11. Pituitary disorder due to hyperactivity/ excessive
secretion of growth hormone, which is also known as
somatotropin characterized by:
Excess growth of body
Average height is approximately 7 – 8 feet
12. Hypersecretion of GH in childhood or
in pre – adult
Tumor of acidophilic cells of Anterior
pituitary(the gland makes more growth
hormone than the body needs).
13.
14. Huge stature : 7 or 8 feet height
Headache due to tumor of pituitary
Very large hands and feet
Thick toes and fingers
A prominent jaw and forehead
Coarse facial features
Weakness
Insomnia and other sleep disorders
15. Visual disturbances
Gigantism ends in
hypopituitarism
(burning of cells of
anterior pituitary )
Diabetes insipidus
(less secretion of
ADH)
Delayed puberty in
both boys and girls
Irregular menstrual
periods in girls
16. Blood test to measure levels of growth hormones.
MRI scan of the gland
Insulin-like growth factor 1 (igf-1), which is a
hormone produced by the liver.
Oral glucose tolerance test:- pt. will drink a special
beverage containing glucose, a type of sugar. Blood
samples will be taken before and after the pt.
drinks the beverage. In a normal body, growth
hormone levels will drop after eating or drinking
glucose. If pt.’s levels remain the same, it means his
body is producing too much growth hormone.
17. Treatments for gigantism aim to stop or slow the
production of growth hormones.
somatostatin analogs such as octreotide or long-
acting lanreotide, which reduce growth hormone
release.
Surgery
Hypophysectomy:-Removing the tumor is the
preferred treatment for gigantism if it’s the
underlying cause.
Radiation therapy
Has also been used to bring growth hormone levels
to normal if surgery and medication fail.
20. Anterior pituitary disorder characterized by:
abnormal growth of the hands, feet, and face,
caused by overproduction of growth hormone
by the pituitary gland.
Enlargement, thickening, and broadening of
bones
Particularly extremities of the body
21. Hypersecretion of GH after fusion of epiphysis
with shaft of bone
Adenomatous tumor of anterior pituitary involving
the acidophilic cells.
22. Striking features are protrusion of :
Supraorbital ridges
Broadening of nose
Thickening of lips
Thickening and wrinkles formation on
forehead
Lower jaw (prognathism)
Face with these features called as acromegalic or
guerilla face
23.
24. Kyphosis : enlargement of hands and feet with
bowing spine
Scalp is thickened and thrown into folds
Overgrowth of body hair
Visceral organs are enlarged
25.
26. Thyroid , parathyroid and adrenal glands shows
hyperactivity
Hyperglycemia and glucosuria
Hypertension
Headache
Visual disturbance – Bitemporal hemianopia
(partial blindness where vision is missing in the
outer half of both the right and left visual field.)
31. Rare disorder
Due to hypersecretion of GH in children,before
fusion of epiphysis with the shaft of bone results in
Gigantism
If hyersecretion of GH is continued after the fusion
of epiphysis the symptoms of Acromegaly
also appear
36. Hypersecretion of glucocorticoids mainly cortisol
Either pituitary origin or adrenal origin
Cushing’s Cushing’s
disease syndrome
37. High levels of cortisol for a variety of reasons,
including:
High stress levels in the final trimester of
pregnancy
Athletic training
Malnutrition
Alcoholism
Depression or panic disorders
Use of corticosteroid medications (like prednisone)
in high doses for a long period of time.
38. Increased secretion of ACTH (Adrenocorticotrophic
hormone) leads to hyperplasia of adrenal cortex
therefore, hypersecretion of glucocorticoids takes
place
ACTH is increased by
Tumor in pituitary cells ( basophilic cells)
Hypothalamic disorder causing hypersecretion of
corticotropin releasing hormone.
39. 1. Disproportionate distribution of body fat results:
Moon face : Fat accumulation and retention of water and
salt .
Torso : Fat accumulation in chest and abdomen but slim
legs and arms.
Buffalo hump : Fat deposit on the back of neck and
shoulder.
Pot belly : Fat accumulation in upper abdomen.
40.
41. 2. Purple striae : Reddish purple stripes on abdomen
due to mainly three reasons:
Stretching of abdominal wall by excess
subcutaneous fat.
Rupture of subdermal tissues due to stretching.
Deficiency of collagen fibres due to protein
depletion.
42.
43. 3. Thinning of extremities
4. Thinning of skin and subcutaneous tissues
5. Aconthosis : Darkening of skin on neck i.e.-
diffuse epidermal hyperplasia.
6. Pigmentation of skin
7. Facial redness (facial plethora)
8. Weakening of muscle
44.
45. 9. Facial hair growth ( Hirsutism ).
10. Bone resorption leads to osteoporosis.
11. Hyperglycemia due to gluconeogeneis leads adrenal
diabetes and glycosuria.
12. Hypertension.
13. Immunosuppression resulting in susceptibility for
infection.
14. Poor healing .
46.
47. Plasma cortisol level—increased(Morning 5-23
micrograms per deciliter (mcg/dL, Afternoon 3-16
mcg/dL )
Blood glucose level—increased.
Serum potassium level—decreased(3.5-5.2 milliequivalents
per liter (mEq/L)
Eosinophils—decreased(0-5%).
Plasma ACTH increased in pt. with pituitary tumor.
Plasma ACTH level low in pt. with adrenal tumor.
X- ray of the skull to detect erosion of the sella turcica by a
pituitary tumor.
C.T. scan and ultrasonography to detect the location of
tumor.
48. Surgical and radiation:- Tumor (adrenal or pituitary)
is removed or treated with irradiation.
Transsphenoidal adenomectomy: remove a tumour
(adenoma) of the pituitary gland is carried out
through the nasal cavity.
Transfrontal craniotomy:- may be necessary when
pituitary tumor has enlarged beyond sella turcica.
Bilateral adrenalectomy:- in case of hyperplasia of
adrenals.
49.
50.
51.
52. Adrenalectomy patients require a lifelong replacement
therapy with the following:-
A glucocorticoid—cortisone.
A mineralocorticoid—fludrocortisones
After pituitary irradiation or hypophysectomy, patient
may require adrenal replacement, plus thyroid,
posterior pituitary, and gonadal replacement therapy.
After transsphenoidal adenomectomy, patient require
hydrocortisone replacement therapy for periods of 12-
18 months.
53. If patient cannot undergo surgery, cortisol synthesis-
inhibiting medications may be used:-
Mitotane :- an agent toxic to the adrenal cortex –
known as medical adrenalectomy. Nausea, vomiting,
diarrhea, somnolence and depression may occur with
use of this medication.
Metopirone :- to control steroid hypersecretion in
patients who do not respond to mitotane therapy.
Aminoglutethimide :- block cholesterol conversion to
pregnenolone, effectively blocking cortisol
production.
57. Reduction in the GH in infancy or early
childhood
Deficiency of GH releasing hormone from
hypothalamus
Atrophy of acidophilic cells in the adenohypophysis
Tumor of chromophobes : nonfunctioning tumor ,
compresses and destroys the normal cells
Panhypopituitarism
58. Stunted skeletal growth
Maximum height approximately 3 feet
Head becomes slightly larger in relation of body
Mental activity is normal without any deformity
Reproductive system is not affected due to lack of GH
but in Panhypopituitarism puberty is not obtained due to
lack of gonadotropic hormone
59. Laron dwarfism (abnormal GH
secretagogue receptors in liver)
Psychogenic dwarfism (Stress
dwarfism)
Dwarfism in dystrophia adiposogenitalis
60. Genetical disorder
Called as GH insensitivity
Occurs due to presence of abnormal GH
secretagogue receptors in liver
GHS becomes abnormal due to mutation in genes
responsible for receptor
Doesn’t depend on amount of GH secretion ,
hormone can’t stimulate the growth due to abnormal
GHS
61. Due to extreme emotional deprivation or stress
Deficiency of GH
Also called as psychosocial dwarfism or Stress
dwarfism
62. Called as Frohlich syndrome
Rare childhood disorder
Characterized by :
o Obesity
o Growth retardation
o Retarded development of genital organs
o Associated with tumors of hypothalamus –
increased appetite and decrease in gonadotropin
hormone.
64. Rare disease in adults characterized by the atrophy
of the extremities of the body.
65. Deficiency of GH in adults
Secretion of GH decreases in the following
conditions:
Deficiency of GH releasing hormone
Atrophy of acidophilic cells in the anterior
pituitary
Tumor of chromophobes
Panhypopituitarism
66.
67. Atrophy and thinning of extremities (
major symptoms )
Associated with hypothyroidism
Hyposecretion of adrenocortical hormone
Person becomes lethargic and obese
Loss of sexual function
69. Rare pituitary disease:- weakness and wasting
of the body due to severe chronic illness.
Also called as cachexia
Occurs mostly in Panhypopituitarism
Atrophy (shrinking and reduced function) of
the cells and organs that are normally
stimulated by pituitary hormones.
70. Tumor
Presses on the optic nerve and surrounding brain
structures.
complication of pregnancy.
Postpartum hypopituitarism or postpartum
pituitary gland necrosis,(decreased functioning of the
pituitary gland), caused by ischemic necrosis due to
blood loss and hypovolemic shock during and after
childbirth
71. Developing senile decay :- due to deficiency
of hormone from target glands of anterior
pituitary e.g. thyroid gland, adrenal cortex and
the gonads
Loss of hair.
The skin on face becomes dry and wrinkled. (
most common )
77. Due to cerebral tumors, lung tumors and lung cancers
because the tumor cells secrete ADH.
Normal secretion of ADH makes the plasma
hypotonic.
Hypotonic solution inhibits the ADH secretion and
restoration of plasma osmolarity takes place.
But in SIADH ,secretion of ADH from tumor is not
inhibited by hypotonic plasma.
78. 1. Loss of appetite
2. Weight loss
3. Nausea and vomiting
4. Headache
5. Muscle weakness , spasm and cramps
6. Fatigue
7. Restlessness and irritability
In severe conditions patient die because of coma and
convulsions
80. Posterior Pituitary disorder characterized by excess
excretion of water through urine
81. Develops due to the deficiency of ADH which occurs in
the following conditions:
Lesion (injury) or degradation of supraoptic and
paraventricular nuclei of hypothalamus.
Lesion in hypothalamo-hypophyseal tract
Atrophy of posterior pituitary
Inability of renal tubules to give response to ADH
hormone. Called as Nephrogenic diabetic insipidus.
82. 1.Polyuria
Excretion of large quantity of dilute urine with
increased frequency of voiding is called polyuria
Daily output is >4litres.
Due to absence of ADH ,the epithelial cells of distal
convoluted tubule in the nephron and the collecting
duct of the kidney becomes impermeable to water
83. 2.Polydipsia
Intake of excess water
Because of polyuria ,thirst center in hypothalamus
results in intake of large quantity of water
84. 3.Dehydration
In some cases ,the thirst center in the hypothalamus is
also affected by the lesion.
Therefore water intake decreases in these patients and,
the loss of water through urine is not compensated.
Dry mouth
Changes in skin elasticity
Low blood pressure (hypotension)
Elevated blood sodium (hypernatremia)
Fever
Headache
Electrolyte imbalance
85. Genetic testing
Genetic testing is used to detect altered genes that may
cause illness or disease. Although genetic testing can
offer important health information, it has limitations.
MRI
MRI uses a magnetic field and radio waves to create
detailed images of the organs and tissues within the
body.
Urinalysis
Urinalysis can be used to assess overall health, detect a
wide range of disorders, or monitor a medical
condition or treatment.
88. Characterized by obesity and hypogonadism affecting
mainly adolescent boys
Also known as Frohlich syndrome or hypothalamic
eunuchism
89. “Adiposogenital Dystrophy, also called Frohlich's
syndrome rare childhood metabolic disorder
characterized by obesity, growth retardation, and
retarded development of the genital organs. It is
usually associated with tumours of the
hypothalamus, causing increased appetite and
depressed secretion of gonadotropin”.
90. Hypoactivity of both anterior and posterior
pituitary
Tumor in pituitary gland and hypothalamic regions
concerned with food intake and gonadal
development
Injury or atrophy of pituitary gland
Genetic inablility of hypothalamus to secrete
luteinizing hormone
91. Obesity (common feature)
Sexual infantilism (failure to develop secondary
sexual characters)
Dwarfism occurs if disease starts in growing age
Called as infantile or prepubertal type of
Frohlich syndrome (in children)
and adult type of Frohlich’s syndrome (in adults)
Other features are loss of vision and diabetes
92.
93. Observe the shape and size of the body, measuring
weight and height, observe the shape and size of
the breast, axillary and pubic hair growth in male
clients, observe also the growth of facial hair .
ability of clients to meet their basic needs.
Palpation of the skin, the woman usually becomes
dry and rough.
94. Disturbed body image related to : enlargement of body
parts as manifested by enlarged hands, feet and jaw.
Ineffective coping related to change in appearance as
manifested by verbalization of negative feeling about the
change in appearance.
Disturbed sensory perception related to enlarged
pituitary gland as manifested by protrusion of eye balls.
Risk for Decreased Cardiac Output related to
Uncontrolled hyperthyroidism, hypermetabolic state.
95. Disturbed sleeping pattern related to soft tissue
swelling as manifested by verbalization of the patient
about insomnia.
Fluid volume deficit related to polyuria as
manifested by excessive thirst of the patient.
Anxiety related to change in appearance and
treatment as manifested by verbalization of the
patient about body appearance.
Knowledge deficit regarding development of disease
and treatment as manifested by repeated questions by
the patient regarding disease and treatment.
96. Reduce metabolic demands and support cardiovascular
function.
Provide psychological support.
Prevent complications.
Provide information about disease process/prognosis
and therapy needs.
97. Monitor BP lying, sitting, and standing, if able. Note
widened pulse pressure.
Investigate reports of chest pain or angina.
Assess pulse and heart rate while patient is sleeping.
Auscultate heart sounds, note extra heart sounds,
development of gallops and systolic murmurs.
Monitor ECG, noting rate and rhythm. Document
dysrhythmias.
Administer medications as indicated
98. Provide comfort measures: touch therapy or
massage, cool showers. Patient with dyspnea will
be most comfortable sitting in high Fowler’s
position.
Provide for diversional activities that are calming,
e.g., reading, radio, television.
Administer medications as indicated: Sedatives:
phenobarbital (Luminal), antianxiety agents:
chlordiazepoxide (Librium)
99. Assess thinking process. Determine attention span,
orientation to place, person, or time
Note changes in behavior.
Assess level of anxiety.
Provide quiet environment; decreased stimuli, cool
room, dim lights. Limit procedures and/or personnel.
Provide clock, calendar, room with outside window;
alter level of lighting to simulate day or night.
Provide safety measures. Pad side rails, close
supervision, applying soft restraints as last resorts as
necessary.
100. Monitor daily food intake. Weigh daily and report
losses.
Encourage patient to eat and increase number of
meals and snacks. Give or suggest high-calorie
foods that are easily digested.
Avoid foods that increase peristalsis and fluids that
cause diarrhea.
102. Incidence of primary cancers and intracranial
tumour recurrences in GH-treated and untreated
adult hypopituitary patients: analyses from the
Hypopituitary Control and Complications Study.
Child CJ, Conroy D, Zimmermann AG,
Woodmansee WW, Erfurth EM, Robison LL
103. OBJECTIVE:
Speculation remains that GH treatment is associated
with increased neoplasia risk. Studies in GH-treated
childhood cancer survivors suggested higher rates of
second neoplasms, while cancer risk data for GH-
treated and untreated hypopituitary adults have been
variable. We present primary cancer risk data from the
Hypopituitary Control and Complications Study
(HypoCCS) with a focus on specific cancers, and
assessment of recurrence rates for pituitary adenomas
(PA) and craniopharyngiomas (CP).
104. DESIGN:
Incident neoplasms during HypoCCS were evaluated in
8418 GH-treated vs 1268 untreated patients for primary
malignancies, 3668 GH-treated vs 720 untreated patients
with PA history, and 956 GH-treated vs 102 untreated
patients with CP history.
METHODS:
Using population cancer rates, standardised incidence
ratios (SIRs) were calculated for all primary cancers,
breast, prostate, and colorectal cancers. Neoplasm rates in
GH-treated vs untreated patients were analysed after
propensity score adjustment of baseline treatment group
imbalances.
105. RESULTS:
During mean follow-up of 4.8 years, 225 primary
cancers were identified in GH-treated patients, with
SIR of 0.82 (95% CI 0.71-0.93). SIRs (95% CI) for
GH-treated patients were 0.59 (0.36-0.90) for breast,
0.80 (0.57-1.10) for prostate, and 0.62 (0.38-0.96) for
colorectal cancers. Cancer risk was not statistically
different between GH-treated and untreated patients
(relative risk (RR)=1.00 (95% CI 0.70-1.41), P=0.98).
Adjusted RR for recurrence was 0.91 (0.68-1.22),
P=0.53 for PA and 1.32 (0.53-3.31), P=0.55 for CP.
106. CONCLUSIONS:
There was no increased risk for all-site cancers: breast,
prostate or colorectal primary cancers in GH-treated
patients during HypoCCS. GH treatment did not
increase the risk of PA and CP recurrences.
