Disorders of pituitarygland

1. PRESENTED TO- MRS. BINDU JOSEPH PRESENTED BY- MS. AMANDEEP KAUR MSC. NSG. 1ST YEAR 1915703

2.  Adenocorticotrophic hormone (ACTH): 9-46pg/ml  Thyroid stimulating hormone (TSH):0.3- 5.0uIU/ml.  Luteinizing hormone (LH) & Follicle stimulating hormone (FSH): decreased at menstrual phase.  Prolactin (PRL): decreased at menstrual phase  Growth hormone (GH) <5.0nanometer/mililiter  Melanocyte-stimulating hormone (MSH)

3. Mainly of 2 reasons:  Hyperactivity  Hypoactivity

4. Parts involved Hyperactivity Hypoactivity Anterior Pituitary 1. Gigantism 2. Acromegaly 3. Acromegalic gigantism 4. Cushing’s disease 1. Dwarfism 2. Acromicria 3. Simmond’s disease Posterior Pituitary Syndrome of inappropriate hypersecretion of ADH (SIADH) Diabetes insipidus Anterior and Posterior Pituitary ……. Dystrophia adiposogenitalis

6. 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

7.  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).

8.  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

9.  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

10.  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.

11.  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.

13. 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

14.  Hypersecretion of GH after fusion of epiphysis with shaft of bone  Adenomatous tumor of anterior pituitary involving the acidophilic cells.

15. 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

16.  Kyphosis : enlargement of hands and feet with bowing spine  Scalp is thickened and thrown into folds  Overgrowth of body hair  Visceral organs are enlarged

17.  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.)

18.  SAME AS GIGANTISM

20.  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

21.  SAME AS GIGANTISM AND ACROMEGALY

23.  Rare disease characterized by obesity

24.  Hypersecretion of glucocorticoids mainly cortisol  Either pituitary origin or adrenal origin Cushing’s Cushing’s disease syndrome

25. 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.

26.  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.

27. 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.

28. 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.

29. 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

30. 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 .

31.  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.

32.  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.

33.  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.

34.  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.

35.  Possibility of recurrence in patients with adrenal carcinoma.

37.  Pituitary disorder in children characterized by stunted growth.

38. 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

39.  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

40. Laron dwarfism (abnormal GH secretagogue receptors in liver) Psychogenic dwarfism (Stress dwarfism) Dwarfism in dystrophia adiposogenitalis

41.  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

42.  Due to extreme emotional deprivation or stress  Deficiency of GH  Also called as psychosocial dwarfism or Stress dwarfism

43. 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.

45.  Rare disease in adults characterized by the atrophy of the extremities of the body.

46.  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

47.  Atrophy and thinning of extremities ( major symptoms )  Associated with hypothyroidism  Hyposecretion of adrenocortical hormone  Person becomes lethargic and obese  Loss of sexual function

49.  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.

50.  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

51.  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 )

54.  Disease characterized by loss of sodium through urine due to hypersecretion of ADH

55.  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.

56. 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

58.  Posterior Pituitary disorder characterized by excess excretion of water through urine

59. 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.

60. 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

61. 2.Polydipsia  Intake of excess water  Because of polyuria ,thirst center in hypothalamus results in intake of large quantity of water

62. 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

63.  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.

64.  Prevent dehydration.  Wear a medical alert bracelet or carry a medical alert card in hand.

66.  Characterized by obesity and hypogonadism affecting mainly adolescent boys  Also known as Frohlich syndrome or hypothalamic eunuchism

67.  “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”.

68.  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

69.  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

70.  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.

71.  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.

72.  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.

73.  Reduce metabolic demands and support cardiovascular function.  Provide psychological support.  Prevent complications.  Provide information about disease process/prognosis and therapy needs.

74.  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

75.  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)

76.  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.

77.  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.

78. ANY QUIRY

79.  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

80.  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).

81.  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.

82.  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.

83.  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.

84. ANY QUIRY

Disorders of pituitarygland

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