Diabetes mellitus.diet, insulin therapy

2. HISTORY:-
 THOMAS GULLUS(1675) was found
some patient come with complain of
Repeated urination in, Greek ward it is called
“Diabetes”. sweetness in the urine & in Latin
ward sweetness of urine called “Mellitus”
 So he name the disease Diabetes Mellitus.
So it is a disorder of carbohydrate
metabolism.
In DM blood sugar level increase.

3. ANATOMY :-
Pancreas has 2 part
1. EXOCRINE PART which release enzyme
2. ENDOCRINE PART:- which release
hormones.
Islets of langerhans is the endocrine part of
the pancreas
It secrets alpha, beta, delta & pancreatic
polypeptides
Alpha cell secrete glucagon
Beta cells secrete insulin
Delta cell secrete somatostatin.

5. TYPES:-
1. Cause related to pancreas(primary)95%
2. Cause related not to pancreas (secondary
DM 5%)

6. 1. CAUSE RELATED TO
PANCREAS(PRIMARY)95%:-
a. According to Beta cell
damage there is decrease
of insulin secretion, patient
need insulin injection. So it
is insulin dependent type 1
(10% people affected)
b. Due to decrease number of
insulin receptors:- It is
called NIDDM also type II .
90% people affected. Occur
mainly among obese &
more then 40 years.

7. 2. Cause related not to pancreas
(secondary DM 5%):- it is secondary DM,
5% people get this
Occur due to GCAT(Glycine C-
acetyltransferase ) hormone increase

8. THE ROLE OF GLUCOSE
Glucose — a sugar — is a source of energy for
the cells that make up muscles and other tissues.
Glucose comes from two major sources: food
and from liver.
Sugar is absorbed into the bloodstream, where
it enters cells with the help of insulin.
Liver stores and makes glucose.
When glucose levels are low, such as when you
haven't eaten in a while, the liver breaks down
stored glycogen into glucose to keep glucose
level within a normal range.

9. HOW INSULIN WORKS
Insulin is a hormone that comes from a
pancreas.
The pancreas secretes insulin into the
bloodstream.
The insulin circulates, enabling sugar to enter
cells.
Insulin lowers the amount of sugar in
bloodstream.

11. CAUSES OF TYPE 1 DIABETES
The exact cause of type 1 diabetes is unknown.
It may due to immune system — which normally fights
harmful bacteria or viruses — attacks and destroys insulin-
producing cells in the pancreas.
This leads to little or
no insulin in body .
Instead of being
transported into
cells, sugar builds up in bloodstream.
Type 1 diabetes can affect children or adults, but was
traditionally
termed "juvenile diabetes" because a majority of these
diabetes cases were in children

12. CAUSES OF TYPE 2 DIABETES
cells become resistant to the action of insulin,
and pancreas is unable to make enough insulin
to overcome this resistance.
Instead of moving into cells where it's needed
for energy, sugar builds up in bloodstream.
it's believed that genetic and environmental
factors play a role in the development of type 2
diabetes too.
Being overweight is strongly linked to the
development of type 2 diabetes,
but not everyone with type 2 is overweight.

13. CAUSES OF GESTATIONAL DIABETES
During pregnancy, the placenta
produces hormones to sustain
pregnancy.
These hormones make cells more
resistant to insulin.
Normally pancreas responds by
producing enough extra insulin to
overcome this resistance.
But sometimes pancreas can't keep
up. When this happens, too little
glucose gets into cells and too much
stays in blood, resulting in gestational
diabetes.

15. PATHOPHYSIOLOGY
• Insulin is released into the
blood by beta cells (β-cells),
found in the islets of
Langerhans in the pancreas, in
response to rising levels of
blood glucose, typically after
eating.
• Lower glucose levels result in
decreased insulin release
from the beta cells and results in the breakdown of
glycogen to glucose.
•This process is mainly controlled by the hormone
glucagon, which acts in the opposite manner to
insulin.

16. PATHOPHYSIOLOGY
•If the amount of insulin available is insufficient
•If cells respond poorly to the effects of insulin
•If the insulin itself is defective
•Then glucose will not be absorbed properly by the
body Cells
•The net effect is persistently high levels of blood
glucose, poor protein synthesis, and break down of
fat storage
•Acidosis.

17. PATHOPHYSIOLOGY
When the glucose concentration in the blood
remains high over time, the kidneys will reach a
threshold of reabsorption Glycosuria.
This increases the osmotic pressure of the urine
Polyuria increased fluid loss
Lost blood volume will be replaced osmotically
from water held in body cells and other body
compartments dehydration
polydipsia

18. CLINICAL MANIFESTATION:-
Increased thirst
Frequent urination
Extreme hunger
Unexplained weight loss
Presence of ketones in the urine
Fatigue
Irritability
Blurred vision
Slow-healing sores
Frequent infections, such as gums or skin
infections and vaginal infections

19. DIAGNOSIS
1. Glycated hemoglobin (A1C) test:-
 This blood test, which doesn't require fasting,
indicates average blood sugar level for the past two to
three months.
 It measures the percentage of blood sugar attached to
hemoglobin, the oxygen-carrying protein in red blood
cells.
The higher blood sugar levels, the more haemoglobin
with sugar attached.
An A1C level of 6.5 percent or higher on two separate
tests indicates diabetes.
An A1C between 5.7 and 6.4 percent indicates
prediabetes.
Below 5.7 is considered normal.

20. 2. Random blood sugar test:-
 A blood sample will be
taken at a random time.
Regardless of when pt last ate, a
random blood sugar level of 200
milligrams per deciliter (mg/dL)
 or 11.1 millimoles per liter
(mmol/L) — or higher suggests
diabetes

21. 3. Fasting blood sugar test.
A blood sample will be taken after an
overnight fast.
A fasting blood sugar level less than 100 mg/dL
(5.6 mmol/L) is normal.
A fasting blood sugar level from 100 to 125
mg/dL (5.6 to 6.9 mmol/L) is considered
prediabetes.
 If it's 126 mg/dL (7 mmol/L) or higher on two
separate tests indicate diabetes.

22. .
4. Oral glucose tolerance test. :-
For this test, pt fast overnight, and the fasting
blood sugar level is measured.
Then pt drink a sugary liquid, and blood sugar
levels are tested periodically for the next two
hours.
A blood sugar level less than 140 mg/dL (7.8
mmol/L) is normal.
A reading of more than 200 mg/dL (11.1
mmol/L) after two hours indicates diabetes.
A reading between 140 and 199 mg/dL (7.8
mmol/L and 11.0 mmol/L) indicates prediabetes.

23. COMPLICATION-
The primary complications of diabetes due to
damage in small blood vessels include damage
to the eyes, kidneys, and nerves
Damage to the eyes, known as diabetic
retinopathy, is caused by damage to the blood
vessels in the retina of the eye, and can result in
gradual vision loss and blindness.
Damage to the kidneys, known as diabetic
nephropathy, can lead to tissue scarring, urine
protein loss, and eventually chronic kidney
disease, sometimes requiring dialysis or kidney
transplant.

24. CONT....
Diabetes-related foot problems (such as
diabetic foot ulcers) may occur, and can be
difficult to treat, occasionally requiring
amputation.
Additionally, proximal diabetic neuropathy
causes painful muscle
wasting and weakness – Diabetic Amyotrophy.

25. AMYOTROPHY

27. EMERGENCY MANAGEMENT:-
Hypoglycemia:-
Initial signs : mood changes,
decreased spontaneity, hunger and
weakness.
Followed by sweating, tachycardia it
Results in unconsciousness,
hypotension, hypothermia, seizures,
coma, even death
15 grams of fast-acting oral
carbohydrate.
Measured blood sugar.
Loss of consciousness: 25-30ml 50%
dextrose solution iv. over 3 min
period.
Glucagon 1mg

28. Severe hyperglycemia:-
Ketoacidosis may develop with nausea, vomiting,
abdominal pain and acetone odor
EMERGENCY MANAGEMENT:-
Hyperglycemia needs medical intervention and
insulin administration.
While emergency, give glucose first Small amount
is unlikely to cause significant harm

30. DIAGNOSIS:-
Can be diagnosed by demonstrating any one of the
following:
Fasting plasma glucose level ≥ 7.0 mmol/l (126 mg/dl)
Symptoms of high blood sugar and casual plasma
glucose ≥ 11.1 mmol/l (200 mg/dl)
Glycated hemoglobin (HbA1C) ≥ 48 mmol/mol (≥ 6.5
DCCT %)

31. MANAGEMENT
Lifestyle:-
Good nutrition
Regular exercise
Diet control to maintain blood pressure
Medications:-
Surgery
1. Pancreas transplant
2. kidney transplantation
3. Weight loss surgery

32. g
INSULIN AND ITS TYPE
1. Rapid acting insulin:-
 Example:- lispro, aspart,
novalog, humalog
Duration of action :- 3 -5 hour
Onset of action :- 15 -30 min
Pick action ( severe
hypoglycemia) :- 1-5 hour
2. Short acting or regular insulin
Example :- novalin –R
Duration of action :- 5 – 8 hour
Onset of action:- 30 -60 min
Peak action:- 1-5 hour

33. 3. Intermediate acting :-
Example :- NPH,lente (novalin –
N)
duration of action :-24 hour
Onset of action:- 1-4 hour.
Peak action:- 6-14 hour
4. Long acting:-
Example:- ultra lente,
protamine, zinc, Glargine,
detemine.
Duration of action:- 36 hour
Onset of action:- 4-8 hour
Peak action:- 12-24 hour

34. COMPLICATION OF INSULIN:-
1.DOWN PHENOMENON:-
Also known as pre-breakfast hyperglycaemia
It occur due to cell less work in rest specially in
night so decrease cell sensitivity.
In rest or night insulin cannot go in to the cell
& glucose metabolism decrease & increase
blood glucose level. (treatment:- increase
evening dose of insulin)

35. 2. Rebound hyperglycaemia:-
It is also known as Smoggy effect
Due to night dose of insulin there is decrease
glucose level at 1-2am.
So pituitary gland identify glucose level &
increase production of glucagon & cortisol
which increase glucose level in morning
( treatment:- provide complex carbohydrate
snacks at night)

36. FOOD AVOIDED :-
SWEET
SUGAR. HONEY
JAM & JELIES
CACKS,
PASTRIES
SOFT DRINK
FRIED FOOD
MANGO, BANANA, GRAPES

37. ESPECIALLY BENIFICIAL FOOD FOR
DIABETES:-
BITTER GUARD
FENUGREEK SEEDS
AMLA
JAMUN
RAGI
DIABETIC ATTA