 Pathogenesis
Type 1 Diabetes
• Absolute deficiency of insulin
– results from an interplay of genetic, environmental, &
autoimmune factors that selectively destroy insulin-
producing β cells
Genetic Factors
• Identical twins show concordance rates of 30 to 40%
• Many of the genes linked to type 1 diabetes have not been
identified
• HLA genes clearly play a dominant role
– 90 to 95% of type 1 patients express DR3 or DR4 class II HLA
molecules

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 Pathogenesis - T1DM(Cont’d)
Environmental Factors
• Diet and toxins have been proposed as triggers of diabetes
• Epidemics of mumps, congenital rubella, and coxsackievirus
infection have been associated with an increased frequency of
type 1 diabetes
Autoimmune Factors
• About 80% of patients with new-onset type 1 diabetes have
islet cell antibodies
– Antibodies to a variety of β-cell constituents have been
identified
• β-Cell destruction is mediated by a variety of cytokines or by
direct T-lymphocyte activity targeting specific β-cell antigens
• Diabetes does not become evident until a majority of beta
cells are destroyed (~80%)
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Temporal model for development of type 1 diabetes

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 Pathogenesis
Type 2 DM
• Insulin resistance and abnormal insulin secretion( with
resultant ralative insulin deficiency) are central to the
development of type 2 DM
• Has a strong genetic component.
– Concordance in identical twins is between 70 and 90%
– Individuals with a parent with type 2 DM have an
increased risk of diabetes;
• Both parents with type 2 DM, the risk approaches 40%
– Environmental factors (such as obesity, nutrition, and
physical activity) modulate genetic predisposition
• Obesity, particularly central , is very common in type 2
DM

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 Pathogenesis T2DM(Cont’d)
Insulin Secretion
• Insulin levels generally appear normal or elevated, but
relatively low to the degree of hyperglycemia due to β-Cell
secretory defect
• As the disease progresses basal insulin levels eventually
decline
Insulin Resistance
• Decreased ability of insulin to act effectively on target tissues
(especially muscle, liver, and fat), is a prominent feature of
type 2 DM and results from a combination of genetic
susceptibility and obesity
• Insulin resistance impairs glucose utilization by insulin-
sensitive tissues and increases hepatic glucose output;

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A proposed sequence of events leading to the
development of type 2 diabetes

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 Clinical Features
Type 1 DM
– Classically, symptoms appear abruptly (i.e., during days
or weeks) in previously healthy, non-obese children or
young adults (Onset usually below 30 yrs of age)
– Polyuria & polydypsia
• Consequence of osmotic diuresis secondary to sustained
hyperglycemia.
• Results in a loss of glucose as well as free water and
electrolytes in the urine
– Weight loss, despite normal or increased appetite,
– Blurred vision, which often develops as the lenses and
retinas are exposed to hyperosmolar fluids.
– May also present with ketoacidosis
– An acute illness (infection ,physical stress etc) may
speed the transition from the preclinical phase to clinical
disease.
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 Clinical Features (Cont’d)
Type 2 Diabetes
• Insidious onset of hyperglycemia and thus relatively
asymptomatic initially
• Presence of obesity or a strongly positive family history of
diabetes suggests type 2 diabetes
• Diabetes may be detected only after glycosuria or
hyperglycemia is noted during routine laboratory studies
• Chronic skin infections & generalized pruritus and symptoms
of vaginitis are frequent initial complaints of women with type
2 diabetes
• Due to long standing(usually decades) asymptomatic
hyperglycemia most patients present with features of chronic
complications
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 Diagnosis
• Classic symptoms of polyuria, polydipsia, and unexplained
weight loss and, a random (or “casual”) plasma glucose
measurement of 200 mg/dL or more
• An 8-hour (overnight) fasting plasma glucose measurement is
most convenient;
– Diabetes is established if fasting glucose levels are 126
mg/dL or higher on two separate occasions
• Alternatively, a 75-g oral glucose tolerance test (OGTT) may be
employed
– Performed after an overnight fast,
– With use of a glucose load containing 75 g of anhydrous
glucose dissolved in water;
– 2-hour postload glucose levels of 200 mg/dL or higher
confirm the presence of diabetes
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 Diagnosis(Cont’d)
Diagnosis of Prediabetes.
• Impaired glucose tolerance (IGT) and impaired fasting glucose
(IFG) refer to intermediate states between normal glucose
tolerance and DM type 2.
• IFG and IGT (designated as Prediabetes) are risk factors for
development of type 2 diabetes and micro- and macrovascular
complications.
– IGT - defined by a 2-hour OGTT, plasma glucose from
140 to 199 mg/dL.
– IFG - defined by fasting plasma glucose of 100 to 125
mg/dL.

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DIAGNOSTIC CATEGORIES: IMPAIRED FASTING GLUCOSE,
IMPAIRED GLUCOSE TOLERANCE, & DIABETES MELLITUS

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 Diagnosis(Cont’d)
Screening
• Widespread use of the FPG as a screening test for type 2 DM
is recommended because:
– Large number of individuals who meet the current criteria
for DM are asymptomatic and unaware that they have the
disorder,
– Type 2 DM may be present for up to a decade before
diagnosis,
– As many as 50% of individuals with type 2 DM have one or
more diabetes-specific complications at the time of their
diagnosis, and
– Treatment of type 2 DM may favorably alter the natural
history of DM

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• ACUTE COMPLICATIONS OF DM
(DDx of coma in diabetic patients)
– Hyperglycemic States
• Diabetic Ketoacidosis (DKA)
• Hyperosmolar Hyperglycemic State (HHS)
– Hypoglycemia

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 ACUTE COMPLICATIONS OF DM
Hyperglycemic States
• Generally classified into two broad clinical syndromes,
Diabetic Ketoacidosis (DKA) & Hyperosmolar Hyperglycemic
Syndrome (HHS)
• DKA is generally seen in type 1 patients, whereas the HHS
affects patients with type 2 diabetes
– lines of distiction are commonly blurred.
• HHS can present with variable degrees of ketosis and
acidosis, and
• DKA is being seen with increasing frequency in obese
type 2 patients
• Despite aggressive treatment, mortality rates remain high for
both conditions, approaching 5% for DKA and 15% for the
HHS.
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 Diabetic Ketoacidosis
• Three cardinal biochemical features of DKA—hyperglycemia,
ketosis, and acidosis—
• Result from the combined effects of absolute deficiency of
insulin and the excessive secretion of counter-regulatory
hormones
• Hormonal imbalances (decreased ratio of insulin to glucagon)
mobilize the delivery of substrates from muscle (amino acids,
lactate, pyruvate) and adipose tissue (free fatty acids,
glycerol) to the liver,
– Where they are actively converted to glucose or to ketone
bodies (β-hydroxybutyrate, acetoacetate, acetone)
• DKA may herald the onset of type 1 diabetes but most often
occurs in established diabetic patients as a result of
intercurrent illness
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PRECIPITANTS OF DKA & HHS

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 DKA :Clinical Manifestations
• Typically involves deterioration during several days, with
advancing polyuria, polydipsia, and other symptoms of
hyperglycemia
• Other common features are weakness, lethargy, nausea and
anorexia
• Abdominal pain in the setting of DKA is classically periumbilical
and can mimic an acute abdomen
• Physical findings in DKA are mainly secondary to dehydration
and acidosis;
– Dry skin and mucous membranes, reduced jugular venous
pressure, tachycardia, orthostatic hypotension, depressed
mental function, and Kussmaul (deep, rapid) respirations
• Ketosis may be recognizable by a sweet, sickly smell on the
patient's breath.
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Manifestations of DKA

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 DKA: Diagnosis
• Timely diagnosis of DKA is crucial and allows for prompt
initiation of therapy
• Initial laboratory tests to be performed include routine serum
chemistries (RFT ,Elecrolytes including divalent cations), CBC
with differential, and urinalysis
• Diagnosis is based on the demonstration of moderate or
severe hyperglycemia, ketonemia, and wide anion gap
metabolic acidosis.
• Urine ketone reaction correlates poorly with ketonemia but is
usually positive in DKA
• Focused search for a precipitating infection is always prudent
• Hyponatremia, hyperkalemia(despite a total-body potassium
deficit), azotemia, and hyperosmolality are other findings
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 DKA: Management
• Preferably be conducted in an ICU
• IV access & supportive measures should be instituted without
delay
• Fluid deficits of several liters are common and the average
degree of dehydration is approximately 7-9% of body weight
– Initial restoration of circulating volume using isotonic (0.9%)
saline
– 1st liter should be infused rapidly and should be followed by
additional fluids at a rate of 1 L/hr until the volume deficit is
corrected
– Next goal is to replenish total body water deficits;
• Accomplished using a 0.45% saline infusion at 150- 300
mL/hr if the corrected serum sodium is normal or
elevated;
• 0.9% NaCl at a similar rate is appropriate if corrected
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serum sodium is low
 DKA: Management(Con’d)
Insulin Therapy:
• Sufficient insulin must be administered to turn off ketogenesis
and correct hyperglycemia.
• IV bolus of regular insulin, 10 - 15 units (0.15 unit/kg)
administered ,followed by a continuous infusion of regular
insulin at rate of 5 - 10 units/hr
• A decrease in blood glucose of 50 - 75 mg/dL/hr is an
appropriate response
• Once oral intake resumes, insulin can be administered SC
– prudent to give the first SC injection of insulin
approximately 30 minutes before stopping the IV route
• Dextrose (5%) should be infused once plasma glucose
decreases to 250 mg/dL and the insulin infusion rate should
be decreased to 0.05 units/kg/hr to prevent dangerous
hypoglycemia
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 DKA: Management(Con’d)
• Potassium deficit should always be assumed or anticipated,
regardless of plasma levels on admission.
– Insulin therapy results in a rapid shift of potassium into the
intracellular compartment
– Potassium should be added routinely to the IV fluids at a
rate of 10 -20 mEq/hr except in pts with hyperkalemia,
renal failure, or oliguria
– Patients with hypokalemia should receive higher doses of
potassium, 40 mEq/hr or greater
Monitoring of therapy
• Measure capillary glucose every 1–2 h; measure electrolytes
(especially K+, bicarbonate, phosphate) and anion gap every 4
h for first 24 h.
• Monitor blood pressure, pulse, respirations, mental status,
fluid intake and output every 1–4 h.
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 DKA: Management(Cont’d)
• Bicarbonate therapy is not routinely necessary and may be
deleterious in certain situations
– Should only be considered in pts with shock or coma, severe
acidosis (pH 6.9 -7.1), plasma bicarbonate <5 mEq/L ,severe
hyperkalemia
• IV antimicrobial therapy should be started promptly for
documented bacterial, fungal, and other treatable infections.
• Complications of DKA include -Lactic acidosis, Arterial
thrombosis , Cerebral edema, Rebound ketoacidosis

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 Hyperglycemic Hyperosmolar State(HHS)
• Occurs primarily in patients with type 2 DM
• Significantly less common than DKA but with a graver
prognosis
Pathophysiology
• Hallmarks of the HHS are severe hyperosmolarity (>320
mOsm/L) and hyperglycemia (>600 mg/dL)
• Hyperglycemia induces an osmotic diuresis that leads to
intravascular volume depletion, which is exacerbated by
inadequate fluid replacement.
• Insulin levels remain sufficient to suppress lipolysis and to
avoid significant keto acid production
– Severely depressed endogenous insulin secretion may be
unable to suppress ketone production fully

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 HHS:Clinical Features
• Elderly individual with type 2 DM, with a several week history
of polyuria, weight loss, and diminished oral intake that
culminates in mental confusion, lethargy, or coma
• Profound dehydration and hyperosmolality and reveals
hypotension, tachycardia, and altered mental status
• Nausea, vomiting, and abdominal pain and Kussmaul
respiration characteristic of DKA are notably absent
• Often precipitated by a serious, concurrent illness such as
myocardial infarction or stroke, sepsis, pneumonia, and other
serious infections

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 HHS(Cont’d)
Laboratory Findings include
• hyperglycemia, often >600 mg/dL;
• plasma osmolality >320 mOsm/L;
• absence of ketonemia; and
• pH >7.3 and serum bicarbonate >20 mEq/L.
• Prerenal azotemia and lactic acidosis can develop
Management
• The goals of therapy are:
– Restoration of hemodynamic stability and intravascular
volume by fluid replacement
– Correction of electrolyte abnormalities
– Gradual correction of hyperglycemia and hyperosmolarity
with fluid replacement and insulin therapy
– Detection and treatment of underlying disease states and
precipitating causes.
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 HHS(Cont’d)
Treatment
• Restoring hemodynamic stability is the first aim.
• Restoration of intravascular volume should be followed by
correction of total body water deficit
• Patients with HHS may require as much as 10 -12 L positive
fluid balance over 24 - 36 hours to restore total deficits
• Despite initial normal or high serum potassium ,rehydration
and insulin therapy usually result in hypokalemia, and should
be corrected.
• Insulin therapy plays a secondary role in the initial
management of HHS
– Administered in similar fashion as in mgt of DKA

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 Hypoglycemia
• Hypoglycemia is the most frequent complication resulting
from insulin therapy
– May also occur in patients who take oral sulfonylureas,
esp. older patients or those with impaired liver or kidney
function
– May result from delay in taking a meal or from unusual
physical exertion without supplemental calories or a
decrease in insulin dose.
Clinical Features
• Symptoms of hypoglycemia can be divided into Autonomic
(adrenergic: palpitations, tremor, and anxiety; cholinergic:
sweating, hunger, and paresthesia) and
• Neuroglycopenic (behavioral changes, confusion, fatigue,
seizure, loss of consciousness,and, if hypoglycemia is severe
and prolonged, death).
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 Hypoglycemia(Cont’d)
• Recurrent episodes of hypoglycemia impair recognition of
hypoglycemic symptoms, (hypoglycemia un-awareness)
– Increasing the risk for severe hypoglycemia.
– Hypoglycemia unawareness results from defective glucose
counterregulation with blunting of autonomic symptoms
and counterregulatory hormone secretion during
hypoglycemia

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Physiology of glucose counterregulation—the mechanisms that normally
prevent or rapidly correct hypoglycemia. In insulin-deficient diabetes, the
key counterregulatory responses—suppression of insulin and increases of
glucagon—are lost, and the stimulation of sympathoadrenal outflow is
attenuated

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 Hypoglycemia(Cont’d)
• Diagnosis of Hypoglycemia is most convincingly documented
by Whipple's triad:
– Symptoms consistent with hypoglycemia,
– A low plasma glucose concentration and
– Relief of those symptoms after the plasma glucose level is
raised.
• The lower limit of the fasting plasma glucose concentration is
normally approximately 70 mg/dL
• Should be considered in any patient with episodes of
confusion, an altered level of consciousness, or a seizure.

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 Hypoglycemia(Cont’d)
• Treatment
– Easily correctable if treated promply but fatal if prolonged
– Any comatose diabetic pt should first be considered to be
hypoglycemic unless proven otherwise
– Readily absorbable carbohydrates (e.g., glucose and sugar-
containing beverages) can be administered orally to
conscious patients for rapid effect
– IV dextrose is indicated for severe hypoglycemia, in
patients with altered consciousness, and during restriction
of oral intakeinitial bolus,
• 20 - 50 mL of 50% dextrose, should be given immediately,
followed by infusion of D5W (or D10W) to maintain blood
glucose above 100 mg/d
– Glucagon, 1 mg IM (or SC), is an effective initial therapy for
severe hypoglycemia
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 CHRONIC DIABETIC COMPLICATIONS
• Chronic complications of DM affect many organ systems and
are responsible for the majority of morbidity and mortality
associated with the disease
• Commonly seen after decades of hyperglycemia
• Pathogenesis of chronic complications of diabetes is complex
and poorly understood
• Microvascular complications of diabetes may affect patients
with type 1 or type 2 diabetes
• Macrovascular complications, which are particularly common
in type 2 diabetes
• Progressively occur over years and decades after onset of
hyperglycemia
• Treatment of chronic complication is usually unsatisfactory
thus the best strategy is prevention through strict control of
glycemia (esp for microvascular comlications)

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Chronic Complications of DM

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 Diabetic Retinopathy
• Refers to progressive pathologic alterations in the retinal
microvasculature,
– leading to areas of retinal nonperfusion, increased vascular
permeability, and the pathologic proliferation of retinal vessels
• One of the leading causes of blindness in adults
Types
• Non-proliferative (background)
– Generally no symptoms but may affect macula and impair vision
– Microaneurysms, hard exudates, dot and blot hemorrhages
• Pre-proliferative
– 10-40% progress to proliferative within one year
– Macular edema, venous shunts and beading, nerve fibre layer
microinfarcts (cotton wool spots)
• Proliferative
– Great risk for loss of vision
– Neovascularization, fibrous scarring, vitreal detachment, retinal
detachment
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hard exudates

blot hemorrhages

Neovascularization
Cotton wool spots

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 Diabetic Retinopathy(Cont’d)
Prevention and management
• Tight glycemic control
• Photocoagulation (eliminates neovascularization)
• Vitrectomy
• Frequent follow-up visits with an ophthalmologist
(immediate referral after diagnosis of type 2 DM;
after 5 years of type 1DM)

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 Diabetic Nephropathy
• One of the leading cause of end-stage renal disease (ESRD).
• 25-45% of pts with type 1 DM develop clinically evident
diabetic nephropathy during their lifetime
– less frequent in type 2 diabetics
• Natural history of diabetic nephropathy in type 1 diabetes is
well described ,less clear inT2DM

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 Diabetic Nephropathy(Cont’d)
Diagnosis
• Screening for microalbuminuria is mandatory
– patients with nephropathy are often asymptomatic
– number of effective intervention strategies can slow
disease progression.
– Measurement of the albumin-to-creatinine ratio (normal,
<30 mg albumin/g cr) in a random urine sample is
recommended for screening
– At least 2 – 3 measurements within a 6-month period
should be performed to establish the diagnosis

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 Diabetic Nephropathy(Cont’d)
Prevention and Treatment
• Intensive control of diabetes and hypertension is an effective
intervention for incipient or established diabetic nephropathy
• Type 1 and type 2 patients with or without hypertension and
micro-albuminuria, ACE inhibitors delay the progression of
nephropathy
• Type 2 patients with hypertension, creatinine >1.5 mg/dL, and
macroalbuminuria, angiotensin II receptor blockers (ARBs)
delay progression of nephropathy

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 Diabetic neuropathy
• Sensorimotor diabetic peripheral polyneuropathy is a major risk
factor for foot trauma, ulceration, and Charcot arthropathy,
– Responsible for 50 - 75% of nontraumatic amputations.
– Types

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 Diabetic neuropathy(Cont’d)
Presentation
• Paresthesias or neuropathic pain
• Motor or sensory deficits (including cranial nerves)
• Orthostatic hypotension
• Impotence
• Voiding difficulties
• Foot ulcers
Prevention and management
• Tight glucose control
• anti-depressants (e.g. amitriptyline), capsaicin, and anti-epileptics
(e.g. Tegretol, Neurontin) for painful neuropathic syndromes
• Erythromycin and metcloromide for gastroparesis
• Foot care education
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 Diabetic Foot Ulcers
• Slowly healing plantar ulcers that result from apparently
insignificant trauma
• Left untreated, superficial ulcers may penetrate to underlying
tissues, leading to complications including cellulitis, abscess
formation, joint sepsis, and osteomyelitis
• Gangrene may occur, and amputation may be required in
severe cases.
• Risk factors include long-standing diabetes, poor glycemic
control, and concurrent diabetic complications.
• To varying degrees, the diabetic foot is characterized by the
combination of chronic sensorimotor neuropathy, vascular
disease, autonomic neuropathy, and impaired immune
function
• Once an ulcer has formed, it should be treated aggressively
with antibiotics, appropriate local wound care, and
debridement of necrotic tissue
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 Pathway to  Diabetic Neuropathy(80% of pts)
Ulceration • 7% annual risk of ulceration
• Sensory, motor, and autonomic
Results from an interaction • Decrease pain sensation and
of a number of component perception of pressure,
causes
• Ms imbalance leading to deformities
Hammer toes ,Claw toes Prominent
metatarsal heads ;
• Reduced sweating, dry skin, and
development of cracks and fissures
 Peripheral Vascular Disease
– Increased incidence by 2-4fold
– Promotes development of critical limb
ischemia, poor wound healing and tissue
loss

57
Site of foot ulcers:
Toes: 51%
Plantar metatarsal head: 28%
Dorsum of foot: 14%
Multiple ulcers: 7%

58
FOOT CARE PRESCRIPTION FOR DIABETIC PATIENTS WITH
LOWER EXTREMITY SENSORY NEUROPATHY

59
Management Of Diabetic Foot Ulcers
Diabetic foot ulcer heals if
 Arterial inflow is adequate.
 Infection is treated appropriately
 Pressure is removed from the wound and the immediate surrounding
area
 Six interventions with demonstrated efficacy in diabetic foot
wounds:
(1) Off-loading,
(2) Debridement,
(3) Wound dressings,
(4) Appropriate use of antibiotics,
(5) Revascularization, and
(6) Limited amputation

60
 Principles of Management of DM
• Therapeutic goals are alleviation of symptoms, achievement
of metabolic control, and prevention of acute and long-term
complications of diabetes
• Patient education is integral to successful management of
diabetes
• Dietary modification
– Total caloric intake can be distributed as follows:
• 45 - 65% of as carbohydrates, 10 - 30% as protein, and <30%
as total fat (<7% saturated fat) with <300 mg/d of
cholesterol
• Exercise improves insulin sensitivity, reduces fasting and
postprandial blood glucose, and offers numerous metabolic,
cardiovascular, and psychological benefits in diabetic patients.

61
 Management of DM:T1DM

• Treatment of type 1 DM requires lifelong insulin replacement.

• Initial insulin dosage for optimal glycemic control is
approximately 0.5 - 1.0 units/ kg/d

62
 Management of DM:T1DM(Cont’d)
• Regimen of multiple daily insulin injections is preferred to obtain
optimal control.
– Provides approximately 40 - 50% of the total daily dose of
insulin as basal insulin supply, using one or two injections of
long-acting or intermediate-acting insulin
– Remainder is given as three doses of rapid-acting insulin
divided across the main meals
• Typically 1 unit of insulin per 10 - 15 g of carbohydrate consumed
is typical
• The conventional insulin regimen uses a mixture of short- and
intermediate-acting insulins administered before breakfast and
before the evening meal
– two-thirds of the total daily dose is injected in the morning and
one-third in the evening.
– Approximately two-thirds of each injection comprises
intermediate-acting insulin and one-third is rapid-acting insulin
• Insulin administration by insulin infusion pump with the basal
insulin and a bolus injection at each meal.
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Representative insulin regimens for the treatment of diabetes
Multiple-component insulin regimen, Injection of two shots of long-
acting insulin, Insulin administration by insulin infusion device,
respectively

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 Management of DM:T2DM
• Oral therapy should be initiated early in patients with T2DM
that failed glycemic control after a short-term trial of diet and
exercise
• Monotherapy with maximum doses of insulin secretagogues,
metformin, or thiazol-idinediones yields comparable glucose-
lowering effects
• Second or third agent including insulin should be added if no
response is achieved with monotherapy
• Insulin therapy in type 2 DM is indicated in:
– Patients in whom oral agents failed to sustain glycemic control
– DKA
– Nonketotic hyperosmolar crisis
– Newly diagnosed patients with severe hyperglycemia
– Pregnancy and other situations in which oral agents are
contraindicated
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Management of DM:T2DM(Cont’d)

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 DERMATOLOGIC MANIFESTATIONS
• The most common skin manifestations of DM are xerosis and
pruritus and are usually relieved by skin moisturizers.

• Protracted wound healing and skin ulcerations are also frequent

complications.

• Diabetic dermopathy, sometimes termed pigmented pretibial

papules, or “diabetic skin spots,” begins as an erythematous
macule or papule that evolves into an area of circular
hyperpigmentation.

• These lesions result from minor mechanical trauma in the pretibial

region and are more common in elderly men with DM.

• Bullous diseases, such as bullosa diabeticorum (shallow ulcerations

or erosions in the pretibial region), are also seen.
• Necrobiosis lipoidica diabeticorum is an uncommon disorder, accompanying
diabetes in predominantly young women.

• This usually begins in the pretibial region as an erythematous plaque or

papules that gradually enlarge, darken, and develop irregular margins, with
atrophic centers and central ulceration. They are often painful.

• Vitiligo occurs at increased frequency in individuals with type 1 DM.

• Acanthosis nigricans (hyperpigmented velvety plaques seen on the neck,

axilla, or extensor surfaces) is sometimes a feature of severe insulin resistance
and accompanying diabetes.

• Generalized or localized granuloma annulare (erythematous plaques on the

extremities or trunk) and scleredema (areas of skin thickening on the back or
neck at the site of previous superficial infections) are more common in the
diabetic population.

• Lipoatrophy and lipohypertrophy can occur at insulin injection sites but are
now unusual with the use of human insulin.