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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.
HORMONES PRODUCED IN THE
BODY
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TESTES: Testosterone, Estrogen, Inhibin.
OVARY:
Estrogens, Progesterone, Relaxin. PLACENTA:
Estrogens, Progesterone, HCG, HPL.
THYMUS:
Thymosin. PINEAL GLAND:
Melatonin
HORMONES PRODUCED IN THE
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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Nursing management for
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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Nursing management for
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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Nursing management for
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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Nursing management for
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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Nursing management for
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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Nursing management for
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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Nursing management for Cushings
syndrome
Nursing management for Cushings
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Nursing management for Cushing s
syndrome
Nursing management for Cushings
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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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General multisystem findings
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
General multisystem findings
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General multisystem findings
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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Categories of insulin preparation
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
Categories of insulin preparation
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Categories of insulin preparation
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
Categories of insulin preparation
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Categories of insulin preparation
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
Categories of insulin preparation
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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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Complication of insulin therapy
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.
Complication of insulin therapy
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Complication of insulin therapy
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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Self injection of insulin
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.
Self injection of insulin
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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