HEAD

• Lies within the curve of the duodenum

• Unicate process  prolongtion of the
head
UCINATE PROCESS
• The part of the head that wraps
behind the superior mesenteric artery
and vein and comes to lie adjacent to
the ascending part of the duodenum
 CONT,
NECK
• A constricted portion to the left of
the head. It abuts the pylorus
above and the beginning of the
portal vein behind
 CONT,
BODY
• Anterior surface separated from the
stomach by the omental bursa
• Posteriorly related to the aorta , splenic
vein, left kidney and renal vessels, left
suprarenal, origin of superior mesenteric
artery and crura of diaphragm
TAIL
• Extends into the lienorenal ligament and
abuts the spleen
 FUNCTION
• DIGESTIVE - produces digestive
enzymes
• HORMONAL - islets of Langerhans
produce insulin needed to control
blood sugar levels
 CLINICAL
CONSIDERATION
• Hypertrophy of the head  portal
or bile duct obstruction
• Degeration of the islets of
Langerhans  DM
• Pancreatitis due to serious
inflammatory condition of the
exocrine pancreas
•DIABETES
( From a Greek work meaning “ to
siphon “, referring to the
increased output of urine. )
•MELLITUS
(From a Latin word meaning
“sweet“ )

The two words together identify the

disease as an outpouring of sweet
urine.
 DEFINITION
•Diabetes is a metabolic disorder
characterized by inappropriate
hyperglycemia ( high levels of
sugar ) caused by a relative or
absolute deficiency of insulin or
by a cellular resistance to the
action of insulin.
 MAJOR
CLASSIFICATION OF
DIABETES
• Type 1 DM – insulin-dependent
diabetes mellitus ( IDDM )
• Type 2 DM – non-insulin-
dependent diabetes mellitus
( NIDDM )
 DIABETES
TYPES 1
INSULIN –
DEPENDENT
DIABETES MELLITUS
( IDDM )
 DEFINATION
• Metabolic condition in which the
beta cells of pancrease no longer
produce insulin:
• Characterized by hyperglycemia,
breakdown of body fats and
protein and development of
ketosis.
• Called JUVENILE onset diabetes or
( IDDM )
 SIGN AND SYMPTOMS
• Hyperglycemia ( elevated
blood glucose levels )
• Development of ketosis
( an accumulation
of ketone bodies produced
during the oxidation of fatty
acids )
 Cont,
• Result of the destruction of the
beta cells of the islets of
Langerhans in the pancreas ( on
cell in the body make insulin ).
• When Beta cell destroyed, insulin
no longer produced.
 Autoimmune or
Idiopathic Disorder
• Begin with insulinitis.
• A chronic inflammatory process that
occurs in response to the autoimmune
destruction of islet cells.
• Slowly destroys beta cell production
of insulin.
 Cont,
• The onset of hyperglycemia occurring when
80% - 90% of beta cell function is lost.
• Usually occur over a long preclinical period.
• Alpha-cell and Beta-cell function are
abnormal, with a lack of insulin a relative
excess of glucagon resulting in
HYPERGLYCEMIA.
 RISK FACTORS
• Genetic predisposition for increased
susceptibility: Human Leukocyte Antigens
(HLA) linkage.
• Environmental triggers stimulate an
autoimmune response.
 Viral infection ( mumps, rubella,
coxsackievirus B4 )
 Chemical toxins.
 ETIOLOGY
• Obesity (overweight)
• Waist size
• Sedentary lifestyle
• Age
• Family history
• Ethnicity
• Gestational diabetes/high birth weight
baby
• High blood pressure/cholesterol
 CLINICAL
MANIFESTATIONS
• Polyuria ( hyperglycemia acts as
osmotic diuretic )
• Glycosuria ( renal threshold for
glucose: 180mg/dl )
• Polydipsia ( thirst from
dehydration from polyuria. )
• Polyphagia ( hunger and eats more
since cell not utilize glucose )
 Cont,
• Weight loss ( body breaking down
fat and protein to restore energy
source )
• Malaise and fatigue ( fron decrease
in energy. )
• Blurred vision ( swelling of lenses
from osmotic effects. )
 POTENTIAL
COMPLICATION OF
DM TYPE 1.
DIABETIC
KETOACIDOSIS
( DKA )
 DEFINITION
• Result from breakdown of fat and
overproduction of ketones by the
liver and loss of bicarbonate.
• Occur when undiagnosed or known
diabetic has increased energy
needs, when under physical or
emotional stress or fails to take
insulin.
 PATHOPHYSIOLOG
Y
• An absolute deficiency of insulin and an increase
in the insulin counterregulatory hormones.

• Glucose production by the liver increase,

peripheral glucose use decrease, fat
mobilization increase, and ketogenesis is
stimulated.
 Cont,
• Increased glucagon levels activate the
gluconeogenic and ketogenic pathways in
the liver.

• Presence of insulin deficiency, hepatic

overproduction of beta-hydroxybutyrate
and acetoacetic acid ( ketone bodies )
 Cont,
• Loss of bicarbonate ( which occurs when the
ketones is formed )

• Bicarbonate buffering does not occur and a

metabolic acidosis occurs

• DKA
DIABETES TYPES
2
NON-INSULIN-
DIPENDENT
DIABETES
MELLITUS
 DEFINITION
• Is a condition of fasting
hyperglycemia that occur
despite the availability of
endogenous insulin.
 • Sufficient insulin production to
prevent DKA

• But insufficient to lower blood

glucose through uptake of glucose by
muscle and fat cells.

• Cellular resistance to insulin

increased by obesity, inactivity,
illness, age, some medication.
 RISK FACTORS
 History of diabetes in parents or siblings.
 Obesity
 Physical inactivity.
 Race / ethnicity
 Women
 Hypertension
 Metabolic syndrome
 CLINICAL
MANIFESTATION
• Not experience weight loss.
• Hyperglycemia.
• Polyuria
• Polydipsia
• Blurred vision
• Fatigue
• Paresthesias
• Skin infection
 POTENTIAL
COMPLICATION OF DM
TYPE 2.
HYPERSOMOLAR
HYPERGLYCEMIC
STATE
( HHS )
 DEFINITION
• Is characterized by a plasma osmolarity of
340 mOsm/L or greater ( the normal range
is 280 to 300 mOsm/L.
• Greatly elevated blood glucose levels (
over 600 mg/dL and often 1000 to 2000
mg/dL), and altered level of consciousness.
• HHS is a serious, life-threatening medical
emergency and has a higher mortality rate
than DKA.
 CAUSES
THERAPEUTIC AGENTS
Glucocorticoids
Diuretics
Beta-adrenergic blocking agent
Immunosuppressant
Chlorpromazine
Diazoxide
 Cont,
THERAPEUTIC PROCEDURE
Peritoneal dialysis
Hemodialysis
Hyperosmolar alimentation ( oral or
parenteral )
surgery
 Cont,
ACUTE ILLNESS
Infection
Gangrene
Urinary infection
Burns
Gastrointestinal bleeding
Myocardial infarction
Pancreatitis
Stroke
 Cont,
CHRONIC ILLNESS
Renal disease
Cardiac disease
Hypertension
Previous stroke
Alcoholism
PATHOPHYSIOLOGY
• Hyperglycemia leads to increased urine
output and dehydration.

• Kidneys retain glucose: glucose and sodium

rise

• Severe hyperosmolar state develops

leading to brain cell shrinkage.
 CLINICAL
MANIFESTATIONS
• Altered level of consciousness.
( Lethargy to coma )
• Neurological deficits:
hyperthermia, motor and sensory
impairment, seizures.
• Dehydration: dry skin and mucous
membranes, extreme thirst.
 INVESTIGATIONS
Blood capillary glucose test
Random blood sugar
Fasting blood sugar
2 hours postprandial
Modified oral glucose tolerance test
Renal profile
Fasting lipid profile
 COMPLICATION
Eye complications (diabetic retinopathy)
Kidney damage (kidney disease)
Nerve damage
Heart disease
Stroke (brain attack)
Urinary incontinence (unable to hold urine)
Intestinal disruptions leading to constipation.
 NURSING CARE PLAN
(1)Anxiety related to hospitalization.
Goal
 -Patient
will verbalize less anxiety
Intervention:
 assess patients level of a anxiety
 explain to patients the important of
completing the treatment.
 explain to patients regarding procedures.
 give emotional support.
 involve patients when planning nursing care.
 Cont,
2)Ineffecive health maintenance
related to management of type 1
diabetes mellitus.
Goal:
 patients will describes feeling about self
management of types1 diabetes mellitus.
 patients will describes disease process.
Interventions:
 -evaluate
the patients understanding of
types1 diabetes mellitus and attitude
about the need to manage it.
 Cont,
 correct any misconceptions about type 1
diabetes mellitus and the therapeutic regimen.
 discuss peer presure.ask the adolescent if
patients feel social pressure that causes to
ignore dieter avoid self administering insulin.
 ask if patients feel depressed about disorder.
 Cont,
3)Nutrition less than body
requirements related to poor of
appetite.
Goal:
 patients will show no further evidence of
weight loss.
 patients will take in calories daily.
Interventions:
-obtain and record patients weight at the
same time every day to obtain accurate
readings.
 Cont,
4)Risk for fluid volume deficit related
to hyperglycemia and osmotic
diuresis.
Goal:
 The diabetic client will exhibit optima
fluid balance as evidence by:
#Blood pressure > 90/60mmHg (or
within the client normal range).
#Firm skin turgor and moist mucous
membranes.
 Cont,
 maintain parental fluids or
ordered to provide patients
with needed fluids and
electrolytes.
 monitor electrolytes level and
report abnormal values.
 Cont,
Intervention:
 Monitor vital signs every 15min until the
client condition is stable for 1hour,then
4 hourly.

 Notify the physician if heart rate is >

120/min,blood pressure is <90/60mmHg
or decreased >20mmHg from baseline,
CVP is <2mmHg and <6mmHg
 Cont,
 Monitor the client for fluid volume
deficit: poor skin turgor, dry mucus
membranes sunken and soft eyeballs.
 Measure intake and output accurately:
report to the physician urine output
<30ml /hour for 2 consecutive hours.
 Weight the client daily on the same
scales.
 Administer IV fluid as described
 Cont,
 Administer antiemetic medications
to the client as prescribed.
 unless contraindicated, maintain oral
intake of at least 2500ml.
 FOOT CARE
• Check the feet daily.
• Monitor for :red
areas,cuts,blister,corns,ingrown
toe nails,calluses,cracks in the
skin and changes in color.
• Check the skin for dry and
changes in skin color.
• Wash feet for lukewarm water
and mild soap.
 Cont,
• Do not soak feet.
• Dry feet thoroughly with a soft towel
and pat gently.*DO NOT RUB*
• Use moisturizing lotion to prevent skin
cracking DO NOT APPLY BETWEEN
TOES-CAN INCREASE RISK OF
INFECTION.
• Use a pumice stone to remove callus
 NUTRITION
 Advice pt to avoid adding sugar to food
 Avoid food that sweetened with sugar or
honey
 Smoking cessation
*** CHECK BLOOD GLUCOSE LEVEL
REGULARLY
*** INCREASE FLUID INTAKE
 Limit intake of saturated fat and
cholesterol in food.
 REFERENCE
• Medical Surgical Nursing – Fourth Edition
Pricilla LeMone & Karen Burke ( Page: 562 – 603 )
 GROUP OF
MEMBERS
SOLEHAH NURFARAHANIMS
IZZATULELLMY UHAIDA
NUR NADIA SITI FATIMAH
TASHA NOOR AZIZAH
NUR FARIHAH SHAMINI DEVI
LATHA ZURAINI