pituitary disorders

1. PITUITARY
DISORDERS
MS SAHELI CHAKRABORTY
1ST YEAR MSC NURSING
RAMAIAH INSTITUTE OF NURSING
BANGALORE

3. PITUITARY DISORDERS
 Pituitary disorders are conditions caused by too
much or too little of one or more of the hormones
produced by the pituitary gland and can produce a
variety of symptoms depending on which hormones
and target tissues are affected.

4. HYPOPITUITARISM
 Hypopituitarism is a rare disorder where there is a
loss of function in the pituitary and the failure to
secrete hormones that affect many of the body's
functions.
 Patients diagnosed with hypopituitarism may be
deficient in one or several hormones or have
complete pituitary failure.

5. ETIOLOGY
 Congenital
 Tumor
 Inflammation
 Infection
 Head injuries
 Lesions
 Surgery
 Tuberculosis
 Radiographic therapy

6. DWARFISM
 It is an endocrine disorder
resulting from hypo
secretion of growth
hormone during critical
development period in
children.
 The term ‘short stature’ or
little people is often used
too.

7. TYPES OF DWARFISM:-

9.  Lesion of the anterior pituitary due to infection or injury
results in hypo secretion of growth hormone.
 Genetic disorders.
 Hereditary.
 Lesion of hypothalamus resulting in hypo secretion of
growth hormone releasing factor.

10. CLINICAL FEATURES:
 Stunted physical and skeletal growth.
 The average height is 4 feet or less than that. But
dwarfism could apply to an adult who is less than 4 feet
10 inch height.
 Low blood glucose level.
 Developmental of gonads may be normal
 IQ may be normal.
DIAGNOSTIC EVALUATION:
 History collection.
 Physical examination.
 CT scan, MRI scan of brain.
 Blood test – to rule out hormone level.

11. MANAGEMENT

12. HYPERPITUITARISM
 Hyperpituitarism is the excessive production of growth
hormone.
 Hyperpituitarism is a chronic, progressive, disease
marked by hormonal dysfunction and startling skeletal
overgrowth.
 Hyperpituitarism appears in 2 forms-
1. Gigantism- affects infants and children.
2. Acromegaly- affects adults after epiphyseal closure.

13. GIGANTISM :-
 Pituitary gland secretes growth hormone (GH) which is
responsible for overall body development during
childhood.
 When too much growth hormone is secreted that
augments the growth of muscle, bones and connective
tissue in childhood or adolescence before the end of
puberty, the condition is called Gigantism.
 The result is an increase in height and formation of
additional soft tissues.
 Some individuals may achieve a height in excess of
eight feet.

14. ETIOLOGY
 In most of the cases, non-cancerous
pituitary gland tumour is behind gigantism.
 Genetic mutation.
 McCune-Albright syndrome is a disorder
that causes unusual growth of bone tissues,
gland irregularities and patches of light-
brown skin.
 Carney complex is a hereditary condition
which is cancerous or non-cancerous
endocrine tumours and spots of darker skin.
 Multiple endocrine neoplasia type 1 is also a
hereditary condition which cause tumours in
the pancreas, parathyroid glands and
pituitary gland.
 Neurofibromatosis is a hereditary disease
that causes tumours in the nervous system.

15. CLINICAL FEATURES:-
 Child will be much taller than other children of the same age.
 Parts of the body may be visibly bigger than other parts.
Common signs of gigantism include:-
 large hands and feet,
 Thick toes and fingers,
 A bulging jaw and forehead.
 Improper facial features.
 Children suffering from gigantism may also suffer from large
heads, lips, or tongues. The symptoms of gigantism depend on
the size of the pituitary gland tumour.
 Some children may experience vision problems, headaches and
nausea from tumour.

16. Other symptoms include:
 Large scale sweating
 Weakness
 Onset of puberty in boys and girls may be delayed
 Irregularity in menstrual cycle
 Deafness.

17. DIAGNOSTIC EVALUATION
 History collection.
 CT scan , MRI scan- to rule out pituitary tumour.
 Oral Glucose Tolerance Test- to rule out
hyperglycaemia.
 Blood test- to rule out growth hormone level, high
prolactin level, increase insulin level, growth factor -
1 levels.

18. MANAGEMENT :-
 Gigantism requires early detection and strong treatment to prevent
excess production of growth hormone and to improve life expectancy.
Surgery include-
 TRANSFENOIDAL ADENECTOMY,
 HYPOPHYSECTOMY
Surgery is the first line of treatment with the objective of
removing the tumour to minimize growth hormone levels and reduce
the pressure on the nerves.
 Radiation therapy is another option if surgery has not provided a
complete cure. It can take several years for radiation therapy to be
effective.
 Half of the patients achieve controlled growth hormone in 5-10 years.
 Though radiation therapy is successful in controlling tumour growth, it
may not reduce growth hormone and insulin-like growth factor 1 levels.

20.  Drug therapy may also be used in certain
circumstances. Drug therapy include:-
 Somatostatin analogs - reduces growth hormone
release.
 Pegvisomant-blocks the effects of growth hormone.
Drug therapy is used -
 Prior to surgery in order to control symptoms and cause
the tumour to shrink.
 Post surgery when growth hormone levels are not
managed.
 While radiation therapy is going on.
 Individuals not qualified for surgical process.
 Regular medical follow-up is required to scrutinize
growth hormone and insulin-like growth factor 1 to
notice any growth of the tumour.

21. ACROMEGALY
 Acromegaly is a chronic
metabolic disorder in
which there is a
secretion of too much
growth hormone and the
body tissues gradually
enlarge.
INCIDENCE:-
 It occurs in about 6 of
every 100,000 adults.
 Occurs in adulthood,
usually during middle
age.

22. ETIOLOGY :-
 Pituitary tumour.
 Benign tumour.
 Adenoma of the pituitary gland.
 Non pituitary tumour.
 Benign or cancerous tumour of the other part of the
body such as lungs, pancreas, adrenal glands.
Excess growth hormone and growth
hormone releasing factor in the blood leads to
changes in the physical appearance and functions
of body

23. SYMPTOMS:-
 Hand swelling , ‘ sausage like’ fingers.
 Increase in shoe size.
 Diaphoresis .
 Thickening of the facial features especial
nose.
 Increase prominence in the jaw and
forehead.
 Thickened skin.
 Swelling of tongue.
 Thickening or swelling of the neck.
 Arthritis .
 Sleep apnoea.
 Headache.
 Partial loss of vision. May occur one eye or
both the eyes.

24.  Pain , numbness, tingling or weakness in hands
and wrists.
 Increased thirst and urination.
 Hyperglycemia.
 Chest pain.
 Shortness of breath.
 Palpitation.
 Heart failure.
DIAGNOSTIC EVALUATION :-
 History collection.
 Physical examination.
 CT scan , MRI scan of head, chest, abdomen,
pelvis, adrenal glands, ovaries,

25. MANAGEMENT:-
 Goal of the treatment is
to relieve and reverse the
symptoms of acromegaly.
 Surgical treatment is the
first line treatment.
Surgery brings remission
and in some people, but
not all.
TRANSSPHENOIDAL
HYPOPHYSECTOMY

26.  Radiation therapy- is an option to reduce the size of the
tumour and hence reduce the production of growth
hormone.
 Radiation therapy focuses on high intensity radiation at
pituitary tumour to destroy the abnormal cells.
 Given in 2 forms. External beam and stereotactic.
 Drug therapy –
 Somatostatin analogs- reduces growth hormone release.
 Dopamine agonists- prevents the release of growth
hormone.
 Growth hormone receptor agonist eg Pegvisomant-
blocks the effects of growth hormone.

27. DIABETES
INSIPIDUS

29. DEFINITION :-
Diabetes insipidus is a disorder of the posterior
lobe of the pituitary gland characterized by a
deficiency of antidiuretic hormone (ADH), or
vasopressin. Great thirst (polydipsia) and large
volumes of dilute urine characterize the
disorder.

31. TYPES OF DI
A) Central diabetes insipidus
B) Nephrogenic diabetes insipidus
C) Psychogenic diabetes insipidus
D) Gestational diabetes insipidus.

32. CAUSES:-
A) Central diabetes insipidus :-
 Head trauma or surgery
 Pituitary or hypothalamic tumour
 Intracerebral occlusion or infection
B) Nephrogenic diabetes insipidus
 Systemic diseases involving the kidney
 Multiple myeloma
 sickle cell anemia
 Polycystic kidney disease
 Pyelonephritis
 Medications such as lithium

33. PATHOPHYSIOLOGY :-
A) Central diabetes insipidus :-
 Loss of vasopressin-producing cells,
 Causing deficiency in antidiuretic hormone (ADH)
 synthesis or release;
 Deficiency in ADH, resulting in an inability to conserve
water,
 leading to extreme polyuria and polydipsia
B) Nephrogenic diabetes insipidus
 Depression of aldosterone release or inability of the
nephrons to respond to ADH,
 causing extreme polyuria and polydipsia

34. SIGNS AND SYMPTOMS
 Polyuria with urine output of 5 to 15 L daily
 Polydipsia, especially a desire for cold fluids
 Marked dehydration, as evidenced by dry mucous
membranes, dry skin, and weight loss
 Anorexia and epigastric fullness
 Nocturia and related fatigue from interrupted sleep

35. DIAGNOSTIC TEST RESULTS
 High serum osmolality, usually above 300 mOsm/kg
of water
 Low urine osmolarity, usually 50 to 200 mOsm/kg of
water;
 low urine-specifi c gravity of less than 1.005
 Increased creatinine and blood urea nitrogen (BUN)
levels resulting from dehydration
 Positive response to water deprivation test: Urine
output decreases and specific gravity increases

36. MANAGEMENT :-
The objectives of therapy are
(1) to replace ADH (which is usually a long-term therapeutic
program),
(2) to ensure adequate fluid replacement, and
(3) to identify and correct the underlying cause.
Treatments
 Replacement of vasopressin therapy with intranasal or
I.V. DDAVP (desmopressin acetate).
 Correction of dehydration and electrolyte imbalances.
 A thiazide diuretic to deplete sodium and increase renal
water reabsorption.
 Restriction of salt and protein intake.

37. SIADH- SYNDROME OF INAPPROPRIATE ANTI
DIURETIC HORMONE.
 SIADH is a disorder of impaired water excretion
caused by the inability to suppress secretion or due
to excessive secretion and action of Antidiuretic
hormone .
 If water intake exceeds the reduced urine output
(concentrated Urine), the ensuing water retention
leads to the development of hyponatremia.
 Most common cause of HYPOOSMOLAR
EUVOLEMIC Hyponatremia.

38. ETIOLOGY:
 Neoplasms
 Carcinomas of
 Lung
 Duodenum
 Pancreas
 Ovary
 Bladder, ureter
 Other neoplasms
 Thymoma
 Mesothelioma
 Bronchial adenoma
 Carcinoid
 Gangliocytoma
 Ewing's sarcoma
 Head trauma (closed and
penetrating)
 Infections
 Pneumonia, bacterial or viral
 Abscess, lung or brain
 Cavitation (aspergillosis)
 Tuberculosis, lung or brain
 Meningitis, bacterial or viral
 Encephalitis
 AIDS
 Vascular
 Cerebrovascular occlusions,
 hemorrhage
 Cavernous sinus thrombosis
 Genetic
 X-linked recessive
 (V2 receptor gene)

39.  Drugs
 Vasopressin or desmopressin
 Chlorpropamide
 Oxytocin, high dose
 Vincristine
 Carbamazepine
 Nicotine
 Phenothiazines
 Cyclophosphamide
 Tricyclic antidepressants
 Monoamine oxidase inhibitors
 Serotonin reuptake inhibitors
 Congenital malformations
 Agenesis corpus callosum
 Cleft lip/palate
 Other midline defects
 Neurologic
 Guillain-Barré syndrome
 Multiple sclerosis
 Delirium tremens
 Amyotrophic lateral
sclerosis
 Hydrocephalus
 Psychosis
 Peripheral neuropathy

40. INVESTIGATIONS SENT FOR DIAGNOSIS
OF SIADH:
 Serum Na+, potassium, chloride, and bicarbonate
 Plasma osmolality
 Urine Sodium
 Urine osmolality
 Serum creatinine
 Blood urea nitrogen
 Blood glucose
 Serum uric acid
 Serum cortisol
 Thyroid-stimulating hormone

41. MANAGEMENT :-
 Fluid restriction — is a mainstay of therapy in most
 patients with SIADH, with a suggested goal intake of
lessthan 800 mL/day .
 The associated negative water balance initially raises
the Serum sodium concentration toward normal and,
with maintenance therapy in chronic SIADH, prevents a
further reduction in serum sodium.
 Intravenous saline — Severe, symptomatic, or
resistant hyponatremia in patients with SIADH often
requires the administration of sodium chloride.
 If the serum sodium concentration is to be elevated, the
electrolyte concentration of the fluid given must exceed
the electrolyte concentration of the urine, not simply
that of the plasma