Download ENDOCRINE SYSTEM 9

ENDOCRINE SYSTEM
ENDOCRINE SYSTEM

Endocrine system maintains homeostasis:
– Growth, maturation, reproduction, energy,
metabolism (physical and chemical changes
that takes place w/i an organism), behavior
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Composed of glands or glandular tissue:
– Synthesize, store, and secrete hormones
Exocrine- secretions passed along ducts
that empty outside body or lumen of
organ
 Endocrine- glands &/or cells are ductless
but highly vascular; secretion hormones
into bloodstream
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HORMONES
 Hormones:
natural chemical
substances secreted
 Carried in bloodstream to “target”
cells/tissues
 Effects are direct or indirect
– Trophic/tropic- stimulate another
endocrine gland
 Cells
response to hormone depends
on genetic make-up
HORMONES
 Characteristics:
– Circulate in blood at low concentrations
– Secreted in minute amounts at variable
rates
– Bind to specific receptors/cells
– Variable effects on rates of responses
– Most not stored, must be produced as
needed
– Activity is of short duration
HORMONES
 Classifications:
– Polypeptides: proteins with genetic
code; bind at cell membrane; stimulates
cellular adenyl cyclase (AMP); FAST
CHANGE (anterior/posterior pituitary)
– Steroids: derived from cholesterol;
diffuse thru cell membrane; enzyme
synthesis; SLOW CHANGE (aldosterone,
sex hormones)
– Amino acids: derived from tyrosine; act
on cell membrane; ( thyroid, dopamine,
HORMONES
 Steroid
and thyroid hormones are
not water soluble; bound to protein,
but only unbound portion is activated
and can be used.
 Peptides and catecholamine are
water soluble; not bound to protein
and can circulate freely in blood
 Lab tests measure both bound and
unbound (free) hormones
SECRETION
 Pituitary-target
gland axis: pituitary
gland regulates endocrine glands
thru tropic hormones. Tropic
hormones get feedback about
specific target glands by constant
monitoring of levels of hormone.
 Works by stimulation or inhibition of
hormones
SECRETION
Hypothalamic-pituitary-target-gland axis:
hypothalamus in brain’s di-encephalon
produces tropic hormones; in particular
the pituitary gland. In turn, pituitary
controls other target glands to produce
hormones. Therefore works indirectly
 Hypothalamus secretes releasing factors
and inhibiting factors
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FEEDBACK MECHANISMS
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Negative- increased levels of substance inhibit
hormone synthesis and secretion; decreased
levels stimulate production and release (heat
thermostat)
Positive- increased levels stimulate hormone
production and release; decreased levels inhibit
synthesis and secretion
Complex- thyroid stimulating hormone (TSH) in
pituitary is activated by thyroid releasing
hormone (TRH) and inhibited by somatostatin (in
hypothalamus). Decreased T3 & T4 leads to
increased TSH release. Increased levels lead to
inhibit TSH secretion
OTHER REGULATORY
MECHANISMS
Nervous system- central nervous system
innervates hypothalamus
 Hypoxia, pain, stress, RX affect ADH and
oxytocin levels
 Hypothalamus helps to control autonomic
nervous system
 Can be used to modify other hormones
 If secreted and transported by bloodHORMONE
 If secreted across synaptic junctionNEUROTRANSMITTER

REGULATORY MECHANISMS
 RHYTHMS-
hormonal levels fluctuate
in a 24 hour period
 Related to sleep-wake periods; darklight
– Diurnal- cortisol rises early in day, falls
toward evening
– Circadian- growth hormone, prolactin
peak during sleep
– Ultradian- menstrual cycle
DYSFUNCTIONS
DEFINITIONS
HYPERFUNCTION: excessive hormone
production/function
 HYPOFUNCTION: deficient hormone
function/production
 HYPERTROPHY: increase in size of organ,
in bulk not in # of cells or tissue elements
as a result of increased function
 HYPERPLASIA: excessive proliferation of
normal cells in normal tissue arrangement
of an organ
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DYSFUNCTIONS
CLASSIFICATIONS
 PRIMARY:
disease within endocrine
gland
 FUNCTIONAL: hormonal imbalances
resulting from disease in an organ or
tissue other than endocrine gland
 SECONDARY: disease in a target
gland
GLANDS
 HYPOTHALAMUS:
– Size of sugar cube
– Autonomic NS and endocrine functions
– Works thru releasing/inhibiting factors
– Hypothalamic-hypophysial portal system
– Functions are visceral, somatic,
behavioral/emotional; temp. regulation,
perspiration, GI secretion/motility,
appetite, thirst, B/P, respiration, sexual
behavior, fear, rage, sleep,& menstrual
cycles
GLANDS
 PITUITARY:
– Size of pea (hypophysis); 1 cm
diameter
– Located in sella turcica
– Anterior- largest lobe; growth hormone,
thyroid stimulating,
adrenocorticortrophic, follicle
stimulating, leutinizing, prolactin
– Posterior- lies behind anterior; antidiuretic, oxytocin
– Connected to hypothalamus by
hypophyseal stalk
GLANDS
 THYROID:
– Located in front of trachea; two lobes
connected by isthmus (“H” shaped)
– HIGHLY VASCULAR
– Secretes thyroxine (T4);
triiodothyronine (T3); thyrocalcitonin
(calcitonin)
– Can store large quantities of hormones
– 99%+ is bound to protein; INACTIVE
THYROID
 Increase
in oxygen use and heat
production
 Requires iodine and protein to
produce hormone
 Is able to store some hormone
GLANDS
 PARATHYROID:
– Oval shaped arranged in pairs behind
thyroid (4 total glands)
– Regulates blood levels of calcium and
phosphorus
– Free from pituitary and hypothalamus
control
GLANDS
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ADRENAL GLANDS:
– Flat, pyramid-shaped structures lying on top of
kidneys, surrounded by thick capsule; crucial
to metabolism, stress response, and fluid & elytes balance
– Cortex- firm, yellow, outer portion; 3 specific
layers
 Outer
layer secretes mineralocorticoids
 Middle layer secretes glucocorticoids
 Inner layer secretes androgens
– Medulla- reddish brown; produces and secretes
catecholamines
ADRENAL GLAND
 MINERALOCORTICOIDS-
aldosterone, maintains extracellular
fluid volume; acts on renal tubule to
promote renal re-absorption of Na+
& excretion of K+; stimulated by
angiotension II, hyponatremia,
hyperkalemia
ADRENAL GLAND
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GLUCOCORTICOIDS- cortisol,
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most abundant,
is necessary to maintain life;
secreted in diurnal pattern;
facilitates hepatic gluconeogenesis; converts
protein to glucose, decrease glucose use in
fasting state
– critical in body’s response to stress;
– anti-inflammatory response;
– maintains vascular integrity
ADRENAL GLAND
 ANDROGENS:
– Steroids secreted in small amounts
– Stimulate pubic and axillary hair growth
– Stimulate sex drive in females
– In post-menopausal women, primary
source of estrogen
Easily remembered
SALT, SUGAR, SEX
3 S’s:
EFFECTS OF AGING

General changes include:
– Increased connective tissue in glands
– Decreased blood supply
– Decreased metabolism resulting in increased
half-life of medications
– Changed:
basal level
 response to stimuli
 Transport
 Target organ responsiveness
 catabolism

ASSESSMENTS
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Hormones affect ALL body tissues
Great diversity in sign/symptoms
s/s are often vague
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Fatigue
Depression
Energy level
Alertness
Sleep patterns
Mood
Affect
Weight
Skin
Hair
Personal appearance
Sexual function
PHYSICAL ASSESSMENT
INSPECTION: use head to toe approach
 PALPATION: only thyroid and testes can
be palpated
 AUSCULTATION: cardiac baseline; bruits
 PSYCHOSOCIAL: coping skills, support
systems; health-related beliefs;
perception of self; need for social services
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DYSFUNCTIONS
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Hypo-functioning: requires hormone
replacement daily; transplants??, diet, etc.
– Purified vs. synthetic: synthetic is a more
precise dosage
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Hyper-functioning: generally harder to
treat; usually tumors removed by surgery,
radiation, or hormone antagonist
– Inhibits action of hormone; propylthiouricil
(PTU) and methimazole (Tapezole) to treat
hyperthyroidism
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Adjunctive: patient education
QUESTIONS TO ASK??
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General state of health: any noticeable changes
Past history
Medications
Past surgeries
Growth and development
Trauma (head/neck)
Size of extremities
Secondary sex characteristics
Visual changes
Menstruation
Changes in: hair, skin, nails, weight, appetite, memory, sleep,
nervous system
Family history
Stressors and coping patterns
System reviews: only endocrine gland that can be palpated is
THYROID; must be experienced to do this
DIAGNOSTIC TESTS
Specific for each hormone
 Measure absolute levels, estimate
production, transport, catabolism-complex
substances converted to simpler
substances- energy release
 May need multiple samples
 Time of sample must always be included
 Patient should be fasting, free from
stressors, no smoking, NPO
 Some samples need preservatives
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DIAGNOSTIC TESTS
 DIRECT:
– Most common; measures as hormone
appears in blood or urine
– Since minute amounts, special
techniques
– May due 24-hour testing (240 urine)
– Radioimmunoassay RIA: radioactively
labeled hormones compete with
unlabeled hormones to binding sites, etc
DIAGNOSTIC TESTS
 INDIRECT:
– Measures the substance the hormone
controls not the hormone itself
– Less costly
– Easier to administer
– EX: glucose measures insulin; calcium
measures PTH
DIAGNOSTIC TESTS
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PROVACATIVE:
– Helps to determine endocrine gland’s reserve
function with tests that show borderline results
– Stimulate an under-active gland or suppress
over-active gland
– Stimulation confirms hypofunction; hormone
given to stimulate target gland
 Stimulus
that increases secretion- hypofunction
 If does not increase despite stimulus- hypofunction
– Suppression
 Hormone
secretion continues despite suppression
confirms hyperfunction
DIAGNOSTIC TESTS
 RADIOGRAPHIC:
– Routine x-rays
 Evaluates
tissue
dysfunction and effect on body
– CAT scans
 Assesses
endocrine gland structure
– MRI
 Helps
to diagnose thyroid disorders
DEFINITIONS
SYNTHESIZE = PRODUCE
 INHIBIT = BLOCK= SUPPRESS
 ANTAGONIZE= goe against; opposite
 SECRETE
 STIMULATE
 ANTAGONIST= substance that inhibits
 AGONIST= Support; help stimulate or
produce

GLANDULAR DYSFUNCTIONS
 PITUITARY:
gland is divided into 2
lobes, anterior and posterior.
Dysfunctions of these hormones can
alter growth, metabolism, or sexual
problems
ANTERIOR PITUITARY
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HYPOPITUITARYISM: caused by deficiency of one
or more of hormones. Decreased production of
all hormones is rare, but referred to as
panhypopituitarism
More commonly, one or two deficiencies are
present
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ACTH: adrenocorticotropic hormone*
TSH: thyroid stimulating hormone*
**Most life-threatening
Deficiencies of gonadotropins (LH,FSH) change sexual
function in men and women
– Testicular failure in men, ovarian failure in women
– Lags in puberty, amenorrhea, and infertility
ETIOLOGY
 Tumors
 Postpartum
hemorrhage: Sheehan’s
syndrome, pituitary enlarges during
pregnancy and if hypotension occurs
may lead to ischemia and infarction
(necrosis) of pituitary gland leading
to hypofunction
GROWTH HORMONE
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GROWTH HORMONE: changes tissue growth
indirectly
GH stimulates liver to produce somatomedins,
which enhances growth in cells and tissues
May lead to dwarfism (growth retardation),
hypoglycemia, and delayed wound healing
May give somatrem (Protropin) to help with linear
growth
In adults, leads to decreased bone
density,(osteoporosis) pathologic fractures,
decreased muscle strength, and increased
cholesterol
GROWTH HORMONE
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ASSESSMENT:
– Changes in secondary sex characteristics,
libido
– Visual changes; diplopia
– Headache
– Weakness, fatigue, apathy
– Mental slowness, poor stress tolerance
– Dry, sallow skin
– Infection
– Orthostatic hypotension
GROWTH HORMONE
 Diagnostic
tests:
– T3 & T 4
– FSH
– TSH
– ACTH
– CT scan or x-ray: changes in structure
– Stimulation tests- insulin increases GH
& ACTH
GROWTH HORMONE
 INTERVENTIONS:
– Replace deficient hormones
– Testosterone
– Estrogen
– Surgical removal of tumor
HYPERPITUITARYISM
 HYPERPITUITARISM:
oversecretion
of hormones (same hormones as
hypo)
ETIOLOGY
 Tumors:
compresses brain tissue;
occur between 40-50 years
 Congenital defects
 Hemorrhage
 Infarction
 Inflammation from TB
 Syphilis
 Prolonged mechanical ventilation
GROWTH HORMONE
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GROWTH HORMONE: produce gigantism or
acromegaly
– Gigantism: excess hormone occurs before puberty
causing rapid proportional growth in bone length. Height
>6’6”
– Most die early with infection or trauma.
– Acromegaly: occurs after puberty producing skeletal
thickness, hypertrophy of skin, enlarged visceral organ
like liver and heart.
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Enlarged hands, feet, paranasal and frontal sinuses,
deformities of spin and mandilble, enlarged tongue, speech
difficulties, hoarseness, hypertension, oily skin, and joint
pain
Cardiomegaly leads to CHF
GH is an insulin antagonist leading to hyperglycemia
Stimulate adrenal cortex- Cushing’s Disease
GROWTH HORMONE
 DIAGNOSTIC
TESTS:
– SAME AS FOR HYPO
– Suppression tests
GROWTH HORMONE
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INTERVENTIONS:
– Surgical removal of tumor
– Radiation
– Drugs
 Bromocriptine
(Parlodel)- dopamine agonists
 Cabergoline (Dostinex)- dopamine agonists
 Octrotide- somatostatin analog that reduces GH w/I 2
weeks(given IM and can cause gallbladder disease)
– Combination therapy
– Prognosis depends on age of onset, age
treatment is started, and tumor size
– No reversal of bone growth, only soft tissue
SURGICAL PROCEDURE:
HYPOPHYSECTOMY
Procedure to remove all or part of
hypophysis;
 Uses transphenoidal approach
 70-90% successful
 Reduces risk of complicatons and death
 No visible scar or loss of hair
 Incision made in inner aspect of upper lip
and gingiva
 Enter sella turcica through floor of
sphenoid sinus
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HYPOPHYSECTOMY
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Teach mouth breathing, mouth care, ambulation, pain control,
activity, and hormone replacement prior to OR
Nasal packing for 2-3 days
Dressing applied to upper lip: “mustache dressing”
Avoid coughing, sneezing, straining at stool to prevent CSF leak
(cerebrospinal fluid leak)
HOB elevated 300 to avoid pressure on sella turcica and reduce HA
Tooth brushing avoided to prevent disruption of suture line
Nasal drainage assessed for CSF (risk for meningitis) c/o HA,
yellow halo on pillow, tests + for sugar; usually resolved w/I 720;
may need patch
S/S of meningitis-HA, nuchal rigidity, temperature,
photosensitivity
Antibiotics started
Hormone replacement started
May develop diabetes insipidus which is usually transient
POSTERIOR PITUITARY
 HYPOFUNCTION:
ADH and oxytocin
 Deficiency of ADH
responsible for
POSTERIOR PITUITARY
 ETIOLOGY:
– Tumors
– Trauma; head injury
– Radiation
– Drugs
– Infection
– Ischemia
DIABETES INSIPIDUS DI
Disorder of water metabolism
 ADH is produced by hypothalamus; stored
and released by post. Pituitary
 Decreased ADH leads to distal renal
tubules not retaining water
 Large volumes of urine excreted (polyuria)
 Massive dehydration
 Increased plasma osmolarity/osmolality
 Stimulates thirst response (if intact)
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CLASSIFICATIONS OF DI
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NEPHROGENIC:
– Inherited disorder where kidneys do not respond to ADH; no
deficiency in hormone
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PRIMARY:
– Defect in pituitary or hypothalamus; lack of ADH production or
secretion
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SECONDARY:
– Tumors of pituitary or hypothalamus; trauma, infection,
surgery, metastasis of oat cell cancer in lung or breast
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DRUGS:
– Any drug that might interfere with kidney’s response to ADH;
lithium carbonate (psych- manic/depressive)
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PSYCHOGENIC:
– Client ingests large quantities of water, usually 5 liters or more
which in turn depresses ADH production/secretion
DI
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ASSESSMENTS:
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Water loss (free water)
Plasma osmolality increases
Serum sodium increases
Urine osmolality decreases
Thirst
Frequent voiding (4 liters/240); 200ml/hr with
specific gravity<1.005
– Abrupt onset (1-2 days after injury)
– Weight loss, fatigue, constipation, anorexia
DI
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DIAGNOSTIC TESTS:
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Serum sodium- increase
Plasma osmolality- increase
Specific gravity of urine- decreased
Water deprivation test- withhold food and water at 6am.
Measure urine volume, osmolality, specific gravity hourly
until osmolality is constant. Measure serum osmolality,
give Vasopressin, and take measurements again. Urine
osmolality >serum before and after test.
– Vasopressin test – used less frequently
– Hypertonic saline test- NS followed by 3% salinesudden decrease in urine output is sign of ADH release
DI
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INTERVENTIONS:
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Maintain fluid and e-lyte balance
Identify and correct cause
IV fluids (hypotonic)
Unrestricted access to fluids
Administer Vasopressin
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Aqueous for short-acting needs
Tannate in oil for long-acting needs
– Diabenese- only used if partial reduction in ADH;
increases action of ADH
– Severe cases administer desmopressin acetate DDAVPsynthetic form of ADH (metered dose inhaler) irritate
nasal mucosa
– Daily weights are a must!!
POSTERIOR PITUITARY
 HYPERFUNCTION
 Oversecretion
of ADH even with low
osmolalities (Schwartz-Bartter
Syndrome)
SYNDROME OF INAPPROPRIATE
ADH SIADH
 Water
is retained but no edema
 Dilutional Hyponatremia
 Sodium loss from kidneys further
leads to hyponatremia
 Positive feedback- elevated ADH
release persists even with increased
plasma volume and decreased
osmolality
SIADH
 ETIOLOGY:
– Cancer
– Cerebrovascular accident- CVA
– Tuberculosis -TB
SIADH
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ASSESSMENTS:
– Changes in LOC:
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 Malaise,
nausea, HA, irritability
Tachycardia
Increased B/P
Water intoxication
Fluid shifts especially in brain lead to LOC
changes
– No dependent edema initially
– Na+ < 130; dilutional hypocalcemia; normal
BUN, creatinine
– Symptoms depend on rate of onset
SIADH
 DIAGNOSTIC
TESTS:
– Serum sodium- decreased
– Serum calcium- decreased
– BUN and creatinine- normal
– Plasma osmolality- decreased
– Urine osmolality- elevated
SIADH
 INTERVENTIONS:
– Restrict fluids to 500-600cc/240
–I & O
– Daily weights
– Diuretics
– Hypertonic saline (3%) use with caution
– Drugs:
 Lithium
carbonate- can cause toxicity
 Declomycin**- more commonly used