THYROID STIMULATING

HORMONE THYROGLOBULIN
-also known as Thyrotropin -a glycoprotein manufactured
-It is composed of 2 mono-covalently exclusively by thyroid follicular cells.
linked alpha and beta subunits. -a form in which hormone is stored in
-It is the first indication of thyroid the gland.
gland failure *Monoiodotyrosine and Diiodotyrosine
Functions are precursors of T3 and T4
-It is the main stimulus for the
uptake of iodine by the thyroid REVERSE T3 is a biologically inactive
gland form of T4.
-Promotes the release of stored
thyroid hormones FUNCTIONS OF THYROID
HORMONE
Diagnostic methods for TSH -Tissue growth
● IMRA (Immunoradiometric -Mental development
assay) -CNS development
-Less than 5 units of TSH are -Increased heat production
sufficient to keep the thyroid gland -Control of oxygen consumption
functioning properly -Influences carbohydrate and protein
-Hypothyroidism – TSH is metablolism
elevated; TSH is the first -Energy conservation
indication of Thyroid Gland
failure HYPOTHALAMIC PITUITARY
THYROID AXIS
● LATS ( Long-Acting -Thyroid hormone is maintained by
Stimulating Substance) Hypothalamic Pituitary Thyroid Axis
-Detectable in the serum of (HPTA).
thyrotoxic patients which imitates -HPTA is a neuroendocrine system
the biologic action of TSH. that regulates production and
secretion of thyroid hormone.
THYROID GLAND -It is the central in regulation of
-Positioned in the lower anterior thyroid hormone production.
nech and shaped like a butterfly. It
is made up of 2 lobes that rest on CARRIER PROTEINS
each side of trachea with a band of  TBG: 70-75%
thyroid tissue (isthmus) running  TBPA OR TTR: 10-25%
anterior to the trachea and bridging  TBA: 10%
lobes. *Less than 1% that is not bound in
protein performs their function and
Thyroid cells are organized into circulates in blood.
follicles.
Follicles are the fundamental MAJOR THYROID HORMONES
structural unit of thyroid gland.  TETRAIODOTHYRONINE/
THYROXINE (T4)
2 TYPES OF CELLS -principal secretory product (80%)
 Follicular cells: T3 and T4 -biologically inactive form of thyroid
synthesis hormone
 Parafollicular Cells: Calcitonin -major fraction of organic iodine in
synthesis circulation
-good indicator of thyroid -biologically active form of thyroid
secretory rate hormone. It has more biologic activity
-prohormone/precursor for T3 than T4.
production. The substance can be -used for diagnosing T3
converted into active hormone. thyrotoxicosis
-helpful in confirming diagnosis of
 FT4 is the biologically active hyperparathyroidism because in
form of thyroxine. The portion hypothyroid, normal values are seen.
that is not bound in protein, it
directly enters the cell that Normal values
affects metabolic process of -Adult: 60-160 ug/dL or 0.9-2.46
body. nmol/L
-Reflect the actual amount of -Child
active hormone available in -1-14: 105-245 ug/dL or 1.8-3.8
tissues and it is the one we nmol/L
measure in laboratory.
*Hypo decreased T3 and T4
Normal values Hyper increased T3 and T4
-Adults: 5.5-12.5 ug/dL or 71-141
nmol/L PRIMARY HYPERTHYROIDISM
-Neonates/Children: -hypermetabolic condition due to
11.8-22.6 ug/dL or 152-292 excessive production of thyroid
nmol/L hormone.
-The latter form of thyrotoxicosis is
 REVERSE called hyperthyroidism.
TRIIODOTHYRONINE (rT3) -Origin: Thyroid gland
-major metabolite of thyroxine (T4)  Grave’s disease is an
-biologically inactive form of T4 autoimmune disease that leads to
product generalized over activity of
-produced by 5- deiodination of thyroid gland
T4
-cannot bind directly to hormone  Toxic multinodular goiter
receptor, which does not stimulate  Toxic adenoma: benign active
metabolic processes. tumor
-high among patients with non-  Thyroiditis: inflammed thyroid
thyroidal illness syndrome gland
(Euthyroid Sick-Syndrome) seen
in neonate patients and taking SECONDARY
propanolol. HYPERTHYROIDISM
- low T3 -Origin: Pituitary gland
-Normal or low T4 -over production of TSH
-TSH is normal to low -over stimulation of thyroid hormones
Causes:
*RT3 and T3 differs in location -Carcinoma
where iodine atom is removed. RT3, -TSH secreting tumors
iodine is removed at the inner part -TRH secreting tumors
of ring of T4 (inactive). T3, iodine is
removed at the outer ring of T4, no Signs Symptoms
binding in hormone receptor. Tachycardia Nervousness,
irritability, anxiety
 TRIIIODOTHYRONINE (T3)
Tremor Tremor DIAGNOSTIC METHODS FOR
Warm, moist, Palpitations THYROID HORMONES
flushed, smooth
skin  SERUM T4 AND T3
Lid lag, widened Fatigue, -radioimmunoassay
palpebral weakness, -cheliminometric assay
fissures decreased -ELISA
exercise tolerance
Ophthalmopathy Weight loss  THYROGLOBULIN
(Graves’ -ideal tumor marker for thyroid
disease) cancer
Goiter Heat intolerance -measured by RIA or ELISA
Brisk deep Hyperdefecation  THYROID AUTOIMMUNITY
tendon reflexes -a test to detect antibodies to the TSH
Muscle wasting Menstrual receptor
and weakness changes  TS Ab: Thyroid stimulating
(oligomenorrhea) antibody
Dermopathy/ Prominence of -can be involved in autoimmune
pretibial eyes thyroid disorders such as Grave’s
myxedema disease.
(Graves’ -targets the Thyroid stimulating
disease) hormone receptor (TSHR) located in
Osteopenia, Nervousness, the surface of the thyroid cells.
osteoporosis irritability, anxiety -the primary role is to mimic the
function of TSH, where they can
stimulate the thyroid gland to
PRIMARY HYPOTHYROIDISM produce T3 and T4 that leads to
-decreased T3 and T4, increased T4 overproduction seen in Grave’s
-deficiency of elemental iodine disease
Causes
-surgical removal of thyroid
-radioactive loan for
hyperthyroidism treatment
-destroys thyroid gland
-drugs such as lithium

 Hashimoto’s disease or
Chronic lymphocytic
thyroiditis: is an autoimmune
disease targeting the thyroid
gland. TPO andtibody testing is
positive in 80-99% of patients
with chronic lymphocytic
thyroiditis
TEST FOR TS ANTIBODIES
1. TRAb (TSH receptor
antibodies)
SECONDARY
-measures the presence of antibodies
HYPOTHYROIDISM that activates or block the TSH
-Origin: Pituitary gland or pituitary receptor.
adenoma
-decreased T3, T4, and TSH
2. TSI (Thyroid stimulating parafollicular C cells. Calcitonin is
Immunoglobulin produced in excess by tumor cells.
-specific form of TRAb associated
with Grave’s disease GONADOTROPINS
-overstimulation of thyroid gland to -secreted by gonadotropic cells and
produce thyroid hormones control the functional activity of
gonads.
OTHER TOOLS FOR THYROID  Gonads are organs in
TESTING reproductive sytem that produces
1. NUCLEAR MEDICINE gametes. Testes in males and
-radioactive materials, to evaluate Ovary for females.
the function and structure of the -Males: LH and FSH is regulated by
thyroid gland. testosterone and inhibin.
-Females: LH and FSH is regulated by
estrogen and inhibin.
*LH and FSH are present in Male and
2. Thyroid ultrasound Female in all ages. It is essential as
-noninvassive technique to asses marker in diagnosis of fertility and
the structure and characteristic of menstrual cycle disorder.
thyroid gland.
-it uses waves to create real time
image of the thyroid gland
FOLLICLE STIMULATING
HORMONE
3. FINE NEEDLE BIOPSY -Produced at the Anterior Pituitary
-used to obtain small sample of gland.
tissue or cell from thyroid nodule for
diagnostic purposes. FEMALES
-used to evaluate if the sample is -It aids in growth and maturation of
benign or malignant and to guide ovarian follicles in females. It is a key
the treatment approach if surgery is hormone for reproductive system
necessary. regulation.
-FSH and LH promotes estrogen
secretion by maturing follicles and
 CALCITONIN triggers ovulation.
-produced by the C cells or -Promotes endometrial changes in
parafollicular cells of the Proliferative Phase of Menstrual
cycle (First phase)
thyroid.
-Normal follicular growth is the result
-The production is stimulated by of complimentary action of FSH and
hypercalcemia. LH. They are essential for regulation
-It has an inhibitory effect on of menstruation and egg maturation.
hypercalcemia that lowers
plasma calcium level and Clinical significance
promotes calcium deposition in -Elevated FSH: diagnosis of
bones and urinary excretion of premature menopause (low estrogen)
calcium.
-Tumor marker for detection of MALES
residual thyroid metastasis in -stimulates testicular growth and aids
medullary thyroid carcinoma in spermatogenesis.
(MTC) *MTC originates from the -production of Androgen Binding
Protein (ABP) by the sertoli cells
 *Sertoli cells are essential for samples, multiple serial blood sample
supporting and nurturing sperm and Timed sample of urine.
cells. -There is a circadian variation of
*ABP is glycoprotein essential secretion of gonadotropin depends on
for male fertility. Where it binds time.
with testosterone in testes that
ensures the local concentration PROLACTIN/LEUTEOTROPIN
of hormone is high enough to -a stress hormone synthesized in
support spermatogenesis and Anterior Pituitary gland specifically in
proper development of sperm lactotroph cells.
cells. -a pituitary lactogenic hormone,
major inhibitor is Dopamine
-Highest serum level is during sleep:
4-8 am or 8-10 pm; lowest at 10 am -
12 noon.
LUTEINIZING HORMONES *During pregnancy, prolactin levels
-synthesized in Anterior Pituitary rise to prepare the mammary glands
Gland for milk production. The milk
-essential in sexual development secretion by prolactin is inhibited by
and functioning. high levels of estrogen and
progesterone during pregnancy. After
MALES childbirth, progesterone and estrogen
-responsible for testosterone levels become low and prolactin
production by the Leydig cells of hormone stimulates the mammary
the testes. gland to begin producing milk
-Maturation of spermatozoa with (Lactogenesis).
FSH
*may cause deficiency in male
FEMALES hormones; high levels of prolactin
-responsible for ovulation and helps reduces testosterone production that
trigger the release of egg from the may lead to infertility because libido
ovary. It is essential for regulation of is lowered or erectile dysfunction may
menstrual cycle seen.
-Corpus luteum formation where it
will secrete the progesterone. -Function in milk production
*Progesterone prepares the -Diagnostic method is
uterus for possible pregnancy Radioimmunoassay
through thickening of
endometrial lining. If pregnancy Increased levels in
does not occur, the corpus -Pituitary adenoma
luteum will degenerate and the -Infertility
progesterone levels will become -Amenorrhea (no menstruation)
low that leads to menstruation. -Galactorrhea
-Acromegaly
DIAGNOSTIC METHOD FOR -Renal failure
GONADOTROPINS -Polycystic ovary syndrome
 Commercial RIA -Cirrhosis
-serum, plasma, urine samples -Primary and Secondary
-Clinical evaluation needs hypothyroidism
determinations in pooled blood
 ADENOCORTICOTROPIC
HORMONE DIAGNOSTIC SIGNIFICANCE
-synthesized in Anterior Pituitary 1. PRIMARY
gland and regulated by corticotropin HYPERPARATHYROIDISM
releasing hormone from the -80% is caused by Parathyroid
hypothalamus. adenoma. It is the most common
-a single chain peptide without cause of hypercalcemia.
disulfide bonds that acts primarily -Occurs when 1 or more of
on adrenal cortex stimulating its parathyroid gland become enlarged
growth and secretion of or tumor is developed.
corticosteroids. *The tumors will secrete excess
-Primary function: Stimulate parathyroid hormone that leads to
adrenal glands/ adrenal cortex increase calcium levels.
to produce cortisol Phosphaturia is also present,
*Cortisol plays a key role to where phosphate levels in urine is
body’s stress response present as compensation for
PARATHYROID GLANDS increased calcium levels in blood.
-smallest endocrine gland in
the body. Diameter per gland is  Osteitis fibrosa cystica
3-4 mm similar to a grain of characterized through formation
rice. of cystic spaces and fibrosis in
-located at the posterior of bones. Typically due to chronic
thyroid consist of tightly packed hyperparathyroidism
secretory cells covered by thin
connective tissue. SIGNS AND SYMPTOMS
*number of parathyroid gland includes bone pain, formation of
varies person by person kidney stones, fatigue, depression,
-It is crucial in regulation of and muscle weakness.
calcium and phosphate balance
that is vital for normal TREATMENT
functioning of muscles, nerves, -Surgery or removal of Parathyroid
and bones. gland.

ROLES OF PARATHYROID 2. SECONDARY

HORMONE HYPERPARATHYROIDISM
-Hypocalcemia and increased -develops in response of decreased
plasma calcium level serum calcium (hypocalcemia). If
stimulates the release of PTH. undetected, severe demineralization
-Promotes bone resorption occurs that causes Osteitis fibrosa
through promoting activity of cystica.
osteoclasts - Vitamin D deficiency where
-Increases renal reabsorption of patients develop severe bone disease
calcium in the kidney, phosphate -Seen in Chronic renal failure at
reabsorption is decreased. This chronic kidney disease where kidneys
will increase calcium levels in are unable to properly balance
blood. Calcium and Phosphate levels that
-Stimulate conversion of inactive leads to overproduction of PTH to
Vitamin D to activated Vitamin raise low level of Calcium.
D3 *Treatment involves addressing
-Indirectly stimulates intestinal underlying condition.
absorption of calcium
Renal failure: Dialysis; Decreased -produces androstenedione (weak
Serum calcium/Vitamin D deficiency: androgens) and
Supplementation dehydroepiandrosterone

3. HYPOPARATHYROIDISM STRUCTURE OF ADRENAL GLANDS

-caused by accidental injury to the
Parathyroid gland due to surgery  ADRENAL CORTEX
-Other causes: Autoimmune -the outer region of adrenal gland
parathyroid destruction. that secretes the steroid hormone.
-Persistent hypocalcemia -Major site of steroid hormone
-Deficiency of blood calcium causes production
neurons and muscle fibers to *Corticosteroids, Glucocorticoids,
depolarize and produce action Mineralocorticoids, sex steroids
potentials spontaneously.
 ADRENAL MEDULLA
-comes from a neural crest origin.
Inner layer of adrenal gland
Symptoms -It stores and secretes
-Muscle cramps, spasm, tetany, catecholamines such as epinephrine,
numbness, seizure, fatigue, anxiety norepinephrine, and dopamine.
-Catecholamines are involved in fight
Treatment or flight response. It is an automatic
-Calcium and Vitamin D suplement physiological reaction to threat or
danger.
ADRENAL GLANDS -The response is triggered by
-pyramid like shape above the sympathetic nervous system and this
kidneys, referred as the suprarenal is reffered as acute stress response.
glands.  CATECHOLAMINES
-Inside the gland is Adrenal medulla -produced in chromaffin cells
and Adrenal cortex which plays vital 1. EPINEPHRINE
role in bodily function such as stress (Adrenaline/Secondary amine)
response, metabolism, immune -called the Flight or Fight hormone
system regulation and electrolyte -It spikes your blood sugar level by
imbalance. helping convert glycogen to glucose
in liver.
3 Layers of Adrenal Gland -Results includes Increased heart
1. Zona glomerulosa rate, thinning of airway, Increases
-outermost layer; consist of 10% blood pressure
-principal source of -Major metabolite:
mineralocorticoid such as VANILLYLMANDELIC ACID (VMA)
aldosterone.
*Aldosterone regulates NaK 2. NOREPINEPHRINE
pump and water. (Noradrenaline/Primary amine)
2. Zona fasiculata -highest concentration in brain (CNS)
-middlemost layer; consisy of 75% -Acts as a neurotransmitter in both
-site of glucocorticoid synthesis. CNS and the Sympathetic nervous
*cortisol increases in stress system.
3. Zona reticularis -Same effect with epinephrine but
-innermost layer; consist of 10% causes narrowing blood vessels
-Major metabolite: 3-methoxy-4- -promotes glycogenesis, lipogenesis,
hydroxyphenylglycol (MHPG) in glycolysis and decreases
CSF and Urine glycogenolysis

DIAGNOSTIC SIGNIFICANCE
 PHEOCHROMOCYTOMA
-tumor of the adrenal medulla or 3. Somatostatin
sympathetic ganglia. -inhibits release of insulin and
-due to overproduction of glucagon
catecholamines (Norepinephrine and -inhibits release of growth hormone
Epinephrine) and other digestive enzymes
Signs and Symptoms
-Hypertension 4. Pancreatic polypeptide
-Tachycardia -involve in regulating pancreatic
-Headache secretion
-Tightness of chest -involve in control of apetite and
-Sweating digestive function.
PANCREAS
-secretes hormone as endocrine DIAGNOSTIC SIGNIFICANCE
gland and digestive juices to the DM 1
digestive tract as an exocrine gland. ONSET Children or teens
-blood sugar regulation RISK Genetic,
ENDOCRINE CELLS: Islets of FACTORS autoimmune
Langerhans C PEPTIDE Decreased or
-excreted in small intestine to LEVELS undetectable
breakdown food SYMPTOMAT Develop abruptly
-Enzyme such as amylase and OLOGY
lipase MEDICATION Insulin absolute
-Alpha: glucagon DM 2
-Beta: insulin ONSET Advancing stage
-Delta: Somatostatim RISK Genetic, obesity,
-F cells: Pancreatic polypeptide FACTORS sedentary lifestyle,
PCOS, dyslipidemia,
1. Glucagon hypertension
-stimulates conversion of stored C PEPTIDE detectable
glycogen to glucose that ca be LEVELS
released into the bloodstream.
SYMPTOMAT Develop gradually
-promotes production of glucose OLOGY
from amino acid molecules and
MEDICATION Manage diet and
released during stress and fasting
exercise, oral agents
states.

2. Insulin
HORMONES SECRETED BY
-primary hormone responsible for
ADRENAL GLAND
glucose entry into the cell
 ALDOSTERONE
-decreases glucose level as it is a
-most potent mineralocorticoid
hypoglycemic agent.
(electro-regulating hormone) due to
-release is stimulated by
its ability to regulate water, sodium,
hyperglycemia
potassium, and chloride.
-main determinant of renal excretion -Increased plasma levels of
of potassium to maintain balance in aldosterone and renin.
sodium-potassium exchange in cells. -Symptoms includes hypokalemia
-acts on renal tubular epithelium to -Treatment includes surgical
increase sodium and chloride removal of tumor or medications such
retention and excretion of as spironolactone (antagonist of
potassium and hydrogen in urine. Aldosterone).
-The synthesis of aldosterone is
controlled by Renin-Angiotensin 1. HYPOALDOSTERONISM
Aldosterone System (RAAS). (ADDISON’S DISEASE)
*Renin converts Angiotensinogen to -due to destruction of adrenal gland
Angiotensin I the ACE will convert it and glucocorticoid deficiency.
to Angiotensin II that stimulates the *usually due to autoimmune
adrenal gland to release disorders or tumors that causes
Aldosterone. the destruction of adrenal glands
-Enzyme needed for synthesis: 18- -Symptoms includes hyperkalemia
hydroxysteroid dehydrogenase and metabolic acidosis, fatigue, low
blood pressure, hyperpigmentation,
DIAGNOSTIC SIGNIFICANCE OF cravings for salt
ALDOSTERONE -Treatment involves hormone
 PRIMARY replacement therapy using
HYPERALDOSTERONISM glucocorticoids such as
(CONN’S DISEASE) hydrocortisone
-caused by aldosterone-secreting
adrenal adenoma  CORTISOL
*Conn’s disease occurs when there -principal glucocorticoid that has an
is excess production of aldosterone anti-inflammatory effect and
due to adenoma. immunosuppressive actions. It
-associated with increased plasma reduces the activity of immune cells
aldosterone and low plasma renin. such as T cells and macrophages, and
it inhibits production of
Symptoms: prostaglandins.
-Hypertension, Hypokalemia, Mild *Therapeutic agent for
hypernatremia, and metablic Rheumatoid arthritis, SLE, and
alkalosis Multiple Sclerosis
*Distal delivery of sodium is -the production is increased in
increased. Increased NaCl response to stress.
reabsorption in cortical collecting -It stimulates gluconeogenesis in the
duct by the action of aldosterone. liver resulting to hyperglycemia (anti-
Inhibits salt reabsorption in proximal insulin effect). Helps to regulate blood
convuluted tubule as result of glucose level by promoting glucose
volume expansion. production from Non-carbohydrate
sources such as amino acids, fats,
 SECONDARY primarily in the liver.
HYPERALDOSTERONISM
-occurs as a result of excessive -High levels in the morning 8-10 am
renin production. This can result due and lowest at night 10 pm to 12 mn.
to heart failure or kidney diseases -Helps to regulate the sleep-wake
where excessive activation of RAAS cycle
system.
*Negative feedback mechanism
controls the release of cortisol.
Cortisol inhibits the secretion of
ACTH.

Hypothalamus releases CRH in

response to stress or low cortisol
level of the body and triggers
Anterior Pituitary to release ACTH.
DIAGNOSTIC SIGNIFICANCE
 HYPERCOTISOLISM
(CUSHING’S SYNDROME)
-excessive production of cortisol and
ACTH, decreased aldosterone and
renin.
-Caused by overuse of
corticosteroids

Signs and Symptoms

-obesity but with thin extremities
-hirutism (excessive hair growth or
coarse hair in face, chest, and back)
-hyperglycemia
-hypertension
-hypercholesterolemia
-thinning of the skin
-poor wound healing
-low WBC (lymphocytes)
-Buffalo hump

 HYPOCORTICOLISM
-due to decreased cortisol
production, aldosterone deficiency,
excess ACTH release.
*Addison’s disease is due to an
autoimmune adrenalitis, TB,
hemmorrhage, HIV-AIDS infection
-adrenal glands are damaged that
leads to reduced production of
cortisol.

Signs and symptoms

-Hypotension
-Hyponatremia
-Hyperkalemia
-Weight loss
-Hyperpigmentation