lecture on endocrine diseases final

8/3/2019 Lecture on Endocrine Diseases FINAL

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The ENDOCRINE SYSTEM


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Anatomy and physiologic Overview

Endocrines: Without ducts: Ductless glands.

A group of glands all of which lack ducts or specificchannels to release their secretions.

All of them secrete or produce ChemicalMessengers or Hormones.

Hormones by definition bring metabolic changes intarget tissues.

The target tissues are usually far away from theendocrine glands.


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WHY ENDOCRINE SYSTEM?

4 MOST IMPORTANT PURPOSES

1. HOMEOSTASIS.

2. COMBATING STRESS.

3. GROWTH & DEVELOPMENT.

4. REPRODUCTION.


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ENDOCRINES ARE USEFUL FOR

1. HOMEOSTASIS

Endocrines help us in

maintaining the

homeostasis of: Temperature:

Thermoregulation or

thermostasis.

Metabolism Nutrition: Glucostasis

Acid Base Balance


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ENDOCRINES ARE USEFUL IN

2. COMBATING STRESS INFECTION

TRAUMA

SHOCK


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ENDOCRINES ARE USEFUL FOR

3. GROWTH & DEVELOPMENT

Increase in the cell

number: Hyperplasia

Increase in cell SIZE:

Hypertrophy.


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ENDOCRINES ARE USEFUL FOR 4.

REPRODUCTION

The Male and femaleGonads secrete:

Sex Hormones

These sex hormonescause the

development of Primary sex organs

Secondary sexualcharacteristics.


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HORMONES

It is important in regulation of the internal

environment of the body and effect every aspect of

life.

Natural chemicals that exert their effects on specific

tissues known as

target tissues

The mechanism for regulating hormone in the bloodstream is called negative feedback


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Target Tissues

usually located some distance from

endocrine glands with no direct

physical connection between the endocrineglands and its target tissue


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Glands Of The Endocrine System

1. Pituitary glands

2. Thyroid glands

3. Parathyroid glands

4. Pancreatic islets

5. Ovaries

6. Testes

7. Adrenal glands


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HORMONES PRODUCED IN THE

BODY

HYPOTHALAMUS:

CRH, TRH, GHRH, GHIH, GnRH, PIH.

ANTERIOR PITUITARY GLAND: GH, ACTH, TSH, FSH, LH, Prolactin.

POSTERIOR PITUITARY GLAND:

ADH, & Oxytocin.

THYROID GLAND:

Thyroxin, T3, Calcitonin.


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ADRENAL CORTEX:

Aldosterone, Cortisol, Sex steroids.

ADRENAL MEDULLA: Epinephrine, Norepinephrine, Dopamine.

ENDOCRINE PANCREAS:

Glucagon, Insulin, Somatostatin, Panpolypeptide.


BODY


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TESTES: Testosterone, Estrogen, Inhibin.

OVARY:

Estrogens, Progesterone, Relaxin. PLACENTA:

Estrogens, Progesterone, HCG, HPL.

THYMUS:

Thymosin. PINEAL GLAND:

Melatonin


BODY


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Excessive Production of hormones due to:

Tumors in the gland.

Excess tropic influence.

Results in: Clinical syndromes with signs/symptoms due to:

Increased blood levels of the hormone

Example: Hyperthyroidism:Thyroxin levels

Clinical features: Fine tremor, Anxiety, PR,BMR

Acromegaly: Growth Hormone.

HYPERSECRETION:


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Drop in the production of hormones dueto:

Excision of gland: Eg: Parathyroids.

Hypofunctioning of gland cells: Eg: Diabetesmellitus.

Decreased tropic influence.

Results in: Clinical features/ syndromes due to

blood levels of the hormone

HYPOSECRETION:


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ENDOCRINE DISORDERS


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Thyroid Hyperfunction Disorder

1. Graves disease: immunological factors,

genetic predisposition, infection, stress,

excessive intake of thyroid medication; occurs8 times more frequently in females

2. Goiter: inadequate intake of iodine, increase

in thyroid demand 3.Thyroid storm: Stress, injury, infection,

surgery


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Causes of Hyperthyroid Disorder

Auto immune response

Neoplasm

Excessive intake of thyroid medication

Excess secretion of TSH from the anterior

pituitary glands


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Pathophysiology

THYROID HYPERFUNCTION DISORDERS

1. Production of thyroid hormone (TH) is

dependent on adequate secretion of

thyroid stimulating hormone (TSH) from

the anterior pituitary gland; The

hypothalamus regulates pituitary

secretion of TSH by negative feedback


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Hyperthyroidism

Hyper function of the thyroid gland

Leads to an excess of thyroid hormone in the

body The presence of excess TH leads to hyper

metabolic state

Which causes increase in metabolic function

Increase in oxygen consumption by tissue,

And heat production


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Graves Disease

The most common cause of hyperthyroidism,

is seen most often in woman under age of 40.

The exact cause is unknown, it is consideredan autoimmune disorder to stimulation of

the thyroid gland from a long acting thyroid

stimulator (LATS) The result in an excess production of TH,

Which leads to hypermetabolic state


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GOITER

It is describes the enlargement or hypertropy of thethyroid gland in attempt to compensate forinadequate TH

It may be present in hyperthyroidism orhypothyroidism

Goiter may be result of response to excess TSHstimulation, excessgrowth stimulatingimmunoglobulins, or presence of substance that

inhibit thyroid hormone synthesis The goiter may become enlarge that compress the

neck and chest


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Toxic Multinodular Goiter

It exist when small, independently

functioning nodules in the thyroid gland

tissue are present and secrete TH hormone The nodule may be benign or malignant

The manifestation developed more slowly

than graves disease. Toxic goiter is most often seen in woman age

60 or older who had goiter for several years.


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Thyroid Storm

Also known as thyroid crisis or thyrotoxicosis

It is life threatening condition which

describes an extreme state ofhyperthyroidism

The presence of excessive TH causes a rapid

increase in metabolic rate Immediate treatment is necessary to avoid

death


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Nursing assessment for

Hyperthyroidism 1. eyes, vital sign, cardiac monitor for rhythm

changes, sign of congestive heart failure,nutritional assessment, complaints of GI

distress, muscle strength and appearance,presence of goiter, reproductive history,integument assessment, weight, fluid status

2. Assessment findings for thyroid storminclude elevated temperature, symptoms ofpain, bowel/GI complaints, neurological,development of seizures, changes in VS,respiratory status


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Nursing management for

Hyperthyroidism1. Medication

A. Antithyroid medication to reduce TH production

1. Methimazole (Tapazole)

2. Propylthioracil (PTU, Propyl-Thracil)B. Propanolol (Inderal) to treat dysrhythmias

C. Glucocorticoids: interfere with conversion of T3 andT4

D. Lugols Solution (iodine) to decrease vascularity andsize of thyroid

E. Antipyretic if needed


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Hyperthyroidism

Educate the client that it may take several

weeks before the therapeutic effects of

antithyroid medications are noticed

a. Instruct to take medication as prescribe and

not abruptly discontinue medication

b. Educate about the signs of hypothyroidism,

which may occur if to much medicine is

taken or dose needs adjusting


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hyperthyroidisn

3. Monitor for cardiac dysthythmias

4.Implement antipyretic measures

5. Elevate head of the bed to decrease eyepressure

6. Teach eye care and monitor for vision

changes if exophthalmos occurs, since it willnot change even after medication have been

started.


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hyperthyroidism

7. Monitor dietary intake: Client may require

up to 4,000 to 5,000 calories a day during

hypermetabolic state 8. Monitor intake and output

9. Monitor weight

10. Keep the environment cool and quietbecause of the symptoms


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Hyperthyroidism

11. Radioactive therapy may be recommended to

destroy thyroid cells in order to reduce production

of TH

A. Give radioactive iodine orally; expect result in 6 to 8

weeks

B. Does not require hospitalization or radiation

precautionC. Contraindicated in pregnant woman

D. Monitor for sign and symptoms of hyperthyroidism


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Hyperthyroidism

12. Preoperative and postoperative care for surgical interventionto remove all or part of the thyroid (thyroidectomy)

A. subtotal thyroidectomy leaves part of the thyroid glandintact in order to produce adequate amounts of TH

B. For total thyroidectomy life long thyroid hormonereplacement is necessary; educate for strict compliance withmedication regimen

C. Preoperative care include administering antithyroid

medications to promote euthyroid state, and iodinepreparation to decrease vascularity of the glands. Teach theclient how to support the neck to reduce strain in the sutureline


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hyperthyroidism

Post operative care includes monitoring for

complication of hemorrhage, respiratory

distress, laryngeal nerve damage, and tetany 13. Priority nursing diagnosis for thyroid

hyperfunction disorders: Activity intolerance;

altered nutrition; hyperthermia; risk for

injury


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Thyroid Hypofunction Disorder

A. Overview

1. Hypofunction of the thyroid glands leads to

an insufficient amount of thyroid hormone(TH), a condition known as hypothyroidism

2. Decrease TH result in a hypometabolic state

manifested by a decrease in metabolicfunction, a decrease in oxygen consumption

by tissue, and decrease in heat production


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Thyroid hypofunction Disorder

A. Hypothyroidism

B.

MyxedemaC. Myxedema coma


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MYXEDEMA HYPOTHYROIDISM


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Classified as primary and secondary

A. Causes of primary hypothyroidism include

congenital defects, loss of thyroid tissue from

surgery or radiation, antithyroid medication,endemic iodine deficiency, or thyroiditis

B. Causes of secondary hyperthyroidism include

peripheral resistance to TH or pituitary TSH

deficiency


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Pathophysiology

1. Hypothyroidism describe an insufficient amount ofTH which leads to a decrease in metabolic rate;manifestation developed slowly over months oryears

2. Myxedema describes a generalized hypometabolicstate occurring with untreated hypothyroidism

A. Accumulation of proteins in the interstitial spaceresult in an increase of interstitial fluid, causing

mucinous edema, (myxedema)B. This non-pitting edema is most commonly found in

the pretibial and facial area


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Pathophysiology of Myxedema coma

Also known as hypothyroid crisis

It is the result of extreme or prolongedhypothyroidism; though rare, it is life threatening

condition A. Characterized by severe metabolic state: lactic

acid acidosis, hypoglycemia, hyponatremia,hypotension, bradycardia, cardiovascular collapse,hypothermia, hypoventilation, coma

B. Precipitated by inadequate thyroid replacement,infection, trauma, exposure to cold temperature,CNS depressant


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Pathophysiology

Iodine deficiency: iodine is necessary for TH

synthesis and secretion

A. Iodine deficiency occurs as a result ofantithyroid drugs, and lithium or iodine

intake

B. In US , thyroid deficiency because of inadequate iodine intake is rare with the use

of iodized salt


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Myxedema Coma

Signs and symptoms:

Hypothermia

Cardiovascular collapse Coma

Hyponatremia

Hypoglycemia

Lactic acidosis


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Nursing Assessment

1. Assessment of hypothyroidism include

neurological assessment, presence of

periorbital edema, presence of goiter,

reproductive history, fluid status, weight,

activity tolerance, respiratory status

2. Assessment in myxedema coma include

cardiac assessment, and other assessment

performed for hypothyroidism


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Priority nursing diagnosis for thyroid

hypofunction disorder Activity intolerance

Altered nutrition

Decrease Cardiac output Hypothermia

Risk for skin integrity

Risk for injury


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Parathyroid disorder

1. The parathyroid glands are located posterior to the

thyroid glands

a. Their major function is to maintain normal serum

calcium levels by secreting TH, which increases

bone reabsorption of calcium

b. PTH respond to decrease calcium levels by

increasing calcium absorption from bone, kidneys,and intestine


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Hyperparathyroidism

It is an Increase in PTH, whichleads to hypercalcemia,hyperposphatemia, bonedamage, and renal damage


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Nursing assessment for

Hyperparathyroidism

1. Includes neurological assessment

including LOC, VS , heart rhythm, GI

assessment, complain of pain, muscle

strength, weight , I and O


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Hypoparathyroidism

It is a decrease in PTH, Which leads to

hypocalcemia, hyperreflexia, and altered

sensorium

The most common cause of

hypoparathyroidism is damage or removal of

the parathyroid gland during surgery


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f


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Nursing Assessment for

hypoparathyroidism


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NURSING MANAGEMENT

P i i i di i f


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Priority nursing diagnosis for

parathyroid disorder

Impaired physical mobility

Risk for injury Altered urinary elimination

Altered nutrition

Ad l C H f i


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Adrenal Cortex Hyperfunction

Disorder

A. Overview

1. The adrenal glands are located superior to eachkidney and composed of the adrenal medulla (the

inner layer of adrenal gland) and the adrenalcortex (the outer layer of adrenal gland

a. The adrenal medulla secretes the catecholomines:epinephrine, norepinephrine and dopamine

b. The adrenal cortex secretes mineralcorticoids(aldosterone), glucocorticoids (cortisol, androgen,andestrogens (sex hormone)


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ADRENAL CORTEX HYPERFUNCTION DISORDER

2. The function of epinephrine and norepinephrine(catecholamines) include increasing metabolic rate,increasing alertness, increasing insulin levels and

the fight or flight response3. The functions of glucocorticoids (cortisol) includes

assisting the bodys response to stress, suppressionof inflammation, increasing serum glucose by acting

as insulin antagonist, it regulates CHO, fat andprotein metabolism, enhancing protein synthesis,and increasing breakdown of protein and fatty acid


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Functions

4. The function of adrenocorticotropic hormone

is for growth and development

5. The function mineralcorticoids (aldosterone)includes sodium (Na) and water retention

and potassium excretion

6. Androgens and estrogens contribute togrowth and development


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ADRENAL CORTEX HYPERFUNCTION

DISORDER

Cushings Syndrome or hypercortisolism

result in excess production of cortisol

(glucocorticoids).

Conns Syndrome or Hyperaldosteronism

result in excess production of aldosterone

f


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Cause of Hypercortisolism

( Cushings syndrome)

Include Adrenal tumors

Adrenal hyperplasia

Or exogenous glucocorticoids

f h ld


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Causes of hyperaldosteronism

( conns syndrome)

Include adrenal lesion

Or condition that stimulate

overproduction of aldosterone: heart

failure, cirrhosis of liver, dehydration,

renal disease


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CUSHINGS SYNDROME


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Pathophysiology of Hypercortisolism

A. The functions of glucocorticoids (cortisol,

ACTH) include promoting gluconeogenesis,

maintaining serum glucose levels,

adaptation to stress, and augmenting

release of catelectomines to increase blood

pressure


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S/S of Hypersecretion of cortisol

N i t f C hi


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Nursing management for Cushings

Syndrome

Includes vital sign: increase BP/ arrhythmias

Neurological assessment

History of GI, renal, and reproductiveproblem

Muscle strength

Integument assessment Weight ; presence of edema, I and O


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N i t f C hi


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syndrome



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Nursing management for Cushing s

syndrome



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Nursing management for Cushing s

syndrome

B. Preoperative and postoperative care is for

adrenalectomy if performed

C. Assist in monitoring effects of radiation ifperformed

D. Monitor for addisonian crisis cause by drug

therapy


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Priority Nursing diagnosis for Cushings

Syndrome Fluid volume in excess

Risk for infection

Activity intolerance

anxiety

Knowledge deficit

Risk for impaired skin

integrity


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CONNS SYNDROME/

HYPERALDOSTERONISM


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Causes of Conns Syndrome or


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Causes of Conn s Syndrome or

Hyperaldosteronism

Adrenal lesion

Any condition that stimulates

overproduction of aldosterone: heartfailure, cirrhosis of liver, dehydration,

renal disease.


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Pathophysiology of Conns syndrome

a. Role of aldosterone ( a mineralcorticoid) is

soduim and water retention

b.

Aldosterone affects tubular reabsorption ofsodium and water also has role in excretion

of potassium and hydrogen ions


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S/S for Conns Syndrome

In secondary hyperaldosteronismhypertension is uncommon

Visual disturbance

Paresthesia

Dysarrythmias

Fluid retention, renal damage, polyuria

Muscle weakness, tetany

Electrolyte and acid-base imbalance

Nursing management for Conns


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Nursing management for Conn s

Syndrome

a. Medication

1. Spironolactone (aldactone) to treat

hypertension and hypokalemia for clientswho will not treat surgically

2. Amiloride (midamor) for those clients

unable to tolerate aldactone

3. Administer glucocorticoids preoperatively as

prescribed to prevent adrenal hyperfunction

Nursing management for Conns


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Nursing management for Conn s

Syndrome

B. Preoperative and postoperative care foradrenalectomy

C. If bilateral adrenalectomy is performed, life

time replacement of glucocorticoid isnecessary

D. Monitor BP, Urine output, electrolytes

E. Low sodium dietF Teach side effects of medications

Priority nursing diagnosis for Conns


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Priority nursing diagnosis for Conn s

syndrome

Altered urinary elimination

Fluid volume in excess

Risk for injury


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Addisons Crisis

It can occur, which is an acute insufficiency of

adenocortical hormone from lack of cortisol

during stress , such as surgery or pregnancy,

or exogenous corticosteroid therapy is

abruptly discontinue

If not treated immediately, circulatory

collapse, shock, and death may occur


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Nursing Management

1. Medication

A. Addisons Disease: administer cortisone,

prednisone, fludcortisone acetate (florinef)

asprescribe

B, Addisonian Crisis, immediate intravenous

glucocticoid replacement and fluids with

sodium


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Anterior Pituitary Disorder

A. Overview

1. The pituitary gland referred to as master

gland is located at the base of the brain

adjacent to hypothalamus, it is responsible

for regulating endocrine function by

producing hormone that affect body system

and stimulating other endocrine glands tosecrete hormone

Hormones Secreted By the Pituitary


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y y

glands

a. Growth Hormone (GH)

b. Thyroid stimulating hormone (TSH)

c. Adenocorticotropic hormone (ACTH)d. FSH

e. LH

f. Prolactin (PRL)


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Anterior Pituitary Disorder

3. Disorder of the anterior pituitary gland resultin excessive or insufficient pituitary hormonedisorder are as not common than other

endocrine disorder4. Growth hormone is the hormone necessary

for growth that regulates cell division and thesynthesis of protein, exerts other metaboliceffects on endocrine organs, skin. Skeletalmuscle, cardiac muscle, and connective issue

Hyperfunction of the Anterior


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Hyperfunction of the Anterior

Pituitary (Hyperpituitarism)

It is the result of excess production and

secretion of one or more hormones: (GH),

FSH, TSH, LH, ACTH: Leading to Tissue over

growth.

The most comm0n cause of hyperpituitarism

is benign adenoma

Hypofunction of the Pituitary Gland


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(hypopituitarism)

1. It is aresult in a deficiency of one or more

pituitary hormones: GH, follicle stimulating

hormone (FSH), TSH, LH, ACTH

2. Causes include surgical removal of the

pituitary gland, pituitary tumors, infection,

trauma, congenital defects, radiation


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Common Disorder

a. Hyperpituitarism ; Giantism

and acromegaly

b. Hyporpituitarism: dwarfism


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dwarfism giantism


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dwarfism giantism

CRETINISM

Hyperpituitarism


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Hyperpituitarism

Giantism Acromegaly


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Pathophysiology of Giantism

a. Giantism is the result of growth hormone

hypersecretion that begins before the closure of

the epiphysicial plates

1. This hypersecretion leads the person to becomeabnormally tall reaching 7 to 8 ft. in height

2. The body proportion are generally normal

3. Early detection, diagnosis, and treatment has madethis disorder rare in occurrence

4. Common cause is tumor


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Acromegaly

It is the result of GH over secretion during continueto grow, leading to adulthood, bone connectivetissue continue to grow , leading todisproportionate enlargement of tissue.

Most common cause is tumor S/S include large hands and feet, protrusion of the

lower jaw, coarse facial features, sign ofosteoporosis, change in hand and shoe and glove

size that slowly progress; systemic symptomshypertension, CAD, CHF, enlarge adrenal gland,thyroid and parathyroid gland


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Dwarfism

Result from deficient secretion of anterior

pituitary hormones

Inadequate secretion of these hormones

leads to growth retardation and

accompanying metabolic disorder

S/S include short stature, obesity, short pitch

voice, slow measuring skeletal system ,

hyperlipidemia, hypercholesteremia


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Nursing assessment

a. Assessment of gigantism includes growth chart for

height and weight by age and visual exam.

b. Assessment of acromegaly includes VS, Visual

disturbances, S/S of CHF or diabetes, growth anddevelopment, symptoms and analysis of pain

c. Assessment for dwarfism include growth chart and

development of sex organ

d. Diagnostic test : bone scan, cholesterol, lipid funnel

, hormone levels


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TRANSSPHENOIDAL HYPOPHYSECTOMY


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d


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Nursing diagnosis

Activity intolerance, body imagedisturbance, sexual dysfunction,

anticipatory grieving, ineffectiveindividual coping; altered growthand development


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P t i it it di d


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Posterior pituitary disorder

A. Overview

1. The posterior pituitary gland secrete

hormones oxytoxin and antidiuretic hormone

(vasopressin), the purpose of antidiuretic

hormone is to control serum osmolarity

Disorder of the posterior pituitary gland are

primarily result of excessive or deficient ADH

secretion

DISORDER OF THE POSTERIOR


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PITUITARY GLAND

A. DIABETES INSIPIDUS (DI) is the result of ADH

insufficiency, resulting to excessive fluid

excretion

B. SYNDROME OF INAPPROPRIATE

ANTIDIURETIC HORMONE SECRETION

(SIADH) is the result of excessive secretion of

ADH and water retention

CAUSES


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CAUSES

Diabetes Insipidus: unknown etiology in most

cases, head trauma with damage to the

pituitary or tumor

SIADH: occurs most often as the result of

ectopic production of ADH by malignant

tumors , but may also occur as the result of

pituitary surgery, head injury, or medicationssuch as diuretics, anesthetics and

barbiturates

N i t f DI


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Nursing assessment for DI

I and O

Complain of thirst

Dry skin Sunken eyeball weakness,

Decreased urinary output

Dry mucous membrane

S/S f DI


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S/S of DI

Polyuria

Excessive Thirst

Polydipsia Dehydration in event the client is unable to

replace fluid loss


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DI and its classification


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DI and its classification

ADH insufficiency leads to the excretion of large

amount of urine (polyuria), up to 12 L/day

Neurogenic DI occurs when there is a decrease in

the synthesis and excretion of ADH : may beidiopathic, or may result from trauma or

dysfunction of the hypothalamus or pituitary gland

Nephrogenic DI occurs when the renal tubules is not

sensitive to ADH

Nursing Management For DI


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a. Medications include vasopressin (pitressin,pressyn) for treatment of nuerogenic DI

b. Administration of hypotonic solution

c. Increase fluid intaked. Treatment is life long for chronic DI

e. Monitor daily weigh

f. Low NA diet and to avoid caffeine since this

increases urine outputg. Educate client for medic alert bracelet


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S/S of (SIADH)


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S/S of (SIADH)

Lethargy

Confusion

Changes in neurological status

Cerebral edema

Muscle cramps weakness, decrease urine

output, fluid retention, weight gain

Assessment of SIADH


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Assessment of SIADH

Assess for nuerological indicator like LOC

I and O

weight

Nursing Management For (SIADH)


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Nursing Management For (SIADH)

Medications include diuretics,

demeclocycline (declomycin)

Administration of hypertonic saline fluids

Oral fluid restriction

I and O and daily weight

Monitor for neurological changes and waterretention

Nursing Diagnosis for disorder of

t i it it di d


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posterior pituitary disorder

Fluid volume in excess

Fluid volume deficit

Altered urinary elimination Risk for Injury

Knowledge deficit


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DIABETES MELLITUS


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DIABETES MELLITUS


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CAUSES OF DM


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CAUSES OF DM

a. Type 1 DM: occurs as a result of genetic,

environmental or immunological factors that

may damage the pancreatic beta cells

b. Type 2 DM Etiology is unknown: however,

obesity is the single most important risk

factor


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S/S of DM


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a. Early manifestation of type 1 DM; polyuria,

polydispia, polypaghia, glycosuria, fatigue,

weight loss, nausea, vomiting, abdominal

pain

b. Early manifestation ofin type 2 Dm :

polyuria, polydipsia, blurring of vision,

weight gain

S/S of DM

General multisystem findings


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1. Sensory/ neurological: diabetic retinopathy,

cataracts, glaucoma, paresthesias, loss of

sensation, peripheral neuropathy

2. Cardiovascular assessment: coronary artery

disease, peripheral vascular disease,

hypertension

3. G I: constipation or diarrhea

4. Musculoskeletal : contractures

S/S of DM



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5. Integumentary : atrophy, foot ulcer, poor

wound healing, chronic skin infections

6. Renal: edema, chronic renal failure,

albuminuria, UTI

7. Reproductive assessment: Sexual

dysfunction, Vaginitis

8. Metabolic: hypergycemia, hypokalemia,

metabolic acidosis

Symptoms of DKA


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Symptoms of DKA

Abdominal pain , nausea and vomiting

Metabolic acidosis

Fruity breath odor

Kaussmauls respiration

Altered LOC

Coma and death if not untreated

Complication of DKA


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Hypoglycemia

Atherosclerosis

CVA, PVD

Retinopathy Paresthesia (especially feet)

Renal failure

Carpal tunnel syndrome,

Peridontal disease

Gangrene, amputation, inability to heal

Diagnostic test for DM


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Diagnostic test for DM

Serum fasting sugar Increase (hyperglycemia)increase to 126 mg/dl

Serum glycosylated hemoglobin levels; increase to 7percent

Urine for glucose, and ketones positive Urine for protein is positive

Serum potassium is decrease

2- hours plasma glucose (after meal) is increase to

200 mg/ dl Cholesterol and triglyceride levels is elevated

Nursing management for DM


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1. Medication include insulin and hypoglycemic agent

a. Type 1 diabetes: regular insulin, NPH insulin such

as 70/30

b. Type 2 diabetes: oral agents such as glipizide(glocotrol), glyburide (micronase), tolazamide

(tolomide), Metformin (glucophage) etc.

2. Monitor I and O, serum glucose, electrolytes

Client education for DM


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Client education for DM

A. Teach sign and symptoms of hypoglycemia

(irritability, fatigue, weakness, tremors,

headache, possible coma) and

hyperglycemia with appropriateinterventions

B. Teach for self administration of insulin or

hypoglycemic agent

Insulin therapy and insulin preparation


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In type I DM exogenous insulin must beadministered for life because the body loses theability to produce insulin

Reaction time of most common insulin preparation

Rapid-acting insulin

Short acting insulin

Intermediate- acting

Long acting insulin Very long acting insulin

Categories of insulin preparation


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Rapid acting it is indicated for rapid

reduction of glucose level, to treat

postprandial hyperglycemia, and/or to

prevent nocturnal hyperglycemia

Agent: lispro (humalog)- onset 10-15 min,

peak 1 hour, duration 2-4 hours

Apart (novolog) onset 5 to 15 min, peak 40-50 min duration 2-4 hours



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Short acting usually administered 20-30 min

before meal; may be taken alone or in

combination with long acting insulin

Agent : Regular (humalog R), Novolin R, Iletin

II regular)

Onset -1 hours, peak 1 hour, duration 4-6

hours



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Intermediate Acting it is usually taken after food

Agent: NPH( neutral protamine hagadorn)

Onset: 2-4 hours, peak: 4-12 hours, Duration 16 to

20 hours Agent: Humalin N, Iletin II lente, Iletin II NPH,

Novolin L (lente) , Iletin II (NPH), Novolin Lente,

Novolin (NPH)

Onset: 3-4 hours , Peak: 4-12 hours, Duration:16 -

20 Hours



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Long Acting Insulin it is used to control fastingglucose level

Agent: Ultra lente ( UL)

Onset: 6-8 h, Peak:12-16 h, Duration: 20-30 h

Very Long Acting it is used for basal dose(Peakless) that is the insulin is absorbed slowly for24 hours and can be given once a day and given HSoriginally, however it is now approved to be givenonce a day at any time of the day but at same timeto prevent overlap of action. It should not mix withother insulin preparation to avoid precipitationbecause of each PH of 4


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Complication of insulin therapy


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Local allergic reaction ( readiness, swelling ,tenderness and indurations or 2-4 cm wheal) mayappear at the injection site

Systemic allergic reaction it is rare, when occur

there is local skin reaction that gradually spreads togeneralized urticaria, treatment desensitization.

Insulin lipodystrophy it refers to a localized reactionin form of lipoatrophy or lipohypertrophy at theinjection site

Resistance to insulin injection.



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Morning hyperglycemiaa. Insulin Wanning it is progressive rise in blood

glucose from bedtime to morning

b. Dawn Phenomenom it is relatively normal blood

glucose until about 3 Am, when the levels begins torise

c. Somogyi Effect it is normal or elevated bloodglucose at bedtime, a decrease at 2-3 AM to

hypoglycemic levels, and a subsequent increasecause by the production of counterregulatoryhormones

Patient Education

Self injection of insulin


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Insulin injection are self administered into

subcutaneous tissue with the use of special insulin

syringe.

Self Injection1. With on hand , stabilize the skin by spreading it or

pinching large area

2. Pick up syringe with the other hand and hold it as

you would a pencil. Insert needle straight into the

skin.



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j

3. To inject the insulin, push the plunger all way

in

4. Pull needle straight out of skin. Press cotton

ball over the injection site for several seconds

5 Use disposable syringe only once and discard

into hard plastic container (with a tight-fitting

top) such as empty bleach container. Followstate regulations for disposal of needle

Selecting and Rotating the injection site


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Selecting and Rotating the injection site

Four main areas for injection

1. Abdomen

2. Upper arms (posterior surface)

3. Thighs (anterior surface)

4. Hips

Note: The speed of absorption is greatest in the

abdomen and decreases progressively in thearm, thight and hip respectively

Patient Education


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Teach the patient how to get CBG or self

monitoring glucose

Teach the client about proper dietary

management for diabetes

Teach proper diabetic foot care and wound

care

Teach for proper exercise for diabetes

lecture on endocrine diseases final

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