Prepared by: Dr.

PA Maroma
Pancreas
 a chronic metabolic
disease characterized by
hyperglycemia
due to disorder of
carbohydrate, fat and
protein metabolism
Predisposing Factors:
 Heredity

 strongly associated with Type II DM

 Obesity
 Adipose tissues are resistant to insulin, therefore glucose
uptake by the cells is poor
 Stress
 Stimulates secretion of epinephrine, nor-epinephrine,
glucocorticoids  increased serum carbohydrates
Predisposing Factors:
Predisposing Factors:
 Viral infection

 increase risk to autoimmune

disorders
 Autoimmune Disorders
 more associated with Type I
DM
 Multigravida Women with
large babies
 Type I
 Type II
 Gestational Diabetes
 Diabetes associated with other
conditions or syndromes
 Pancreatic disease, Cushing’s
syndrome
 Use of certain drugs

 Steroids
 Type I (IDDM)
 Juvenile – onset, Brittle DM, Unstable DM
 Onset is less than 30 years
 Common in children or in non-obese
adults
NO insulin
production
 Prone for DKA
 Management:

 Diet
 Exercise
 Insulin
 Type II (NIDDM)
 Maturity – onset, Stable DM, Ketosis – resistant DM
 Onset is 40 years
 Common in obese adults

Inadequate insulin production or

cells do not respond to insulin
 Prone for HHNKS
 Management:

 Diet
 Exercise
 OHA, Insulin in STRESSFUL situation
HYPERGLYCEMIA

Polyuria
Polydipsia
Polyphagia
 HYPERGLYCEMIA

Large amount of glucose

pass through the kidney

It will exert high osmotic

pressure w/in the renal tubules
OSMOTIC
DIURESIS

POLYURIA
 Hyperglycemia

POLYURIA
Polydipsia
 Due to blood osmolarity, water moves from inside
to outside the cell (ICF dehydration)
 There will be hypovolemia (ECF dehydration)
 Glycosuria will occur if glucose in the blood is
>220mg/dl (renal threshold)
Glucose insulin cell

cellular starvation

Hunger &  appetite  Polyphagia

Glucose cell

cellular starvation
Protein

Fats ketones
Polyphagia
Glucose cell
Protein cellular starvation
Osmoti
Fats  Lipolysis ketonuria
diuresis

Ketones ketonemia
Acetone breath
hyperlipidemia
Metabolic acidosis
atherosclerosis Ketones are acid bodies
(Acetone, acetoacetic acid,
ß-hydroxybutyric acid)
Ketones act as CNS
depressants and may
decrease brain pH
leading to coma
Glucose cell
Fats cellular starvation
 protein breakdown
Protein
Negative nitrogen balance
 BUN and serum creatinine
Tissue wasting
Weight loss
Debilitation
 Due to increased blood viscosity
 Sluggish circulation
 Proliferation of microorganisms

 Infections, Periodontal, UTI, Vasculitis, Cellulitis,

Vaginitis, Furuncles, Carbuncles, Retarded
Wound Healing
Complications:

 Macroangiopathy

 Microangiopathy

 Neuropathy
Complications:
 Macroangiopathy
Brain
 Cerebrovascular accident
Heart
 Myocardial infarction
Peripheral arteries
 Peripheral vascular disease
Complications:
 Microangiopathy
Kidneys
 Renal failure due to nephropathy
Eyes
 Cataract due to retinopathy
Complications:
 Microangiopathy
Complications:
 Neuropathy
 Spinal Cord/ ANS
 Peripheral neuropathy
 involves damage to
the PNS
 affect movement,
sensation and bodily
functions
(numbness/ tingling)
Complications:
 Neuropathy

 Paralysis
 Gastroparesis
(delayed gastric
emptying)
 Neurogenic bladder
(bladder does not
empty properly)
 Decreased Libido,
impotence
 Diagnostic test:
 Random Blood Sugar (RBS)

 Blood specimen is drawn without preplanning

 ≥200mg/dl + symptoms is suggestive of DM
 Fasting Blood Sugar (FBS)
 Blood specimen after 8 hours of fasting
 No DM (70-110 mg/dl)
 Postprandial Blood Sugar
 Blood sample is taken 2 hrs after a high CHO meal
 No DM (70-110mg/dl), DM (≥140)
 Diagnostic test:
 Oral Glucose Tolerance Test (OGTT)
 Client then fast for 8 hours. A baseline blood sample is
drawn & a urine specimen is collected
 An oral glucose solution is given
 Blood is drawn at 30 minutes & 1, 2, and 3 hours after the
ingestion of glucose solution. Urine is collected
 No DM (glucose returns to normal in 2-3 hours & urine is
negative for glucose)
 DM (blood glucose returns to normal slowly; urine is
positive for glucose)
 Diagnostic test:
 Glycosylated hemoglobin

(HbA1c)
 The amount of glucose stored
by the hemoglobin is elevated
above 7% in the newly
diagnosed client with DM, in
one who is
noncompliant, or
in one who is Inadequately
treated
 DIET
 Low caloric diet specially
if obese
 Diet should be in
proportion
 20% CHON
 30% Fats
 50% CHO
 Consume complex CHO
and HIGH fiber diet
 inhibits glucose
absorption in the
intestines
 EXERCISE

 Increases CHO uptake by the cells

 Decreases insulin requirements
 Maintains ideal body weight, serum carbohydrates &
serum lipids
Medications:
 Insulin
 for Type I & II
 Oral Hypoglycemic Agents (OHA)
 for Type II
 Sulfonylureas
 Nonsufonylureas
 Biguanides
 Alpha-glucosidase inhibitors
 Thiazolidinediones
 Meglitinides
 Insulin Onset Peak Duration
Rapid acting
-Lispro(Humalog) 5 minutes 30 mins - 2 to 4 hrs
-Aspart (Novalog) 1hr
Short acting
-Regular (Humulin R, 30 min to 1 hr 2 t0 4 hrs 6 to 8 hrs
Novolin R, Iletin II
regular)

Intermediate
-NPH 1 to 2 hrs 6 to 12 hrs 18 to 24 hrs
-Humulin N 1 to 2 hrs 8 to 12 hrs 18 to 24 hrs
-Lente, Humulin L 1 to 2 hrs 8 to 12 hrs 18 to 28 hrs
Long acting
-Ultralente 5 to 8 hrs 14 to 20 hrs 30 to 36 hrs
-Lantus UK UK 24 hrs
Nursing Responsibilities in Insulin Therapy:
 Route: Subcutaneous
 slow absorption, less painful, 90° (thin) 45° obese clients, no
need to aspirate, do not massage site of injection
 IV insulin: given in emergency cases (DKA)
 Administer insulin at room temperature
 Cold insulin can cause lipodystrophy
 Lipoatrophy- loss of subcutaneous fat usually
caused by the utilization of animal insulin
 Lipohypertrophy- development of fibrofatty
masses, usually caused by repeated use of
injection site
Nursing Responsibilities in Insulin Therapy:
Nursing Responsibilities in Insulin Therapy:
 Store vial of insulin in current use at RT
 Insulin can be stored at RT for 1 month
 Other vials should be refrigerated
 Rotate the site of injection
 To prevent lipodystrophy
 Lipodystrophy inhibits insulin
absorption
 Gently roll vial in between
the palms to redistribute
insulin particles
Nursing Responsibilities in Insulin Therapy:
 DO NOT Shake
 bubbles make it difficult to aspirate exact amount
 Observe for side effects of insulin therapy
 Localized: Induration or Redness, Swelling, Lesion at the
site, Lipodystrophy
 Generalized:
 Edema
 due to sudden resolution of hyperglycemia
 Hypoglycemia
 Somogyi phenomenon
 Sulfonylureas “insulin releasers”
 Stimulate the beta cells to secrete more insulin
 Increases the ability of insulin cell receptors to bind insulin
 SE: weight gain, hypoglycemia, secondary failure of
pancreas due to overstimulation
 Tolbutamide (Orinase)
 Acetohexamide (Dymelor)
 Tolazamide (Tolinase)
 Chlorpropamide (Diabenese)
 Glipizide (Glucotrol)
 Glyburide (micronase, Glynase)
 Glimepiride (Amaryl)
 Nonsulfonylureas
 Biguanides
 Metformin (Glucophage)
 Help tissues use available
insulin more efficiently
 “insulin sensitizers”
 SE: Stomach upset,
flatulence, diarrhea
 no weight gain, no
hypoglycemia unlike
sulfonylureas
 Nonsulfonylureas
 Alpha-glucosidase inhibitors
 Miglitol (Glyset), Acarbose (Precose)
 Alpha-glucosidase is an intestinal enzyme
that breaks down carbohydrates into glucose,
when this enzyme is inhibited, the process of
forming glucose is slowed and glucose is
absorbed more slowly from the small
intestine
 Taken 15 minutes before meal
  Overdose of
insulin,
omission of
meals,
Strenuous
exercise, G.I.
upset (N&V)
 Assessment:
 <60 mg/dl
 Simple Sugars p.o.
 3-4 oz regular soft-drink, 8 oz fruit juice, 5-7 pcs lifesaver’s
candies, 3-4 pcs hard candies, 1 tblsp sugar, 5 ml pure
honey/ karo syrup
 10-15 gm CHO
 D5W 20-50 ml IV push ( if unconscious) or 1 mg glucagon
 Monitor BS (blood sugar)
 Acute complication of DM characterized by
Hyperglycemia
 accumulation of ketones in the body; causes metabolic
acidosis
 frequently occurs in DM Type I (IDDM)
 Precipitating factors:
 undiagnosed diabetes
 neglect of treatment
 infection, cardiovascular disorder
 other physical or emotional stress
Assessment Findings:
3 P’s
 N&V, abdominal pain
 warm, dry, flushed skin
 dry mucous membranes; soft eyeballs
 Kussmaul’s respirations or tachypnea;
acetone breath or fruity breath
 Altered LOC
 Hypotension
 tachycardia
 Diagnostic Test:
 Serum glucose (up to 600 mg/dL) and ketones elevated
(positive urine ketones)
 BUN, Creatinine, Hematocrit are elevated (due to
dehydration)
 Serum sodium decreased, potassium (elevated due to the
acidosis)
 ABGs: metabolic acidosis with compensatory respiratory
alkalosis
 Maintain a patent airway.
 Maintain F&E balance.
 Administer IV therapy as ordered.
 Normal saline (0.9% NaCl), then hypotonic
(0.45% NaCl) sodium chloride
 When blood sugar drops to 250 mg/dl, may add
5% dextrose to IV
 Potassium will be added when the urine output
is adequate.
 Observe for fluid and electrolyte imbalances, especially
fluid overload, hypokalemia & hyperkalemia
 Administer insulin as ordered.
 ONLY Regular insulin is given IV (drip or push) and/or
subcutaneously (SC).
 If given IV drip, give with small amounts of albumin since
insulin adheres to IV tubing
 Monitor blood glucose levels frequently.
 Check urine output every hour
 Monitor vital signs
 Assist client with self-care
 Provide care for the unconscious client if in a coma
 Discuss with client the reasons ketosis developed
and provide additional diabetic teaching if indicated
 A complication of DM characterized by
 Hyperglycemia
 Hyperosmolar state without ketosis
 Occurs in Type II DM
 Precipitating factors are:
 undiagnosed diabetes
 Infections, major burns, other stress
 certain medications (Dilantin, Thiazide diuretics)
 Dialysis, Hyper-alimentation, pancreatic
disease
Assessment findings:
 Similar to ketoacidosis but without Kussmaul

respirations and acetone breath

Laboratory tests
 Blood glucose level extremely elevated
 BUN, creatinine, Hct elevated (due to dehydration)
 Urine positive for glucose

Nursing interventions
 treatment and nursing care is similar to DKA, excluding
measures to treat ketosis and metabolic acidosis
 Composed of ductless
glands that releases
hormones directly into
the bloodstream
 Hypothalamus control
most of the endocrinal
activity of the pituitary
gland
 Secretes RELEASING
HORMONES: GHRH,
CRH, TRH, GnRH, PRH
PITUITARY GLAND (HYPOPHYSIS)
Divided into 2 lobes:
 Anterior Pituitary (Adenohypophysis)
 70% of the gland
 Found in the sella turcica, a depression in the
sphenoid bone at the base of the brain
 Secretions: GH, PRL, ACTH, TSH, LH, FSH,
MSH
 Posterior Pituitary (Neurohypophysis)
 Stores & secretes ADH & Oxytocin produced by
the hypothalamus
 Disorders are generally grouped into:
 HYPER - when the gland secretes excessive
hormones
 HYPO - when the gland does not secrete
enough hormones
 Hyper and Hypo can be classified as:
 PRIMARY - when the Gland itself is the
problem
 SECONDARY - when the problem is the
pituitary or the hypothalamus
Growth hormone
(Somatotropin)
 Growth of body tissues
and bone
 Hyper-secretion:
 GIGANTISM
(children)
 ACROMEGALY
(adults)
 Hypo-secretion of GH:
Dwarfism
Prolactin (Mammotropic/
Lactotropic Hormone)
 Mammary tissue growth
and lactation.
 Hypersecretion:
 galactorrhea (abnormal
breast-milk production)
 Hypo-secretion:
 absence of milk during
lactation
ACTH (Adrenocorticotropic
Hormone)
 Stimulates adrenal cortex to

secrete the adrenal

hormones cortisol and
aldosterone
 Hyper-secretion:

 Cushing’s Syndrome
 Hypo-secretion:
 Addison’s Disease
TSH (Thyroid Stimulating
Hormone)
 Stimulates the
thyroid gland to
secrete T3 and T4
 Hyper-secretion:
 Hyperthyroidism
 Hypo-secretion:
 Hypothyroidism
Gonadotropin (FSH/ LH)
 Affect growth, maturity and functioning of primary

and secondary sex characteristics

 They influence the gonads (ovaries and testes) to

secrete gonadal hormones- estrogen, progesterone,

testosterone
 Hyper-secretion:

 precocious puberty
 Hypo-secretion
 Males: impotence,  production of spermatozoa
 Females: no ovulation, no menstruation, infertility
MSH (Melanocyte
Stimulating Hormone)
 Stimulates the skin

melanocytes to produce
the pigment melanin
 Hypersecretion:

 Bronze appearance of the

skin (hyperpigmentation)
 Hyposecretion:
 Albinism
(hypopigmentation)
ADH (Antidiuretic Hormone / Vasopressin)
 causes the renal retention of water (not affecting

sodium) in the renal tubules

 It can also cause vasoconstriction; “vasopressin”

 Hyper-secretion:

 SIADH - excessive retention of water by the renal tubules:

 Hypo-secretion:
 DI - inability of the renal tubules to retain water
 Diagnostic Test: Water deprivation test
Oxytocin
 released during

childbirth to cause
uterine contraction
 responsible for the

“let-down” reflex
of milk ejection
Hyperpituitarism
Hypopituitarism
 Hyperpituitarism
 Etiologic factors:
 Tumor and hyperplasia (Benign pituitary
adenoma, hyperplasia of pituitary tissue)
 Prolactinomas (prolactin-secreting tumors)
account for 60 to 80% of all pituitary tumors
 GH-producing adenomas
Hyperpituitarism
Assessment findings:
 Acromegaly
 gradual, marked enlargement
of the bones of the face, jaw,
hands and feet.
 Gigantism
 proportional overgrowth of all
body tissues with remarkable
height
Hyperpituitarism
Assessment findings:
 Neurologic manifestations

 Headache
 Somnolence, Behavioral changes, seizures
 Signs and symptoms of increased ICP
 Disturbance in appetite, sleep, temperature
regulation and emotional balance due to
hypothalamic involvement
 Visual disturbances due to the compression of
the optic chiasm above the pituitary gland:
 Hemianopsia or scotomas or blindness
Hyperpituitarism
Assessment findings:

SCOTOMA “blindspot in vision”

Hyperpituitarism
Assessment findings:
 Diagnostic tests:

 skull x-ray, CT scan,

MRI (tumor or
pituitary
enlargement)
 Plasma GH levels
determination:
increased
Hyperpituitarism
Medical Management:
 Surgery

 Removal of
pituitary gland
 Transphenoidal
hypophysectomy
 Radiation
Hyperpituitarism
Medical Management:
 Pharmacotherapy
 Bromocriptine (Parlodel)

 inhibit the synthesis of GH (acromegaly) &

prolactin
Hyperpituitarism
Nursing Management: Surgery
 Pre-operatively: Health Teaching

 explain to the patient that this surgery will

remove the tumor from the pituitary gland
 A nasal catheter and nasal packing are expected
in the nasal cavity for a day
 Indwelling catheter will be inserted (to monitor
UO) – Diabetes Insipidus can be a
complication of the surgery
 Review all patient’s medication regimen and
provide routine pre-op care
Hyperpituitarism
Nursing Management:
Surgery
 Post-operatively:

 Strictlykeep the
patient on BED rest
for 24° and encourage
ambulation on day 2
 position the patient
fowler’s to avoid
tension on the suture
line and to avoid
increased intracranial
pressure
Hyperpituitarism
Nursing Management: Surgery
 Post-operatively:

 Remind the patient NOT to

sneeze, forcefully cough,
bend over and blow the
nose for several days to
avoid disturbing the suture
lines
 Mild analgesic can be
given for headache
Hyperpituitarism
Nursing Management: Surgery
 Post-operatively:
 Anticipate the patient to manifest signs and symptoms of
DI after surgery
 Be alert for  thirst and  UO w/ low
SG
 Replace fluids and administer IV vasopressin as
ordered. DI should resolve in 72°
 Report outputs above 900 ml / 2 hours or specific
gravity below 1.004 (D. Insipidus)
Hyperpituitarism
Nursing Management: Surgery
 Post-operatively:

 Be alert for potential leakage

of CSF from the operative site
 If rhinorrhea is present, test
the discharge for glucose
and if positive, report to the
physician of the CSF leakage
Hyperpituitarism
Nursing Management:

 Provide safety measures because

pituitary tumor can cause visual
disturbances. Approach the
patient to the unaffected side if
he has hemianopsia.
Hypopituitarism
 Hypo-function of pituitary gland causing
deficiencies in both the pituitary hormones
and the hormones of the target glands
 Clinical manifestation:
 Observed when 75% of the pituitary gland is
dysfunctional
 Metabolic dysfunction
 Sexual immaturity
 Growth retardation
Hypopituitarism
 Absence of all pituitary secretions
 Panhypopituitarism (Simmond’s disease)
 Postpartum pituitary necrosis
 severe bleeding, hypovolemia and
hypotension at the time of delivery
 Sheehan’s syndrome
Hypopituitarism
Causes:
 Trauma
 Tumor
 Surgery /
radiation of
pituitary gland
 Congenital
Hypopituitarism
Assessment:
 Hemianopsia / headache (if due to tumor)
 Weight loss, emaciation
 Varying signs of hormonal disturbances
depending on which hormones are being
under-secreted
 menstrual dysfunction
 hypometabolism
 adrenal insufficiency
 growth retardation
Hypopituitarism
Diagnostic tests
 Skull x-ray, CT scan, MRI

(reveal pituitary tumor)

 Blood examination:

 plasma hormone
levels (depending on
specific hormones
under-secreted)
Hypopituitarism
Collaborative Management:
 specific treatment depends on cause

 Tumor: surgical removal or irradiation of

the gland
 Regardless of cause, treatment will include
replacement of deficient hormones (HRT):
 Corticosteroids
 Thyroid hormone
 Sex hormones, gonadotropins