Diabetes mellitus is a syndrome where the body either does not produce enough insulin or the cells ignore the insulin, resulting in high blood sugar levels. The pancreas normally produces insulin to regulate blood sugar levels, but in diabetes the pancreas produces little or no insulin or the body develops resistance to insulin. The three main types of diabetes are type 1, type 2, and gestational diabetes. Type 1 is an autoimmune disease where the pancreas stops producing insulin, type 2 is due to insulin resistance often associated with obesity, and gestational diabetes develops in pregnancy and increases risks for both mother and baby. Complications of diabetes include kidney damage, eye damage, nerve damage, foot damage, and heart disease. Tight control

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2. Diabetes mellitus
is a syndrome of disordered metabolism, usually
due to a combination of hereditary and
environmental causes, resulting in abnormally
high blood sugar levels (hyperglycemia).
often referred to simply as diabetes ( Greek: to
pass through <urine>).
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3. Normal Glucose Metabolism
the sugars and starches within the foods we eat are
broken down into glucose, and are absorbed into the
blood stream. This absorption causes a rise in the
blood glucose level.
As the blood containing elevated glucose levels
circulates, it comes into contact with the pancreas, and
certain other specific parts of the pancreas, which are
contained in a sub structure called the islets of
Langerhans.
These other specialized parts are the alpha, beta, and
delta cells, which produce particular homones, which
drastically affect blood sugar levels.
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4. When an inreased blood sugar level is sensed
by the beta cells, they secrete insulin directly
into the bloodstream. Insulin is a powerful
hormone which allows cell membranes to
change, (become more permeable to glucose),
so that they allow the glucose molecule to be
pulled into the cell interior, where it can be
broken down into energy.
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5. In another example, when you've just gotten
done with a bunch of work, and your blood
sugar level begins to fall, the other type of cell,
the alpha cell, senses a low blood sugar
condition, and it releases another hormone,
called glucagone. Glucagone goes out into the
blood stream in the same fashion as the insulin
did, however, the glucagone tells the liver cells
to release some of their stored sugars back
into the blood stream, thus raising the blood
sugar levels back into an operating range.
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6. Insulin is also the principal control signal for
conversion of glucose to glycogen for internal
storage in liver and muscle cells. Lowered glucose
levels result both in the reduced release of insulin
from the beta cells and in the reverse conversion of
glycogen to glucose when glucose levels fall. This is
mainly controlled by the hormone glucagon which
acts in an opposite manner to insulin. Glucagon and
insulin are part of a feedback system that keeps
blood glucose levels at a stable level.
Glucose thus recovered by the liver re-enters the
bloodstream; muscle cells lack the necessary export
mechanism.
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7. When energy is required, glycogen stores in
the liver are converted into glucose via
glycogenolysis, elevating blood glucose levels
and providing the needed cellular energy
source.
The liver also produces glucose from fat (fatty
acids) and proteins (amino acids) through the
process of gluconeogenesis. Glycogenolysis
and gluconeogenesis both serve to increase
blood glucose levels. Thus, glycemia is
controlled by a complex interaction between
the gastrointestinal tract, the pancreas, and
the liver.
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8. Multiple hormones may affect glycemia.
Insulin is the only hormone that lowers
blood glucose levels. The counter-
regulatory hormones such as glucagon,
catecholamines, growth hormone, thyroid
hormone, and glucocorticoids all act to
increase blood glucose levels, in addition
to their other effects .
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9. Abnormal Glucose Metablolism
The destruction of beta cells by a virus or an auto-immune
response from our own bodies, are two reasons which
have so far been found for beta cell destruction in clinical
studies.
When this sort of destruction occurs, it impairs the body's
ability to manufacture insulin. In the case of someone with
type 1, insulin-dependent diabetes, the beta cell
destruction may be complete and may never be repaired
by the body. In the case of type 2 diabetes, some beta
cells remain, however they may not be able to keep up
with the body's demand for insulin unless a low
carbohydrate or complex carbohydrate diet is followed.
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10. Other conditions
Steroid diabetes(also "steroid-induced diabetes") is a medical term
referring to prolonged hyperglycemia due to glucocorticoid therapy
for another medical condition. It is usually, but not always, a
transient condition.
The most common glucocorticoids which cause steroid diabetes are
prednisolone and dexamethasone given systemically in
"pharmacologic doses" for days or weeks. Typical medical
conditions in which steroid diabetes arises during high-dose
glucocorticoid treatment include severe asthma,
organ transplantation, cystic fibrosis, inflammatory bowel disease,
and induction chemotherapy for leukemia or other cancers.
Topical steroids can also cause hyperglycemia if used in large
quantities and high doses over prolonged time periods, but this
usually resolves with discontinuation of the medication.
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11. Types of Diabetes
• Type 1 diabetes. results from autoimmune destruction
of insulin-producing beta cells of the pancreas.
• Type 2 diabetes: The bodyproduces insulin, but the
cells have developed a resistance to it, often because
the pt is overweight or obese. Watching fat intake is a
necessary part of losing weight and keeping diabetes
under control.
• Gestational diabetes. It usually develops during the
third trimester and significantly increases perinatal
morbidity and mortality. the pathophysiology of
gestational diabetes is associated with increased insulin
resistance.
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12. Impaired Glucose Tolerance and Impaired
Fasting Glucose
The conditions known as impaired glucose tolerance (IGT) and
impaired fasting glucose (IFG) represent metabolic states
lying between diabetes and normoglycemia. People with IFG
have increased fasting blood glucose levels but usually have
normal levels following food consumption.
they are risk factors for future diabetes. Pathophysiology of
IFG and IGT is related primarily to increased insulin
resistance whereas endogenous insulin secretion is normal
in most patients. Approximately 30 to 40% of individuals with
IGT or IFG will develop type 2 diabetes within 10 years after
onset.
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13. Diabetes and Fat Intake
people with diabetes need to limit their fat intake to
decrease their risk of developing heart disease.That is
diabetes slowly damages the arteries in the body
unless blood sugar is very tightly controlled.
The increased risk of cardiovascular disease exists no
matter which of the three types of diabetes the pt has.
Obesity contributes greatly to insulin resistance, even in
the absence of diabetes. In fact, weight loss is a
cornerstone of therapy for obese type 2 diabetic
patients. Insulin resistance generally decreases with
weight loss.
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14. There is some evidence that fat cells are more
resistant to insulin than muscle cells. If a person
has more fat cells than muscle cells, then the
insulin becomes less effective overall, and
glucose remains circulating in the blood instead
of being taken in to the cells to be used as
energy.
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15. Why Do Type 1 Diabetes Patients Slim Down Even
Eating Much
Due to the fact that Type 1 Diabetes patients lack insulin in
body, patients’ body cannot make the best of glucose. This
stimulates protein and fat in body to acceleratory
decomposition, which contributes to supplying energy and
heat for body. By this, large quantity of carbohydrate,
protein and fat will be consumed. Besides, Type 1 Diabetes
patients are always in a state of water loss; even they have
had more water. when the sugar levels are high, they will
want to pass urine quite a few times. This will naturally
result in dehydration. The loss of sugar in the urine means a
loss of calories which provide energy and therefore many
people with high sugars lose weight.
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16. Polyuria,polydipsia,polyphagia
When the glucose concentration in the blood is raised
beyond the renal threshold, reabsorption of glucose in
the proximal renal tubuli is incomplete, and part of the
glucose remains in the urine ( glycosuria). This increases
the osmotic pressure of the urine and inhibits the
reabsorption of water by the kidney, resulting in
increased urine production ( polyuria) and increased fluid
loss. Lost blood volume will be replaced osmotically from
water held in body cells, causing dehydration and
increased thirst(polydipsia).
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17. reason for polyphagia is the intracellular
starvation. As in diabetes either there is absence
or the resistance to insulin action so glucose
cannot move into the cells and thus cells are
starved of glucose.
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18. Permanent Teeth Erupt Early in Diabetic
Children
The reasons for the speedier tooth eruption may have to do
with gum inflammation, which tended to be greater in
children with diabetes. Gum inflammation may diminish the
mass of the bones supporting the teeth, shortening the
distance that developing teeth need to progress to break
through the gums. This could potentially increase their risk
of dental problems liket they could raise the odds of
misaligned or crowded teeth, which, lead to cosmetic
effects, and can make it harder to clean the teeth and keep
the gums healthy.

19. Clinical differentiation between
hypoglycemia and hyperglycemia
hypoglycemia
• hunger and weakness followed
bysweating.
• Rapid pulse
• Shakiness, dizziness,
weakness
• Decreased coordination
• Difficulty concentrating
• Blurred vision
• Headache
• Trouble performing routine
tasks
• Note: Symptoms can vary
from person to person and
episode to episode.
hyperglycemia
• Warm, dry skin that does not
sweat
• Dry, parched mout
• Extreme thirst
• Frequent urination
• General weakness
• Loss of appetite
• Fruity breath
• Nausea and vomiting
• Abdominal pain
• Deep, rapid breathing
• High fever
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20. Diabetic ketoacidosis
People with type 1 diabetes are highly susceptible to diabetic
ketoacidosis. Because the pancreas produces no insulin, glucose
cannot enter cells and remains in the bloodstream. To meet cellular
energy needs, fat is broken down through lipolysis, releasing
glycerol and free fatty acids. Glycerol is converted to glucose for
cellular use. Fatty acids are converted to ketones, resulting in
increased ketone levels in body fluids and decreased hydrogen ion
concentration (pH). Ketones are excreted in the urine, accompanied
by large amounts of water. The accumulation of ketones in body
fluids, decreased pH, electrolyte loss and dehydration from
excessive urination, and alterations in the bicarbonate buffer system
result in diabetic ketoacidosis (DKA). Untreated DKA can result in
coma or death.
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21. Many patients with type 1 diabetes are initially
diagnosed with the disease following a hospital
admission for DKA. In a known diabetic patient,
periods of stress or infection may precipitate DKA.
More often, however, DKA results from poor daily
glycemic control. Patients who remain severely
hyperglycemic for several days or longer due to
inadequate insulin administration or excessive
glucose intake are prone to developing DKA.
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22. ORAL COMPLICATIONS OF DIABETES
• Gingivitis and periodontal disease.
• Salivary gland dysfunction and xerostomia.
• Candidiasis.
• Burning mouth syndrome.
• Lichen planus.
• Acute oral infections
• delayed wond healing
• Early tooth loss in IDDM.
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23. Gingivitis and periodontal disease
Is related to the altered response to infection,
microvascular changes and, possibly, increased
glucose concentrations in the saliva (salivary
hyperglycemia) and gingival crevicular fluid.
Increased salivary glucose results in additional
bacterial substrate and plaque formation.29
Increased gingival crevicular fluid glucose may
diminish the ability of periodontal fibroblasts to
contribute to periodontal healing.
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24. Salivary gland dysfunction and xerostomia.
Is due to polyuria, or an underlying metabolic or endocrine
problem. When the normal environment of the oral cavity is
altered because of a decrease in salivary flow or alteration
in salivary composition, a healthy mouth can become
susceptible to dental caries and tooth deterioration. Dry,
atrophic and cracking oral mucosa is the eventual
complication from insufficient salivary production.
Accompanying mucositis, ulcers and desquamation, as well
as an inflamed, depapillated tongue, are also common
problems. Difficulty in lubricating, masticating, tasting and
swallowing are among the most devastating complications
from salivary dysfunction and may contribute to impaired
nutritional intake.
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25. Candidiasis
Salivary dysfunction, compromised immune function
and salivary hyperglycemia that provides a potential
substrate for fungal growth are the major
contributing factors for oral candidiasis in patients
with diabetes. Oral lesions associated with
candidiasis include median rhomboid glossitis
atrophic glossitis, denture stomatitis, (thrush) and
angular cheilitis.
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26. Mechanism of increased risk of
infection
• Macrophage metabolism alteration occurs, with inhibition of
phagocytosis.
• Immunological defect and deficient leucocytes functions.
Functions of immune cells, including neutrophil, monocytes and
macrophages are altered.
• Decrease production of antibodies.
• Peripheral neuropathy and poorperipheral circulation.
• All steps of PMN functioning which include PMN chemotaxis,
spontaneous activation of PMN cells, increased free radical
production; after stimulation are altered, which may increase
the risk of vascularcomplications and infectious episodes.
• Neutrophil adherence, chemotaxis and phagocytosis are also
impaired thus inhibiting bacteria killing.

27. Infection is a possible consequence of
wounds that remain open for an
extended period to time. Another
complication of poorly controlled
diabetes is a decreased immune
response. So diabetes makes
infections both more likely to occur and
harder for the body to fight off.
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28. DELAYED HEALING OF WOUNDS
• Microangiopathy and utilization
of protein for energy may retardthe repair of tissues.
• There is altered cellular activities and failure of
PMNs to migrate toward the area ofwound
healing.
• Collagen synthesis isdecreased. Decreased
crosslinking and glycosylation of collagenrenders
collagen produced inDM more soluble and
possiblywith a decrease remodelingtime.
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29. Burning mouth syndrome
in uncontrolled or marginally controlled diabetes,
these etiologic factors can include salivary
dysfunction, candidiasis and neurological
abnormalities such as depression. Neuropathy
may lead to oral symptoms of paresthesias and
tingling, numbness, burning or pain caused by
pathological changes involving the nerves in the
oral region.
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