ANTERIOR PITUITARY DISORDERS
HYPERPITUITARISM
• May be due to over activity of the gland
or the result of an adenoma
• Characterized by:
excessive serum concentration of
pituitary hormone ( GH, AGH, PRL)
morphologic and functional changes in
the anterior pituitary
• GROWTH HORMONE
HYPERSECRETION
• Gigantism – prior to closure of
epiphyses; proportional growth
• Acromegaly – after closure of the
epiphyses; disproportional growth
• CLINICAL MANIFESTATIONS:
Arthritis
Chest barreled shape
Rough facial features
Odd sensations: hands and feet
Muscle weakness & fatigue
Enlargement of organs
Growth of course hair
Amenorrhea; breast milk
production
Loss of vision; headaches
Impotence; increased
perspiration
Snoring
• Management:
o Medication: Bromocriptine
cabergoline
-dopamine agonist
GH
hypersecretion and
prolactinoma
Ocreotide
sematostatin
-GH
hypersecretion
o Radiation: Indicated for larger
tumors
o Surgery:
trans-sphenoidal
hypophysectomy
Medication: hormonal substitution
post-surgery nursing care ( maybe for life)
semi to high fowler’s Corticosteroids
position Levothyroxine
protect from infection Androgen/estrogen
and stressful situation Growth hormone
Hormone
replacement o Radiation: Indicated for larger
Constant neurologic tumors
checks o Surgery:
Monitor I&O to check trans-sphenoidal hypophysectomy
for diabetes Incipidus POSTERIOR PITUITARY DISORDERS
Encourage deep DIABETES INCIPIDUS
breathing but not coughing
• Characterized by massive polyuria due to
Institute measures to
either lack of ADH or rnal insensitivity
prevent constipation
• CENTRAL DI
Watch out for CSF
- due to deficiency in ADH production
leak
• NEPHROGENIC DI
HYPOPITUITARISM - due to defect in the kidney
tubules that interferes with H2O
• Deficiency of one or more anterior
pituitary hormones absorption
- polyuria is unresponsive to
• Causes:
Infections/inflammatory disorsers ADH, which is secreted normally
Autoimmune diseases • DIAGNOSTIC
Tumors Fluid deprivation test
Surgery/radiation theraphy Administration of desmopressin
SIMMOND’S DISEASE 24-h urine collection for volume, glucose
- Panhypopituitarism and creatinine
- Complete absence of Serum for glucose, urea, nitrogen, calcium,
pituitary hormones uric acid, potassium and sodium.
CACHEXIA • MANAGEMENT:
- most prominent feature CENTRAL DI
follows destruction of the Desmopressin, lypressin
pituitary by surgery, infection, (intranasal)
injury or tumor Vassopresine tannate in oil (IM)
SHEEHAN’S SYNDROME NEPHROGENIC DI
-post partum pituitary necrosis Indomethacin
- a complication of delivery -hydrochlorothiazide
results from severe blood loss and -desmopressin
hypovolemia -amiloride
• CLINICAL MANIFESTATIONS: Clofibrate chlorpropamide
HYPO-thermia, glycemia, tension
Loss of vision, strength, libido &
secondary sexual characteristics
• MANAGEMENT

SYNDROME OF INNAPROPRIATE ADH
• Disorder due to excessive ADH
release
• CLINICAL MANIFESTATION
Persistent excretion of concentrated
urine
Signs of fluid overload
Hyponatremia
LOC changes- increased ICP
• DIAGNOSTIC
Low serum sodium
Low serum osmolality
High urine osmolality
High urine sodium excretion
Normal renal function
• MANAGEMENT
Maintain fluid balance
MIOW
Fluid restriction
Loop diuretic
Lithium or democlocycline
Maintain Na balance
Increased Na intake
Emergency treatment of 3% NaCl
followed by furosimide
Excessive rapid correction of
hyponatremia: central pontine myelinolysis
THROID DISORDERS
• Function test
Fine needle aspiration biopsy
-Sampling of thyroid tissue to detect
malignancy. Initial test for evaluation of
thyroid masses
NURSING INTERVENTION
o Determine whether the patient has
taken medications or argents that
contains iodine because they may
alter the test results
o Assess allergy to iodine or shellfish
o For scans, tell patient that radiation
is only minimal
HYPERTHYROIDISM
• Increased basal metabolic rate
• CAUSES:
o Grave’s disease
o Initial manifestation of
thyroiditis
o TSH-screening pituitary
tumor
o Toxic adenoma
o Factitious thyrotoxicosis
o Amiodarone theraphy
CLINICAL MSNIFESTATION
o GI Hypermotility
o Rapid weight loss
o Apphrehension
o Volume deficit;voracious appetite
o Exopthalmos; erratic menses
o Systolic BP elevated;sweating
o TSH decreased in primary
disease
o Increased in secondary disease
TYROID STORM/ THYROTOXIC CRISIS
o Marked delirium
o Severe tachycardia
o Vomiting
o Diarrhea
o Dehydration
o High fever
-occurs in patient with exsisting but
unrecognized thyrotoxicosis, stressful
illness, thyroid surgery,RAI
Increased systemic adrenergic activity
severe hypermetabolism
MANAGEMENT
o Anti-thyroid drugs
o Prophylthiouracil (PTU);
methimazole
o Blocks thyroid hormones
synthesis
o Use for pregnant women and patients
who have refused surgery or RA1
treatment
o During pregnancy, PTU is DOC.
o 1% of infants born to mothers on
antithyroid theraphy will be hypothyroid
o WOF agranulocytosis
RAI (131I), K or Na iodide, SSKl (Lugol’s)
Adjuct to other anti-thyroid drugs in preparation
for thyroidectomy
Treatment for thyroroxic crisis
Inhibits release and synthesis of TH
MEDICATIONS:
Digitalis,proprandol (inderal)Phenobarbital
Well balance, high calorie diet with vitamin and
mineral supplement
Subtotal or total thyroidectomy
NURSING IMPLICATION
o NPO post midnight
o Initial dose:
o Urine and saliva slightly radioactive
o 24h vomitus highly radioactive x 6-8h
o Institute full radiation precations
o Instruct the patient to use appropriate
disposal methods when coughing and
expectorating
o Dilute oral doses in water or fruit juices
and give witm meals to prevent gastric
irritation
o LUGOL’s Solution
o Decreased vascularity of thyroid
gland
o Discoloration of the teeth provide
straw for the patient when drinking
o Encourage for increased H2O
intake
o May caused tyrotoxic crisis
HYPOTHYROIDISM
o State of low serum thyroid hormone in the
blood resistance to TH
Autoimmune
Developmental
 Dietary o Decreased all body function o Phenitoin or laxative abuse
Iodine o Decreased v/s CLINICAL MANIFESTATION
Oncologic o Precipitating Factors: o Constipation
Drugs induce Acute illness o Apathy
Iatrogenic Rapid withdrawal to medication o Lordosis
Nonthyroidal anesthesia o Cardiac dysthemia
Endocrine Thyroidectomy o Upset GI tract
o COMMON CAUSES: Opiod use o Low energy level Increased BP
o Autoimmune hypothyroiditis aka MANAGEMENT SYMPTOMS
hashimoto disease Prevention o Increased calcium
o Failure of the hypothalamus Prophylaxis o Increased parathyroid hormone
o Failure of the pituitary gland Hormonal replacement
MANAGEMENT
o Inborn errors of EH synthesis Levothyroxine (syncroid)
o Decreased calcium intake
o History of thyroidectomy Liothyronine (cytomel)
o Increased phosphorus intake
o Expose to radiation Liothrix (thyrolar)
Doses increased every 2-3 weeks o Calcitonin
o Antithyroid theraphy o Surgery to remove adenoma
o COMMON CAUSE: iron Watch out for:
o Chest pain o Furosemides
Deficiency o Biphosponates
CLASSIFICATIONS o Palpitation
o Profuse sweating HYPOPARATHYROIDISM
o CRETINISM – in infants and Auto immune
young children o Nervousness
o Drink meds at exact time each Injury to the parathyroid theraphy
o LYMPHOCYTIC Ischemic thyroid surgery
THYROIDITIS – self limiting day
CLINICAL MANIFESTATION
and appears after 6 yrs of o May develop insomia if taken at
Dypsnea, dysrrhytmia
age and peak during night
Extremities tingling
adolescent o Monitor bp and apical pulse
Fhotophobia
o HYPOTHYROIDISM W/O o If pulse morethan 100 bpm-stop Increased bone density
MYXEDEMA- mild thyroid NURSING IMPLICATION Cramps; chvostek sign
failure common in older o Low calorie Trousseau sign; tetany
children and adult o Warm environment MANAGEMENT
CLINICAL MANIFESTATION o Stool softener o IV calcium gluconate-drug of choice
Dry brittle hair, dry course skin o Maintain patent airway o Oral calcium salts
Edema in periorbital HYPERPARATHYROIDISM o Vit d supplementation
Reduce BMR Primary o Elevated serum phosphate
Apathy, anorexia, anemia o Single adenoma o Low calcium
Increased weight, intolerance to food o Genetic disorders
Lethargy, loss of libido o Trousseau & chvostek sign
o Multiple endocrine neoplasias o Elevated serum phosphate
Enlarged tongue Secondary
Drooling saliva o Low calcium
o Rickets
TSH increased in primary o Akalosis/arrhythmias
o Vit. D deficiency
Decreased in secondary o Narrowing of airways
o Chronic renal failure
MYXEDEMA COMA o Irritability
 o Cramps o Monitor Weight and glucose
o Parathormone injection o 24h urine specimen collection
o High calcium diet-spinach o Bronze skin discoloration
o Low phosphate o Avoid stress
PHEOCHROMOCYTOMA o Avoid contacts
Adrenal tumor CUSHING SYNDROME
Increased epinephrine and norepinephrine Enlargement of adrenal gland
Tumor in the adrenal corex which is Increased stimulation
responsible for the regulation of BP CLINICAL MANIFESTATION
Buffalo hump
CLINICAL MANIFESTATION Unusual behavior
Headache Facial features; moon facesfat; trunkal
Anxiety obesity
Nausea ACTH is elevated
Eye disturbances Loss of muscle mass
Sever hypertension Over extended skin
Dilate blood vessels by nitroprussside Hypertension, hypernatrimia
Monitor bp Urinary cortisol elevated
Monitor I & o Menstrual irregularity
Fluid replacement Pourosity of the bone
Decreased environment stimulation MANAGEMENT
Stress o Remove steroids
Maintain dosage of steroids o Irradiation
Follow up check up o Hypophesectomy
ADDISON’S DISEASE o Adrenalectomy
Hyposecretion of adenocortical hormones o DRUGS
Idiophatic atrophy o Cyproheptadine
SIGNS AND SYMPTOMS
(perjactine)
o Weakness
o Nysodrine
o Excess stress
o Aminoglutethamine
o Anorexia, vomiting, nausea
( cytadrin)
o Low sodium o Monitor V/S
o Decreased potassium o Monitor I & O
o Decreased bp o Stress reduction
MANAGEMENT
o Replacement of
hormones:hydrocortisone
o Increased carbohydrate and protein
o Potassium
o Sodium
o Monitor v/s 4x a day
o Monitor I & O