Endocrine 2

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ENDOCRINE SYSTEM  is a control system in which a stimulus

 Plays a vital role in orchestrating initiates a response that reverses or


cellular interactions, metabolism, reduces the stimulus, thereby stopping
growth, reproduction, aging, and the response until the stimulus occurs
response to adverse conditions again and there’s a need for response.
 Composed of endocrine glands and  As the hormone exerts its effects, the
specialized endocrine cells stimulus for secretion is reverse, and
 Disorders of the endocrine system are the secretion of hormone decreases.
common and are manifested as  Ex: of NFM: Insulin is secreted by the
hyperfunction and hypofunction Pancreas when the blood glucose is
high; that is, Hyperglycemia is the
ENDOCRINE GLANDS stimulus for secretion of insulin. Insulin
 Are glands that secrete hormones in enables cells to remove glucose from
the blood. Hormones (travel through the blood so that it can be used for
blood circulation) exert their effort on energy production and enables the liver
target organs or tissues or effectors. to store glucose as glycogen. As a result
 Target tissues are specific sites where of these actions of insulin, the blood
hormones produce a particular glucose decreases, reversing the
response of the target tissues. stimulus for secretion of insulin.
 These glands are the ff: Pituitary gland,
POSITIVE FEEDBACK MECHANISM
thyroid gland, Thymus, parathyroid
 A control system that requires an
gland, Pineal, adrenal glands,
external event to stop or reverse the
 Organs: Pancreas, ovaries and testes.
stimulus; may become a self-
REGULATION OF HORMONES perpetuating cycle that causes harm.
 Endocrine glands are composed of  The response to the stimulus does not
secretory cells known as ACINI. A rich stop or reverse the stimulus, but
blood supply provides a vehicle for the instead keeps the sequence of event
hormones produced by the endocrine going.
glands to enter the bloodstream  The release of oxytocin from the
rapidly. posterior pituitary gland during labor is
 Hormones are secreted when there is a an example of positive feedback
need for their effects on their target mechanism. Oxytocin stimulates the
organs. Each hormone has specific muscle contractions that push the baby
stimulus for their secretions. Remember through the birth canal. The release of
that the amount of circulating oxytocin result in stronger or
hormones depends on their unique augmented contractions during labor.
function and the body needs. In healthy
physiologic state, hormone CLASSIFICATION OF HORMONES
concentration in the blood stream is Hormones maybe classified into three groups
maintained at constant level.
a. AMINES
 To prevent accumulation, the secretion
 Structural variations of the amino acids
of most hormones must be regulated or
 tyrosine, thyroxine (from thyroid gland)
inactivated by NEGATIVE FEEDBACK
and epinephrine and norepinephrine
MECHANISM so that when the
(from adrenal medulla).
hormone concentration increases,
further production of hormone is b. PROTEINS
inhibited. Or when the hormone  Are chains of amino acids
concentration decreases, the rate of  Insulin (pancreas), growth hormones
production of that hormone increases. (from APG) and calcitonin (from the
thyroid gland) are all proteins
NEGATIVE FEEDBACK MECHANISM  Short canes of amino acids are called
 Negative means “to decrease” PEPTIDES
 Reverses a change in the variable to
bringing it back to “normal”
 Antidiuretic hormones and oxytocin Corticotropin Releasing Hormone(CRH)
(synthesized by hypothalamus) are  Causes the release of ACTH from the
peptide hormones. anterior Pituitary Gland
 TRH, FSH, GH  Adrenocorticotropic hormone in turn
travels in the bloodstream to the
c. STEROIDS.
adrenal glands, where it causes the
 penetrate cell membrane and interact
secretion of the cortisol.
with cellular receptors.
 CRH is produced during physiological
 Includes cortisol, corticosteroids and
stress situation such as injury, disease,
aldosterone produce by adrenal cortex),
exercise and hypoglycemia
estrogen and progesterone (ovaries)
Somatostatin
and testosterone (testes)
 Inhibits the GH and TSH
Dopamine
d. Fatty acid derivatives
 Inhibits the prolactin, FSH and LH
 Ex: eicosanoids and retinoids
 Eicosanoids - include prostaglandins,
leukotrienes that mount or inhibit
PITUITARY GLAND
inflammation, allergy, fever and other  Hangs from the hypothalamus and
immune responses; enclosed by sella turcica of the the
 Retinoids- reduce fine lines and sphenoid bone. (the bonny floor that
wrinkles by increasing the production of supports the brain)
collagen. They also stimulate the  It is composed of two Parts: Anterior
production of new blood vessels in the Pituitary Gland and Posterior Pituitary
skin, which improves skin color. Gland

HYPOTHALAMUS Hormones of Anterior Pituitary Gland


 The part of the brain superior to the  Secretes GH, ACTH,TSH, FSH, LH,
pituitary gland and inferior to the Prolactin
thalamus 1. Growth Hormones
 It releases and inhibit hormones  Known as somatotropin or
 It regulates body temperature and somatotropic hormones
regulates the secretions of the  Regulated by GHRH (hypothalamus) -
pituitary gland stimulates secretion
 Thyrotropin-releasing hormone(TRH,  GHIH (Somatostatin)
Gonadotropin-Releasing - inhibits secretion
Hormone(GnRH), Corticotropin Functions
Releasing Hormone(CRH), somatostatin,  Promotes growth of body tissues. It
dopamine , PIH, PRH concerns with growth of cells, bones
and soft tissues
Thyrotropin-releasing hormone (TRH)  Stimulate cells to produce insulin
 is a hormone produced by the  Increase the rate of CHON synthesis and
hypothalamus that stimulates the increases the use of fats as energy
release of thyroid-stimulating hormone metabolism.
(TSH) and prolactin from the anterior  It increases blood glucose levels by
pituitary. reducing glucose utilization (insulin
Gonadotropin-Releasing Hormone (GnRH) antagonist)
 causes the APG in to secrete and  GH increases the transport of amino
release the luteinizing hormone (LH) acids into cells and increases the rate of
and follicle-stimulating hormone (FSH).
CHON synthesis. Amino acid cannot be
 In men, these hormones cause the
restored by the body, so when they are
testicles to make testosterone. In
available, they must be used in protein
women, they cause the ovaries to make
estrogen and progesterone. synthesis.
2. ADENOCORTICOTROPIC HORMONES (ACTH)  Increases the secretion of testosterone
 Stimulates the adrenal cortex to secrete 6. PROLACTIN
cortisol  AKA mammotropic hormone, lactotropic
 Corticotropin releasing hormone (CRH)- hormone or luteotrophic hormone
stimulate the APG to increase the secretion  Stimulates milk production by the
of ACTH mammary gland
 CRH is produced during physiological stress  It is necessary for breast development and
situation such as injury, disease, exercise lactation
and hypoglycemia  If mothers continue to breastfeed, prolactin
 Cortisol is a steroid hormone made by the levels remain high.
adrenal cortex that is important for  Prolactin Releasing Hormone (PRH)-
regulating glucose, protein, and lipid stimulate the secretion from the
metabolism, suppressing the immune hypothalamus.
system's response, and helping to maintain  Prolactin Inhibiting Hormone- inhibits the
blood pressure secretion from the hypothalamus

7. MELANOCYTE STIMULATING HORMONE (MSH)


3. THYROID STIMULATING HORMONE/TSH
 Necessary for skin pigmentation (skin,
 AKA thyrotropin and the target organ is the
retina)
Thyroid gland
 Increases melanin production in
 Increases the secretion of thyroxine (T4)
melanocytes to make skin darker;
and thriodothyronine T3 by the TG
 Stimulus: Thyrotropin Releasing Hormone POSTERIOR PITUITARY GLAND
(TRH)- stimulates the secretions of TSH  There are two hormones of PPG,
from the hypothalamus. When metabolic  the ADH and Oxytocin
rate decreases, TRH is produced.  Their release is stimulated by nerve
GONADOTROPHIC HORMONES impulses from the hypothalamus.
TWO TYPES
ANTI-DIURETIC HORMONE
4. Follicle Stimulating Hormone (FSH)  AKA VASOPRESSIN
 Its effects is on the gonads (ovaries and  Increases the reabsorption of water by
testes kidney tubules which decreases the amount
 GNRH- stimulated the secretion of FSH. of urine formation
In women:  It decreases sweating
 stimulates the growth of ovarian follicle,  The water is reabsorbed in the blood, so
ovulation urinary output is decrease, blood volume
 Increases secretion of estrogen by follicle increase that maintain normal BP.
cells  If too much water is loss through sweating
In Men or diarrhea, Osmoreceptors in the
 Initiates sperm production in the testes hypothalamus detect the increase
“saltiness” of the body fluids, the
5. LUTEINIZING HORMONE hypothalamus transmit impulses to the PPG
In women to increase the secretion of ADH and
 Responsible for ovulation (aids in egg decrease the loss of water
maturation and provides the hormonal  Any type of dehydration stimulates the
trigger to cause ovulation and the release secretion of ADH to conserve body water
of eggs from the ovary)  In case of Hemorrhage- ADH (in large
 Causes the rupture ovarian follicle to amount) is release that will cause
become and develop corpus luteum which VASOCONSTRICTION in arterioles to raise
secretes progesterone. or maintain BP. (Vasopressin)
Progesterone  Ingestion of alcohol inhibits the secretion
 prepares the uterus for pregnancy of ADH and it increases the UO.
 After you ovulate each
month, progesterone helps thicken the OXYTOCIN
 Cause contraction of myometrium of the
lining of the uterus to prepare for a
uterus after labor has begun.
fertilized egg. If there is no fertilized
 Stimulus: nerve impulses from the
egg, progesterone levels drop and hypothalamus as cervix is stretched and as
menstruation begins infants suck the nipple
In Men
 As labor begins, the cervix of the uterus is T4
stretched which generates sensory impulses  weak hormone, maintains body metabolism
to the hypothalamus, which in turn in a steady rate
stimulates the PPG to release oxytocin. This  contains 4 iodine atoms
causes the strong uterine contraction to  NV: 5.4-11.5ug/dl or 57-148nmol/L
bring about delivery of the baby and the T3
placenta. (positive feedback mechanism).  five times potent as T4 and has more
The external break or shutoff of the metabolic action
feedback cycle is the delivery of the baby  contains 3 iodine atoms
and the placenta.  80-200ng/dl or 1.2-3.1 nmol/L
 Promotes release of milk “let down” reflex Functions: plays a huge role in:
from the mammary glands.  Main function: to control the cellular
metabolic activity
PINEAL GLAND  burning calories (Regulates energy
 Located at the back of the third ventricle of production and protein synthesis)
the brain  how new cells replace dying cells
 Secretes melatonin  how fast we digest food
 stimulate sympathetic nervous system
MELATONIN (alertness, quick responsiveness/reflexes)
 A hormone produced by the pineal gland  increases body temperature and heart rate
that stimulates the onset of sleep, brings  important in brain development and normal
sleep growth
 muscle contraction and fertility
THYROID GLAND  regulates TSH (thyroid-stimulating
 Is located in front and on the side of the hormones through the negative feedback
trachea just below the larynx. loop)
 produces thyroid hormones that play a big  Necessary for normal physical, mental and
role in body metabolism, regulation of body sexual development.
temperature, and growth/development.  Increase cell respiration of all food types to
 Thyroid follicles- the structural units of the increase energy and heat production
thyroid gland that produces  Regulate CHON, CHO and fat metabolism
T3 Triiodothyronine, T4 Thyroxine (most  Act as insulin antagonist
important when talking about hypo/hyper  Maintain growth hormone secretion and
thyroidism), and Calcitonin. promote skeletal maturation
 Thyroid can NOT make thyroid hormones  Affects CNS development CR, force and
without iodine (Iodine is necessary for the output
synthesis of these hormones ) which comes  Stimulate SNS activity
from foods (if you don’t have enough iodine  Stimulus: TSH from APG
in your diet…low t3 and t4…this leads to Regulation of Thyroid Hormone
hypothyroidism and if you have too much TSH (Thyrotropin):
hyperthyroidism)  produced from the anterior pituitary gland
 Secretion of T3 and T4 is stimulated by TSH that stimulates T3 and T4 production
from APG.  Controls the rate of hormones release
 When metabolic rate decreases, the though negative feedback mechanism.
hypothalamus detect this changes, which  The level of thyroid hormone in the blood
secretes the Thyrotropin releasing determines the release of TSH. If the
Hormone (TRH). TRH stimulate thyroid hormone in the blood decreases
the APG to secrete TSH. TSH will stimulate the release of TSH increases, which causes
increase of T3 and T4.
the thyroid gland to release T3 and T4,
Negative Feedback Loop of Thyroid Hormone
which raise the metabolic rate by
Production
increasing energy production. (Negative  Hypothalamus produces -
feedback mechanism) then shut off TRH > TRH (Thyrotropin-releasing hormone)…
from the hypothalamus until metabolic rate this causes the Anterior Pituitary Gland to
decreases again. produce ->TSH (thyroid-stimulating
hormone)….this cause the thyroid gland to
HORMONES SECRETED BY THYROID GLAND produce-> T3 & T4
1. T4 (Thyroxine) and T3 (Triodothyronine)
 Produced by thyroid follicles Note: There can be problems with the feedback
 Both are amino acids that contain iodine system where the pituitary gland is not stimulating
molecules the thyroid gland enough so hormones are not
produced or the thyroid is not receptive to the TSH EXOCRINE Function
from the pituitary gland.  the secretions of the exocrine pancreas are
digestive enzymes high in protein content
CALCITONIN (Thyrocalcitonin) and electrolytes rich in fluid
 Amylase- aids in digestion od CHO
 Produced by parafollicular cells
 Trypsin- aids on digestion of CHON
 acts to reduce calcium levels in
 Lipase- aids in digestion of fats
the blood/ lowers blood calcium levels
 It inhibits osteoclastic activity ENDOCRINE PANCREAS
 It lowers phosphate levels ISLET of LANGERHANDS
 It decreases CA and Phosphorous in the GI  The endocrine portion of the pancreas that
tract secretes insulin and glucagon.
 It helps maintain stable and strong bones  Contain alpha, beta and delta cells
matrix.  ALPHA CELLS- produce glucagon
 Stimulus: hypercalcemia  Beta Cells- produce insulin
 Relationship of Calcitonin and Calcium  Delta cells- secrete somatostatin
 Calcitonin is High, Calcium is Low
 Calcitonin is Low, Calcium Is High HORMONES OF THE PANCREAS
A. GLUCAGON
PARATHYROID GLANDS  Secreted by alpha cells, its effect is to raise
 are located in the neck behind the thyroid the blood glucose by converting the
where they continuously monitor and glycogen to glucose in the liver
regulate blood calcium levels.  Stimulates the liver to change glycogen to
 Four parathyroid glands on the back of the glucose (Glycogenolysis)- glycogen
thyroid gland that secretes parathormone. breakdown)
 Enhances gluconeogenesis (breakdown of
PARATHYROID HORMONE fats and proteins into glucose) and elevates
 The hormone produced by parathyroid blood glucose levels
gland  The secretion of glucagon is stimulated by
 Is an antagonist to calcitonin hypoglycemia.
 PTH regulates CA and phosphorus balance  Result: Raises blood glucose level
 PTH elevates Ca levels by withdrawal of ca
from the bones and inversely, lowers GLYCOGEN- a polysaccharide that is storage from for
phosphorus levels excess glucose in the liver and muscles.
 Increases the reabsorption of calcium and GLYCOGENESIS- conversion of glucose to glycogen to
phosphate from bone to blood be stored in the liver as potential energy.
 Increases the reabsorption of calcium and GLYCOGENOLYSIS- the conversion of stored
the excretion of phosphate by the kidneys; glycogen into glucose to be use for energy
activates Vit D. production.
 Hypocalcemia stimulate the secretion of GLYCOLYSIS
PTH, Hypercalcemia inhibit the secretion of
 Increases the conversion of glycogen to
PTH
glucose in the liver
 Hypersecretion of PTH- Hypercalcemia,  Increase the use of fats and excess amino
Hypophospatemia acids for energy production
 Hyposecretion of PTH- Hypocalcemia,
Hyperphosphatemia INSULIN
 Secreted by BETA CELLS
PANCREAS  The action is to lower the blood glucose by
 Located in the left upper quadrant of the permitting entry of glucose into the cells of
abdominal cavity the liver, muscle and other tissues
 It has both exocrine (secreting externally,  Promotes the storage of fat in adipose
hormonal secretions from excretory ducts tissue and the synthesis of proteins in
and endocrine (secreting internally, various body tissues
hormone secretion of a ductless gland)  Increases the transport of glucose from the
 Exocrine functions includes secretions of blood into the cells. In the absence of
pancreatic enzymes into the GI tract insulin, glucose cannot enter the cells and
through the pancreatic duct. excreted in the urine. This condition called
 The endocrine functions include secretion Diabetes- high levels of glucose in the
of insulin, glucagon and somatostatin blood. In diabetes, stored fats and proteins
directly in the blood stream
are used for energy instead of glucose  Increases the reabsorption of Na and
causing loss of body mass. excretion of K by kidney tubules
 Increases the use of glucose by cells to  Aldosterone is Pro NA (retain NA), ANTI K
produce energy. Once inside the cell, (excretes K)
Glucose is used in cell respiration to  High Aldosterone- Hypernatremia,
produce energy. Hypokalemia:
 Stimulates the liver and muscles cells also  Low Aldosterone- Hyponatremia,
change glucose to glycogen (glycogenesis- Hyperkalemia
means glycogen production)  When BP decreases, secretion of
 Increases the cellular intake of fatty acids aldosterone stimulates the reabsorption of
and amino acids to use for synthesis of Na ions by the kidneys. Water follows
lipids and CHON sodium back to the blood to maintain
 Stimulated by hyperglycemia normal blood volume and blood pressure.
 Results: lowers blood glucose level  Sodium ions return to the blood while the
potassium ions are excreted in urine
C. SOMATOSTATIN  Stimulus: decreased Na in the blood,
 Exerts hypoglycemic effect by interfering or elevated potassium, decrease blood volume
inhibiting the release of growth hormone, or blood pressure.
insulin and glucagon from the pancreas  Low BP or blood volume activates the
 Inhibits the secretion of insulin and RENIN ANGIOTENSIN MECHANISM of the
glucagon kidneys to secrete the enzyme RENIN.
 RENIN splits the plasma protein
ADRENAL GLANDS/ Supra renal glands angiotensinogen to Angiotensin I
 One on top on each kidney  Angiotensin I is converted into Angiotensin
 Each has an INNER ADRENAL MEDULLA and II by an enzyme (converting enzyme) causes
OUTER ADRENAL CORTEX vasoconstriction and stimulates secretions
ADRENAL MEDULLA of aldosterone by the adrenal cortex that
 the inner part of an adrenal gland, controls will cause increase in BP.
hormones that initiate the flight or fight
response. CORTISOL
 Produces catecholamines in stress  Group of hormones called glucocorticoids
situations such as epinephrine and  Increases use of fats and amino acids for
norepinephrine energy.
 Stimulus: sympathetic impulses from the  Decrease the use of glucose because it
hypothalamus conserves glucose for use by the brain.
 cortisol provides the body with glucose by
1. NOREPINEPRINE/ NOR-ADRENALIN
tapping into protein stores via
 Stimulates vasoconstriction and raises BP
gluconeogenesis in the liver. This
2. EPINEPHRINE/ADRENALIN
energy can help an individual fight or flee a
 Increases the HR and force
stressor. However, elevated cortisol over
 Causes vasoconstriction in skin and viscera
the long term consistently produces
and vasodilation in skeletal muscles
glucose, leading to increased blood sugar
 Dilates bronchi
levels
 Slows peristalsis
 Anti-inflammatory effect- during
 Causes the liver the to change glycogen into
inflammation, histamine from damage
glucose to raise blood glucose level
tissue makes capillaries more permeable
 Increases the use of fats for energy
and the lysosomes of damage cells release
their enzymes which help breakdown
ADRENAL CORTEX
damage tissue.
 is the outer region and also the largest part
 Inflammation, more damage on the tissue,
of an adrenal gland.
there will be secretion of cortisol to brake
 Secretes three types of steroids hormones
or limit the inflammation process, which is
 Mineralocorticoids (ex: Aldosterone),
useful for tissue repair and to prevent tissue
Glucocorticoids, and very small amount of
destruction.
sex hormones
 it blocks the effect of histamine and
 It control the 3 S, Sugar, Salt and Sex
stabilize lysosomes to prevent excessive
tissue damage.
ALDOSTERONE
 Too much cortisol decreases the immune
 Most abundant mineralocorticoids
response leaving the body susceptible to
 Target organs are the kidneys
infection and slows the healing of damage PROSTAGLANDIN
tissues.  Synthesized by cells from the phospholipids
 ACTH- direct stimulus of corstisol from APG. of their cell membranes
 Involve in inflammation and pain,
HISTAMINE reproduction, nutrient metabolism, changes
- An inflammatory chemical release by damage in blood vessels, blood clotting
tissues as part of innate immunity; stimulates THYMUS GLAND
increased capillary permeability and vasodilation.
 located behind your sternum and
OVARIES between your lungs, is only active until
 Located in the pelvic cavity on the either puberty.
side of the uterus  After puberty, the thymus starts to
 Estrogen, progesterone, and inhibin slowly shrink and become replaced by
fat.
a. ESTROGEN  Thymosin is the hormone of the
 Secreted by follicles cells in the ovary thymus, and it stimulates the
 Promotes the maturation of the ovum in development of disease-fighting T cells.
the ovarian follicle and stimulates the  Thymopoietin and thymulin- assist in
growth of blood vessels in the the process where T cells differentiate
endometrium. into different types
 Affects the development of female sex
organs and Stimulates the development of DIAGNOSTIC TEST
secondary sex characteristics THYROID FUNCTION TEST
 Promotes the closure of epiphysis of long
bones.
TSH ASSAY
 Lowers blood levels of cholesterol and
triglycerides.  Serum TSH concentration is the primary
 Stimulus: FSH from APG screening tests for thyroid function
b. PROGESTERONE  TSH has a high sensitivity (98%) and
 Produced by corpus luteum of the ovary specificity (92%) use to confirm thyroid
and placenta disease
 “Hormone of pregnancy”  It is also used for monitoring patients
 Responsible for the growth of endometrium with thyroid replacement therapy
and maintenance of pregnancy.
 The normal range for TSH is between
 Prepares uterus for implantation
0.5 mU/l and 5.0 mU/l.
 Promotes storage of glycogen and growth
 A high TSH suggests your thyroid is
of secretory cells of mammary glands.
underactive (hypothyroid) and not
 Decreases uterine contraction
 Stimulus: LH from APG
doing its job of producing enough
thyroid hormone. TSH levels will be
c. INHIBIN- inhibits secretion of FSH increased, if the thyroid gland is not
working due to infection or
TESTES –located in the scrotum between the upper inflammation, as in Hashimoto's
thighs thyroiditis, or autoimmune thyroiditis.
 A low TSH suggests your thyroid is
TESTOSTERONE overactive (hyperthyroid) and
 Produced by interstitial cells producing excess thyroid hormone. If
 Promotes maturation of sperm the thyroid gland is secreting levels of
 Stimulates the development of secondary hormones that are too high, the
sex characteristics among males pituitary gland produces less TSH.
 Promotes the closure of epiphysis of long  High TSH– Hypothyroidism
bones  Low TSH- Hyperthyroidism
Inhibin  No preparation is required
 Inhibits the secretion of FSH to maintain
constant rate of sperm production. T4
 weak hormone, maintains body metabolism
Other Hormones in a steady rate
 NV: 5.4-11.5ug/dl or 57-148nmol/L
T3  Instruct patient to fast overnight before
 five times potent as T4 and has more administration, food delays absorption.
metabolic action  It will take several weeks (usually 6
 contains 3 iodine atoms
weeks) before Therapeutic effects
 80-200ng/dl or 1.2-3.1 nmol/L
become noticeable
 No preparation is required
INTERPRETATION
 Urine and saliva are slightly radioactive
 Increased- Hyperthyroidism
for 24 hours after administration.
 Decreased- hypothyroidism  SE. Metallic taste in the mouth, nausea,
swollen salivary glands.
Radioactive Iodine Uptake (RAIU) Thyroid Antibodies
 Detects hyperthyroidism and  Indicated to diagnose autoimmune
hypothyroidism thyroid diseases both hypothyroid and
 Involves the ingestion of tracer dose hyperthyroid conditions
iodine (123 0r 131) followed in 24  Positive anti thyroid antibodies in
hours by a scan of a thyroid gland autoimmune thyroid disease,
 Gradually shrinking your ultimately Hashimoto’s thyroiditis, and Grave’s
destroying the gland leaving the thyroid disease
unable to produce enough hormones Serum Thyroglobulin
 is a permanent and more reliable cure  Can be measured by radioimmunoassay
for hyperthyroidism  Radioimmunoassay- a technique for
 Anti-thyroid, limits thyroid hormone determining antibody levels by
secretion introducing an antigen labeled with a
radioisotope and measuring the
 Patient with hyperthyroidism exhibit a
subsequent radioactivity of the
high iodine uptake and patient with
antibody component.
hypothyroidism exhibit a very low  Used to detect persistence or
iodine uptake. recurrence of thyroid carcinoma
 High Iodine uptake- Hyperthyroidism Fine Needle Aspiration Biopsy
 Low Iodine Uptake- Hypothyroidism  A small gauge of needle to get sample
from the thyroid tissue to accurately
Patient Teaching detect malignancy
 Radioactive dose is small and harmless  Initial test for evaluation of thyroid
 Collect 24 hours urine specimen after masses
tracer dose is given  Results: Negative- benign, Positive-
 Thyroid scan after 24 hours malignant, Indeterminate – suspicious,
 Contraindicated in pregnancy this can Inadequate- non diagnostic
lead to fetal hypothyroidism, mental
retardation and increased malignancy Diagnostic Imaging Studies
risk in the infant THYROID SCAN
 Avoid Sea foods may elevate or alter  Determine the location, size, shape and
the result anatomic function of TG
 Avoid Drugs that may elevate the  Radioactive iodine (123 and 131)is
results- Barbiturates, Lithium, taken orally; dose is harmless
Phenothiazines, topical antiseptics, food  Scanning is done after 24 hours
supplement that contain seaweeds,  Avoid iodine containing foods, dyes and
estrogen, salicylates, amiodarone, medication
antibiotics, corticosteroids and diuretics  Cold nodules- CANCER
 Avoid Drugs that may decrease the  Hot Nodules- BENIGN
results- Lugol’s solution, Saturated ULTRASOUND
Solution of Potassium Iodide, Anti  No preparation
thyroid, Aspirin, and Anti histamines
 Normal HR; Adequate sleep
 The total cathecholamine value
MRI decreases at least 40% from the client’s
 Test cannot be done in clients with baseline
metal implants (pacemakers, 4. CT scan, MRI, Ultrasound
arthroplasties, skull plates)  To locate pheochromocytoma
 Ask for allergy to contrast media
CT SCAN TEST for PANCREATIC DISORDERS
 if with contrast medium, note for 1. FBS/FBG
allergy history  Detects DM
 Normal value: 70-110mg/dl
Diagnostic For Parathyroid Disorders  A blood sugar level of more than
1. Total Serum Calcium (8.5-10.5mg/dl) 140mg/dl for two consecutives readings
 Venous blood is collected  Preparation: Instruct the client to be on
 Increased- Hyperparathyroidism NPO
 Decreased- Hypoparathyroidism 2. Two Hour Post Prandial Blood Sugar/ 2hrs
2. PTH Radioimmunoassay PBBS
 Venous blood is collected  Initial venous blood is withdrawn
 NV: 11-51 pg/mL  100 gm of CHO in diet is taken from the
 Increased- Hyperparathyroidism client
 Decreased- Hypoparathyroidism  2 hours after meal, blood is withdrawn-
 When elevated in conjunction with blood sugar returns to normal level
serum calcium levels, this is the most
specific test for Hyperparathyroidism. 3. Oral Glucose Tolerance Test/ OGTT
 Done when FBS and 2hr PBBS are
TEST for Adrenal Medullary Disorders BORDERLINE
1. VANILLYMANDELIC ACID TEST (VMA TEST)  Take high CHO diet (200-300g) for 3
 VMA is a metabolite of epinephrine days
 NV- 0.7- 6.8mg/24hr  Avoid alcohol, coffee or smoking for 36
 24 hour urine collection is collected hours before the test
 Avoid the following- Coffee, Chocolate,  NPO for 8-12 hours
Tea, Bananas, Vanilla, Aspirin  Initial blood specimen or urine is
2.TOTAL PLASMA CATHECOLAMINE collected
CONCENTRATION
 150-300 gm of glucose per orem or IV is
 To detect the level of cathecholamine
given
levels
 Series of blood specimen is collected
 Supine position
after administration of glucose (30
 Butterfly needle is inserted 30 minutes
minutes, 1 hr, 2hrs, if required 3hrs, 4
before specimen is collected- to
hrs, 5 hrs after)
prevent elevation of cathecholamine
 If glucose is higher than normal at 1 to 2
levels by stress and venipuncture
hours after ingestion or injection of
 Epinephrine- 100pg/ml or 590pmol/L
glucose and are SLOWER than
 Noradrenaline- 100-550pg/ml
Normal to return to fasting levels, DM is
3. CLONIDINE SUPPRESSION TEST
confirmed.
 Clonidine (Catapress)- a central acting
4. HbA1C/ Glycosylated Hgb
adrenergic blocker suppresses the
 The Most accurate indicator of DM
release of cathecholamines
 It reflects serum glucose for the past 3-
 In PHEOCHROMOCYTOMA- clonidine
4 months
does not suppress the release of
 Glycated hemoglobin is a form of
cathecholamines
hemoglobin that is chemically linked to a
 Normal response- 2-3 hrs after a single sugar. Most monosaccharides, including
dose of clonidine. glucose, galactose and fructose,
spontaneously bond with hemoglobin,
when present in the bloodstream of
humans

 Normal Value: 4%-7% for Non Diabetics


 The goal for the client with DM is 7.5%
or less
 If there are excess glucose in the blood
 Glucose is attached to hemoglobin
 Hgb is a component of RBC that has a
lifespan of 90-120 days
 Nursing Preparation: NPO 6-8 hours
prior to procedure
Water Deprivation Test
 the patient is deprived of fluids under
strict medical supervision for 8-12 hours
or 3%-5% of the body weight is lost
 Weight the patient frequently
 frequent (q2h) monitoring of plasma
and urine osmolality follows.
 The test is generally terminated when
plasma osmolality is >295 mOsm/kg or
the patient loses ≥3.5% of initial body
weight.
 DI is confirmed if the plasma osmolality
is >295 mOsm/kg and the urine
osmolality is <500 mOsm/kg or the
urine specific gravity is decrease.
 jjjjjj
SIADH Diabetes Insipidus (DI)
 Inappropriate continued release of ADH in the absence of  Hyposecretion of ADH/Deficit of ADH
stimuli resulting water intoxication/excessive water  Inability of the kidneys to retain water/
retention by the kidney tubules.  water deficit
 More water will be reabsorbed by the kidneys leading to  absence of ADH allows the filtered water to excreted in the
decrease urine output and fluid overload. urine instead of being reabsorbed, and the patient excrete
 as the fluids build up in the blood stream, Osmolality large quantities of urine
decreases and the blood becomes diluted  Disordered regulation of water balance due to impaired
 Feedback system is impaired and posterior pituitary urinary concentrating ability secondary to inadequate
continues to release ADH secretion of ADH or resistance to ADH.
 Renal tubules continue to reabsorb free water regardless Central/Neurogenic
of the serum osmolality  Inadequate secretion of ADH due to loss or malfunction of
 Excessive activity of the neurohypophyseal system r/t neurosecretory neurons that make up the posterior pituitary.
brain disease  Vasopressin Sensitive

Serum Osmo below 280 mOsm/L Nephrogenic


 water excess  Inadequate response by the kidneys to ADH. A disorder of
 Amount of particles or solute is too small in proportion to renal tubular function resulting in the inability to respond to
the amount of water OR ADH in absorption of water.
 Too much water for the amount of solute  Vasopressin Resistant

CAUSES OF SIADH Dispogneic


 Trauma  Suppression of ADH secondary a defect or damage to the
 Stroke thirst mechanism located in the hypothalamus resulting in
 Hodgkin’s disease increased fluid intake or psychogenic causes
 Stress
 Pancreatic cancer Normal Serum Osmolality
 Lung Cancer  280-295 mOsm/L blood
 Drugs
Serum Osmo above 295 mOsm/L
CLINICAL MANIFESTATION  water deficit
-Mental confusion- initial sign  Concentration is too great or
-Edema- over retention of water  Water concentration is too little
-Weight gain- over retention of water
-Oliguria- More water will be reabsorbed by the kidneys CAUSES OF DI
leading to decrease urine output and fluid overload.  drugs-cause abnormalities secretion of ADH(clonidine, dilatine
-Hypertension- vasopressin causes vasoconstriction  Injury –cause abnormalities in ADH secretion
-Concentrated Urine  Kidney failure- less common cause to respond to ADH
-Hallucination  Lesion such as tumor, removal of PG, aneurysm, thrombus
-Anorexia and infection can interfere with ADH transport or release.
-Absent Tendon Reflex
-Dilutional hyponatremia- excessive retention of water CLINICAL MANIFESTATION
-N/V  POLYURIA- most common sign, 20L-30L of urine/day
-Weakness  POLYDIPSIA- extreme thirst and consumption of water.
-Cramps  Weight loss
-Seizures  Hypotension
LABORATORY DATA  Diluted
 Serum Na-low Na below 120mEq/L  Dehydration
 Hypo osmolality-below 280 mOsm/L  Constipation
 High specific gravity- higher 1.025  Dizziness

NURSING DIAGNOSIS
 Fluid volume excess r/t excessive amount of ADH LAB DATA
 Altered elimination pattern r/t decrease urine output  Serum Na- High 147mE/L, Hypernatremia
 Altered Nutrition  Hyperosmolality-above 290mOSm/L
 Disturbed Thought Process  H2o Deprivation test- Fluids are withheld for 4-18 hrs. If no
 Fluids and Electrolytes Imbalance increase urine concentration, it confirms DI.
 Low specific gravity-below 1.005- urine is diluted
INTERVENTIONS
NURSING DIAGNOSIS
 Fluid restriction-500ml-1000ml/day
 Fluid volume deficit r/t decrease secretion of ADH
 Assess for signs of hyponatremia- 3% NS may be given
 Altered Fecal elimination pattern r/t to constipation
 Diuretics- to reduced body fluids
INTERVENTIONS
 Demeclocycline- inhibit ADH. DOC. Produce water diuresis
 Maintain adequate fluid intake
 Monitor V/S, cardiac and neurologic status- Water
 Monitor urine specific gravity
intoxication may cause CHF and increase ICP
 Administer desmopressin acetate intranasal- affects
 Monitor I and O
prolonged Anti diuretic activity/long acting
 Weigh daily- Same time each day, same scale, same
 Lypressin-short acting nasal spray vasopressin
clothes.
 Administer VASOPRESIN- to control fluid balance and prevent
dehydration

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