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Dow University of Health Sciences

Institute of Nursing
Diabetic Mellitus
(IDDM)

Badil Dass
Lecturer
1st April, 2013

Objectives:
By the end of this lecture, the students will
be
able to:
Define Diabetes Mellitus.
List the types of Diabetes Mellitus
Understand the pathophysiology of Type1 Diabetes Mellitus
Identify the clinical features of Type-1
Diabetes Mellitus
Describe the insulin interim of
Types, dose, peak hours and duration

Diabetes Mellitus
Diabetes mellitus is metabolic disorder of
carbohydrate, protein, and fat characterized
by elevated levels of glucose in the blood
(hyperglycemia) resulting from defects in insulin
secretion, insulin action, or both

Classification of Diabetes mellitus


Type

-1 Diabetes (IDDM)
Type -2 Diabetes (NIDDM)
Gestational diabetes mellitus
Diabetes mellitus associated with other
conditions or syndromes/ secondary diabetes
mellitus

Type -1 Diabetes (IDDM)


Type

-1 (5%10% of all diabetes)


Type-1 Diabetes Mellitus is cased by destruction
of beta cells by autoimmune process.
It is thought that combined genetic,
immunologic, and possibly environmental (e.g.,
viral) factors contribute to beta cell destruction.
Virus are rubella, mumps, Coxsackievirus
etc..
DR3 and DR4 deficiency

Conti:

If

the concentration of glucose in the blood


exceeds the renal threshold for glucose, usually
180 to 200 mg/dL (9.9 to 11.1 mmol/L).
The kidneys may not reabsorb all of the filtered
glucose; the glucose then appears in the urine
(glucosuria).
When excess glucose is excreted in the urine, it
is accompanied by excessive loss of fluids and
electrolytes. This is called osmotic diuresis.

Conti
Insulin normally inhibits glycogenolysis
(breakdown of stored glucose) and
gluconeogenesis.
Due to insulin deficiency the gluconeogenesis
process occurs that cause the fat breakdown.
The end product of fat breakdown is ketone.
Excessive ketones cause the DKA

( Diabetes Ketoacidosis)

Ketone
Ketone

bodies are acids that disturb the acid


base balance of the body when they accumulate
in excessive
amounts.
The resulting DKA may cause signs and
symptoms such
as abdominal pain, nausea, vomiting,
hyperventilation, a fruity breath odor, and, if left
untreated, altered level of consciousness, coma,
and death.

Conti

Initiation

of insulin treatment, along with fluid


and electrolytes needed, is essential to treat
hyperglycemia and DKA and rapidly improves
the metabolic abnormalities.

Clinical characteristics and implications


Onset any age, but usually young (<20 yrs)
Usually thin at diagnosis
Recent weight loss
Etiology includes genetic, immunologic, or

environmental factors (e.g., virus).


Often have islet cell antibodies
Little or no endogenous insulin
Need insulin to preserve life
Ketosis-prone when insulin absent
Acute complication of hyperglycemia: diabetic
ketoacidosis

The Discovery of Insulin


1869,

a German medical student, Paul


Langerhans, found pancreatic cells named
the islets of Langerhans
Beta cells produce insulin
Functions was unknown

Conti.
In

1889 in Germany, physiologist Oskar Minkowski


and physician Joseph von Mering, showed that if the
pancreas was removed from a dog, the animal got
diabetes.
But if the duct through which the pancreatic juices
flow to the intestine was ligated - surgically tied off so
the juices couldn't reach the intestine - the dog
developed minor digestive problems but no diabetes.
So it seemed that the pancreas must have at least two
functions:
To produce digestive juices
To produce a substance that regulates the sugar glucose

Banting's Idea
In

October 1920 in Toronto, Canada, Dr.


Frederick Banting, surgeon with a bachelor's
degree in medicine, had the idea that the
pancreatic digestive juices could be harmful to
the secretion of the pancreas produced by the
islets of Langerhans.
ligate the pancreatic ducts in order to stop the
flow of nourishment to the pancreas.
This would cause the pancreas to degenerate,
making it shrink and lose its ability to secrete
the digestive juices.

Conti..
Early

in 1921, Banting took his idea to


Professor John Macleod at the University
of Toronto, who was a leading figure in
the study of diabetes in Canada

Conti.
The Experiment Begins
Banting and Best began their experiments
by removing the pancreas from a dog.
This resulted in the following:
It's blood sugar rose.
It became thirsty, drank lots of water, and
urinated more often.
It became weaker and weaker.
The dog had developed diabetes

Conti.
Experimenting on another dog
Banting and Best surgically ligated the pancreas,
stopping the flow of nourishment, so that the
pancreas degenerated.
sliced it up, and froze the pieces in a mixture of
water and salts. When the pieces were half frozen,
they were ground up and filtered. The isolated
substance was named "isletin."
The extract was injected into the diabetic dog. Its
blood glucose level dropped, and it seemed
healthier and stronger. By giving the diabetic dog a
few injections a day, Banting and Best could keep it
healthy and free of symptoms.

Conti.
January

1922 in Toronto, Canada, a 14-yearold boy, Leonard Thompson, was chosen as


the first person with diabetes to receive
insulin.
The test was a success.
The Nobel Prize
The news of the successful treatment of
diabetes with insulin rapidly spread outside
of Toronto, and in 1923 the Nobel Committee
decided to award Banting and Macleod the
Nobel Prize in Physiology or Medicine.