SEMINAR ON :

INTRODUCTION
• DEFINITION
• CLASSIFICATION
• ETIOLOGY
• RISK FACTORS

PRESENTED BY-
 INTRODUCTION
Chronic disease of carbohydrate
metabolism
Chronic systemic disease
characterized by either a deficiency
of insulin or decrease in ability of
body to use insulin.
Commonly called high sugar by
both client and health care
provider.
 DEFINITION
Chronic systemic disease
characterized by either a
deficiency of insulin or decrease
in ability of body to use insulin.
 DEFINITION
• Diabetes mellitus is a chronic systemic
disease characterized by either deficiency
of insulin or a decreased ability of the body
to use insulin resulting in elevated levels of
glucose in blood
 DEFINITION
DM is a chronic metabolic
systemic disease characterized by
either a deficiency of insulin or a
decreased ability of body to use
insulin .
OR
It is a syndrome complex cause
due to a absolute or relative
deficiency of insulin leading to
 STATISTICS
• In 2003- 189 million
• It is double in period 2000-2005 & may
reach a level of almost 324 million people
• Top ten countries with DM:India,China,
Russia, Brazil, Indonesia, Pakistan,
Mexico,Ukraine ,Egypt & Japan
• In India in1997-14.7%,2005-17.4%
 CLASSIFICATION
TYPE I DIABETES MELLITUS

TYPE II DIABETES MELLITUS

GESTATIONAL DIABETES

SECONDRY DIABETES
 TYPE I DM
Autoimmune disorder
Beta cell destruction
Occurs in genetically susceptible
individuals.
Prone to develop ketoacidosis
 TYPE II DM
Also called NIDDM or adult onset
DM
Etiology remain unclear
It is not a single disease but
result from many conditions that
produce hyperglycemia
 Contd…
Contribute to hyperglycemia due to
• Excessive glucose production by liver
• Impaired insulin secretion
• Peripheral insulin resistance primarily
occurs in liver,muscle & adipose tissue.
 CHARACTERISTICS OF
TYPE I&II DM
FACTOR TYPE-I TYPE-II
Age of onset Common in young but can >35yr.
occur at any age

Type of onset s/s abrupt, but disease Slow

process may appear at any
age
Prevalence Accounts 5-10% of all DM 90% of DM

Environmental Virus, toxins Obesity, lack of

factors exercise.
Islet cell Often present at onset Absent
antibodies
Nutritional Thin, catabolic state Obese or normal
status
 CHARACTERISTICS OF
TYPE I&II DM
FACTOR TYPE-1 TYPE-2
Endogenous Minimal/absent Excessive, delayed
insulin secretion or decrease
utilization
Symptoms Thirst,polyuria, None /mild
polyphagia,fatigue

Ketosis Prone at onset/during Resistant except during

insulin deficiency infection or stress

Nutritional essential essential

therapy
OHA Not beneficial Usually beneficial

Vascular/ frequent frequent

neurological
complication
GESTATIONAL DIABETES

Gestational diabetes
generally develops in
pregnancy & resolves
itself.
 GESTATIONAL
DIABETES
GDM is defined as carbohydrate
intolerance occurring during pregency
Occurs in approx. 4% of pregnancies
&usually disappear after delivery.
Women with GDM are at higher risk of
diabetes at later stage
Associated with increase risk of fetal
morbidity.
 SECONDARY
DIABETES
Not true Diabetes Mellitus .
CAUSES
• another chronic illness such as
pancreastitis or cystic fibrosis
•Genetic defects
•Endocrinopathy
•Drug or chemical -induced
 Contd…..
• Infection
• Genetic syndrome associated
with diabetes

Usually resolve when underlying

cause is treated.
• SIGN AND SYMPTOMS
• PATHOPHYSIOLOGY
• DIAGNOSTIC TESTS

PRESENTED BY-
 RISK FACTORS
DIABETES MELLITUS I

Hypertension

Genetically recessive HLA gene

Ist degree relatives(1in 20)

 RISK FACTORS
DM II
Family h/o diabetes
Obesity
Origin
Age-45+
Previously identified impaired
glucose tolerance
 Contd…
HDL<35mg/dl

triglycerides<250mg/dl

H/o gestational mellitus

Insulin promotes glucose transport from the blood
stream across cell membrane to cytoplasm of cell.

During meal, plasma insulin increases.

• Stimulate storage of glucose as glycogen in

liver and muscles.
• Inhibits gluconeogenesis.
• Inhibits fat depletion in adipose tissue.
• Increases protein synthesis.
ON FASTING
Insulin level falls

Facilitates the release of store glucose,

proteins & fats
 RISKY OR TARGET
GROUP
• Family history
• Old age
• Sedentary life style
• Obesity
• Having high saturated fat
• Stressed
• Alcoholic
• Previously identified IFG or IGT
• Polycystic ovary syndrome
 CAUSES(DM TYPE I)
• GENETIC –
Certain HLA antigens
located on chromosome no.6
predispose the client to IDDM.

• IMMUNOLOGIC FACTOR-
Certain islet cells
antibodies & anti insulin
antibodies are responsible.
 CAUSES(DM TYPE I)
• ENVIRONMENTAL FACTORS:
- Certain viruses as coxacie cause DM

- BOVINE SERUM ALBUMIN, a major constituent

of cow’ milk triggers DM-1.

- Various nitrosamines found in smoked & cured

meats are diabetogenic toxins.
 CAUSES(DM TYPE II)
• GENETIC-

- Identical twins have 70-90%

risk of developing DM-2.

- TRANSCRIPTION FACTOR . 7
has been associated with DM-2

• ENVIRONMENTAL FACTORS-

- obesity & under activity.

- over eating
 NORMAL INSULIN
METABOLISM
Insulin is a hormone that is produced by B-
cells in islet of langerhans of pancreas as its
precursor PROINSULIN

Send to liver and forms insulin .

Normal insulin is continuously released into the

blood stream and maintains the blood glucose
level.
 NORMAL PHYSIOLOGY
CHO eaten
break &form glucose
absorbed into blood stream with the help
of insulin
insulin comes in connect with cell
membrane
it combine with receptor that allow
activation of special glucose transmitter
in memb.
help glucose to enter into cell
low blood glucose level
Insulin also help the body to store
glucose
HOMEOSTATIS
 DIABETES MELLITUS I
Genetic predisposition(have gene markers
DR3&DR4 HLA)
Env. Trigger with viral diseases

Active autoimmunity against beta-cells & their

products

ICAs &insulin antibodies progressively decrease

circulating insulin level

Can result in abrupt onset of diabetes

PATHOPHYSIOLOGY DMII
PATHOPHYSIOLOGY OF
IDDM
Environmental trigger (viral inf.)
↓
Autoimmunity
↓
Progressive beta cell destruction.
↓
Decreased circulatory insulin level
↓
IDDM
• Destruction of beta cells results in fasting hyperglycemia.

• Glucose cannot be stored in the liver & contributes to

postparandial hyperglycemia.

• Concentration of glucose in the blood exceeds the renal

threshold for glucose (180-200 mg/dl),results in glucosuria.

• Excess glucose excreted in urine leads to osmotic diuresis.

• Formation of ketone bodies due to fat breakdown.

PATHOPHYSIOLOGY OF NIDDM
Insulin resistant factor

Insulin secreted normally by pancreas

Body tissues do not respond to action of insulin

Entry of insulin impeded into cell

 …contd

hyperglycemia

Initially pancreas compensates

Hyperinsulinemia with hyperglycemia

Insulin resistance syndrome(Syndrome X)

INTRACELLULAR EXTRACELLULAR

HYPOGLYCEMIA HYPERGLYCEMIA
 INTRACELLULAR HYPOGLYCEMIA

Breakdown of fats Dec.protein synthesis

Inc. levels of ketones Wasting of muscles

•Diabetic ketoacidosis Inc.N2 & K levels in

blood

Release of K & BUN in

 EXTRACELLULAR HYPERGLYCEMIA

Blood glucose > renal Chronic elevation in blood glucose

Threshold
• Neuropathy

Glucosuria • Nephropathy

• Retinopathy
Osmotic diuresis

Polyuria • Impaired immune function

•
• Polydipsia
• Hypokalemia • Accelerated atherosclerosis
• Hyponatremia
 CLINICAL MANIFESTATIONS
• POLYURIA
• POLYDIPSIA
• POLYPHAGIA
• BLURRED VISION
• DELAYED WOUND HEALING
• WEAKNESS
• FATIGUE
• CONSTIPATION
• RECURRENT ULCERTATION
• WEIGHTLOSS
 CLINICAL
MANIFESTATIONS
POLYDIPSIA

POLYURIA
UNHEALING WOUND

WEIGHT LOSS
BLURRED VISION
 CLINICAL
MANIFESTATIONS
DM TYPE 1-
• Polyuria
• Polydypsia 3 P’s
• Polyphagia
• Weakness
• Diabetic ketoacidosis
• Dehydration
• Postural hypotension
 POLYDIPSIA
(Excessive thirst )
Increased blood glucose level

Water is osmotically attracted from body cells

Intracellular dehydration

Stimulation of thirst in hypothalamus

 POLYPHAGIA
(Excessive hunger )
Depletion of cellular stores of CHO,
fats and proteins

Cellular starvation

Increased hunger
 POLYURIA
(FREQUENT URINATION )
HYPERGLYCEMIA
(acts as osmotic diuretic)

Glycosuria

Water not reabsorbed from renal tubules

Polyuria
 WEIGHT LOSS
• Fluid loss in osmotic diuresis

Loss of body tissues as fat and protein

 Fatigue
• Metabolic changes

• Poor use of food products

• Lethargic and fatigue

 CLINICAL
MANIFESTATIONS

DM TYPE II

• Recurrent infections
• Prolonged wound healing
• Pruritis
• super infections
• Ketone urea
• Postural hypotension
 Gestational Diabetes Symptoms

Symptoms
• Increased thirst
• Increased urination
• Weight loss in spite of increased appetite
• Fatigue
• Nausea and vomiting
• Frequent infections including those of the bladder, vagina, and
skin
• Blurred vision
• Note: Usually there are no symptoms.
Signs and tests
• An oral glucose tolerance test between the 24th and 28th
weeks of pregnancy is the main test for gestational diabetes.
• (From National Institute of Health)
 DIAGNOSTIC TESTS
FASTING BLOOD GLUCOSE-
FBS> 126 mg/dl→ diabetes

CASUAL BLOOD GLUCOSE-

RBS>200 mg/dl→ diabetes
 DIAGNOSTIC TESTS….
ORAL GLUCOSE TOLERANCE TEST-
Done if FBG < 140 mg/dl.

• <140mg/dl - normal

• 140-200mg/dl - impaired
•

• >200mg/dl – diabetes

POSTLOAD BLOOD GLUCOSE-

• samples are drawn 2 hours after a
standard meal.

• Reflects the efficiency of insulin

mediated glucose uptake.

• PBG> 200 mg / dl - diabetes

 Preparation
• The patient is instructed not to restrict carbohydrate intake in
the days or weeks before the test.

• The test should not be done during an illness, as results may

not reflect the patient's glucose metabolism when healthy.

• A full adult dose should not be given to a person weighing less

than 43 kg (94 lb), or exaggerated glucoses may produce a
false positive result.

• Usually the OGTT is performed in the morning as glucose

tolerance can exhibit a diurnal rhythm with a significant
decrease in the afternoon.

• The patient is instructed to fast (water is allowed) for 8–12

hours prior to the tests.
 Dose of glucose

• The WHO recommendation is for a

75g oral dose in all adults: the dose
is adjusted for weight only in
children. The dose should be drunk
within 5 minutes.
 Procedure
• A zero time (baseline) blood sample is drawn.
• The patient is then given a measured dose (below) of
glucose solution to drink within a 5 minute time frame.
• Blood is drawn at intervals for measurement of glucose
(blood sugar), and sometimes insulin levels.
• The intervals and number of samples vary according to the
purpose of the test.
• For simple diabetes screening, the most important sample is
the 2 hour sample and the 0 and 2 hour samples may be the
only ones collected.
• Sometimes other laboratory continuous to collect blood up
to 3 hours depending on the requesting physician
 1999 WHO Diabetes criteria - Interpretation
of Oral Glucose Tolerance Test
Glucose NORMAL
levels
Diabetes mellitus (DM)

Venous Fasting 2hrs Fasting 2hrs

Plasma

(mmol/l) <6.1 <7.8 >7.0 >11.1

(mg/dl) <110 <140 >126 >200

 DIAGNOSTIC TESTS….
• GLYCOSYLATED HEMOGLOBIN-
• The A1C is an average blood glucose level.
• Measured over the previous 3 months.
• For evaluating long term hyperglycemic
control.

• GLYCOSYLATED ALBUMIN-
Represents the average blood glucose level
over the previous 7-10 days.

• CONNECTING PEPTIDE-
C peptide and insulin are formed in the equal
amounts, test indicates the amount of
endogenous insulin production.
 DIAGNOSTIC TETS....
KETONE UREA-
Urine levels of
ketone can be tested
by clients by use of
dip strips or tablets.
The presence of
ketones indicates
that body is using fat
as a major source of
energy.
 DIAGNOSTIC TESTS.....
• PROTEINURIA-
The presence of protein
(microalbuminuria) in the
urine is an early
manifestation of kidney
disease.

• SELF MONITORING BLOOD

GLUCOSE
 MEDICAL
MANAGEMENT
PRESENTED BY-
 EXERCISE

MEDICAL
MANAGEMENT DIET
OHA

INSULIN THERAPY
 WEIGHT MAINTAINANCE DIET

INSULIN REGIMENS
• multiple injections
NON once or twice a day.
OBESE
TYPE 1 •Insulin in combination
INSULIN
•Continuous
DIABETES subcutaneous insulin
OBESE infusions.

LOW ENERGY DIET

INSULIN + DIET
 DIET MONOTHERAPY COMBINED
THERAPY

Weight
management diet
I
SULFONYL N
NON SULFONYL UREA
OBESE UREA S
TYPE 2 +
U
DIABETES METFORMIN
OBESE METFORMIN L
+
I
Thiazolidinedione
Low energy diet N
•α-glucosidase
inhibitor
DIET
 DIET
Diabetic diet depend on
the client’s sex, weight,
height and age.

AIM of diabetic diet

1. To abolish symptoms of
hyperglycemia
2. To reduce blood glucose
and avoid fluctuations in
blood glucose levels
3. To reduce insulin
resistance by reducing
weight
4. To avoid weight gain.
 DIABETIC DIET DEPENDS
ON?
• BMI
• Cultural
background
• Activity
• Age & sex
• Stage of diabetes
IDDM (Insulin dependent, exogenous
insulin is required for survival)

• For Children, underweight individuals and pregnancy, sufficient

calories are required for growth/weight gain, or fetal growth, so added
calories to basal meals are to be planned.

• Caloric break up in divided meals is organised to cover insulin

injection, so timing of meals is important.

• Consistency of eating pattern and meal composition is very

important.
•Greater consideration is to be given to carbohydrates content
of diet.
 NIDDM
• Usually obese, so reduction in excess of energy intake or low

calorie diet is to be followed

• The absorption of nutrients may be slowed with fibre or bitter. This

provides uniform blood glucose pattern through out the day.

• Fasting or exercise is beneficial, timing is not so crucial.

• Diet should be lower in fat and cholesterol content so as to obviate

the risk of atherosclerotic disease.

 Present Recommendations of diet
constituents
• Diabetics are permitted carbohydrates upto 65-75% of
total calories. Higher amounts carbohydrates in daily
diet increase insulin sensivity and as well lower blood
lipids.

• Simple carbohydrates (glucose, sucrose containing)

rapidly elevate blood glucose and so are not
recommended.

• Complex carbohydrates such as from coarse cereals,

grain starches, dextrins, and legumes in equal amounts
do not induce abrupt rise of blood glucose and should
form the bulk source.
 Fibre content
• Fibre content modifies glucose tolerance,
fibre enriched meals decrease glycaemia,
effect the transit time and tend to gel
formation that sequester glucose and
insulate carbohydrates from digestive
enzymes.

• The content of fibre recommended is

approximately 30 g/day.
 Fats
• Ratio of saturated fats as from animal fats, hydrogenated fat,
e.g. meat, ghee : polyunsaturated fats e.g. vegetable oils,
sunflower, gingely, maize or til oil and monosaturated fats as olive
oil, poultry and certain fat oils should be in order of-1 : 1 : 1.
Saturated fats are atherogenic and epidemiologically diets with
high proportion of fats and relatively low proportion of
carbohydrates can be related to cardiovascular mortality.

• Total calories from fat sources should not exceed 30% of calories.

• Cholesterol intake should be reduced to 300 mg day (HDLC

should be elevated, low value having a direct relationship to CAD).
 Proteins
• Proteins are good stabilizers, daily requirement is 0.9
g/kg b.w. and should form 15- 20% of total calories

• Proteins affect gut hormones and insulin secretion and

in this manner glucose tolerance. At level of central
nervous system, protein diet lower serotinin level, that
modulates chemical signals for satiety.

• Children/pregnant diabetics require more proteins

than proportion recommended for adult/Kg.

• Formulation proteins are not recommended, they have

lower biological value and certain side effects.
 The common denominators of food groups
are as follows :

• 1. Cereals and cereal products.

• 2. Milk and milk products.
• 3. Meat and meat products.
• 4. Legumes and grams
• 5. Oils and fats.
• 6. Leafy and other vegetables
• 7. Fruits
•Cereal and cereal products contain mainly carbohydrates
and starches and therefore can be taken in
supplementation with pulses and grams to improve the
nutritive value in terms of proteins and fibre.
•Soya bean is a good example.
•Milk and milk products have a good quality protein and
use of low fat milk is recommended for diabetics to bring
down the fat and caloric content.
• Meat and its products are a rich source of
proteins and should be taken in the grilled or
tandori form to avoid the extra cooking fat
commonly used in their preparation in the
Indian manner.
• Green and leafy vegetables are rich source of
vitamins and minerals.
• In fats and oils, vegetable oils like safola, corn
til, or gingely are recommended, these being
the unsaturated fats. Oils, like coconut, palm,
deshi ghee or vanaspati are rich in saturated
fats.
Supplement foods recommended consists of
micronutrients, as :-
vitamins and minerals
Vit. B complex :
IDDM patients with uncontrolled
diabetes loose water soluble vitamins, need
replenishment. Obese diabetics on weight
reducing diet also benefit from vitamin
supplement.

Iron : Pregnant diabetics need additional iron

as others.

Zinc : Zinc is of no value, and its intake

does not modify glucose metabolism.
.
Few comments are included on other dietary items :-

• Sweeteners : Non-nutritive sweeteners include saccharin and cylamates.

These are banned in some countries though in the amount consumed seem
safe. Nutritive sweetners consist of sorbital, xylitol, aspartame, i.e. yields 4
calories and these items are expensive.

• Alcohol : This is best avoided. However 35 ml/day can be allowed with- out
upset of glycaemic control. Caloric content of alcohol is 7 K cal/g and so one
helping will be 135 C and this should be borne in calculation of total calorie
intake
. Alcohol has antabuse like effect with sulphonylureas. In an alcoholic, coma
can be mistaken and diagnosis of hypoglycaemia missed completely

Use of alcohol may as well provoke hypertriglyceridaemica

 Diet Counselling
(a) Practice of Art
(b) Behaviour modification
(c) Preparedness for situations wherein
routine meal is not practical.
(d) Causes of failure of diet therapy
I. Communication Gap
II. Lack of individual approach
III. Rigidity of meal pattern
IV. Cheating with treatment
 Exercise helps
control type 2 diabetes by:

• Improving your body's use of insulin.

• Burning excess body fat, helping to decrease
and control weight .
• decreased body fat results in improved
insulin sensitivity.
• Improving muscle strength.
• Increasing bone density and strength.
• Lowering blood pressure.
• Helping to protect against heart and blood vessel
disease by lowering 'bad' LDL cholesterol and
increasing 'good' HDL cholesterol.
• Improving blood circulation and reducing your risk
of heart disease.
• Increasing energy level and enhancing work
capacity.
• Reducing stress, promoting relaxation, and
releasing tension and anxiety.
 WHY EXERCISE IN
DIABETES ?
• Increases carbohydrate metabolism.
• Lowers the blood glucose levels b’coz:
glucose transporting receptors allow the skeletal
muscles to take glucose from blood independent of
insulin and provides energy during exercise and
lowers the blood sugar.
• Increases insulin sensitivity.
• Improves circulation of blood deficient in diabetic
clients.
• Lowers cholesterol and triglyceride level.
 DIABETES ! A FEW ALERTS!!
Do Not Exercise
• In full or empty stomach
• When insulin action is at
peak
• Under extremes of
temperature
• During other illnesses
• If blood sugar is over 250
and ketones present
• Is chest pain occurs during
exercise
TYPES OF EXERCISES
 Effect of exercise
• After 5 min -
blood glucose & Muscle
glycogen is used
• After 15 min -
Liver Glycogen is used.

• After 30 min -
Fatty Acids are used

• After exercise-
insulin rebuilds in 4-6 hrs
extremes in 12-24 hrs
 OHAs
Used when the client is not responding to the
diet and exercise modifications.
INDICATIONS:
1. FBS <200 mg/dl
2. Insulin requirement < 40 U/day
CONTRAINDICATIONS:
1. No ketoacidosis
2. No renal/hepatic disease
 CLASSIFICATION

INSULIN AUGMENTORS
•SULFONYLUREAS
•MEGLITINIDES

OHA
ALFA GLUCOSIDASE
INSULIN ASSISTING
AGENTS INHIBITORS
•BIGUANIDES •ACRABOSE
THIAZOLIDINEDIONE
• MIGLITOL
 INSULIN AUGMENTING AGENTS
• Increase the secretion of endogenous insulin, as
long as pancreatic Beta cell function remains

• Poorly effective in adults who are Type 1 DM

TYPES:
• Sulfonylureas
– Glipizide
– Glyburide
– glimepiride
• Meglitinides
– Repaglinide
– Nateglinide
– mitiglinide
 INSULIN -ASSISTING
AGENTS
• Also called Insulin sensitizers
• Enhance the effectiveness of insulin

Insulin – Assisting Agents are:

• Bigunides
– Metformin
• Thiazolidinedione
– Pioglitazone
– troglitazone
 ALPHA GLUCOSIDASE
INHIBITORS
• Acrabose
• Miglitol

Mode of action
• Delay CHO Absorption
• Reduces PP Hyperglycemia without
increasing insulin level
 SULPHONYLUREAS
• Sulphonylureas were the First OHA .
• They work by PROMOTING INSULIN
RELEASE.
• Sulphonylureas are derivatives of the
SULFONAMIDE antibotics , but lack
antimicrobial activity .
• Sulphonylureas cause increased secretion
of insulin from beta cells.
 Contd……..
• Sulphonylureas fall into 2 Groups
First generation agents
eg.Talbutamide ( orinase )
Second generation agents
Both generations reduce
GLUCOSE levels to the same
extent. But second generation
agents produce its effect at
much lower dose.
 First generation……..
Drug Duration Dose Special
comment
Tolbutamide 6-12 hrs. 500mg Safest for the
elderly

Acetohexamide 12-18hrs. 250mg Safest for the

elderly

chlorpropamide 24-28hrs. 100- Prolonged

500mg in one hypoglycemia &
dose avoid in renal
disease
tolazamide 12-14hrs. 100-
1000mg in 1-2
doses
 Second generation……..
Drug Duration Dose Special
comment
Glibenclamide 12-24hrs. 2.5-20mg Hypoglycemia
more readily
appear because
of higher patency

Glipizide 12-24hrs. 2.5-40mg Prolonged

hypoglycemia is
less common
Gliclazide 12-24hrs. 40- Possible decrease
320mg in platelet count
 Mechanism of action
Sulphonylureas bind with there receptors
present close the potassium channels of the
cell membrane of the beta cells

This cause closing of these channels, there is

stoppage of potassium efflux from the
interior of the cell . As a result accumulation
of potassium ions.
 Cell membrane is now depolarized

Opening of the calcium channels in the

same cell membrane will occur

Thus entry of calcium ions from ECF to

ICF
This calcium entry causes release of
INSULIN
 Sulphonylureas also increases the
concentration of INSULIN
RECEPTORS on the target cell &
reduce the output of GLUCAGON
from the alpha cell of the islets.
THERAPEUTIC USE:-
• Indicated only for type 2 DM
• no help to patient with type 1 DM

PRECAUTIONS
• hypoglycemia
• Use in pregnancy and lactation
• Cardiovascular toxicity.
• not recommended in the treatment of
DKA or post surgical glycemic patients
 Therapeutic nursing
interventions…
• Assess V/S, weight, condition of skin &
nails, serum & urine glucose levels,
glycosylated Hb & ABG.
• Assess for long term complications related
to development of atherosclerosis
( hypotension, heart disease, stroke)
• Monitor for drugs therapeutic & adverse
side effects.
• Teach client & family the symptoms,
prevention & treatment of hypoglycemia.
 Client education………..
• Perform self glucose testing to monitor
therapeutic benefit.
• Adhere to other regiments prescribed to ctrl
diabetes, such as nutrition & exercise plan.
• Donot ingest alcohol when taking this
medicine.
• wear long sleeves to prevent side effects of
photosensitivity side effects.
BIGUANIDES
 Mechanism of action
They increase glycol sis at peripheral
tissue

By potentiating the action of insulin at

the target cells

Thus , the need of insulin is reduced

NOTE:- They oppose the development of
hyperglycemia but if the blood sugar is normal
they cannot produce hypoglycemia. So, they are
EUGLYCEMIC agents
 Indications…
Metformine are only used in NIDDM
cases who are:-
• obese i.e. have resistant to insulin
action
• where sulphonylurea alone is not
providing effective i.e in such cases
use metformine & sulphonylurea.
 metformine
Dose duration Side effect Contra-
• Daily 1-3 gm in divided doses.
indications

1-3 gm in about 12 diarrhoea Renal failure,

divided doses hrs. ,lactic acidosis, emphysema,
GI symptoms CMF, anemia.
i.e. nausea
 MEGLITINIDES

• A non sulphonnylurea which facilitates the

pancreas to produce more insulin right
after the meal
• Important drug :- Repalginide (Prandin)
 indications Side effects
• Monotherapy in the treatment of Hypoglycemia
type 2 DM
GI disturbances

• Secondary DM when pancreas is UTI

capable of insulin production.
weight gain

• combination therapy in the arthralgia

treatment of DM 2
 Nursing intervention..
• monitor the drugs therapeutic & adverse side
effects.
• teach clients & families about the signs ,
symptoms, preventions & treatment of
hypoglycemia.
• dosing is “MEAL BASED” with maximum doses not
to be exceed 16 mg daily.
• Assess renal functions & evidence of renal
insufficiency
• Assess for early signs of lactic acidosis.
• assess for long term complications of DM.
 THIAZOLAMIDES…
• Thiazolamides also know as “
GLITAZONES” reduce glucose level
by decreasing insulin resistance.
• These agents are not related
chemically or functionally to
biguanides , sulfonylureas , or alpha
glycosidase inhibitors.
• they only used in type 2 DM.
 Action & uses…
• Rosiglitazone ( avandia) acts primarily
by decreasing insulin resistance,
• The drug increases the ability of target
cells to respond to insulin.
• in animal models of diabetes glitazone
increase uptake of glucose by muscle &
decrease glucose production by the
liver
 INSULIN THERAPY
“The ultimate
approach.”
SOURCES:
• Human insulin
• Pigs & sheep
INSULIN
 ALTERNATE METHOD OF
INSULIN DELIVERY METHOD
Insulin pump
Prepartion Action Onset Peak Duration

Humalog Rapid 5-10 1 hr 2-4 hrs

Novolog acting min

Humilin (R) Short ½-1 hr 2-4 hrs 4-6 hrs

acting

Humilin N Intermediate 2-4 hrs 4-10 10-16hrs

(NPH) - acting hrs

Humulin (U)Long acting 6-10 None 18-20

hrs hrs
INSULIN EFFECTS:-
• Glucose transporters
• Liver cells
• Muscles
• Fat cells
Methods of Delivery-
• Pens,
• Jet injectors,
• Pumps,
• Inhalers
 Storage of insulin

• All insulin preparations are required to be

stored in a cool and dark place
• The extremes of temperature, that is, <2
and >30 degree C should be avoided.
• Therefore, keep insulin preparations away
from direct sunlight, in a cool and dark
place.
• Do not keep in a freezer compartment
 INSULIN PUMP THERAPY
ADVANTAGES OF PUMP
THERAPY:
• Exercise want –
without having to eat
first
• Free from multiple
daily shots
• Reduced risk of eye,
kidney & nerve
disease
 INSULIN PENS
ADVANTAGES OF INSULIN PENS:
• Easy to carry
• Accurate dose administration
• Less painfull
• Patient can be trained for self injection
PARTS OF INSULIN PENS:
 Moving injection sites
• Inject insulin at the same area for 1-2 weeks
• Each time put the needle into different spot
• At the end of 1-2 weeks, move to another area of the body
• It is no good idea to change from arm one to abdomen the next
day
• This may cause fluctuations in blood glucose levels
• It is not a good idea to use only arms and legs
• If you only inject in the abdomen, inject in the new spot each time
• Try to use each spot only once a month
 Complications of Insulin
Therapy

• Hypoglycaemia
• Allergy (Localised/Generalised).
• Lipoatrophy and Lipohypertrophy.
• Insulin oedema.
• Immunological insulin resistance.
• Insulin antibodies.
• Insulin resistance.
• Obesity and weight gain.
• Atherosclerosis
 NURSING MANAGEMENT
1. HISTORY
• Biodata
• Occupation
• Recent changes in weight, food habbits,
voiding pattern
• Past history
• Medications if any significant past history
• Family history
• Life style
PHYSICAL ASSESMENT:
NURSING DIAGNOSIS:
1.Risk for fluid volume deficit related to
polyuria and dehydration

Goal :- To maintain fluid and electrolyte balance

Interventions:-
• Intake and output should be measured
• Skin turgor should be checked
• Amount of urine passed uot should be measured so
as to replace equal volume of fluids
• Iv fluids should be encouraged
• Laboratory values (Na,K ) should be monitored
• Vital signs (BP) for signs of dehydration to be check
• 2.Imbalanced nutrition
related to imbalance of
nutrition, physical activity

Goal:-To improve nutritional intake

Interventions :-
• Asses the food fads of the patient.
• Diet is planned according to
patient’s lifestyle
• Extra snacks should be provided
before physical activity.
• Exchange list should be offered.
• Diet high in calories should be
given.
• Serve diet in an attractive way.
 3.Risk for complications related to
disease condition
Goal:- To prevent complications

Interventions:-
• Early identification of the acute
complications should be done
• Maintain optimal control of
blood glucose
• Maintain skin integrity
• Perform periodic foot care
• Take dietary precautions
• Take medications as and when
prescribed
 3.Knowledge deficit
related to self care skills

Goal:-To improve self care

Interventions:-
• Patient and family is taught regarding diabetes
• State normal and target glucose levels
• Describe major treatment modalites-diet,
exercise, medication
• Verbalize appropriate schedule for eating
snacks and medication
 PANCREAS TRANSPLANT

SURGICAL MANAGEMENT

ISLET CELL TRANSPLANT

UMMM….. WHICH SURGERY SHOULD I
PERFORM...
“PANCREAS TRANSPLANT” OR “ISLETS
CELL TRANSPLANT” !!!!!
 DIABETIC FOOT
Precipitating features and causes:-
• Friction of ill fitting or new shoes
• Untreated callus
• Foot injuries
• Burns
• Nail infections
• Heal friction in pt. confined to bed
 The foot is especially affected by
diabetes because:
• diabetes damages the nerves (damage can occur to the foot and not
be detected) - this is called peripheral neuropathy.
• diabetes also affect the circulation. Poor circulation can affect the
ability of the body to heal when damage occurs.
• those with diabetes are more prone to infection - the body's processes
that normally fight infection respond slower and often have trouble
getting to infections due to the poor circulation.
• diabetes can also affect the joints, making them stiffer
• other diabetes complications that can also affect the foot, for example,
kidney disease (affects proteins that are involved in wound healing)
and eye disease (can't see the foot to check for damage).
 Diabetic Foot Care Guidelines
• Inspect your feet daily.
• Wash your feet in lukewarm (not hot!)
water.
• Be gentle when bathing your feet.
• Moisturize your feet – but not between
your toes..
• Cut nails carefully
• Never treat corns or calluses yourself.
 Diabetic Foot Care Guidelines

• Wear clean, dry socks.

• Avoid the wrong type of socks.
• Wear socks to bed.
• Shake out your shoes and feel the inside
before wearing.
• Keep your feet warm and dry.
• Never walk barefoot
• Take care of your diabetes.
• Don’t smoke
• Get periodic foot exams.
 ACUTE
COMPLICATIONS OF
DIABETES MELLITUS
• Diabetic ketoacidosis
• Hyperglycemic
hyperosmolar
nonketotic syndrome
• Hypoglycemia
 DIABETIC KETOACIDOSIS
DEFINITION: It is a type of metabolic acidosis
when there is an acute insulin deficiency or
an inability to use insulin secreted by
pancreas.
This deficit in available insulin results in
disorders in metabolism of CHO, protien & fat
leading to three main clinical features:
• Hyperglycemia
• Dehydration & electrolyte loss
• Acidosis
CAUSES
• Previously undiagnosed diabetes
• Interruption of insulin therapy
• Stress of intercurrent illness
eg.MI
• Infection
• Drugs (Antipsychotic
drugs,corticosteroids, glucagon,
interferon etc.)
• Other causes(Acromegaly
,arterial thrombosis ,CVA,
pancreatitis etc.)
 LACK OF INSULIN

INCREASED BREAKDOWN
•DECREASED UTILISATION OF OF FATS
GLUCOSE
•INCREASED PRODUCTION OF
GLUCOSE BY LIVER
INCREASED F.A.

•Acetone breath
•Poor appetite INC. KETONE
HYPERGLYCEMIA •Nausea BODIES

BLURRED POLYURIA
ACIDOSIS
VISION •Nausea
•WEAKNESS •Vomiting
DEHYDRATION
•HEADACHE •Abd. Pain
RAPID
POLYDIPSIA RESPIRATIONS
 Clinical features
• Thirst Metabolic features:
• Polyuria leading to • Hyperglycemia
oliguria • Ketonemia
• Dehydration • hyperkalemia
• Hypotension
• Ketosis
• Hyperventilation
• Vomiting
• Abd. Pain
• Drowsiness, coma
DIAGNOSTIC TESTS

• Blood glucose levels

• Blood test for
ketones (>5mmol/L
-ketoacidosis)
• Urine test for
ketones
• Blood pH(<7.3-
metaolic acidosis)
 MANAGEMENT
• Replace fluid loss
• Replace electrolyte losses
• Restore acid base
balance
• Replace deficient insulin
• Monitor blood glucose
• Replace energy losses
 MANAGEMENT - ALBERTI'S REGIME

0.9% Saline IV
Start with 10-20 cc/kg NS bolus
• 1.5 litres per hour for 2 hours

• 0.5 litres per hour over the

next 4 hours
• 1 litre, 4 hourly.

• Goal is to replace deficits over 48

hours

• Continually re-evaluate status of

hydration
IV soluble insulin

• Do NOT give initial bolus

of insulin
• IV insulin drip at 0.1
units/ kg/ hour
• May decrease to 0.05
u/kg/hr if BG decreasing
too quickly
– To get control of balance
with IV fluids
– Prevent hypoglycemia
• Monitor BG at least q 1 hr
POTASSIUM

• Plasma potassium should be

kept at
4-5 mmol/L
• If K+ < 3, give 40 mmol
K /hr in IV NS
• If K+ 3-5, give 20 mmol K/
hr in IV NS
• If K+ above 5, stop
potassium
 NURSING
MANAGEMENT
• Urine Volumes
• Naso-gastric aspiration
• Central Line
• CVP Monitoring
• Cardiac Monitor
• Oxygen Therapy
• Pulse Oxymetry
• Blood gas monitoring
• Electrolyte monitoring
• Conservative care.
 PREVENTION
• Diabetic education
• Blood glucose
monitoring
• Home monitoring
of ketones
• Supplemental short
acting insulin
regimens.
• Easily digestible
liquid diets
 HYPEROSMOLAR
HYPERGLYCEMIC NONKETOTIC
SYNDROME
HHNKS ,an acute complication of
diabetes ,is characterised by
hyperglycemia without ketoacidosis.
Blood glucose levels are usually>500
mg/dl accompanying fluid &
electrolyte imbalances but pH
remains normal.
 ETIOLOGY
• Undiagnosed clients
with type 2dm
• Old clients with DM-2
• Drugs that elevate
blood glucose
• Clients on dialysis
• TPN
 PATHOPHYSIOLOGY
Metabolic needs exceeds the limits of available insulin

Some insulin is persistent hyperglycemia

still secreted

Transport of glucose ICF moves to ECS

Into cells

Minimal fat metabolism diuresis

(ketosis will not develop)
loss of sodium &
potassium
CLINICAL MANIFESTATIONS
• Hypotension
• Dehydration
• Polydipsia
• Neurological
symptoms
• High blood sugar
level
• Low sodium &
potassium levels
 DIAGNOSTIC TESTS
• Blood glucose
• Electrolyte
• BUN
• Complete blood
count
• ABG
• Serum osmolarity
 MANAGEMENT
• Insulin
administration
• Correction of
fluid and
electrolyte
• CVP monitoring
 NURSING
MANAGEMENT
•Measure clients blood glucose levels
•Evaluate hydration status, intake
output , skin turgor , vital signs &
electrolyte studies.
•Implement medical orders for insulin ,
fluids & electrolyte electrolyte
replacement.
•Observe neurologic & cognitive
symptoms.
 HYPOGLYCEMIA
Hypoglycemia (abnormal low
blood glucose level )occurs when
blood glucose level falls to < 50-60
mg/dl.
It is a adverse reaction when
administering medication for
diabetes.
 ETIOLOGY
• Not eating at all
and continous to
take insulin or OHA
• Not eating
sufficient calories
to compensate
glucose lowering
medications.
• Vigorous exercises
 DIAGNOSTIC TESTS
• Check blood glucose
level
• If client had taken
insulin and has not
eaten meals –
hypoglycemia
• If client has not
taken insulin and has
taken meals – DKA
 MANAGEMENT
•Administration of simple
CHO as soon as possible.
•Sources for quickly
available concentrated
CHO include honey ,
candy , sugar , sweetened
fruit juice ,or glucose
tablets.
•If the client is
unconscious , glucose gel
can be applied in buccal
mucosa
 MANAGEMENT…..

• IV administration of 20-50ml
of 50% glucose if client is not
responding.
• Once hypoglycemic symptoms
are relieved, complex CHO can
be given to sustain & prolong
an adequate level of blood
glucose.
 NURSING MANAGEMENT
• If the client is conscious &
can swallow, nurse gives an
oral source of glucose.
• Administer IV glucose or
glucagon as prescribed.
• Stay with client until the
symptoms are corrected.
CHRONIC COMPLICATIONS
OF

DIABETES MELLITUS
 MACROVASCULAR

CHRONIC COMPLICATIONS

MICROVASCULAR
 ACUTE COMPLICATIONS OF
DM
Hypoglycemia
It is blood glucose level less
than 60 mg/100ml .
It results from:
• An over dose of insulin.
• Omitting a meal
• Overexertion
• Nutritional and fluid imbalance
• Alcohol intake
CLINICAL MANIFESTATIONS
In mild hypoglycemia:
☺ Sweating
☺ Tremor
☺ Tachycardia
☺ Palpitation
☺ Hunger
☺ Nervousness
In mild hypoglycemia:
☺ Headache
☺ Confusion
☺ Memory lapses
☺ Numbness of lips and tongue
☺ Inability to concentrate
In severe hypoglycemia
☺ Disorientation
☺ Seizures
☺ Unconsciousness
 MANAGEMENT
• Provide quick acting CHO 15-20
gm.
• Provide 1 tbs of honey, 8 oz low
fat milk.
• Commercial dextrose products.
• Repeat treatment after 15 mins.
• Notify to the physician.
 CHRONIC
COMPLICATIONS

Microvascular Macrovascular
Microvascular
Retinopathy

Neuropathy

Nephropathy
Macrovascular

CAD

Cerebro vascular disease

Peripheral vascular diseas

 RETINOPATHY
DEFINITION
Deterioration of small blood
vessels that nourish the retina.
TYPES
@ Proliferative
@ Pre Proliferative
• PROLIFERATIVE:
PROLIFERATIVE It represents increased
destruction of retinal blood vessels..
• PRE PROLIFERATIVE:
Abnormal growth of new blood vessels
of the retina.
↓
rupture of new vessels, leads to bleeding in
vitreous.
↓
Blocking light
↓
rupture of B.V in the vitreous, form scar
tissue, which detach the retina.
CLINICAL MANIFESTATIONS
• Blurred vision
• Macular edema
• Floaters
• Spotty or hazy vision
• Complete loss of vision
 DIAGNOSTIC TEST
• Assessment
• Direct visualization with
ophthalmoscope.
• Fluorescent Angiography
 MANAGEMENT
MEDICAL MANAGEMENT
• Control of hypoglycemia
• Control of hypertension
• Control of hyperlipidemia.
SURGICAL MANAGEMENT
• Photocoagulation
• Virectomy
 NEPHROPATHY
Definition
Damage to the small blood
vessels that supply glomerulus of the
kidneys.
Risk factors
• HTN
• Genetic predisposition
• Smoking
• Chronic hyperglycemia
Clinical manifestation
• Hypoglycemia
• Fatigue
• Edema
• Decreased micturation
Diagnostic test
• Blood test
• RFT
• Glycated Hb
Treatment
• Strict glycemic control
• Prevent UTI
• Avoid nephrotoxic substances
• Lipid control
• Low sodium diet
• Control B.P
• Low protein diet
• Hemodialysis
• Renal Transport
 NEUROPATHY
Definition
Damage of peripheral, autonomic
and spinal nerves.

Risk factors
• Increasing age
• Genetic risk
• Cigarette smoking
• Alcohol use
• High B.P
Sign and Symptoms
• Numbness
• Tingling sensation
• Indigestion
• Nausea
• Vomiting
• Wt. loss
• Dizziness
• Fatigue
Diagnostic Test
• CBC
• Electromyography
• USG
• Check reflex
• Assess vibration perception
• Thyroid function test
Treatment
• Control Blood sugar
• Walk regularly
• Take warm bath
• Wear elastic stockings
 CAD
Definition
Narrowing of the arteries
that supply the heart.
Risk factors
• Smoking
• Increasing age
• Obesity
• High fat diet
Clinical Manifestation
• Pain in left side radiates to shoulder,
arm and left jaw.
• Decreased tissue perfusion
• Breathlessness
Prevention and treatment
• Stop smoking
• Decrease intake of fat
• Control blood glucose
• Regular exercise
CEREBRO VASCULAR DISEASE
Definition
Inadequate blood supply to brain
which leads to hge.
Risk factors
• Smoking
• Obesity
• Hypertension
• Dyslipidemia
Sign and Symptoms
• Slurred speech
• Aphasia
• Weakness
• Paralysis
• Blindness
• Loss of coordination
• Numbness
Treatment and Prevention
• Stop smoking
• Decrease intake of fat
• Control blood glucose
• Regular exercise
 PERIPHERAL ARTERIAL
DISEASE
Definition
Fat deposit in the arteries of lower
extremities lead to decrease blood flow.

Risk factors
• Smoking
• Obesity
• Hypertension
• Dyslipidemia
Sign and Symptoms
• Pain
• Slow healing
• Blister formation
• Tissue death
Prevention and Treatment
• Stop smoking
• Antiplatelet drugs
• Anti anginals
• Anti hypertensive drugs
 HYPERTENSION
DEFINITION
Systolic B.P ≥140mmHg
and diastolic ≥ 90 mmHg.
Risk factors
• Age
• Alcohol intake
• High fat diet
• Obesity
• Family history
Clinical manifestations
• Fatigue
• Dizziness
• Palpitations
• Headache
Diagnostic study
• History and Physical examination
• CBC
• Serum lipid profile
• Serum uric acid
Prevention
• Maintain wt.
• Reduce salt and sodium intake
• Do regular exercise
• Limit consumption of alcohol
• Monitor B.P regularly.
 MACROVASCULAR
DISEASES

1.Coronary artery disease

2.Cerebrovascular disease
3.HTN
4.Peripheral vascular disease
5.infection
 MICROVASCULAR
DISEASES

DIABETIC RETINOPATHY

DIABETIC NEPHROPATHY

DIABETIC NEUROPATHY
1.CORONARY ARTERY
DISEASE:-

• Atherosclerotic changes in
the coronary artery leads to
increase in the occurrence of
MI in persons with DM

• Typical ischemic symptom

may be absent

• Patient may not experience

the early signs of decrease
coronary blood flow and may
have silent MI in which chest
pain and other symptoms
were not experienced.
CEREBROVASCULA
R DISEASE:-

• Atherosclerotic changes in
cerebral blood vessels or
the formation of an
embolus in the
vasculature lead to
ischemic attack and
stroke.

• Symptoms include
dizziness, decreased
vision and blurred vision
and weakness
3 .HYPERTENSION:-
• 40% increase rate of
HTN in diabetic patients
is noticed
• It is major risk factor of
stroke and nephropathy
• Pharmacological
treatment for HTN is
greater than 130/80
mm of Hg suggests for
diabetic client.
5 . INFECTION:-

• Once infection occur ,they

are difficult to treat .
Three Factors contribute to
develop infection are :
 Impaired polymorph
nuclear
leukocyte function
 Diabetic neuropathies
 Vascular insufficiency
• UTI are common
• Diabetic foot
1 DIABETIC RETINOPATHY:-

• It is progressive disorder of
retina , characterized by
microscopic damage retinal
vessels resulting in occlusion
of vessels

• It is one of the leading cause

of blindness worldwide

• All the persons suffering from

DM from last 15-20 yrs have
80-90% of chances of
developing retinopathy
 ETIOLOGY:-

• Damage of blood vessels that

nourish retina as a result of
inadequate blood glucose
level

• Inadequate blood supply

• Decreased vision & then it is

permanently lost .
CLINICAL MANIFESTATIONS

• Blurred vision

• Cloudy vision

• Black spots

• Complete loss of vision

PATHOPYSIOLOGY
Damage of blood vessels that nourish
retina

Weak vessels of retina

Hyperpermeability & leakage

Microhaemorrhages , retinal swelling &

exudative deposit

Progressive retinal ischemia

 Neovascularization

New vessels are fragile & may rupture

Sub retinal dot hemorrhage / bleeding

into vitreous bodies

May form vascular bands that contract

resulting in retinal detachment
TYPES OF DIABETIC RETINOPATHY

A ) BACKGROUND OR NON
PROLIFERATIVE

B) PREPROLIFERATIVE

C) PROLIFERTIVE
A) BACKGROUND OR NON-
PROLIFERATIVE
• It occurs due to long term DM .
90% people are affected
.
• Retinal vessels become dilated

• Multiple hemorrhages form

vessels

• Retinal edema occur

• Hard exudates form & ischemia

contribute to impaired vision
(C)PROLIFERATIVE
It is the final & most vision
threatening type
 The weakened & damaged
vessel

 That have proliferate or

formed in
response to ischemia may
rupture
causing retinal hemorrhage
& exudates
DIABETIC NEPHROPATHY

• It is the simple most ,common

cause of end stage renal disease
( ESRD)

• About 35 –45% of clients with

DM 1 are found to have
nephropathy 15 –20 yrs after
diagnosis
• Nephropathy
involves damage to
& eventual
obliteration of the
capillaries that
supplies the
glomeruli of the
kidney
• About 20 % of client
with DM 2 are found
to have nephropathy
5-10 yrs after
diagnosis
 RISK FACTORS
• Poor control
• HTN
• Long duration of disease
CLINICAL
MANIFESTATIONS
• Intercapillary
glomerulosclerosis
• HTN
• Albuminuria
PATHOPYSIOLOGY
Renal hypertrophy

Increased GFR

Damage glomerular capillaries

Increased shearing forces

Mesangial cell hypertrophy & increase

secretion of extracellular mesangial
matrix material.
 Glomerular sclerosis

Thickening of basement membrane

Disruption of protein cross linkage

Progressive leakage of large molecules

into the urine (protein urea)
3. DIABETIC
NEUROPATHY

• A disease process of
nerve degeneration &
loss of function.

• It is the most
common chronic
complication of about
60% of diabetes.
 ETIOLOGY

• Vascular insufficiency
• Chronic elevation in blood
glucose level
• Hypertension
• Cigarette smoking

 TYPES

• Mononeuropathy
• Polyneuropathy
• autonomic neuropathy
(A) MONONEUROPATHY

• It involves a single or a group

of nerves

• It produce sharp , stabbing

pain

• It is caused by an infarction of
the blood supply

• Treatment includes surgical

decompression for
compression lesions
(B) POLYNEUROPATHY

• It involves sensory &

autonomic nerves
• Sensory neuropathy is
most common
• It commonly effects the
lower extremities
• A client describes tingling
, numbness , burning &
mild to total sensory loss
• Treatment include foot
care to prevent trauma &
ulcer
(C)AUTONOMIC
NEUROPATHY

It demonstrates itself its effect in

pupillary,CVS,GI, and GU functions

 PUPILARY
It interferes with the pupils ability
to adapt to the dark
 CARDIOVASCULAR
It is evidenced by an response to exercise
• A fixed heart rate

• Orthostatic hypotension

• Resting tachycardia

 GI
• Dysphagia , abd pain , vomiting , diarrhea ,
malabsorption , constipation & stomach
fullness

• Gastroparasis
 GU
• Bladder hypotonicity

• Staining with urination

• Decreased urinary strain

• Sexual dysfunction
PATHOPYSIOLOGY

Diabetes

Decreased nourishment of nerve fibers

Axons & dendrites are not nourished

Transmission of impulses slow

.
Sorbital accumulation in nerve tissue

Dec. both sensory & motor funtion

Temporary & permanent neurological problem

 Nursing management
• Assessment
History
Visual defects
Motor coordination
Neurologic defects
 Conti…..
2 DIAGNOSIS
 Risk for fluid volume deficit related to polyuria &
dehydration
 Imbalanced nutrition related to insulin, food and
physical activity
 Deficient knowledge about DM, self care skills and
information
 Conti…..
 Potential self care deficit related to
physical impairment or social factors.
 Anxiety related to loss of control , fear
of inability to manage DM ,
misinformation related to DM and fear
of diabetic complication
POTENTIAL COMPLICATION
Fluid overload ,pulmonary edema , heart failure .
o
Hypokalemia
o
Hyperglycemia and ketosis
o
Hypoglycemia
o
Cerebral edema
o
 Conti ……..
PLANNING AND GOALS
oMaintain fluid electrolyte balance
oOptimal control of BGL
oAbility to perform self care
activities
 NSG INTERVENTION
MAINTAIN FLUID ELECTROLYTE
BALANCE
•Intake and output to be measured
•IV and electrolytes administration
•Oral fluid intake
•Lab values
•Vitals monitored
 Conti……
IMPROVING NUTRITONAL
INTAKE
•Diet planned with control of
glucose
•Maintain desired weight
•Encourage to eat full diet
 Conti…….
REDUCING ANXIETY
•Emotional support
•To focus on learning self care
•Teach glucose monitoring
•PROVIDING SELF CARE
 HEALTH TEACHING TO
PATIENT
1) Simple pathology
 definition of DM
 Normal blood glucose level and
target
 Effect of insulin and exercise
 Effect of food and stress
 Basic treatment approaches
 Feet care
 CONTI…..
TREATMENT MODALITIES
Administer insulin & oral
antidiabetic drug
Diet information
Monitoring blood glucose and
ketones
 Conti…….

RECOGNITION TREATMENT AND

PREVENTION
Hypoglycemia
Hyperglycemia

PRAGMATIC INFORMATION
Where to buy insulin syringe
When and how to reach physician
 SUMMARIZATION
•INTRODUCTION
•DEFINITION
•CLASSIFICATION
•TARGET GROUP
•PATHOGENESIS OF TPPE 1 DIABETES
•TREATMENT
•DIAGNOSTIC TEST
•COMPLICATION
•MEDICAL MANAGEMENT
 CONTI….

NURSING MANAGEMENT
HEALTH TEACHING
 RECAPTUALIZATION
• DEFINE DM
• WHAT ARE THE TYPES OF DM?
• ENLIST THE ORAL HYPO GLYCEMIC
AGENT
 BIBLIOGRAPHY
Brunner & Suddarth et -al. Text Book of MEDICAL
SURGICAL NURSING,Virginia: A wolters kluwer
company;2007:volume 2 :pp 1150-1200
Joyce M. Black, Hawaks et-al. Medical
Surgical Nursing. Web Saunders Company :Newyork
publishers : volume 1;pp 1277-1280

 Braunwald ,fauci, kasper et-al. Harrison’s Principle

of Internal Medicine,USA:Grawhill Medical Publishing
Division,1998;pp2109-2135
 CONTI..
 Richland s.(online-2007(cited NOV 17)
available from
google:http//www.palmeto
health.org/body.com,id=77//
 Yoga & Diabetes

• Sun salutation

• Asanas

• Pranayama

• Meditation

• Yoga Nidra

• Cleansing Processes
 Sun Salutation
• It increases the blood supply to various
parts of body,
• improving insulin administration in the
body,
• it gives all the benefits of exercise if
practiced at 4 rounds per minute.
• If practiced at slow speed, it offers the
benefits of asanas.
 Asanas
• Due to various twists, stretches and
strains in the body, the internal organs are
stretched and subjected to strain.
• This increases the blood supply, oxygen
supply to the organs increasing the
efficiency and functioning of the organ.
• Stretching various glands result in
increased efficiency of the endocrine
system
Pranaya
ma
 Pranayama
• One of the basic preparations for
Pranayama is Nadi Shodhan
Pranayama or alternate nostril
breathing, this type is found useful in
diabetes as Alternate nostril
breathing has calming effect on
nervous system, which reduces
stress levels, helping in diabetes
treatment
 Meditation
•
Concentration on pancreas during the
meditation practice has shown positive
effects on sugar levels.
• One can even visualize the proper
functioning of pancreas, proper insulin
administration in the body can help in
treatment of diabetes.
 Yoga Nidra
• Yoga Nidra is very important process
of deep relaxation.

• It helps alleviate the stress and has

very good positive effects on the
entire body – mind complex.