ENDOCRINE SYSTEM

The endocrine
system integrates
body functions by
ENDOCRINE SYSTEM the synthesis and
release of hormones.
‹ The functions of the
endocrine and the
nervous system are
interrelated.
‹ Hypothalamus:
link between the
nervous system
and the endocrine
system.

ENDOCRINE GLANDS Endocrine System

‹ Pituitary ‹ Endocrine Glands
Gland • secrete their products directly into
‹ Adrenal the bloodstream
Glands • different from exocrine glands
‹ Pancreas • Exocrine glands: secrete through
‹ Thyroid
ducts onto epithelial surfaces or
into the gastrointestinal tract
Glands
‹ Parathyroid

Glands
‹ Gonads

Hormones Hypothalamus and

Pituitary Gland
‹ are chemical substances that are
secreted by the endocrine glands.
‹ can travel moderate to long
distances or very short distances.
‹ acts only on cells or tissues that
have receptors for the specific
hormone.
‹ Target Organ: The cell or tissue
that responds to a particular
hormone

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 Regulation of Hormones:
Negative Feedback Mechanism
‹ If the client is healthy, the
concentration or hormones is
maintained at a constant level.
‹ When the hormone concentration
rises, further production of that
hormone is inhibited.
‹ When the hormone concentration
falls, the rate of production of that
hormone increases.

Diseases of the Endocrine System

‹ Primary”
Primary” Disease Æ problem in
target gland; autonomous Disorders of the Anterior
Pituitary Gland
‹ “Secondary”
Secondary” disease Æ problem
outside the target gland; most often Hypopituitarism
due to a problem in pituitary gland Hyperpituitarism

Hypopituitarism Causes of Primary Hypopituitarism

‹ pituitary tumors
‹ Caused by low levels of one or more ‹ inadequate blood supply to pituitary
anterior pituitary hormones. gland
• e.g. Sheehan syndrome
‹ Lack of the hormone leads to loss of
‹ infections and/or inflammatory
function in the gland or organ that it diseases
controls. • sarcoidosis
• amyloidosis
‹ radiation therapy

‹ surgical removal of pituitary tissue

‹ autoimmune diseases

‹ congenital absence

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 Causes of secondary
hypopituitarism (affecting the Signs and Symptoms
hypothalamus):
‹ Tumor: bitemporal
hemianopia on
‹ tumors of the hypothalamus visual
‹ inflammatory disease confrontation
‹ head injuries ‹ Varying signs of
hormonal
‹ surgical damage to the pituitary
disturbances
and/or blood vessels or nerves depending on
leading to it which hormones
are being under
secreted

Signs and Symptoms Signs and Symptoms

Gonadotropin Deficiency
Thyroid-
Thyroid-stimulating (TSH)
‹
‹
• Congenital onset
‹ Delayed or absent secondary sexual
deficiency
characteristics • Causes hypothyroidism with
‹ May have micropenis, cryptorchidism manifestations such as fatigue,
• Acquired weakness, weight change, and
‹ Loss of body hair hyperlipidemia
‹ Infertility, decreased libido, impotence in
‹ Adrenocorticotropic hormone
males, amenorrhea in females
‹ Osteopenia, muscle atrophy
(ACTH) deficiency
• results in diminished cortisol secretion.
‹ Prolactin Deficiency
• Symptoms include weakness, fatigue,
• Failure to lactate
weight loss, and hypotension.

Signs and Symptoms Diagnostics

‹ Growth hormone ‹ X-ray, MRI or CT
(GH) deficiency scan: pituitary
• In childhood: failure tumor
to grow ‹ Plasma hormone
• In adulthood: mild levels: decreased
to moderate central
obesity,
obesity, increased
systolic blood
pressure, and
increases in LDL
cholesterol

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 Treatment
Hormonal Substitution: may be for life
‹
• Corticosteroids
• Levothyroxine
• Androgen for males
• Estrogen for females
• Growth hormone
‹ Radiation therapy for tumors
‹ Surgery for tumors: Transsphenoidal
hypophysectomy
Pituitary Tumor:
‹ Prolactinoma
Growth Hormone Hypersecretion
‹ Gigantism: GH ‹ Acromegaly: GH
hypersecretion
prior to closure of
epiphyses;
proportional
growth
Hyperpituitarism
‹ Hyperfunction of the anterior
pituitary gland Æ oversecretion of
one or more of the anterior
pituitary hormones
‹ Usually caused by a benign
pituitary adenoma
‹ 2 most common hormones
affected:
• Prolactin
• Growth hormone
Prolactinoma
‹ Female: galactorrhea
menstrual disturbances,
infertility, signs of estrogen
deficit (vaginal mucosal
atrophy, decreased vaginal
lubrication and libido)
‹ Male: Decreased libido and
possible impotence,
reduced sperm count and
‹ Somatotropinoma infertility, gynecomastia
Gigantism vs. Acromegaly
hypersecretion
after closure of
epiphyses;
disproportional
growth
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 Growth Hormone Hypersecretion:
Signs and symptoms
‹ Enlarged hand and feet; Carpal tunnel
syndrome common
‹ Coarsening of features esp. in
acromegaly; prominent mandible, tooth
spacing widens,
‹ Macroglossia Æ OSA
‹ Hypertension, cardiomegaly, heart failure
‹ Insulin resistanceÆ
resistanceÆ DM
‹ Visual field defects: bitemporal
hemianopsiaÆ
hemianopsiaÆcomplete blindess
‹ Headaches
‹ Arthritis
‹ Hypogonadism
Nursing Interventions
‹ Provide emotional supportÆ
supportÆ striking
body change can cause psychological
stress.
‹ Perform or assist with range-
range-of-
of-
motion exercises to promote
maximum joint mobility and prevent
injury.
‹ Evaluate muscle weakness, especially
in the patient with late-
late-stage
acromegaly.
‹ Keep the skin dry. Avoid using an oily
lotion because the skin is already oily.
Transsphenoidal hypophysectomy
Endoscopic, transnasal, transsphenoidal
pituitary microsurgery.
Removal of adenoma while preserving
anterior pituitary function in most patients.
Surgery is usually well tolerated, but
complication occur in about 10%
Treatment
‹ Medication
• Bromocriptine and cabergoline (dopamine
agonist) for prolactinoma and GH
hypersecretion
• Octreotide (somatostatin) for GH
hypersecretion
‹ Surgery
• Surgical remission is achieved in about 70% of
patients followed over 3 years.
• Growth hormone levels fall immediately;
diaphoresis and carpal tunnel syndrome often
improve within a day after surgery.
‹ Radiation Therapy for large tumors
‹ Diet
Nursing Interventions
‹ Be aware that pituitary tumor may cause visual
problems. If there is hemianopia, stand where he
can see you.
‹ Warn relatives that hyperpituitarism can cause
inexplicable mood changes
‹ If the patient is a child, explain to the parents
that surgery prevents permanent soft-soft-tissue
deformities but won’
won’t correct bone changes that
have already occurred.
‹ After an operation, emphasize the importance of
continuing hormone replacement therapy.
Postoperative Care
‹ WOF: Bleeding
• Operative site is patched with muscle or fat Æ
sutures easily disrupted
• Keep the patient on bed rest for 24 hours after
surgery and encourage ambulation thereafter
• Keep the head of bed elevated (300) to avoid
placing tension or pressure on the suture line.
• Instruct patient not to sneeze, cough, blow his
nose, or bend over for several days to avoid
disturbing the suture line.
• Arrange for visual field testing as soon as
possible because visual defects can indicate
hemorrhage
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 Postoperative Care
‹ WOF: CSF leak and infection ‹ WOF: Post-
• Reinforce measures to prevent increased
ICP
• Oral care, BUT the patient should not brush
his teeth for 2 weeks to avoid suture line
disruption
• Signs of CSF leak
‹ Frequent clearing of the throat and swallowing
‹ Presence of halo ring on gauze
‹ Test for glucose
Postoperative Care
Post-op pain
• Mild analgesics for headache caused
by CSF loss during surgery or for
paranasal pain.
• Paranasal pain typically subsides
when the catheters and packing are
removed, usually 24 to 72 hours after
surgery.

• Signs of infection
‹ Fever, headache, nuchal rigidity

Postoperative Care Postoperative Care

‹ WOF: Diabetes insipidus ‹ WOF: S/sx
S/sx of hypopituitarism
• Due inadequate release of ADH • Patient may need hormonal replacement
• usually happens 24 to 48 hours after therapy due to decreased pituitary secretion
of tropic hormones.
surgery and may resolve within 72
hours. • Necessary: cortisol immediate post-
post-op
• Be alert for increased thirst and • Maintenance hormonal replacement as
necessary
increased urine volume with a low
Cortisol
specific gravity. ‹

‹ Thyroxine
• Management ‹ Estrogen or testosterone

‹ I & O, urine sp.gr.

sp.gr. and daily weight ‹ Vasopressin
monitoring
‹ Fluid replacement

‹ aqueous vasopressin, sublingual

desmopressin acetate

Vasopressin or Antidiuretic
Hormone
‹ Regulates water
Disorders of the Posterior ‹
metabolism
Released during
Pituitary Gland stress or in response
to an increase in
plasma osmolality to
Diabetes Insipidus stimulate reabsorption
of water and
SIADH decreased urine
output

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 DIABETES INSIPIDUS DIABETES INSIPIDUS
‹ Central Diabetes Insipidus :
‹ Disorder characterized
Deficiency of vasopressin
by massive polyuria
• Primary diabetes insipidus (without an
due to either lack of identifiable organic lesion noted on MRI of
ADH or kidney’
kidney’s the pituitary and hypothalamus)
insensitivity to it ‹ May be familial, occurring as a dominant trait, or
sporadic (“
(“idiopathic”
idiopathic”).
‹ Types: • Secondary diabetes insipidus
• Central DI ‹ Due to damage to the hypothalamus or pituitary
stalk by tumor, anoxic encephalopathy, surgical
• Nephrogenic DI or accidental trauma, infection (encephalitis,
tuberculosis, syphilis), sarcoidosis, or multifocal
Langerhans cell (eosinophilic) granulomatosis
(“histiocytosis X”
X”).

DIABETES INSIPIDUS DIABETES INSIPIDUS

Signs and Symptoms
‹ “Nephrogenic”
Nephrogenic” ‹ Polyuria Æ enormous daily output of very
Diabetes Insipidus dilute, water-
water-like urine with a specific gravity
• Due to defect in the of 1.001 to 1.005
‹ Intense thirst (patient tends to drink 4 to 40
kidney tubules that
liters of fluid daily), especially with a craving
interferes with water for ice water,
reabsorption. ‹ Dehydration Æ weight loss, poor tissue turgor,
turgor,
• Polyuria is dry mucous membranes, constipation, muscle
unresponsive to weakness, dizziness.
‹ Inadequate water replacement results in
vasopressin.
• Hyperosmolality (irritability, mental
• Patients have normal dullness, coma, hyperthermia) because of
secretion of dehydration and hypernatremia
vasopressin • Hypovolemia (hypotension, tachycardia,
and shock eventually)

DIABETES INSIPIDUS DIABETES INSIPIDUS

Diagnostics Medications
‹ For central DI
‹ Fluid deprivation test Æ to differentiate
• Desmopressin (DDAVP): intranasal
between psychogenic polydipsia and DI • Lypressin: intranasal
‹ Administration of desmopressin Æ to • Vasopressin tannate in oil: IM
differentiate between central DI and ‹ For nephrogenic DI:
nephrogenic DI • Indomethacin-
Indomethacin-hydrochlorothiazide (with
potassium supplementation)
‹ 24-
24-hour urine collection for volume, • indomethacin-
indomethacin-desmopressin
glucose, and creatinine • indomethacin-
indomethacin-amiloride
‹ serum for glucose, urea nitrogen, ‹ Clofibrate, chlorpropamide and thiazide
calcium, uric acid, potassium and diuretics (mild DI)
sodium.
sodium. ‹ Psychotherapy

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 DIABETES INSIPIDUS: Nursing
Management
‹ Maintain fluid and sodium balance
• Record I and O. Weight patient daily.
• Maintain fluid intake to prevent severe
dehydration.
• WOF: Dehydration and shock
• Keep the side rails up and assist with
walking if the patient is dizzy or has muscle
weakness.
• Monitor urine specific gravity between
doses. Watch for decreased specific gravity
with increased urine output Æ need for the
next dose or a dosage increase.
DIABETES INSIPIDUS: Nursing
Management
• Add more bulk foods and fruit juices to
the diet Æ to prevent constipation.
Laxative (milk of magnesia) prn.
prn.
• Provide meticulous skin and
mouth care, and apply a lubricant
to cracked or sore lips.
• Diet: low in sodium
‹ Carry out drug therapy
• Caution must be used with
administration of vasopressin if
coronary artery disease is present Æ
causes vasoconstriction.
‹ Assist in searching for the underlying
pathology

Syndrome of Inappropriate Antidiuretic

Syndrome of Inappropriate
Hormone (SIADH): Causes of SIADH
Antidiuretic Hormone (SIADH)
‹ Tumors: bronchogenic carcinoma, lymphoma,
‹ Disorder due to pancreatic cancer, mesothelioma
excessive ADH release ‹ Pulmonary: TB, pneumonia, lung abscess,
‹ Signs and symptoms: COPD, pneumothorax, HIV infection
• Persistent excretion ‹ CNS: meningitis, head injury, subdural
of concentrated urine hematoma, subarachnoid hemorrhage,
• Signs of fluid neurosurgery
overload ‹ Drugs: Some medications (vincristine,
• Change in level of phenothiazines, tricyclic antidepressants,
consciousness thiazide diuretics, and others) and nicotine
• NO EDEMA have been implicated in SIADH; they either
• HYPONATREMIA directly stimulate the pituitary gland or
increase the sensitivity of renal tubules to
circulating ADH

Syndrome of Inappropriate
Syndrome of Inappropriate Antidiuretic
Antidiuretic Hormone (SIADH):
Diagnostic Tests
‹ low serum sodium (<135 meq/L0
‹ low serum osmolality
‹ high urine osmolality (urine
osmolality >100 mosmol/kg)
‹ high urine sodium excretion (>20
mmol/L)
‹ Normal renal function (low BUN <10
mg/dL), absence of hypothyroidism
and glucocorticoid deficiency and
recent diuretic therapy.
Hormone (SIADH): Management
‹ Maintain fluid balance
• Restriction of water intake (<1,000
ml/day).
‹ Takes 3-
3-10 days to work
• If the patient has evidence of fluid
overloading, a history of CHF, or is
resistant to treatment, loop diuretics
(Furosemide) may be added as well.
• Chronic treatment: lithium or
demeclocycline which inhibit ADH
action.
• Monitoring of body weight

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 Syndrome of Inappropriate Antidiuretic
Hormone: Management

‹ Maintain sodium balance

• Increase sodium intake
Disorders of the Adrenal
• If the serum sodium is below 120 or if the
patient is seizing, emergency treatment: Glands
3% NaCl.
NaCl. May be followed by furosemide.
• Excessively rapid correction of
hyponatremia may cause central pontine
myelinolysis. Cushing’
Cushing’s Syndrome
• Patients with a plasma sodium Hyperaldosteronism
concentration greater than 125 Adrenal Insufficiency
mmol/l rarely need specific therapy Pheochromocytoma
for hyponatremia.

Adrenal Cortex Hormones

‹ Glucocorticoids
• Cortisol, Corticosterone
‹ Increase blood glucose levels by
increasing rate of gluconeogenesis
‹ Increase protein catabolism

‹ Increase mobilization of fatty acids

‹ Promote sodium and water

retention
‹ Anti-
Anti-inflammatory effect
‹ Aid the body in coping with stress

Adrenal Cortex Hormones

‹ Mineralocorticoids
• Aldosterone, Corticosterone,
Deoxycorticosterone
• Regulate fluid and electrolyte balance
• Stimulate reabsorption of sodium, chloride and
water
• Stimulate potassium excretion
‹ Under the control of the Renin-
Renin-
Angiotensin-
Angiotensin-Aldosterone system

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 Summary: Adrenal Cortex
Adrenal Cortex Hormones
Hormones
‹ Sex Hormones ‹ Sugar
• Androgens, Estrogens ‹ Salt
• Influences the development of sexual
‹ Sex
characteristics

Hypercortisolism (Cushing’
(Cushing’s
Adrenal Medulla
Syndrome)
‹ Releases ¾ Cluster of physical
catecholamines abnormalities due to
• Epinephrine excessive cortisol release
• Norepinephrine ¾ Cortisol excess is due
‹ Released during either to:
“fight or flight”
flight” ¾ autonomous steroid release
situations Æ from adrenals
SYMPATHETIC ¾ Increased ACTH release from
effect pituitary
¾ complication of exogenous
steroid therapy

Hypercortisolism (Cushing’
(Cushing’s
Syndrome)
Altered metabolism of
‹ CHO: hyperglycemia
‹ CHON: muscle wasting, thin,
fragile skin, impaired wound
healing
‹ Fats: central obesity, moon face,
buffalo hump
‹ Na and water retention

‹ Hypokalemia, hypocalcemia

‹ Acne, hirsutism,
hirsutism, menstrual
changes, decreased libido
‹ Weakness, emotional lability

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 Complications Cushing’
Cushing’s Syndrome: Diagnostics
‹ ACTH Levels Æ determine whether the
‹ Osteoporosis syndrome is ACTH dependent
‹ Peptic Ulcer (from steroid intake) ‹ 24-
24-hr urine collection for cortisol, midnight
‹ Immune and inflammatory response is serum cortisol
also compromised ‹ Dexamethasone Suppression Test Æ 1 mg
dexamethasone given at 11 pm and serum
‹ Hypertension cortisol taken at 8 AM the next day
‹ Diabetes mellitus ‹ Cortisol level <5ug/dl excludes Cushing’
Cushing’s
‹ sexual and psychological complications syndrome with 98% certainty
‹ Radiologic evaluation
• tumor in the pituitary or adrenal gland

Cushing’s Syndrome : Nursing

Cushing’
Cushing’
Cushing’s Syndrome: Management
Considerations
‹ Transsphenoidal resection of pituitary ‹ Monitor VS, WOF for HPN
Safety Precaution:
tumor ‹
• Maintain Muscle tone
‹ Medications: • Prevent accidents or falls and provide adequate rest
‹ Protect client from exposure to infection, monitor
• Aminogluthetimide:
Aminogluthetimide: adrenal enzyme inhibitor WBC
• Metyrapone and ketokonazole:
ketokonazole: suppress ‹ Maintain skin integrity
hypercortisolism in unresectable adrenal tumor ‹ Minimize stress
‹ Antihypertensives ‹ Provide diet low in calories, sodium and high in
protein, potassium, calcium and vitamin D
‹ Adrenalectomy as needed ‹ Monitor for urine glucose and acetone, administer
insulin if necessary
‹ Prepare client for adrenalectomy if needed

Hyperaldosteronism Hyperaldosteronism : Causes

‹ hypersecretion of aldosterone from the
adrenal cortex
‹ Two types:
• primary disease of the adrenal cortex
• secondary condition due to increased
plasma renin activity
Primary hyperaldosteronism: Autonomous
secretion of aldosterone from adrenals
‹ Benign adrenal adenoma (Conn’
Conn’s syndrome)
‹ Bilateral adrenortical hyperplasia
Secondary hyperaldosteronism: High renin
stateÆ
stateÆ stimulating aldosterone release
‹ Renal artery stenosis

‹ Wilms’
Wilms’ tumor
‹ Causes:
‹ Pregnancy
• excessive reabsorption of sodium and water
‹ Oral contraceptive use
• excessive renal excretion of potassium
‹ Nephritic syndrome

‹ Cirrhosis with ascites

‹ Idiopathic edema

‹ Heart failure

‹ Extrarenal sodium loss

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 Hyperaldosteronism: Signs and
Symptoms
‹ Hypertension
• Headache and visual disturbance
‹ Hypokalemia
• Muscle weakness and Fatigue
• Paresthesia and Arrhythmias
• Polyuria and Polydipsia
• Tetany from alkalosis
‹ Hypernatremia
Hyperaldosteronism: Treatment
‹ Primary hyperaldosteronism:
• unilateral adrenalectomy
‹ After adrenalectomy, WOF:signs of
adrenal insufficiency
‹ potassium-
potassium-sparing diuretic (such as
spironolactone or amiloride)Æ
amiloride)Æ may lead to
decreased libido, gynecomastia, impotence
‹ antihypertensives
‹ aminogluthetimide Æ inhibits synthesis of
aldosterone.
‹ Diet: sodium restriction, increased potassium
‹ Treatment of secondary hyperaldosteronism:
include correction of the underlying cause.
Adrenal Insufficiency: Causes
‹ Autoimmune destruction of the adrenal gland,
tuberculosis, bilateral adrenalectomy,
hemorrhage into the adrenal gland, neoplasms,
or fungal infections
Secondary adrenal hypofunction is caused by
‹
• Hypopituitarism
• abrupt withdrawal of long-
long-term corticosteroid
therapy
In a patient with adrenal hypofunction, adrenal
‹
crisis occurs when the body’
body’s stores of
glucocorticoids are exhausted by trauma,
infection, surgery, or other physiologic stressors.
Hyperaldosteronism: Diagnostics
‹ Hypokalemia (<3.5 meq/L)
meq/L)
‹ Hypernatremia (>145 meq/L)
meq/L)
‹ Elevated serum bicarbonate and pH
‹ Hypomagnesemia
‹ Elevated plasma and urinary aldosterone
‹ ↓Renin in primary hyperaldosteronism
‹ ↑Renin in secondary hyperaldosteronism
‹ Low specific gravity urine (diluted urine)
Adrenal Insufficiency
‹ Addison’
Addison’s disease
• the most common form of adrenal hypofunction
• Autoimmune process, circulating antibodies react
specifically against the adrenal tissue
• Decreased secretion of androgen, glucocorticoids,
and mineralocorticoids.
• Symptoms occur when more than 90% of the
adrenal gland is destroyed.
‹ It may also be caused by a disorder outside
the gland, in which case aldosterone secretion
frequently continues.
‹ Acute adrenal insufficiency, or adrenal
crisis (Addisonian crisis), is a medical
emergency requiring immediate, vigorous
treatment.
Adrenal Insufficiency: Signs and
Symptoms
‹ Weakness, fatigue,
‹ weight loss, nausea and
vomiting, anorexia
‹ chronic constipation or diarrhea
‹ cardiovascular abnormalities
• postural hypotension,
decreased heart size and
cardiac output
• weak, irregular pulse
• decreased tolerance for even
minor stress
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 Adrenal Insufficiency: Signs and Adrenal Crisis
Symptoms Liver
Decrease in hepatic Hypoglycemia Profound
Hypoglycemia
‹ conspicuous bronze skin coloration, especially in Glucose output

hand creases and over the metacarpophalangeal Cortisol

Stomach
joints, elbows, and knees Absent or low
Decrease in Digestive
Vomiting, Cramps
And Diarrhea
Enzyme
‹ poor coordination
Brain
‹ fasting hypoglycemia; and craving for salty food. Adrenal Gland
Coma and Death

‹ Amenorrhea Destruction of
the adrenal cortex

‹ Adrenal crisis
Kidney
• profound weakness and fatigue, shock, severe Na and H2O loss with
K retention
nausea and vomiting, hypotension, Aldosterone Hypovolemia
dehydration and high fever. Absent or Low And
Hypotension
Shock

Heart
Arrhythmias and
Decrease CO

Adrenal Insufficiency: Diagnostic Adrenal Insufficiency: Treatment

tests ‹ Corticosteroid replacement, usually
‹ Decreased plasma cortisol and serum with cortisone or hydrocortisone Æ
sodium levels primary lifelong treatment
‹ Increased ACTH (in Addison’
Addison’s), ‹ Fludrocortisone acetate: acts as a
serum potassium, and blood urea mineralocorticoid to prevent
nitrogen level dehydration and hypotension.
‹ Adrenal crisis : prompt I.V. bolus

of corticosteroids, 3 to 5 L of
I.V.fluids,
I.V.fluids, dextrose

Adrenal Insufficiency: Nursing Adrenal Insufficiency: Nursing

Management Management
‹ WOF: adrenal crisis ‹ If patient has diabetes, check blood
• Hypotension and signs of shock glucose levels periodically because
(decreased level of consciousness and steroid replacement may necessitate
urine output). changing the insulin dosage.
• Watch for hyperkalemia before
treatment and for hypokalemia after
treatment (from excessive
mineralocorticoid effect).

13
 Adrenal Insufficiency: Nursing
Management
‹ Diet: maintain sodium and potassium
balance, high protein and
carbohydrates.
‹ If the patient is anorexic, suggest six
small meals per day to increase
calorie intake
‹ Observe the patient receiving
steroids for cushingoid signs, such as
fluid retention around the eyes and
face.
Adrenal Insufficiency: Nursing
Management
‹ Instruct on lifelong cortisone replacement
therapy: “Do not omit medications”
medications”. Give
2/3 of dose in AM and 1/3 in PM.
‹ Instruct the patient that he’
he’ll need to
increase the dosage during times of
stress.
‹ Warn that infection, injury, or profuse
sweating in hot weather may precipitate a
crisis.

Pheochromocytoma Pheochromocytoma
‹ Rare disorder, a chromaffin-
chromaffin-cell tumor of
the sympathetic nervous system, usually
in the adrenal medulla, secretes an excess
of the catecholamines epinephrine and
norepinephrine.
‹ This causes episodes of hypertension and
symptoms of catecholamine excess.
‹ The tumor is usually benign but may be
malignant in as many as 10% of patient.

Pheochromocytoma:
Signs and symptoms
‹ Think Sympathetic!!!
• persistent or paroxysmal hypertension
• palpitations, tachycardia, headache, visual
disturbances, diaphoresis, pallor, warmth or
flushing, paresthesia, tremor, and excitation
anxiety, fright, nervousness, feelings of
impending doom, abdominal or chest pain,
tachypnea, nausea and vomiting, fatigue,
weight loss, constipation, postural
hypotension, paradoxical response to
antihypertensives (common), hyperglycemia
Pheochromocytoma:
‹ Diagnostic tests:
• Increased plasma levels of
catecholamines, elevated blood sugar,
glucosuria
• Elevated urinary catecholamines and
urinary vanilylmandelic acid (VMA)
levels
‹ avoid coffee, nuts, chocolate, banana
• Tumor on CT scan

14
 Pheochromocytoma: Treatment ADRENALECTOMY
‹ Surgical removal of the tumor with
sparing of normal adrenals, if possible ‹ Resection or removal of one or both
• WOF: hypo or hypertension post-
post-op adrenal glands.
‹ Antihypertensives: ‹ The treatment of choice

• Alpha-
Alpha-adrenergic blocker • for adrenal hyperfunction and
(phentolamine, prazosin, or hyperaldosteronism
phenoxybenzamine) • adrenal tumors, such as adenomas and
• Beta-
Beta-adrenergic blocker (e.g
(e.g pheochromocytomas,
propranolol)
• Calcium channel blockers
‹ Metyrosine may be used to block
catecholamine synthesis

Adrenalectomy:
Adrenalectomy: Postoperative
Adrenalectomy: Pre-op
Care
‹ Correct electrolyte imbalance ‹ Monitor ABCs, vital signs
• Potassium, sodium, calcium ‹ Watch out for:
‹ Manage hypertension • shock from hemorrhage
• postoperative hypertension Æ
common because handling of the
adrenal glands stimulates
catecholamine release.

Adrenalectomy:
Adrenalectomy: Nursing interventions
‹ WOF: adrenal crisis
• Hypotension, hyponatremia, hypoglycemia,

‹
hyperkalemia
Remember, glucocorticoids from the
Disorders of the Thyroid
adrenal cortex are essential to life and
must be replaced to prevent adrenal Gland
crisis until the hypothalamic, pituitary,
and adrenal axis resumes functioning.
‹ Instruct the patient to take prescribed Hyperthyroidism
medication as directed.
‹ If patient had unilateral adrenalectomy, Hypothyroidism
explain that he may be able to taper his
medication in a few months,
‹ Inform patient that sudden withdrawal of
steroids can precipitate adrenal crisis

15
 The Thyroid Gland
‹ Thyroid gland is a butterfly-
butterfly-shaped organ
located in the lower neck anterior to the
trachea.
•It consists of two lateral
lobes connected by an
isthmus.
•The gland is about 5 cm
long and 3 cm wide and
weighs about 30 g.
•It produces three
hormones: thyroxine (T4)
and triiodothyronine
(T3), and calcitonin.
Tests of Thyroid Function
Thyroid-
Thyroid-Stimulating Hormone
‹ Single best screening test of thyroid function
because of its high sensitivity.
‹ Values above the normal range of 0.38 to 6.15
uU/mL are indicative of primary hypothyroidism,
and low values indicate hyperthyroidism
‹ If TSH is normal, there is a 98% chance that the
free thyroxine (FT4) is also normal.
‹ Used for monitoring thyroid hormone
replacement therapy and for differentiating
between disorders of the thyroid gland and
disorders of the pituitary or hypothalamus.
Tests of Thyroid Function
Thyroid scan, Radioscan, or Scintiscan
‹ In a thyroid scan, a scintillation detector or
gamma camera moves back and forth across the
area to be studied and a visual image is made of
the distribution of radioactivity in the area being
scanned.
‹ Isotopes used:
• 123I Æmost commonly used isotope,
• technetium-
technetium-99m pertechnetate, thallium, and
americium
‹ Scans are helpful in determining location, size,
shape, and anatomic function of the thyroid gland,
particularly when thyroid tissue is substernal or
large.
‹ Identifying areas of increased function (“(“hot”
hot”
areas) or decreased function (“ (“cold”
cold” areas) can
assist in diagnosis.
Function of Thyroid Hormones
T4 and T3
‹ Control the cellular metabolic activity.
‹ T4, a relatively weak hormone, maintains body
metabolism in a steady state.
‹ T3, is about five times as potent as T4 and has a more
rapid metabolic action.
‹ Accelerates metabolic processes.
‹ Influence cell replication and are important in brain
development.
‹ Necessary for normal growth.
‹ Controlled by TSH
Calcitonin
‹ Or thyrocalcitonin, secreted in response to high plasma
levels of calcium and it reduces the plasma level of
calcium by increasing its deposition in bone.
Tests of Thyroid Function
Serum Free Thyroxine
‹ Test used to confirm an abnormal TSH is FT4.
‹ FT4 is a direct measurement of free (unbound) thyroxine,
the only metabolically active fraction of T4.
‹ The range of FT4 in serum is normally between 0.9 and 1.7
ng/L (11.5 to 21.8 pmol/L).
Serum T3 and T4
‹ Normal range for T4 is between 4.5 and 11.5 ug/dL (58.5
to 150 nmol/L).
‹ Although serum T3 and T4 levels generally increase or
decrease together, the T3 level appears to be a more
accurate indicator of hyperthyroidism, which causes a
greater rise in T3 than T4 levels.
‹ Normal range for serum T3 is 70 to 220 ng/dL (1.15 to
3.10 nmol/L)
Tests of Thyroid Function
Radioactive Iodine Uptake
‹ Measures the rate of iodine uptake by the thyroid
gland.
‹ The patient is administered a tracer dose of
iodine-
iodine-123
‹ Measures the proportion of the administered dose
present in the thyroid gland at a specific time
after its administration.
‹ Affected by the patient’
patient’s intake of iodide or
thyroid hormone; therefore, a careful preliminary
clinical history is essential in evaluating results.
‹ hyperthyroidism Æ high uptake of the 123 I
‹ hypothyroidism Æ very low uptake.
16
 Tests of Thyroid Function Tests of Thyroid Function
Fine-
Fine-Needle Nursing Implications of Thyroid Tests
Aspiration ‹ It is necessary to determine whether the
Biopsy patient has taken medications or agents
‹ Sampling thyroid that contain iodine because these alter the
tissue to: detect results of some of the scheduled tests.
malignancy. ‹ Assess for allergy to iodine or shellfish
‹ Initial test for ‹ For the scans, tell patient that radiation is
evaluation of minimal
thyroid masses.

Hyperthyroidism: Signs and

Hyperthyroidism
symptoms
‹ Or Thyrotoxicosis ‹ Enlarged thyroid gland
‹ Increased metabolic rate ‹ Tachycardia Æ atrial fibrillation, heart
‹ Causes: failure
• Grave’
Grave’s disease ‹ Hypertension
• Initial manifestations of thyroiditis ‹ Heat intolerance, diaphoresis
(Hashimoto’
(Hashimoto’s and subacute thyroiditis) ‹ Smooth, soft, warm skin
• Toxic Adenoma ‹ Fine, soft hair
• TSH-
TSH-secreting pituitary tumor ‹ Diarrhea, weight loss inspite of increased
• Factitious thyrotoxicosis appetite
• Jodbasedow disease ‹ Nervousness and fine tremors of hands
• Amiodarone-
Amiodarone-induced ‹ Hyperactive reflexes, body weakness
‹ Personality changes, mood swings
‹ Osteoporosis
‹ Clubbing and swelling of fingers, Plummer’
Plummer’s
nails

Signs and symptoms of Grave’

Grave’s
Thyroid Storm
Disease
‹ A medical emergency : high
‹ All s/s of mortality
thyrotoxicosis ‹ Marked delirium, severe
tachycardia, vomiting, diarrhea,
‹ Grave’
Grave’s dehydration, high fever
exophthalmos Æ ‹ Occurs in patients with existing
vision loss, but unrecognized thyrotoxicosis,
diplopia stressful illness, thyroid surgery,
RAI administration
‹ Pretibial
‹ increased systemic adrenergic
myxedema activity Æ epinephrine
overproduction and severe
hypermetabolism

17
 Hyperthyroidism: Diagnostics
‹ Radioimmunoassay test shows
elevated T4 and T3.
‹ Thyroid scan reveals increased
radioactive iodine (123 I) uptake
‹ ↓TSH in Primary hyperthyroidism
‹ ↑ TSH in secondary hyperthyroidism
‹ Orbital sonography and computed
scan confirm subclinical
ophthalmopathy
Hyperthyroidism: Management
‹ Radioactive iodine (131 I), potassium or
sodium iodide (potassium iodide SSKI),
strong iodine solution (Lugol’
(Lugol’s solution)
‹ Adjunct with other antithyroid drugs in
preparation for thyroidectomy
‹ Treatment for thyrotoxic crisis
‹ Mechanism of action:
• Inhibits the release and synthesis of thyroid hormones
• Decreases the vascularity of the thyroid gland
• Decreases thyroidal uptake of radioactive iodine
following radiation emergencies or administration of
radioactive isotopes of iodine
Hyperthyroidism: Nursing
Management of RAI treatment
Radioactive iodine (sodium iodide or 131I
• Category X
‹ Food may delay absorption. The patient should
fast overnight before administration
‹ After dose for hyperthyroidism, the patient’
patient’s
urine and saliva are slightly radioactive for 24
hours; vomitus is highly radioactive for 6 to 8
hours.
‹ Institute full radiation precautions during this
time
‹ Instruct the patient to use appropriate disposal
methods when coughing and expectorating.
Hyperthyroidism: Management
Antithyroid drug therapy
‹ Propylthiouracil (PTU) and
methimazole
‹ Used for pregnant women and patient
who refuse surgery or 131I treatment.
‹ During pregnancy PTU, is the preferred
therapy
‹ A few (1%) of the infants born to
mothers receiving antithyroid
medication will be hypothyroid.
‹ Mechanism of action
• Blocks thyroid hormone synthesis
‹ WOF: Agranulocytosis
Hyperthyroidism: Nursing
Management
Potassium or sodium iodide, (potassium
iodide solution, SSKI), strong iodine
solution (Lugol’
(Lugol’s solution) Category D
‹ Dilute oral doses in water or fruit juice and give
with meals to prevent gastric irritation, to
hydrate the patient, and to mask the very salty
taste
‹ Warn the patient that sudden withdrawal may
precipitate thyrotoxicosis
‹ Store in a light-
light-resistant container
‹ Give iodides through a straw to avoid tooth
discoloration
‹ Force fluids to prevent fluid volume deficit
Hyperthyroidism: Nursing
Management of RAI treatment
) ‹ After dose for thyroid cancer, isolate the
patient and observe the following
precautions:
• Pregnant personnel shouldn’
shouldn’t take care
of the patient
• Disposable eating utensils and linens
should be used
• Instruct the patient to save all urine in
lead containers for 24 to 48 hours so
amount of radioactive material excreted
can be determined.
• Or flush the toilet twice after urination
18
 Hyperthyroidism: Nursing
Management of RAI treatment
• The patient should drink as much fluid
as possible for 48 hours after drug
administration to facilitate excretion.
• Limit contact with the patient to 30
minutes per shift per person the 1st
day; may increase time to 1 hour on
2nd day and longer on 3rd day.
Hyperthyroidism: Nursing
Management of RAI treatment
‹ If the patient is discharged less than
7 days after 131 I dose for thyroid
cancer, warn patient
• to avoid close, prolonged contact with
small children
• not to sleep in the same room with his
spouse for 7 days after treatment Æ
increased risk of thyroid cancer in
persons exposed to 131 I.

Hyperthyroidism: Management Hyperthyroidism: Management

Surgery: Thyroidectomy
‹ B-blockers, Digoxin, anticoagulation ‹ Preop:
Preop: give Lugol’
Lugol’s iodide to prevent thyroid
‹ Prednisone for ophthalmopathy storm
‹ Treatment for thyroid storm: ‹ Care of Post-
Post-thyroidectomy client
• Monitor for respiratory distress
• PTU • Have tracheotomy set, oxygen, and suction
• I.V. propranolol to block sympathetic effects at bedside
• Corticosteroids to replace depleted cortisol • Semi-
Semi-Fowler’
Fowler’s position
levels • Monitor for laryngeal nerve damage
(respiratory obstruction, dysphonia,
dysphonia, high-
high-
• Iodide to block release of thyroid hormone pitched voice, stridor, dysphagia,
restlessness)
• Monitor for signs of hypocalcemia and
tetany
‹ Prepare to administer calcium gluconate
or calcium chloride as prescribed for
t t

Hyperthyroidism: Nursing Hyperthyroidism: Nursing

Management
‹ Record vital signs and weight.
‹ Monitor serum electrolyte levels, and check
periodically for hyperglycemia and glycosuria.
‹ Monitor cardiac function.
‹ Check level of consciousness and urine output
‹ If patient is in her first trimester of pregnancy,
report signs of spontaneous abortion (spotting
and occasional mild cramps) to the doctor
immediately.
‹ Diet
• high protein, high calorie diet, with six meals per day
and vitamin supplements.
• Low sodium diet for the patients with edema.
• No stimulants like coffee, tea
Management
‹ For exophthalmos
• suggest sunglasses or eye patches to protect his
eyes from light
• Moisten the conjunctivae often with artificial tears
• Warn the patient with severe lid retraction to avoid
sudden physical movement that might cause the lid
to slip behind the eyeball.
• Elevate the head of the bed to reduce periorbital
edema
‹ Stress the importance of regular medical
follow-
follow-up after discharge because
hypothyroidism may develop from 2 to 4
weeks postoperatively.
‹ Drug therapy and 131 I therapy require careful
monitoring and comprehensive teaching.

19
 Hypothyroidism: Signs and
Hypothyroidism
symptoms
A state of low serum thyroid hormone levels
or cellular resistance to thyroid hormone, ‹ Weakness
Causes ‹ Fatigue
‹ may result from thyroidectomy ‹ Forgetfulness
‹ radiation therapy ‹ Cold intolerance
‹ chronic autoimmune thyroiditis (Hashimoto’
(Hashimoto’s ‹ Unexplained weight
disease) gain
‹ inflammatory conditions such as amyloidosis and ‹ Constipation
sarcoidosis ‹ Goiter
‹ pituitary failure to produce TSH ‹ Slow speech
‹ hypothalamic failure to produce thyrotropin-
thyrotropin-
releasing hormone (TRH). ‹ Decreasing mental
‹ Inborn errors of thyroid hormone synthesis
stability
‹ an inability to synthesize thyroid hormone because ‹ Cool, dry, coarse,
of iodine deficiency flaky, inelastic skin
‹ use of antithyroid medications such as
propylthiouracil.

Hypothyroidism: Signs and Myxedema Coma

symptoms
‹ Congenital
Hypothyroidism ‹ Manifests as hypotension,
‹ Puffy face, hands and
feet bradycardia, hypothermia,
‹ Dry, sparse hair hyponatremia, hypoglycemia,
Thick, brittle nails
respiratory failure, coma
‹

‹ Slow pulse rate

‹ Anorexia ‹ Can be precipitated by acute illness,
Abdominal distention
‹

‹ Menorrhagia
rapid withdrawal of thyroid
‹ Decreased libido medication, anesthesia, surgery,
‹ Infertility hypothermia, use of opioids
‹ Ataxia
‹ Intention tremor

Hypothyroidism: Diagnostics Management

‹ Radioimmunoassay tests: ↓ T3, T4
‹ ↑TSH level with primary hypothyroidism
‹ ↓ TSH in secondary hypothyroidism
‹ Serum cholesterol and triglyceride levels
are increased
In myxedema coma
‹
• low serum sodium levels
• respiratory acidosis because of hypoventilation
Prevention: Prophylactic iodine
supplements to decrease the
incidence of iodine deficient goiter
Symptomatic Cases:
‹ Hormonal replacement: Synthroid
(synthetic hormone (levothyroxine))
• Dosage is increased q 2-2-3 weeks esp. if
the patient is an elderly

20
 Nursing Management of Nursing Management of
replacement therapy replacement therapy
‹ Different brands of levothyroxine may not be
‹ Instruct the patient to take thyroid
bioequivalent. hormones at the same time each day to
• After the patient’
patient’s condition has been stabilized on maintain constant hormone levels.
one brand, warn patient not to switch to another, as
this may affect drug bioavailability. Avoid generic ‹ Suggest a morning dosage to prevent
levothyroxine.
insomnia
‹ Warn the patient (especially the elderly) to
tell the doctor if with ‹ Monitor apical pulse and blood pressure.
• chest pain, palpitations, sweating, If pulse is >100 bpm, withhold the drug.
nervousness, or other signs or symptoms Assess for tachyarrhythmias and chest
of overdosage pain.
• signs and symptoms of aggravated
cardiovascular disease (chest pain,
dyspnea, and tachycardia).

Nursing Management of Hypothyroidism:

Hypothyroidism: Nursing
replacement therapy Interventions
Diet: high-
high-bulk, low-
low-calorie diet
Thyroid hormones alter thyroid function
‹
‹
‹ Encourage activity
test results. ‹ Maintain warm environment
• For 123I uptake studies ‹ Administer cathartics and stool softeners, as
• D/C levothyroxine 4 weeks before the test. needed.
‹ To prevent myxedema coma, coma, tell the patient
• D/C liothyronine 7 to 10 days before the test. to continue his course of thyroid medication
‹ Monitor prothrombin time; a patient even if his symptoms subside.
• maintain patent airway
taking these hormones usually requires
• administer medications – Synthroid,
Synthroid,
less anticoagulant. glucose, corticosteroids
• WOF: unusual bleeding and bruising • IV fluid replacement
• Wrap patient in blanket
• Treat infection or any underlying
illness

Hyperaparathyroidism Hyperaparathyroidism: Causes

‹ Characterized by ‹ Primary hyperparathyroidism:
excess activity or
one or more of the • single adenoma, genetic disorders, or
four parathyroid multiple endocrine neoplasias.
glands, resulting in ‹ Secondary hyperparathyroidism:
excessive secretion
of parathyroid • rickets, vitamin D deficiency, chronic
hormone (PTH). renal failure, or phenytoin or laxative
‹ May be primary or abuse.
secondary.

21
 Hyperaparathyroidism:
Hyperaparathyroidism
Signs and symptoms
‹ Effect of PTH secretion: ↑Calcium Think of Hypercalcemia:
• Through increased bone resorption, increased ‹ CNS: psychomotor and
GI and renal absorption of calcium personality disturbances, loss of
‹ Complications memory for recent event,
• renal calculi Æ renal failure depression, overt psychosis,
• Osteoporosis
stupor and, possibly, coma.
‹ GI: anorexia, nausea, vomiting,
• Pancreatitis
• peptic ulcer
dyspepsia, and constipation.
‹ Neuromuscular: fatigue; marked
muscle weakness and atrophy,
particularly in the legs.

Hyperaparathyroidism: Hyperaparathyroidism:
Signs and symptoms Diagnostics
Renal: symptoms of recurring
↑serum PTH levels
‹
nephrolithiasis Æ renal insufficiency ‹

‹ Skeletal and articular: chronic lower ‹ Increased serum calcium

back pain and easy fracturing from and decreased phosphorus
bone degeneration, bone tenderness, levels
joint pain
‹ X-rays may show diffuse
Others: skin pruritus, vision
‹
impairment from cataracts,
demineralization of bones
subcutaneous calcification. ‹ Elevated Alkaline
phosphatase

Hyperaparathyroidism: Treatment
Hypoparathyroidism
‹ Surgery to remove the adenoma
‹ Force fluids; limiting dietary calcium ‹ A deficiency of parathyroid hormone
intake
(PTH).
‹ For life threatening hypercalcemia:
promote sodium and calcium ‹ PTH primarily regulates calcium
excretion, using normal saline
solution (up to 6 L in life-
life-threatening balance; hypoparathyroidism leads
situations), furosemide; and to hypocalcemia and produces
administering oral sodium or neuromuscular symptoms ranging
potassium phosphate, Calcitonin
‹ Postmenopausal women: estrogen from paresthesia to tetany.
supplements

22
 Hypoparathyroidism: Causes Hypoparathyroidism: Signs and
symptoms
‹ Congenital absence or malfunction of the
parathyroid glands ‹ Neuromuscular irritability
‹ Increased deep tendon reflexes, positive Chvostek’
Chvostek’s and
‹ autoimmune destruction Trousseau’
Trousseau’s signs
‹ removal of or injury to one or more ‹ Dysphagia
parathyroid glands during neck surgery ‹ Paresthesia
Psychosis
rarely, from massive thyroid radiation therapy.
‹
‹
‹ Mental deficiency in children
‹ Ischemic infarction of the parathyroids during ‹ Tetany seizures
surgery ‹ Arrhythmias
‹ diseases, such as amyloidosis or neoplasms ‹ Abdominal pain
‹ Dry, lusterless hair, spontaneous hair loss
‹ suppression of normal gland function caused ‹ Brittle fingernails that develop ridges or fall out.
by hypercalcemia (reversible) ‹ Dry and scaly skin
‹ hypomagnesemia-
hypomagnesemia-induced impairment of ‹ Weakened tooth enamel may cause teeth to stain, crack,
hormone secretion (reversible). and decay easily

Hypoparathyroidism: Diagnostic
Hypoparathyroidism: Treatment
tests
‹ Vitamin D with supplemental calcium
‹ Decreased PTH and serum calcium ‹ Lifelong therapy, except for patient with
the reversible form of the disease.
levels
‹ Acute life-
life-threatenting tetany calls for
‹ Elevated serum phosphorus levels
immediate I.V. administration of calcium
‹ X-rays reveal increased bone density ‹ Sedatives and anticonvulsants are given
‹ ECG: prolonged QTi,
QTi, QRS-
QRS-complex to control spasms until calcium levels rise.
and ST-
ST-elevation changes ‹ Seizure precautions

Hormones of the Pancreas

‹ Insulin
• Decreases blood sugar by:
Disorders of the Pancreas ‹ Stimulating active transport of glucose
into muscle and adipose tissue
‹ Promoting the conversion of glucose to
glycogen for storage
‹ Promoting conversion of fatty acids into
Diabetes Mellitus fat
‹ Stimulating protein synthesis

• Secreted in response to high blood

sugar
• Found in β cells of the Islets of
Langerhans

23
 Hormones of the Pancreas
‹ Glucagon
• Increases blood glucose by
‹ causing gluconeogenesis and glycogenolysis
in the liver
• Secreted in response to low blood sugar
• Found in the α-cells of the Islets of
Langerhans
Diabetes Mellitus
‹ Chronic disease characterized by
hyperglycemia
‹ It is due to total or partial insulin
deficiency or insensitivity of the cells
to insulin
‹ Characterized by disorders in the
metabolism of CHO, FAT and CHON
as well as changes in the structure
and function of blood vessels

Types of DM Pathophysiology
‹ Type 1 or IDDM ‹ Lack of insulin causes hyperglycemia
• Usually occurs in children or in non-
non-obese (insulin is necessary for the transport
adults
of glucose across the membrane)
‹ Type 2 or NIDDM
‹ Body excretes excess glucose
• Usually occurs in obese adults over age 40
‹ Gestational DM through kidneys Æ osmotic diuresis
‹ Secondary DM
Æ polyuria Æ dehydration Æ
• Induced by trauma, surgery, pancreatic
polydipsia
disease or medications ‹ Cellular starvation Æ polyphagia
• Can be treated as either type 1or type 2

Cont. Pathophysiology Chronic Complications

‹ Microangiopathy:
Microangiopathy: retinopathy,
‹ The body turns to fats and protein nephropathy
for energy; but in the absence of ‹ Macroangiopathy:
Macroangiopathy: peripheral
glucose in the cell, fats cannot be vascular disease, atherosclerosis,
completely metabolized and ketones CAD
are produced
‹ Neuropathy

24
Instruction in the Care of the Feet
Hygiene of the feet
‹ Wash feet daily with mild soap and
lukewarm water. Dry thoroughly
between the toes by pressure. Do
not rub vigorously, as this is apt to
break the delicate skin.
‹ Rub well with vegetable oil to keep
them soft, prevent excess friction,
remove scales, and prevent
dryness.
‹ If the feet become too soft and
tender, rub them with alcohol about
once a week.
Instruction in the Care of the Feet
Hygiene of the feet
‹ When rubbing the feet, always rub upward
from the tips of the toes. If varicose veins
are present, massage the feet very gently;
never massage the legs.
‹ If the toenails are brittle and dry, soften them
by soaking for 11/2 hour each night in
lukewarm water containing 1 tbsp of
powdered sodium borate (borax) per quart.
Clean around the nails with an orangewood
stick. If the nails become too long, file them
with an emery board. File them straight
across and no shorter than the underlying
soft tissue of the toes. Never cut the corners
of the nails.

Instruction in the Care of the Feet Instruction in the Care of the Feet

‹ Wear low-
low-heeled shoes of soft leather
that fit the shape of the feet correctly.
The shoes should have wide toes that
will cause no pressure, fit close in the
arch, and grip the heels snugly. Wear
new shoes one-
one-half hour only on the
first day and increase by 1 hour each
day following. Wear thick, warm, loose
stockings.
Treatment of Corns and Calluses
‹ Corns and calluses are due to friction
and pressure, most often from
improperly fitted shoes and stockings.
Wear shoes that fit properly and cause
no friction or pressure.
‹ To remove excess calluses or corns, soak the
feet in lukewarm (not hot) water, using a mild
soap, for about 10 minutes and then rub off
the excess tissue with a towel or file. Do not
tear it off. Under no circumstances must the
skin become irritated.
‹ Do not cut corns or calluses. If they need
attention it is safer to see a podiatrist.
‹ prevent callus formation under the ball of the
foot (a) by exercise, such as curling and
stretching the toes several times a day; (b) by
finishing each step on the toes and not on the
ball of the foot; and (c) by wearing shoes that
are not too short and that do not have high
heels.

Diagnostics: Glycosylated
Diagnostics: FBS and OGTT
hemoglobin
Normal Impaired Diabetes
‹NV= 7.5% or less, good control
glucose glucose Mellitus
tolerance tolerance ‹ 7.6% -- 8.9% fair control
Fasting <110 110-
110-125 > 126 ‹ 9% or greater, poor control
Plasma mg/dl mg/dl mg/dl
Glucose
2 hours < 140 > 140 > 200
after mg/dl but < mg/dl
glucose 200

25
 Therapeutic interventions:
ƒ Life-
Life-style changes
• Weight control and Exercises
• Planned diet
‹ 50 – 60 % of calories are complex
carbohydrates, high fiber
‹ 12 -20 % of daily calories is protein, 60 –
85 g/day
‹ Fat intake not to exceed 30% of daily
calories, more of
polyunsaturated/monounsaturated fats
‹ Basic tools: food exchange groups, using
the exchange system of dietary control,
food composition tables
• Self-
Self-monitoring of blood glucose
Cont. Therapeutic interventions:
‹ Insulin Administration
• For type 1 IDDM and type 2 DM when diet
and weight control therapy failed
• Aspirin, alcohol, oral anticoagulants, oral
hypoglycemics, beta blockers, tricyclic
antidepressants, tetracycline, MAOIs
increase the hypoglycemic effect of
insulin
• Glucocorticoids, thiazide diuretics, thyroid
agents, oral contraceptives increase blood
glucose level
• Illness, infection, and stress increase the
need for insulin

Insulin Onset Peak Duration

Ultra rapid
10 - 15 min 1 hour 3 hours Complications of insulin therapy
Acting
Insulin analog
(Humalog)
Humalog) ‹ Local allergic reaction, lipodystrophy,
SAI
Insulin resistance
½-1 hr 2-4 hrs 4-6 hours ‹ Dawn phenomenon
(Humulin regular)

IAI
• increase in blood sugar because of
3-4 hrs 4-12 hrs 16-
16-20 hrs release of growth hormone at around 3
(Humulin lente,
lente,
Humulin NPH) AM;
• Tx:
Tx: give at 10 pm, intermediate-
intermediate-acting
LAI
6-8 hrs 12-
12-16 20-
20-30 insulin
(Protamine Zinc,
Humulin hrs hours ‹ Somogy effect
Ultralente)
Ultralente) • rebound hyperglycemia at 7 am after a
Premixed Insulin bout of hypoglycemia at around 2-2-3 AM.
½-1 hour 2-12 hrs 18-
18-24 hrs
(70% NPH, 30% Tx:
Tx: decrease the evening dose of
Regular) intermediate-
intermediate-acting insulin

Complications of insulin therapy Oral Hypoglycemic Agents

Hypoglycemia
ƒ If awake, give 10-
10-15 g of fast-
fast-acting ‹ For DM type 2
simple carbohydrate (glucose tablets, ‹ May have to be shifted to insulin
fruit juice, and soda).
when sick, under stress, during
ƒ If unconscious, glucagon SQ or IM.
surgery.
ƒ If in the hospital, 25-
25-50 cc of D50%.
‹ Necessary to shift to insulin when

pregnant.

26
 ORAL HYPOGLYCEMICS
ORAL HYPOGLYCEMICS
‹ Sulfonylureas ‹ Biguanides
• promotes inc. insulin secretion from
pancreatic beta cells through direct • reduces hepatic production of
stimulation (requires at least 30 % glucose by inhibiting glycogenolysis
normally functioning beta cells)
• First-
First-Generation Agents: • decrease the intestinal absorption
‹ Tolbutamide,
Tolbutamide, Acetohexamide,
Acetohexamide, of glucose and improving lipid
Tolazamide,
Tolazamide, Chlorpropamide profile
• Second-
Second-Generation Agents
‹ Glypizide,
Glypizide, Glyburide • Agents
‹ Phenformin , Metformin , Buformin

ORAL HYPOGLYCEMICS ORAL HYPOGLYCEMICS

‹ Alpha-
Alpha-glucosidase inhibitors
‹ Thiazolidinediones
• Inhibits alpha-
alpha-glucosidase enzymes
in the small intestine and alpha • Enhances insulin action at the cell
amylase in the pancreas and post-
post-receptor site and
decreasing insulin resistance
• Decrease rate of complex
carbohydrate metabolism resulting • Agents
to a reduced rate postprandially.
postprandially. ‹ Pioglitazone (Actos),
Actos),
• Agents Rosiglitazone (Avandia)
Avandia)
‹ Acarbose (precose),
precose), Miglitol (glyset)
glyset)

Acute Complication: DKA DKA: Signs and Symptoms

‹ Characterized by hyperglycemia and
accumulation of ketones in the body
causing metabolic acidosis
‹ Occurs in Insulin-
Insulin-Dependent Diabetic
Client
‹ Precipitating Factors: Undiagnosed
diabetes, neglect of treatment,
infection, other physical or emotional
stress
‹ Onset slow, maybe hours to days
‹ Polydipsia, polyphagia and polyuria
‹ Nausea and Vomiting, Abdominal pain
‹ Skin warm, dry and flushed
‹ Dry mucous membrane
‹ Kussmaul’
Kussmaul’s respirations or
hyperventilation; acetone breath
‹ Alterations in LOC
‹ Hypotension, tachycardia

27
 Hyperglycemic Hyperosmolar
Nonketotic Coma (HHNK)
‹ characterized by hyperglycemia and
a hyperosmolar state without ketosis
‹ Occurs in NIDDM or non-
non-diabetic
persons (typically elderly persons)
‹ Precipitating factors: undiagnosed
diabetes, infection or other stress;
certain medications, dialysis,
hyperalimentation,
hyperalimentation, major burns
Emergency Management:
‹ For both DKA and HHNK, treat
dehydration first with 0.9% or 0.45%
saline.
• Shift to D5W when glucose level is down
to 250-
250-300 mg/dl.
• WOF too rapid correction, it can cause
rapid fluid shifts (brain edema and
increased ICP, ARDS)
‹ IV Regular Insulin 0.1 unit/kg bolus and
then 0.1 u/k/h drip
‹ Correcting electrolyte imbalance. Watch
out for hypokalemia as a result of
treatment. For severe acidosis (pH < 7.1),
DKA patients may have to be given
NaHCO3.
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