Anatomy of pituitary glands,its secretions and disorders due to its imbalance. Adrenal gland anatomy,its secretions and tumors of adrenal gland and disorders associated with it.

1. PITUITARY
DISORDERS
&
ADRENAL TUMORS
 Anita ma’am
 Faculty of C.O.N
 VMMC &
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 Sirsha De
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2. Pituitary gland is referred to as the
master gland because of the
influence it has on secretions of
hormones by other endocrine
gland.

7. CAUSES OF DISORDER OF
PITUITARY GLAND
Mainly of 2 reasons:
 Hyperactivity
 Hypoactivity

9. HYPERPITUITARISM
(HYPERACTIVITY)
 Having an overactive pituitary gland is called hyperpituitarism.
 Most commonly caused by noncancerous tumors.
 This causes gland to secrete too much of certain kinds of
hormones related to growth,reproduction and metabolism.
DISORDERS CAUSED :
 Gigantism
 Acromegaly
 Acromegalic gigantism
 Cushing syndrome

10. GIGANTISM

11.  Pituitary gland secretes growth hormone,which is responsible
for overall growth and development of human body 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 the puberty, this condition is
called Gigantism.
 The result is an increase in height and formation of additional
soft tissues.
Characterized by :
• Excess growth of body(sometimes more in trunk and limbs).
• Average height is approximately 7-8 feet.

12. ETIOLOGY
In most of the cases,non cancerous pituitary gland tumor is
caused due to gigantism.
 Mc Cune-Albright syndrome is a disorder that causes
unusual growth of bone tissues, gland irregularities and
patches of light and brown skin.

13.  Carney complex is a rare hereditary condition which is
characterised by multiple benign tumors most often
affecting heart,skin and endocrine system and
abnormalities in skin pigmentation resulting in spotty
appearance to the skin of affected areas.

14.  Multiple Endocrine Neoplasia Type1 is also a
hereditary condition which cause tumors in the
pancreas,parathyroid glands and pituitary gland.
 Neurofibrinomatosis is a hereditary disease that
causes tumors in nervous system.

15. CLINICAL FEATURES
Child will be much taller than other children of the same age.Parts of body may be
visibly bigger than others.
1. Large hand and feet
2. Thick toes and fingers
3. A bulging jaw and forehead
4. Improper facial features
5. Children suffering from gigantism may show large heads,lips or tongue.
6. Some may experience vision problems, headaches and nausea from tumors.
7. Onset of puberty in children may be delayed.
8. Irregularities in menstrual cycle
9. Deafness
The symptoms of gigantism depend on the size of pituitary gland tumors.

16. DIAGNOSTIC EVALUATION
 History collection
 CT scan
 MRI scan (to rule out pituitary tumor)
 Oral Glucose Tolerance Test (to rule out hyperglycemia)
 Blood test (to rule out growth hormone level,high prolactin
level, increase in insulin level& growth factors)

17. MANAGEMENT
 Gigantism requires early detection & strong treatment to prevent
excess production of growth hormone and to improve life
expectancy.
 Surgeries include-
 Transfenoidal Adenomectomy
 Hypophysectomy
Surgery is the first line of treatment with the objective of removing
the tumor to minimize growth hormone levels & reduce the
pressure on the nerves.
 Radiation Therapy is another option if surgery cannot be
implemented. Radiation therapy can take several years.
 ½ of the clients get controlled growth hormone in 5-10 years.

18. ACROMEGALY

19. Acromegaly is a chronic metabolic disorder in which there is a
secretion of too much growth hormone & the body tissues
gradually enlarge.
ETIOLOGY:
 Pituitary tumors Benign tumor,adenoma of pituitary gland
 Non Pituitary tumors Benign or cancerous tumor of the
other part of body such as lungs,pancreas,adrenal
glands.
 Excess growth hormone & growth hormone releasing factors in the
blood levels results in changes in the appearance & functions of the
body.

20. SYMPTOMS
 Hand swelling,sausage like fingers
 Increase in shoe size
 Diaphoresis
 Thickening of the facial features
 Increase prominence in jaw & forehead
 Thickened skin
 Swelling of tongue
 Arthritis
 Sleep apnoea
 Headache
 Partial loss of vision
 Pain,numbness,tingling weakness in hands & wrists
 Increased thirst n urination,hyperglycemi,heart failure etc

21. CONTINUED:
• Thyroid, parathyroid and adrenal glands shows hyperactivity.
• Hyperglycemia and glycosuria
• Hypertension
• Headache
• Visual disturbance-BITEMPORAL HEMIANOPIA

22. DIAGNOSTIC EVALUATION
 History collection
 Physical examination
 CT scan,MRI scan of head,chest,abdomen, pelvis,adrenal gland &
ovaries.
MANAGEMENT:
 Goal of treatment is to relieve & reverse the symptoms of acromegaly.
 Surgical treatment is the 1st line treatment
 TRANSPHENOIDAL HYPOPHYSECTOMY
Transsphenoidal means through the sphenoid sinus. This is the air sinus
(cavity) at the back of your nose. We remove the pituitary tumour through
the nose. Hypophysectomy refers to the pituitary gland.

24.  RADIATION THERAPY: Is an option to reduce the size of the
tumor & hence reduce the production of growth hormone.
Radiation therapy focuses on high intensity radiation at pituitary tumor to
destroy the abnormal cells.
 Given in 2 forms: External beam & stereotactic
 DRUG THERAPY:
 Somatostatin analogs: reduce growth hormone release
 Dopamine agonist: prevents the release of growth hormone
 Growth hormone receptor antagonist: blocks the effect of growth
hormone eg,Pegvisomant

26. HYPOPITUITARISM(HYPOACTIVI
TY)
 Hypopituitarism(pituitary insufficiency) is a rare condition in
which your pituitary gland doesn’t make enough of certain
hormones.
 Can be caused due to pituitary tumors which when increases
its size may compress and damage pituitary tissues, interfering
with hormone production.
 DISORDERS CAUSED:
• Dwarfism
• Acromicria
• Simmond’s disease

27. DWARFISM
It is an endocrine disorder resulting from hyposecretion of growth
hormone during critical developmental period in children.

28. TYPES OF DWARFISM
1. Proportionate
2. Disproportionate
 Short limb
 Short trunk
3. Asymmetry

29. CAUSE OF DWARFISM
 Reduction in the growth hormone in
infancy or early childhood.
 Occurs because of following reasons:
 Tumor of pituitarygland,which compress &
destroys the normal cell secreting growth
hormone
 Def of GHRH by hypothalamus
 Def of somatomedinC
 Atrophy or degeneration of acidophillic cells
in the anterior pituitary
 Lesion of anterior pituitary due to infection or
injury results in hyposecretion of growth
hormone
 Genetic disorder
 Hereditary

30. SIGNS AND SYMPTOMS
 Stunted skeletal growth
 Maximum height approximately 3 feet
 Head becomes slightly larger in relation to body
 Mental activity is normal without any deformity
 Reproductive system is not affected due to lack of growth
hormone but in Panhypopituitarism puberty is not obtained due
to lack of gonadotrophic hormone.

32. DIABETES INSIPIDUS
 Diabetes insipidus is a disorder of the posterior lobe of the pituitary gland
characterized by a deficiency of ADH or vasopressin.
 Great thirst,polydipsia & large volume of dilute urine characterize the
disorder.

33. TYPES OF DIABETES INSIPIDUS
1. Central diabetes insipidus
2. Nephrogenic diabetes insipidus
3. Psychogenic diabetes insipidus
4. Gestational diabetes insipidus

34. CAUSES
 Central diabetes insipidus:
 Head trauma or surgery
 Pituitary or hypothalamic tumor
 Intracerebral occlusion or infection
 Nephrogenic diabetes insipidus:
 Systemic disease involving kidney:-
 Multiple myeloma
 Sickle cell anemia
 Polycystic kidney diseases
 Pyelonephritis
 Medication such as lithium

35. PATHOPHYSIOLOGY
 Central diabetes insipidus:
 Loss of vasopressin producing cells
 Causing deficiencies in ADH synthesis
 Deficiency in ADH,resulting in an inability to conserve water
 Leading to extreme polyuria& poiydipsia
 Nephrogenic diabetes insipidus:
 Depression of aldosterone release or inability of nephrons to respond to
ADH,causing extreme polyuria and polydipsia.

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

37. DIAGNOSTIC TEST RESULTS
 High serum osmolarity,usually above 300mosmol/kg of water.
 Low urine osmolarity,usually 50 to 200 m osmol/kg of water.
 Low urine –specific gravity of less than 1.005.
Management: the objective of therapy are:
1. To replace ADH,which is usually a long term therapeutic
programme.
2. To ensure adequate fluid replacement
3. To identify & correct the underlying cause.

38. TREATMENT:
 Replacement of vasopressin therapy with intranasal or I.V
DDAVPC(desmopressin acetate).
 Correction of dehydration and electrolyte imbalance.
 Thiazole diuretic increase renal water reabsorption
 Restriction of salt & protein intake.
NURSING MANAGEMENT: The nurse reviews the patient history&
physical assessment.
 The nurse is responsible to educate the patient, family & other caregivers
about follow up care,prevention of complication & emergency measures.
 The nurse should demonstrate and make the client understand about his
medical condition.

39. SIADH-SYNDROME OF
INAPPROPRIATE ANTI DIURETIC
HORMONE
 SIADH,is a disorder of impaired water excretion
caused by the inability to suppress secretions or due
to excessive secretions & actions of anti diuretic
hormone.
 If water intake exceed the reduced urine output i.e
conc urine,the ensuring water retention leads to the
development of hyponatremia.
 Most common cause of Hypo osmolar Euvolemic
Hyponatremia.

40. ETIOLOGY
1. Neoplasms
2. Carcinomas of lung,duodenum,ovary,bladder,ureter,any
other neoplasms.
3. Thymoma
4. Mesothelioma
5. Bronchial adenoma
6. Carcinoid gangliocytoma
7. E wing’s carcinoma

41. PATHOPHYSIOLOGY

43. DRUGS
1. Vasopressin or demopressin
2. Chloropropamide
3. Oxytocin high dose
4. Vineristine
5. Carbamazepine
6. Nicotine phenothiazines
7. Cyclophosphamide
8. Serotonin reuptake inhibitor ,etc.

44. INVESTIGATION TESTS FOR
DIAGNOSIS OF SIADH
1. Serum Na+,KCl and bicarbonate
2. Plasma osmolarity
3. Urine sodium
4. Urine osmolarity
5. Serum creatinine
6. Blood urea nitrogen
7. Blood glucose
8. Serum uric acid
9. Serum cortisol
10. Thyroid stimulating hormone

45. MANAGEMENT
 Fluid restriction:
Is a mainstay of therapy in most patient with SIADH,with a suggested
goal,intake of less than 800ml/ day.
The associated -ve water balance initially raises the serum Na conc
towards normal &with maintenance therapy in chronic SIADH,prevents
further reduction in serum sodium.
 Intravenous saline:
Symptomatic or resistant=Hyponatremia in patient with SIADH often
requires the administration of NaCl.

46. NURSING MANAGEMENT
 Close monitoring of fluid intake& output
 Daily weight check up
 Urine and blood investigations to be measured on regular
basis,in order to indicate any risk for the client.
 Supportive measures and explanation of procedure and
treatment will assist the patient in managing this disorder.

47. ADRENAL GLAND

48. INTRODUCTION
 Each person has 2 adrenal gland ,one attached to
superior part of each kidney.
 Each adrenal gland is,in reality,two endocrine glands
with separate independent function.
 Adrenal gland consist of 2 parts:
1. Adrenal medulla
2. Adrenal cortex

49.  Adrenal medulla: Present at the centre of the gland ,
secreted catecholamines and the outer portion of gland.
 Adrenal cortex: it secretes steroid hormones.The secretion
of hormone from the adrenal cortex is regulated by the
hypothalamus-pituitary –adrenal axis.
Hypothalamus secretes corticotrophin releasing
hormone(CRH), which stimulates the pituitary gland to
secrete ACTH, which in turn stimulates the adrenal cortex to
glucocorticoid hormones (cortisol).
Increased level of adrenal hormone inhibit the production of
CRH&ACTH.
This system is an example of –ve feedback mechanism.

50. ANATOMICAL STRUCTURE OF
ADRENAL GLAND
 Right adrenal gland is triangular in shape
 Left adrenal gland is crescent in shape.
 Left adrenal gland is more elongated than right & lie in more superior position
than the right one.
 3 TYPES OF STEROID HORMONE PRODUCED BY ADRENAL CORTEX
ARE:-
1. Glucocorticoids
2. Mineralocorticoid
3. Sex hormones
 ADRENAL CORTEX IS DIVIDED INTO 3 ZONES:-
1. Zona glomerulosa
2. Zona fasciculata
3. Zona reticularsis

51. ADRENAL GLAND TUMORS
Divided into tumors arising from adrenal gland cortex &
arising from medulla:-
 Adrenal cortex:-
1. Cushing syndrome
2. Primary hyperaldosteronism(Conn’s disease)
3. Adrenal carcinoma
 Adrenal medulla:-
1. Pheochromocytoma
2. Neuroblastoma

52. CUSHING SYNDROME

53.  Hypersecretion of cortisol caused by endogenous production
of corticosteroids is known as Cushing’s syndrome.
 Themost common cause is ACTH dependent cushing
syndrome,resulting from pituitary adenoma that secrete
excessive amount of ACTH.
 Adrenocortical carcinoma & bilateral macronodular hyperplasia
represent rare cause of hypercorticolism.
CLINICAL SYMPTOMS:-
A typical patient is characterized by
 A facial plethora
 A Buffalo hump
 A moon face

54. CLINICAL FEATURES OF CUSHING
SYNDROME
 Weight gain/central obesity
 Diabetes
 Hirusitism
 Hypertension
 Skin changes(abdominal striae)
 Muscle weakness
 Menstrual irregularity
 Depression
 Osteoporosis
 Hypokalemia

55. DIAGNOSIS
 Biochemical test
 Radiological investigation
NURSING MANAGEMENT
 Decrease risk of injury
 Decreasing risk of infection
 Preparing the patient for allergy test.
 Encouraging rest & activity
 Promoting skin integrity
 Improving body image

56. PRIMARY HYPERALDOSTERONISM
(CONN’S DISEASE)
 Primary aldosteronism (PA), also known as primary
hyperaldosteronism or Conn's syndrome, refers to the excess
production of the hormone aldosterone from the adrenal glands, resulting
in low renin levels.[1] This abnormality is caused by hyperplasia or tumors.
Many suffer from fatigue, potassium deficiency and high blood
pressure which may cause poor vision, confusion or headaches.

57. Primary hyperaldosteronism (PHA) is defined by hypertension,
hypokalemia & hypersecretion of aldosterone.
 In PHA ,plasma renin activity is suppressed.
 Among pateients with hypertension the incidence of
hypokalemia.
 PHA is approximately 2% recent studies have revealed that
upto 12% of hypertension patient have PHA ,with normal
potassium levels.
CAUSES OF PHA:-
1. Aldosterone producing adencema.
2. Bilateral adrenal hyperplasia(ideopathic
hyperaldosteronism)
3. Aldosterone-producing adrenocortical carcinoma.

58. CLINICAL FEATURES
1. Most patient are between 30-50 years of age with female
predominance.
2. Apart from hypertension & hypokalemia, patient complains
of non specific symptoms.
3. Headache,muscle weakness,cramps,polyuria, intermittent
paralysis,polydipsia & nocturia.
DIAGNOSIS
 Assessment of potassium levels
 Antihypertensive & diuretic therapy
 Once biochemical diagnosis is confirmed,MRI or CT scan
can be performed.

59. ADRENOCORTICALCARCINOMA

60.  Adrenocortical carcinoma is a rare malignancy with a
incidence of 1-2 cases per 10lakhs population per year.
 A variable but generally poor prognosis.
 A slight female predominance is observed (1:5:1)
 1st peak in childhood & a second between 4th or 5 th decade.

61. PATHOLOGY
1. Criteria for malignancy are tumor size,the presence
of necrosis or haemorrhage & microscopic features
such as capsular or vascular invasion.
2. These should be assessed in terms of microscopic
diagnostic score.
3. Additional information is provided by immuno histo
chemistry.
4. Macroscopic features commonly multinodularity &
hexogenous structure.

62. DIAGNOSIS
1. Dexamethasone suppression test
2. MRI & CT scan
3. MRI angiography
4. WHO classification-
1. Tumor < 5 cm (stage1)
2. > 5 cm(stage2)
3. Locally invasive tumor(stage 3)
4. Tumor with distant metastasis (stage 4)
TREATMENT
 Complete tumor resection
 Laproscopic adrenalectomy
 Adjuvant radiotherapy

64. PHEOCHROMOCYTOMA

65.  A tumor begins when healthy cells change & grow out of
control forming a mass.
 A tumor can be cancerous or benign.
 A cancerous tumor is malignant, measuring it can grow &
spread to other parts of body.
 A benign tumor means the tumor can grow but will not
spread.
 The adrenal gland tumor can sometimes produce too much
of hormone, When it does,the tumor is called”functioning
tumor”.
 It is catecholamines-secreting neoplasms associated with
hypertension of chromaffin cells of adrenal medulla.

66. ETIOLOGY
 Medullary thyroid carcinoma
 Parathyroid hyperplasia
 Emotional & physical stress
 General factor
 Increased or decreased
secretion of hormone.

68. CLINICAL FEATURES
 Hypertension
 Postural hypotension,this results from volume contraction
 Weight loss
 Pallor
 Fever
 Tremor
 Neurofibromas
 Patches of cutaneous pigmentation
 Tachyarrhythmias
 Pulmonary oedema
 Cardiomyopathy

69. LABORATORY SIGNS
 Hyperglycemia
 Hypercalcaemia
 Erythrocytosis
5’H’s SYMPTOMS
1. Hypertension
2. Headache
3. Hyperhidrosis
4. Hypermetabolism
5. Hyperglycemic
Classically, pheochromocytoma shows Swiss cheese
configuration.

70. NURSING MANAGEMENT
 Educating patient about self care
 During pre operative & post operative phases of care ,the nurse
educate the patient about follow up monitoring to ensure that
pheochromocytoma does not reactivate.
 Nurse provide verbal & written instructions about
 The procedure for collecting 24 hrs urine specimen to monitor
urine for catecholamines level.
 Continuing care
 The patient is scheduled for periodic follow up appointments to
observe for return of normal blood pressure & plasma for urine
levels of catecholamines.

71. TREATMENT
1. Laparoscopic resection is now a routine treatment
for pheochromocytoma.
2. If the tumor is larger than 8-10 cm or radiological
signs of malignancy are detected an approach
should be co

73. SUMMARY
 The presentation includes the
Pituitary disorders
 Gigantism
 Acromegaly
 Dwarfism
 Diabetes insipidus
 SIADH
Adrenal tumors
 Cushing syndrome
 Primary hyperaldosteronism
 Adrenocortical carcinoma
 Pheochromocytoma
Their causes,clinical features,diagnosis,treatment and
management have also been covered.

74. BIBLIOGRAPHY
 Brunner’s & Suddharth’s text
book of MEDICAL SURGICAL
NURSING 13th edition.
 https://www.endocrinweb.com
 https://www.cancer.org.com
 www.slideshare.com