WHAT IS DIABETES ?
DIABETES
Diabetes is chronic metabolic disorder that prevents the body to
utilize glucose completely or partially. It is characterized by raised
glucose concentration in the blood and alterations in
carbohydrate, protein and fat metabolism. This can be due to
failure in the formation of insulin or liberation or action.
CAUSES OF DIABETES
IDDM (Insulin dependent diabetes mellitus) :
Genetics :
The inheritance of human IDDM is polygenic. It has been estimated that over 50% of the
heritability is contributed by the HLA class 2 nd genes(chromosome 6).
Environmental factor :
Infections: Infections
cause a non- specific outpouring of catabolic hormones
antagonise insulin action and then may trigger the onset of disorder.
which
The virus may trigger an autoimmune reaction in the pancreatic islets and this impairs
insulin secretion and ultimately destroys the beta cells.
Acute stress:
The body releases adrenaline, noradrenaline, and cortisol hormones that
raise blood glucose levels to provide a quick source of energy for coping with stress
In acute cases of stress blood glucose levels may rise and in extreme cases diabetic ketosis
and coma also may result .
Diet: Wheat and milk protein
have the strongest diabetogenic effect and one evidently
capable of triggering the string of events which result ultimately in destruction of pancreatic
islet insulin secreting cells.
Immunological factors :
IDDM is a slow autoimmune disease. IDDM is associated with other autoimmune disorders.
NIDDM ( Non insulin dependent diabetes mellitus)
Genetics :
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NIDDM is commonly associated with obesity , hypertension , and hyperlipidemia .
It Occurs in subjects who are obese insulin- resistant accompanied by impaired beta cell
function.
It represents a combination of major and minor genes affecting insulin secretion, insulin
action , and obesity.
Environmental factors :

life style: NIDDM is associated with people who are obese and underactive usually they

over eat.
Obesity probably acts as a diabetogenic factor through increasing resistance to the action
of insulin.

Age : it is principally
a disease of the middle aged and elderly.
Abdominal fat : people with high waist / hip ratio
has greater risk of diabetes than
people with a similar amount of fat distributed peripherally.
This probably relates to the insulin insensitivity which is caused by a high flux of free fatty
acids in the portal circulation, because intra- abdominal fat cells can release fatty acids very
rapidly.
Pregnancy :
During normal pregnancy the level of plasma insulin is raised by the action of
placental hormones thus placing burden on the insulin secreting cells of the pancreatic
islets.
The pancreas may be unable to meet these demands in women genetically predisposed to
develop both types of diabetes.
Insulin resistance :
Insulin resistance may be due to an abnormal insulin molecule, an excessive
amount of circulating antagonists and target tissue defects.
The last is the common cause of insulin resistance in NIDDM and seems to be the
predominant abnormality in those with more severe hyperglycemia.
INSULIN
Insulin a hormone produced by the beta
cells of the pancreas that is necessary for
the use or storage of body fuels.
FUNCTIONS OF INSULIN
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In addition to its role of regulating glucose metabolism, insulin also
Stimulates lipogenesis
Diminishes lipolysis s
Increases amino acid transport into cells
Modulates transcription
Altering the cell content of numerous mRNAs
Stimulates growth
DNA synthesis
Cell replication
INSULIN AND COUNTER REGULATORY HORMONE
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Optimal control of diabetes requires the restoration of normal
carbohydrates, protein, and fat metabolism.
Insulin is both anti catabolic and anabolic and facilitates cellular transport.
In general , the counter regulatory hormones have the opposite effect of
insulin .
ACTION OF INSULIN ON CARBOHYDRATES, PROTEIN , FAT
METABOLISM
EFFECTS
CARBOHYDRATES
PROTEIN
FAT
Anti catabolic
(prevents
breakdown)
Decrease breakdown
and release of glucose
from glycogen in the liver
Inhibits protein
degradation
diminishes
gluconeogenesi
s
Inhibits lipolysis
prevent excessive
production of
ketones and
ketoacidosis
Anabolic
(promote
storage )
Facilitates conversion of
glucose to glycogen for
storage in liver and
muscle
Stimulates
protein
synthesis
Facilitates
conversion of
pyruvates to free
fatty acids
stimulating
Lipogenesis
Transport
Activates the transport
system of glucose in to
muscle and adipose cells
Lower blood
amino acids in
parallel with
blood glucose
level
Activate lipoprotein
lipase, facilitating
transport of
triglyceride into
adipose tissue
INSULIN THERAPY
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When the islets of langerhans are unable to produce insulin it must be
supplied by injection.
Persons with type 1 diabetes depend on insulin to survive and with
type 2 diabetes, insulin may be needed to restore glycemia to near
normal.
Insulin has four properties : action , concentration, purity, and source.
These properties determine its onset, peak , and duration.
TYPES OF INSULIN AND THEIR ACTION
INSULIN
ONSET
PEAK
DURATION
Short acting insulin (clear)
 Lispro
 Regular
5-15 minutes 30-75 minutes 2-3 hours
30-45minutes 2-3 hours
4-6 hours
Background insulin (cloudy)
 NPH (neutral protamine
hagedorn)
LENTE
 ULTRALETE
2-4 hours
2-4 hours
3-5 hours
4-10 hours
4-10 hours
8-14 hours
10-18 hours
10-18 hours
18 hours
Premixed insulin
70/30 or 50/50
60 minutes
2-12 hours
Up to 18 hours
TYPES OF INSULIN
Regular and Lispro insulin:

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Short -acting
Regular insulin needs to be taken 30 to 45 minutes before eating.
Lispro insulin, an analogue with two amino acids reversed in position. Starts to work very
quickly. So it should be taken immediately before eating.
Both insulins may be used in combination with a background or intermediate –acting insulin,
may also be used independently during acute illness , in insulin pumps , and in multiple daily
injection regimen .
Background or intermediate–acting insulins:
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It include NPH, LENTE AND ULTRALENTE
Their appearance is cloudy. And their onset ,peak, duration are similar.
Ultralente is a slightly longer-acting insulin than the intermediate –acting insulins.
Premixed insulins:
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70/30 which is 70% NPH and 30% regular
50/50 which is 50% NPH and 50 % regular
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Human or highly purified animal insulin are now standard and contain less than
1ppm of impurities.
They are associated with fewer insulin antibodies, less insulin allergy.
The source of insulin is important because it affects the speed of absorption, peak,
and duration of action.
Animal insulin come from the pancreas of the cows and pigs.
Human insulin has been produced synthetically.
Human insulins are generally absorbed more rapidly, peak earlier, and have a
shorter duration time than animal insulins.
A major advantage of human insulin is that it produce fewer antibodies and as a
result, can also be used for insulin treatment.
TYPES AND TIMING OF INSULIN
REGIMEN
A short –acting and
background insulin
• Given twice a day
• The breakfast dose
consist of about one third
regular and two third NPH
A short acting and
background insulin
• Prebreakfast a short –
acting insulin presupper
and background insulin
such as NPH, at bedtime.
Intensive insulin
regimen
• It consist of multiple daily
injection or insulin
infusion pump therapy .
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A short- acting insulin is given before meals to provide bolus insulin
replacement.
A background insulin is given once a twice a day.
These types of regimens allow increased flexibility in the type and timing of
meals.
The amount of short-acting insulin can be adjusted based on composition of
meals.
INSULIN INFUSION PUMP THERAPY
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It provide basal short-acting insulin pumped continuously by a mechanical device in micro
amounts through a subcutaneous catheter that is monitored 24 hours a day .
Boluses of the short-acting insulin are then given before meals.
Pump therapy requires a motivated person who is willing to do a minimum of four blood
glucose test per day.
Keep blood glucose and food records and learn the technical features of pump usage.
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Pump therapy is also more expensive than other insulin regimen.
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DOSE:
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35% Before breakfast
25% before lunch and dinner
15% before bed time
In addition to closer control of blood glucose levels, use of the insulin pump is reported
to lower elevated level of serum cholesterol and triglycerides and to permit greater
flexibility in timings of meals.
Environmental influence
Genetic influence
Insulin resistance
•Deficiency of nutrients
•Excessive calorie intake
•Low physical activity level
Hyperinsulinemia
Increased
plasma
triglyceride
s
Increased
LDL
cholester
ol
Atherosclerosis
Decreased
HDL
cholesterol
Increased
uric level
Gout
Glucose
intoleranc
e
Diabetes
Increased
lipogenesis
Obesity
Pathaphysiology of insulin resistance
Increased
blood
pressure
Hyperte
nsion
Metabolic syndrome
A collection of health risks, including excess fat in the abdominal region, high
blood pressure, elevated blood triglycerides , low high- density lipoprotein
cholesterol and high blood glucose that increases the chance of developing
heart disease , stroke, and diabetes, the condition is also known by others
names including syndrome x , insulin resistance syndrome ,dysmetabolic
syndrome.
HYPERINSULINEMIA OR SYNDROME X
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Syndrome x refers to a clusters of metabolic disorders, including type 2 diabetes,
hypertension and dyslipidemia and often include obesity.
A major factor in syndrome X is insulin resistance, which is cellular resistance to insulin.
Resistance to insulin mediated to glucose uptake may be more common.
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Factors that have a positive impact on insulin :
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Exercising
Reducing calorie intake
Reducing body weight
A defensive nutrition plan for middle-aged adults emphasizes food that supply
glucose to the cells at a steady rate and moderate insulin demands.
One useful tool for measuring the rate at which foods provide glucose to the
blood and then stimulate insulin release is the glycemic index .
COMPLICATIONS
Without effective insulin hyperglycemia occurs, which can lead to both the short
term and long term complication of diabetes mellitus.
Short term or acute complication:
1) Hyperosmolar hyperglycemic nonketotic syndrome
2) Hyperglycemia/ diabetic ketoacidosis
3) Hypoglycemia
4) Hyperglycemia after hypoglycemia
5) Dawn phenomenon
HYPEROSMOLAR HYPERGLYCEMIC
NONKETOTIC SYNDROME
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HHNK syndrome is defined as a extremely high blood glucose level, absence or
only small amounts of ketones and profound dehydration.
Patient who have HHNK syndrome have sufficient insulin to prevent lipolysis
and ketosis.
This condition occurs rarely, usually in older patients with type 2 diabetes
Clinical manifestation
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Hypotension
Profound dehydration
Tachycardia
Variable neurological signs
TREATMENT:
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Hydration
Small doses of insulin
.
HYPERGLYCEMIA/DIABETIC KETOACIDOSIS
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It is characterized by severe disturbance in carbohydrate, protein and fat metabolism.
DKA
Acidosis
Inadequate insulin for glucose utilization
Increased production and decreased
utilization
Body depends on fat for energy
Ketones are formed
Acetoacetic acid , 3 beta hydroxy butyric
acid from fatty acid
These ketones split into the urine the reliance on urine testing for ketones
DKA is characterized by elevated blood glucose level and the presence of
ketones in the blood and urine.
Symptoms:
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polyuria
polydipsia
hyperventilation
dehydration
fatigue
TREATMENT:
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Supplemental insulin
Fluid and electrolyte replacement
Medical monitoring
Acute illness such as flu , colds, vomiting, and diarrhea. If not manage
appropriately can lead to the development of DKA.
HPOGLYCEMIA
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Hypoglycemia is a common side effect of insulin therapy.
SYMPTOMS:
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Shakiness
Sweating
Palpitation
Hunger
Hypoglycemic symptoms are related to neuroglycopenia
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Headaches
Confusion
Lack of coordination
Blurred vision
Anger
Seizures
Coma
CAUSES
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Medication errors
Excess insulin or oral medication
Inadvertent or deliberate errors in insulin doses
Improper timing of insulin in relation to food intake
Intensive insulin therapy
Inadequate food intake
Omitted or inadequate meals or snacks
Delayed meals or snacks
Unplanned activities
Alcohol intake
TREATMENT
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15 grams of carbohydrate commercially available glucose tablets .
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Parents, roommates , and spouses should be taught how to mix , draw up , and
administer glucagon.
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Patients need to be reminded of the need to treat hypoglycemia , even in the
absence of symptoms
HYPERGLYCEMIA AFTER HYPOGLYCEMIA
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Hypoglycemia followed by “ rebound” hyperglycemia is also called the somogyi
effect.
This phenomenon originates during hypoglycemia with the secretion of counter
regulatory hormones hepatic glucose production is stimulated thus raising blood
glucose levels.
If rebound hyperglycemia goes unrecognized and insulin doses are increased, a
cycle of over insulinization may result.
DAWN PHENOMENON
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The amount of insulin required to normalize blood glucose levels during the night is
less in the predawn period (from 1 to 3 am ) than at dawn (4 to 8 am )
The rise in blood glucose levels may be increased if insulin level declines between
predawn and dawn or if hypoglycaemia occurs during the predawn period.
Blood glucose level is monitored at bed time and at 2 to 3 am to identify the dawn
phenomenon.
Taking intermediate acting insulin at bed time or substituting it with a longer-acting
insulin may also be effective.
Retinopathy
Micro vascular
diseases
Neuropathy
Nephropathy
Long term
complications
Macro vascular
diseases
Coronary artery disease
Cerebrovascular disease
Peripheral vascular disease
MACROVASCULAR DISEASES
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Macro vascular disease result from changes in the medium to large blood vessels. In
this blood vessel walls thicken, and become closed by plaque that adheres to the
vessel walls . Eventually blood flow is blocked.
Coronary heart disease , peripheral vascular disease , cerebrovascular disease
Lipid abnormalities are one of the risk factors contributing to accelerated
atherosclerotic vascular disease .
Generally , total cholesterol and LDL cholesterol are comparable between persons
with diabetes and the general population.
Patients with type 2 diabetes have smaller , more dense LDL particles, which
increase atherogenecity .
Elevated plasma triglyceride and very low density lipoprotein cholesterol levels and
lower HDL cholesterol level.
SYMPTOMS
•Chest pain
•Dyspnea
Coronary •Orthopnea
heart
•Paroxysmal nocturnal
disease
•Foot ulcers
Peripheral •Pain in buttock, thigh,
vascular
disease
•Transient blindness,
Cerebrova •dysarthria, or
scular •unilateral weakness
disease
TREATMENT
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It is based on LDL cholesterol levels. With CHD, PVD, OR CVD , Medical nutrition
therapy and drug therapy is initiated.
When LDL cholesterol levels exceed 100mg/dl , with a goal of reducing this value ,
MNT is initiated.
Drug therapy is appropriate at LDL cholesterol levels of 130mg/dl or higher.
MANAGEMENT
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Diet and exercise are important in managing obesity, hypertension , and
hyperlipidemia.
Use of medications to control hypertension and hyperlipidemia
Smoking cessation is essential
Control of blood glucose levels
Patients may require increased amounts of insulin or may need to switch from oral
antidiabetic agents to insulin during illness.
MICROVASCULAR DISEASES
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Micro vascular complications of diabetes affect small blood vessels and nerves of
the body.
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Retinopathy
Neuropathy
Nephropathy
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RETINOPATHY
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The eye pathology refer to as diabetic retinopathy is caused by changes in the small blood
vessels in the retina, the area of the eye that receives images and sends information to the
brain.
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Nearly all patients with type I diabetes and more than 60% of patients with type II diabetes
have some degree of retinopathy after 20 years.
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Changes in the micro vasculature include micro aneurysms, intra retinal hemorrhage, hard
exudates, focal capillary closure.
There are three main stages of retinopathy:
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Nonproliferative retinopathy
Preproliferative retinopathy
Proliferative retinopathy
Nonproliferative retinopathy
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It is the earliest stage of retinopathy where structural changes began to occur in
various structures of the eye.
It is divided into three stages mild, moderate and severe.
Mild NPDR is characterized by microaneurysms
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The residue of protein and lipid components that leak from the blood vessels are
present.
Intra-retinal hemorrhage appearing as dots or flame shapes and soft exudates or
‘cotton wool spots’, areas of infraction in the nerve fiber layer of the retina.
Moderate NPDR
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It is characterized by microaneurysms, dot and blot hemorrhages and exudates.
The retinal veins becomes dilated and intra retinal micro vascular abnormalities
which appear as a clusters of micro aneurysms and hyper cellular vessels develops.
Severe NPDR:
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It is characterized by hemorrhages and microaneurysms in all of the retina, IRMA in
one, and venous beading in another quadrants signify high for development of PDR.
Preproliferative retinopathy
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In this retinopathy there are more wide spread vascular changes and loss of nerve
fibers.
10-50% of patients with preproliferative retinopathy will develop proliferative
retinopathy within a short time.
PROLIFERATIVE RETINOPATHY
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It is characterized by the proliferation of new blood vessels growing from the retina
into the vitreous. These new vessels are prone to bleeding.
The visual loss associated with proliferative retinopathy is caused by the vitreous
hemorrhage or retinal detachment.
The vitreous is normally clear, allowing light to be transmitted to the retina.
When there is a hemorrhage, the viterous becomes clouded and cannot transmit
light resulting in loss of vision.
Another consequence of vitreous hemorrhage is that resorption of the blood in the
vitreous leads to the formation of fibrous scar tissue.
Clinical manifestations
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Retinopathy is a painless process.
Blurry vision secondary to macular edema occurs in some patients.
Symptoms:
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Floaters or cobwebs in the visual field.
Sudden visual changes including spotty or hazy vision or complete loss of vision.
Medical management
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For advanced cases , the main treatment of diabetic retinopathy is argon laser photo
coagulation.
The laser treatment destroys leaking blood vessels and areas of neovasclarization.
For patients at increased risk for hemorrhaging, pan- retinal photo coagulation may
significantly reduce the rate of progression to blindness.
Nephropathy:
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It is characterized by albuminuria, hypertension, and progressive renal insuffiency.
It can lead to end stage renal disease, a serious condition in which a patient’s
survival depends on either dialysis or kidney transplantation.
Characteristics
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Decrease in glomerular filtration rate
Increase in glomerular capillary pressure
Clinical manifestations
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Proteinuria
Fluid retention
SIGNS AND SYMPTOMS
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Weight gain ,peripheral edema , and pulmonary edema
Elevated blood urea nitrogen (BUN) and creatinine levels
Fatigue and shortness of breath
Uncontrolled hypertension
Uremia due to accumulation of metabolic wastes
GI manifestations : anorexia, nausea, vomiting
Neuromuscular disturbance : fatigue, muscle cramps, seizures, coma
Hematologic symptoms: anemia fatigue, decreased white blood cell count ,
increased risk of infection.
TREATMENT
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HbA1c<7%
Control blood pressure
Appropriate diet
Manage kidney infections
Avoid nephrotoxic drugs
Test regularly for microalbuminuria
Smoking cessation
NEUROPATHY
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Damage to the nerves that allow feeling sensation, diminished transmission of nerve
impulses that affect muscle function and sensory perceptions in various parts of the
body.
Autonomic dysfunction
Diabetic foot, ulceration, amputation
Types of diabetic neuropathy
Distal symmetric sensorimotor
Diabetic autonomic
Diabetic proximal
Focal neuropathy
DISTAL SYMMETRIC SENSORIMOTOR
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Most commonly legs and foot are affected .
Nerve damage in the feet can result in loss of foot sensation, increasing foot
problems.
Symptoms:
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Tingling
Numbness
Burning sensation and pain
Peripheral neuropathy leads to
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Small fiber damage
Large fiber damage
Motor nerve damage
Prevention:
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Examine your foot daily
Apply lotion on dry feet
Wear proper fitting footwear, corns should never be cut and keep them clean.
DIABETIC AUTONOMIC NEUROPATHY

It commonly affects the digestive system especially the stomach, blood vessels,
urinary system and sex organs
Its affects on
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Upper GI
Intestinal
Bladder
Sexual dysfunction
Cardiovascular
.
DIABETIC PROXIMAL NEUROPATHY
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It is usually causes pain in one side in the thighs, hips or buttocks
It can also leads to weakness in legs.
Treatment
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Medication and physical therapy
Keep blood glucose level under control
FOCAL NEUROPATHY

It affect specific nerve , most often in the head , legs causing muscle weakness or
pain.
symptoms
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Double vision , pain in eye
Severe pain in lower back, legs, chest
Abdominal pain
DIABETIC FOOT
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Foot ulcers are one of the main complication of DM.
With damage to the nervous system, a person with diabetes may not be able
to feel his or her feet properly.
Normal sweat secretion & oil production that lubricates the skin of the foot
is impaired
These factor together can lead to abnormal pressure on the skin, bones,
and joints of the foot during walking and can lead to breakdown of the skin
of the foot.
Sores may develop.
Damage to blood vessels and impairment of the immune system from
diabetes makes it difficult to heal these wounds.
Bacterial infection of the skin connective tissues, muscles and bones can
occur.
These infection can develop into gangrene.
FEET SHOULD BE LABELED AS HIGH RISK IF:
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If any deformity ids observed.
Sensory examination revels loss of sensation.
Absence of foot pulses.
Previous history of ulcer.
FOOT CARE DO’S AND DONT’S FOR PATIENT
DO
DO NOT
Inspect feet daily using mirror
Walk barefoot
Wash feet daily in the tepid water
Smoke
Apply lotion to the feet after drying
Expose to extreme temperature
Have your feet check at each clinical visit
Use chemical agents e.g. corn plaster to
treat corns or calluse
Inspect foot wear daily for detects
/foreign bodies, change footwear often
Wear new foot wear for more than a hour
or two at a time
THANKYOU