Adrenal medulla

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INTERFERENCES TO NUTRITIONAL
NEEDS DUE TO REGULATORY
MECHANISM DYSFUNCTION:
ENDOCRINE DISORDERS
Adrenal and Pituitary Dysfunction
2009
ENDOCRINE SYSTEM
• FUNCTION:
• Works with the nervous system
• Coordinates the response of the body to
internal and external stimuli
• Goal: to maintain homeostasis
ENDOCRINE GLANDS
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Pituitary
Thyroid
Parathyroid
Adrenals
Islets of Langerhans in pancreas
Ovaries
testes
WHAT DO ENDOCRINE GLANDS DO?
• Secrete their products directly into the
bloodstream
• Differ from EXOCRINE GLANDS which secrete
through ducts onto epithelial surface or into
the GI tract
HORMONES
DEFINED: Chemical substances secreted by the
endocrine glands
WHAT DO THEY DO?
• Hormones help regulate organ function
• They work with the nervous system
GOAL OF HORMONES
• Keep concentration of hormones in bloodstream
constant
• When levels drop: rate of production increases
• When levels are high: rate of production decreases
• NEGATIVE FEEDBACK SYSTEM: mechanism for
regulation of hormone concentration in the
bloodstream
EXAMPLE OF NEGATIVE FEEDBACK
SYSTEM
CONTROL OF INSULIN SECRETION:
• When blood glucose levels
hormone insulin secreted
• Insulin glucose uptake by the cells
blood glucose levels
• THUS: the action of insulin ( blood glucose levels) is
the opposite of the condition that stimulated insulin
secretion ( blood glucose levels)
HYPOTHALMUS
• Link between the nervous system and
endocrine system
• It controls both the posterior and the anterior
pituitary gland
ABNORMALITIES
• Based on overproduction and
underproduction
PITUITARY GLAND: ANTERIOR AND
POSTERIOR
• ANOTHER NAME: hypophysis
• Master gland of endocrine system
• Secretes hormones that control the secretion
of hormones by other endocrine glands
• It is controlled by the hypothalmus
POSTERIOR PITUITARY
HORMONES SECRETED:
• Vasopressin (or ADH or antidiuretic hormone)
STIMULATED BY:
• Increase in osmolality of the blood
• Decrease in blood pressure
PRIMARY FUNCTION:
• To control the excretion of water by the kidney
POSTERIOR PITUITARY
HORMONES SECRETED:
• Oxytocin
STIMULATED BY:
• Pregnancy
• childbirth
PRIMARY FUNCTION:
• Facilitate milk ejection during lactation
• Increase force of uterine contractions during L&D
POSTERIOR PITUITARY: QUICK
SUMMARY
• DI (Diabetes Insipidus)
ADH
urine
• SIADH (syndrome of inappropriate antidiuretic
hormone)
ADH
– Dilute urine
– Water retained
– Low sodium
ANTERIOR PITUITARY
HORMONES SECRETED control growth, metabolic
activity and sexual development:
• FSH – Follicle Stimulating Hormone
• LH – Luteinizing Hormone
• Prolactin
• ACTH - Adrenocorticotropic hormone
• TSH – Thyroid stimulating hormone
• GH – Growth hormone,or somatotropin
• MSH - Melanocyte stimulating hormone
PITUITARY: QUICK SUMMARY
ANTERIOR PITUITARY:
• Hypopituitarism: deficiency of one or more hormones
resulting in metabolic and sexual dysfunction
• Panhypopituitarism: decreased production of all anterior pituitary
hormones
• Hyperpituitarism: hormone oversecretion
– ACTH
secretion of MSH
– PRL(prolactin)
inhibits secretion of gonadotropins and sex
hormones
galactorrhea , amenorrhea, infertility
– GH
gigantism and acromegaly
ADRENAL GLANDS
There are two glands
Each has two parts
• Adrenal medulla
• Adrenal cortex
HORMONE SECRETION: is regulated by the
pituitary ACTH
ADRENAL GLANDS
Adrenal medulla at the center of the gland
secretes catecholamines
Catecholamines regulate metabolic pathways to
promote catabolism of stored fuels to meet
caloric needs
• (dopamine, epinephrine, and norepinephrine)
• EPINEPHRINE: fight or flight response
ADRENAL GLANDS
Adrenal cortex at the outer portion of the gland
secretes steroids and sex hormones:
STEROIDS:
• Glucocorticoids (cortisol)
• Mineralocorticoids (aldosterone)
PURPOSE OF STEROIDS:
• Regulate body’s response to physical and
psychological stress
ADRENAL CORTEX HORMONES AND WHAT
THEY DO
GLUCOCORTICOIDS: important to glucose metabolism
• Eg: increased secretion results in elevated blood
glucose
Glucocorticoids are often administered to patients to
reduce inflammatory response to tissue injury and to
suppress allergic manifestations
• SE: diabetes, osteoporosis, peptic ulcer, poor wound
healing
ADRENAL CORTEX HORMONES AND WHAT
THEY DO
MINERALOCORTICOIDS (aldosterone):
• Acts on the kidney and GI tract to increase Na
absorption in exchange for excretion of K or
hydrogen ions
• Secretion occurs in the presence of
angiotensin II
ADRENAL CORTEX HORMONES AND WHAT
THEY DO
SECRETION OF ADRENAL SEX HORMONES are
controlled by ACTH
ANDROGENS:
Exerts effects similar to those of male sex
hormones
ESTROGEN:
Adrenal gland secretes small amounts of female
sex hormones
ADRENAL GLAND: QUICK SUMMARY
OF DYSFUNCTION
ADRENAL CORTEX
• function adrenal insufficiency adrenal crisis,
Addison’s crisis loss of aldosterone and cortisol
• function cortisol (hypercortisolism or Cushings)
– Mineralocorticoids hyperaldosteronism
– androgens
ADRENAL MEDULLA
– Pheochromocytoma:
catecholamines
PHEOCHROMOCYTOMA
• Tumor, usually benign on the adrenal medulla,
unknown cause
• Affects men and women equally, runs in families
• Causes *****hypertension
• Severity of symptoms depends on the amount of
epinephrine and nor-epinephrine secretion
PHEOCHROMOCYTOMA S&S
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Tremor
Headache
Flushing
Anxiety
Hyperglycemia
palpitations
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Profuse diaphoresis
Chest pain
N&V
Heat intolerance
Wgt loss
DRUGS WHICH PROMOTE HYPERTENSIVE CRISIS
IN PHEOCROMOCYTOMA
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Trycyclic antidepressants
droperidol (Inapsine): sedative/hypnotic
glucagon (GlucaGen)
metoclopramide (Clopra): antiemetic
phenothiazines (Melloril): antipsychotic
Naloxone (Narcan): opiod antagonist
Foods high in tyramine
PREPARE FOR SURGERY
• Stabalize BP with IV antihypertensives of long acting
alpha adrenergic blockers: phenoxybenzamine
(Dibenzyline)
• Control tachycardia and dysrhythmias: propanolol
(Inderal)
• Suppress catecholamine synthesis: calcium channel
blockers: nicardipine (Cardene)
DIAGNOSTIC EVALUATIONS
FOR PHEOCROMOCYTOMA
• Measurement of urine and plasma levels of
catecholamines: elevated with pheochromocytoma
24 hour urine for
– VMA (vanillylmandelic acid - product of catecholamine
metabolism)
– Metanephrine
– Catecholamines
All are elevated with pheochromocytoma
PREP FOR 24 HOUR URINE TEST FOR VMA: Avoid for 2-3
days: coffee,tea,cola,cocoa,bananas,citrus fruits, chocolate,
vanilla,licorice,aspirin,antihypertensives prior to the VMA test
SURGICAL REMOVAL OF
PHEOCROMOCYTOMA TUMOR
REMOVAL OF TUMOR WITH ADRENALECTOMY
• Anesthesia and Manipulation of the tumor during
surgery may cause release of stored epinephrine and
norepinephrine
hypertensive crisis and changes of HR
• If both adrenal glands are removed: corticosteroids
replacement is necessary
POSTOP AFTER REMOVAL OF
PHEOCHROMOCYTOMA
• Hypotension, hypoglycemia may occur because of
the sudden withdrawal of excessive amounts of
catecholamines
• Urine and plasma levels of catecholamines are
measured to determine whether surgery has been
successful
• Receive volumn expanders for possible hypovolemia,
hemorrhage and shock
ADDISON’S DISEASE
• Adrenocortical insufficiency
• Results when adrenal cortex function is inadequate
to meet the patient’s need for cortical hormones
CAUSED BY:
• Decrease secretion of ACTH
• Dysfunction of hypothalamic-pituitary control
• Dysfunction of adrenal gland tissue
• Removal of both adrenal glands
STEROIDS AND ADRENAL
INSUFFICIENCY
• MOST COMMONLY CAUSED BY therapeutic use of
corticosteroids
• Corticosteroids therapy suppresses production of
glucocorticoids through negative feedback by causing
atrophy of the adrenal cortex
• Glucocorticoids MUST BE WITHDRAWN gradually to
allow for pituitary production of ACTH and activation
of adrenal cells to produce cortisol
WHAT HAPPENS WITH ADDISON’S
DISEASE?
• Insufficiency of adrenocortical steroids causes
problems through loss of aldosterone and
cortisol
WHAT HAPPENS WITH CORTISOL IN
ADDISONS
Cortisol
– gluconeogenesis (making of glucose from
proteins)
hypoglycemia
– depletion of liver and muscle glycogen
WHAT HAPPENS WITH DECREASED
ALDOSTERONE?
• ALDOSTERONE
– K EXCRETION HYPERKALEMIA
DYSRRHYTMIAS AND CARDIAC ARREST
– Na and water excretion
• Hyponatremia; craves salt, low BP
• Hypovolemia
– Hyperkalemia reabsorption of hydrogen ions
acidosis
S&S OF ADDISON’S DISEASE
• ****Muscular weakness, fatigue, emaciation
• Anorexia, GI symptoms(N,V,D) dehydration/wgt loss
• melanocyte stimulating hormone
– Dark pigmentation of skin, knuckles, knees, elbows and
mucous membranes
• c/o BEING TIRED AND WEAK (CARDINAL SYMPTOM)
– increased during stress from hypoglycemia
LABORATORY EVAL FOR ADDISON’S
DISEASE
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Low blood glucose
Low serum sodium
elevated serum potassium
High WBC (leukocytosis)
***low levels of adrenocortical hormones in
bld/urine
• Low serum cortisol levels
TEACHING PT WITH ADDISON’S
DISEASE
• Teach increase Na to prevent hyponatremia:
illness/heat/stress
• Lifelong hormone replacement
• Teach to prevent stress, prevent fatigue
• Teach to increase CHO and protein to prevent
hypoglycemia
• Lifelong problem
ADDISONIAN CRISIS
Disease at it’s worst
• Severe hypotension and shock
• Fever
• N/V, abdominal pain, diarrhea
WITH SLIGHT OVEREXERTION, EXPOSURE TO COLD,
INFECTIONS OR DECREASE IN SALT: leads to
circulatory collapse, shock, death
TO PREVENT CRISIS
• Must replace corticosteroids
• No salt restriction - leads to crisis
• No diuretics - leads to crisis
MANAGEMENT OF ADDISON’S CRISIS
• IV fluids, glucose and
electrolytes and
sodium for
dehydration
• Replace missing
cortisol and
aldosterone
deficiency:
hydrocortisone
• For Na and K imbalance
give mineralocorticoids
hormone: fludrocortisone
(Florinef)
• Glucagon for
hypoglycemia
CUSHINGS SYNDROME
(Hypercortisolism)
Increased production of ACTH
DISEASE RESULTS from too much corticosteroids
being secreted by the adrenal cortex
CAUSE; adrenocortical tumors, or pituitary
tumor secreting ACTH causing increased
secretion of glucocortiocoids
IF CAUSE OF CUSHINGS IS PITUITARY
TUMOR
• Pituitary tumor causes increased production
of ACTH
• treatment of choice is removal of pituitary
gland
WHAT IS HAPPENING IN CUSHINGS?
• Problems with nitrogen, CHO, mineral metabolism
• Slow turnover of fatty acids:
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total body fat
Truncal obesity, thin arms and legs
Buffalo hump: fat pads on neck, back, shoulders
Moon face
Pendulous abdomen
PROBLEMS IN CUSHINGS
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BREAKDOWN OF TISSUE PROTEIN
urine nitrogen excretion
1. muscle mass (muscle wasting, weakness),
edema
2. Thin skin
3. Bone density loss
PROBLEMS IN CUSHINGS:
•
levels corticosteroids
1. killing of lymphocytes
2. Shrinks organs
3. eosinophils and macrophages
ALL IMMUNE RESPONSE; leading to increased
infections
PROBLEMS IN CUSHINGS:
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1.
2.
3.
4.
5.
ANDROGEN PRODUCTION
Acne
Hirsuitism ( hair growth)
Masculination of women
Oligomenorrhea
Decreased libido
PROBLEMS IN CUSHINGS:
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1.
2.
3.
4.
SKIN CHANGES FROM BLOOD VESSEL
FRAGILITY:
Bruises
Thin skin
Wound won’t heal
Reddish striae on abdomen, thighs, and
upper arms from degrading effect of
cortisol on collagen
PROBLEMS IN CUSHINGS:
PSYCHOSOCIAL:
• Emotional lability
PROBLEMS IN CUSHINGS:
• Hypertension from water and sodium
retention
DIAGNOSIS OF CUSHINGS SYNDROME
• Cortisol levels
• Hypernatremia – increased Na leads to fluid
retention
• Hypokalemia – leads to arrhythmias
• Hyperglycemia
from cortisol
• 24 hour urine test measure cortisol levels:
NURSING CARE PT WITH CUSHINGS
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Protect from infection
Skin care
Decrease stress
ROM
VS check for hypertension
Check for edema
I&O, daily wgts, fluid
restriction
• Low cal, low Na, high
protein, high
potassium, high
calcium and high vit D
• Accuchecks: insulin
prn
• Sores won’t heal
because of increased
sugar
NON-SURGICAL MANAGEMENT:
DRUG THERAPY:
• mitotane (Lysodren): adrenal cytotoxic agent used to interfere
with ACTH production
• aminoglutethimide (Elipten): decreases cortisol production
RADIATION THERAPY: tx pituitary tumor if that is the cause
SURGERY: remove the pituitary tumor causing the adrenal
hyperfunction total hypophysectomy (removal of the
pituitary gland)
HYPER-ALDOSTERONISM
(CONN’S SYNDROME)
•
secretion of aldosterone
mineralocorticoid
CAUSED BY: secretion of aldosterone from one or
both adrenal glands caused by a tumor
RESULT: aldosterone affects the renal tubules
hypernatremia, hypokalemia, metabolic acidosis:
Hydrogen ion excretion
Conn’s syndrome continued
• Hypernatremia blood volume
BP
PITUITARY GLAND
• Master gland of endocrine system
• Secretes hormones that control the secretion
of hormones by other endocrine glands
• Pituitary controlled by the hypothalmus
HYPOPITUITARISM
RESULTS from disease of pituitary gland or of the
hypothalamus, tumor, trauma, radiation
RESULTS in deficiencies of 1 or more anterior pituitary
hormones
to metabolic problems
Sexual dysfunction
TX: replacement of deficient hormones: corticosteroids,
thyroid hormone, sex hormones, gonadotropins
DX: skull xray, CT scan (pituitary tumor)
CHANGES IN OTHER HORMONES
• ACTH and TSH are the most life threatening
because they lead to in secretion of
hormones from the adrenal and thyroid gland
• gonadotropins (LH and FSH)
changes
sex function in men and women (sterility and
infertility)
CHANGES IN OTHER HORMONES
• GH in children
• GH in adults
(osteoporosis)
growth retardation
bone destruction
SURGICAL TX FOR PITUITARY
TUMOR
HYPOPHYSECTOMY (partial or complete removal
of pituitary gland)
TWO APPROACHES:
• Craniotomy
• Transphenoidal (through the nose and into the
floor of sinuses
TRANSPHENOIDAL POSTOP CARE
• HOB up to decrease headache
• Look for CSF leak: clear drainage from nose or
postnasal drip (constant swallowing); check for
glucose in drainage. If + then means CSF
• Leak usually resolves in 72 hours
• May need spinal tap to decrease CSF pressure
• Antibiotics to prevent meningitis
POSTOP TEACHING FOR REMOVAL OF
PITUITARY GLAND
• No bending
• No straining at stool for 2 mo postop
• No toothbrushing until sutures removed and
incision heals; 10 days
• If gland removed client has permanent
diabetis insipidis
ABSENCE OF PITUITARY GLAND
Alters function of many body systems:
• Menstruation ceases
• Infertility occurs
REPLACEMENT THERAPY WITH STEROIDS AND THYROID
HORMONE NECESSARY
• Replacement hormones: cortisone and thyroid
hormones, testosterone for impotence in men and
estrogen for women for atrophy of vagina, human
pituitary gonadotropin may restore fertility in
women
FUNCTION OF POSTERIOR
PITUITARY: ADH DIABETES INSIPIDUS
HYPOFUNCTION OF THE POSTERIOR PITUITARY
of ADH or vasopressin
• Water metabolism problem caused by an ADH
• polyuria, dilute urine, dehydration, increased thirst,
low specific gravity (less than 1.005)
• Tx: lifelong aqueous vasopressin (Pitressin) therapy
TREATMENT
TX: fluid and electrolytes, I&O, wgts, IV’s to
replace losses
Administer hormone replacement: vasopressin
(Pitressin) and vasopressin tannate IM;
Lypressin nasal spray
POSTERIOR PITUITARY: ADH
SIADH: syndrome of inappropriate antidiuretic hormone
• SIADH involves hypersecretion of ADH from the
posterior pituitary gland
• With continual secretion of ADH the body retains
water leading to water intoxication
• CAUSE: bronchogenic carcinoma (malignant lung
cells synthesize and release ADH
• ALSO occurs following brain surgery, brain tumors,
infection
PROBLEMS:
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elevated urine specific gravity
Decreased urinary output (retaining fluids)
Serum Na decreases (dilutional problem)
May have respiratory/cardiac problems
May develop cerebral edema which leads to seizures
Limbs are small (no edema) gaining wgt only in body
SIADH SYMPTOMS AND
TREATMENT
TX:
• lithium carbonate (Lithobid) uncommon use ,
demeclocycline (Declomycin) commonly used
• diuretics,
• restrict fluids to promote fluid loss and
gradual increase in serum sodium
NURSING CARE
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I&O
Wgt
Blood chemistries
Keep HOB flat or slightly up to decrease the
secretion of ADH
• Neuro checks
• CONSIDER THIS SERIOUS PROBLEM
HYPERPITUITARISM
• Hormone oversecretion that occurs with
pituitary tumors
• Tumors occur most often in the anterior
pituitary cells that produce GH, Prolactin (PRL)
and ACTH
OF GH
GIGANTISM
• Slow progression
• If dx early changes preventable
• If not dx early changes in soft tissue, face,
hands, feet, skin are irreversible
• After tx changes in all but skeletal ones
• If occurs before puberty causes rapid
growth in length of all bones
GH
ACROMEGALY
• CAUSES:
– skeletal thickness,
– hypertrophy of skin
– Enlargement of visceral organs
– GH blocks action of insulin
Hyperglycemia:
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