endocrine function tests
DESCRIPTION
ENDOCRiNE FUNCTION TESTS. MA. LOURDES TILBE, D,F,PSP. Objectives. Review hormone regulation in health and disease Types of endocrine testing Basic principles behind test Considerations in patient preparation and specimen handling Interpretion of tests applying acquired knowledge. - PowerPoint PPT PresentationTRANSCRIPT
ENDOCRINE
FUNCTION TESTS
MA. LOURDES TILBE, D,F,PSP
Objectives Review hormone regulation in health and
disease Types of endocrine testing
Basic principles behind test Considerations in patient preparation and
specimen handling Interpretion of tests applying acquired
knowledge
Endocrine System
Composed of different glands that secrete hormones directly in the blood
Some hormones are regulatory in nature Trophic hormones, releasing hormones
Synthesis and secretion of each hormone is under continous feedback control in normal physiologic conditions
HYPOTHALAMUS
PITUITARY GLAND
EFFECTOR ORGAN
Feed back
External stimuli
Releasing hormones
Trophic hormones
Diagnosis of Endocrine Disorders
Normally, hormone concentration in circulation falls within a predictable range
Most hormones are conveniently measured by RIA or other immunoassays.
Direct measurement of individual hormones in plasma or serum allows for screening and establishing diagnosis of most endocrine disorders. Determine hyperfunction or hypofunction Localize the diseased organ
Effector organ (primary) Pituitary Gland (secondary) Hypothalamus (tertiary)
Endocrine disorders
1o excess high target organ hormones; low trophic hormone
1o deficiencylow target organ hormone; high trophic hormone
2o excess high trophic hormone and hormones of target gland
2o deficiency low trophic hormone and hormones of the target gland
3o deficiency low trophic hormone and hormones of the target gland
Assessment of Hormone Function
1. Direct measurement of hormone concentrationA. Basal serum hormone levelsB. Hormone measurement in the urine.
Urinary excretion of hormone or its metabolite Corrects for fluctuations in blood levels Integrates value over longer period
2. Dynamic testsA. Suppressive tests for hormone excess (DST; Glucose ST)B. Stimulation test for hormone deficiency (Insulin Induced
Hypoglycemia to evaluate Hypothal-PG axis3. Image Studies
Anterior PG Post. PG.
Ad. cortex
Thyroid
Gonads
Breast
Multiple tissues of the body
Hypothalamus
TSH
GH
PRL
LH
FSH
ACTH
Cortisol
Male testosterone
Female estrogens/progesterones
ADH
Oxytocin
T4
T3
RF
HYPOTHALAMIC HORMONES
HORMONE REGULATION PHYSIOLOGIC ACTION
Corticotropin Releasing H
Negative feedback by ACTH and adrenal cortisol
Stimulates secretion of ACTH
Thyrotropin RH Negative feedback by TSH and thyroid H
Stimulates secretion of TSH and prolactin
HORMONE REGULATION PHYSIOLOGIC ACTION
GH Inhibiting H Positive feedback by GH
Inhibits secretion of GH and TSH
Gonadotropin RH Negative feedback by FSH and LH
Stimulates secretion of FSH and LH
Prolactin IH Positive feedback by prolactin, TSH, FSH, LH and GH
Inhibits secretion of prolactin, TSH, FSH, LH and GH
Growth H RH(Somatocrinin)
Negative feedback by GH
Stimulates secretion of GH
ANTERIOR PITUITARY HORMONES
Adrenocorticotrophic H (ACTH)
Regulation: Corticotrophic releasing hormone (CRH) causes
secretion in response to biorhythms with circadian variation
Production is regulated by glucocorticoid concentration via the negative feedback mechanism
Physiologic action: Stimulate secretion of adrenocorticoids
Glucocorticoids (cortisol) Mineralocorticoid (aldosterone) Androgens)
Causes sedation, increased pain threshold, autonomic regulation of respiration, BP and HR
Adrenocorticotrophic H ( ACTH ) Episodic secretion in respose to
1. Falling levels of active glucocorticoids Cortisol ( predominant) 90% inactive bound to
CBG(Cortisol binding globulin) 2. Stress 3. Cycles of sleeping and waking
Display circadian rhythmPeak: bet 4 am and 8amnadir: at midnight
Adrenocorticotrophic H
Patient preparation: Stressful venipuncture inc levels
Specimen collection/handing: Collected in prechilled plastic tubes with EDTA or
heparin Place immediately on ice Store at -20 C within 15 min of collection
TSH or Thyrotropin
Regulation: TRH from hypothalamus causes secretion
in response to low levels of thyroid hormones (T3, T4)
Physiologic Function: Stimulates secretion of T3, T4
TSH Serum TSH is single best screening test for
thyroid fxn followed by FT4 Useful for evaluating both thyroid and pituitary
function Elevated serum level:
sensitive and specific indicator of primary HYPOTHYROIDISM
Normal or decreased level: secondary or tertiary hypothyroidism
Growth Hormone
AKA : somatotropin Most abundant hormone of ant PG
Growth Hormone Regulation:
GHRH and GHIH regulates its secretion in response to exercise stress, hypoglycemia Amino acids testosterone estrogen levels
Physiologic Function: Promotes growth of soft tissue , cartilage and bone Stimulates Pr synthesis , fat and CHO metabolism
Growth Hormone Increase GH gigantism in children acromegaly in adults
Decrease GH in children dwarfism
Secreted in pulsatile bursts with very short half life single random determination ( limited
usefulness) 24 hours hormone secretion level (better
measurement)
Growth Hormone
Patient preparation: Patient should be fasting Complete rest for 30 min before collection.
Spikes occur 3 hr after meals, stress, or exercise and 90 min after onset of sleep,
Specimen: Serum preferred; refrigerate immediately; stable at 2-8C
for 8 hr.
Prolactin Hormone
Biochemical properties similar with GH and placental GH
Main target organ: adult female mammary gland
Regulation: Regulated by TRH, dopamine
Physiologic Function: Increased in pregnancy, sucking Initiates lactation ; growth of mammary
tissues; controls osmolality, fat , CHO , Vit D metab and steroidogenesis in the ovary and testis
Effects : Suppresses ovulation Stimulates growth of prostate
Hypersecretion : Females: hypogonadism , infertility,
oligo/amenorrhea , galactorrhea Males: inhibits testosterone secretion, decrease
spermatogenesis , infertility and galactorrhea
Prolactin Hormone
Levels fluctuate; fluctuations occur Q 95 min,
Long half life ( approx 50 min ) Physiologically stimulated by :
Pregnancy, breast feeding, sleep, dietary Pr, hypoglycemia, exercise and stress
Prolactin Hormone Patient Preparation:
Collect 3-4 hr after awakening; levels increased during sleep and peak in early morning. Avoid emotional stress, exercise, ambulation, protein
ingestion ( can increase levels). Specimen:
fresh nonhemolyzed serum; stable at 4 C for 24 hr.
Follicle Stimulating and Luteinizining H
Regulated by GnRH from hypothalamus Controls the functional activity of gonads Exhibit episodic, circadian and cyclic variations– best to use
serial blood tests or timed urine collection Specimen:
Serum, plasma and urine acceptable; Stable 8 days at room temp; two weeks at 4C
HYPOTHALAMIC-PITUITARY FUNCTION TESTS
Hyperpituitarism Most are due to benign tumors that are autonomous
and do not respond to negative feedback control GHsecreted by pituitary adenoma is not suppressed by
glucose Exception to the rule of suppressibility:
Prolactinoma and Pit adenoma that secrete ACTH(Pituitary Cushing); both are partially autonomous
GH Excess: Acromegaly
1. Serum GH Elevated basal or random levels in most acromegalics Basal and random GH may also be inc in
Normal patients due to episodic secretion Malnourished patients Anorexia nervosa Patients on estrogen therapy
Best test to confirm acromegaly: Measurement of GH following a glucose load. GH is normally suppressed to <2ng/ml one hour after a 75 -
100g glucose load. Failure to suppress means a functioning pituitary adenoma
Pituitary Hyperpituitarism
2. Serum Somatomedin C Synthesized mainly in the liver Mediates most of the major growth promoting effects of GH Involved in negative feedback regulation of Normal GH secretion Serum level of SM-C is a good screening test for acromegaly
Basal SM-C is elevated in acromegaly Maybe elevated in adolescents during the peripubertal growth
spurt and during pregnancy
Hypopituitarism : GH deficiency
GH testing: Shd be routinely included in evaluating children with short stature Not indicated in adults suspected of hypopituitarism
Basal GH levels: not reliable to distinguish deficiency from normal;
Baseline measurement : fasting morning sample Factors that increase GH secretion:
Low serum glucose, dopamine, exercise
Laboratory diagnosis : Hypopituatarism : GH deficiency
Screening tests for GH deficiency: GH measurement after 15 min exercise Measurement of somatomedin:
Laron Dwarf: normal GH but low somatomedin
Stimulation Test to confirm GH deficiency
Stimuli 1. Insulin 2. Arginine 3. L-dopa 4. Clonidine
GH should be measured every 30 mins for 2-3 hours Normal: GH increment above baseline >5ng/ml or
a maximal GH>7ng/ml GH deficiency: failure to respond to at least two
independent stimuli; hypothalamic or pituitary gland dysfunction
Stimulation test:
Insulin induced hypoglycaemia to investigate suspected GH deficiency.
A reduced or absent response is seen in a GH deficient patient (B)
Insulin decreases plasma glucose concentrations and in a normal person this stimulates the release of GH (A)
Stimulation Test to confirm GH deficiency
GH stimulation test (After CRH): A CRH injection is given followed by
measurement of the blood level Normal: GH elevated Hypopituitarism: no response
PITUITARY GLAND
Measure Growth Hormone
Feed back
Bolus injection of releasing hormone
HypothalamusHypothalamus
No response or delayed peak response (60 mins vs 20 mins)
ADRENAL FUNCTION TESTS
Hormones of Adrenal Gland :
Hormones of adrenal cortex (adrenal corticosteroids) : Glucocorticoid ( cortisol ) secreted by cells in zona
fasciculata – Mineralocorticoid ( aldosterone ) secreted by cells in z.
glomerulosa- Sex hormones (testosterone and estradiol ) secreted
by cells in zona reticularis Catecholamines (dopamine, epinephrine and
NE) secreted by chromaffin cells of adrenal medulla
Glucocorticoid (Cortisol) Physiologic action:
Affects metabolism of proteins, CHO and lipids Stimulates gluconeogenesis by the liver, inhibits the
effects of insulin and decrease the rate of glucose use in the cells
Regulation: Secreted in response to stress and ACTH Normally: secretion higher in early morning (6-8am) lower in the evening (4-6pm);
lowest at midnight Cortisol excess (Cushing’s Syndrome and in patients under
stress): loss of diurnal variation in secretion
Circadian rhythm of cortisol secretion
Feedback control of Adrenal Corticosteroid synthesis and release
Decreased blood levels of adrenal corticosteroids, stress
Hypothalamus secretes corticotrophin releasing hormone (CRH)
Ant Pit g gland secretes ACTH
Adrenal cortex secretes hormones (cortisol)
Hormone secretion suppressed via negative feedback
Corticosteroid Excess : Cushing Syndrome:
Hyperadrenalism with production of excess cortisol
Clinical Presentation: 1. Glucocorticoid Effects: “cushingoid
habitus”, bone dimineralization, glucose intolerance
2. Mineralocorticoid effects: HPN, edema, hypokalemic alkalosis
3. Sex steroid effects: hirsutism, acne, amenorrhea, gynecomastia
Cushing Syndrome: Causes
Exogenous glucocorticoid therapy (most common cause)
Other causes: 1. ACTH Producing pituitary adenoma (60%)
( Cushing disease) 2. Glucocorticoid producing adrenal neoplasm(20%)
(adenoma or carcinoma) 3. Ectopic ACTH-producing neoplasm(20%)
Tests for Adrenal Hormone Function
1. Serum cortisol -Secretion is episodic and pulsatile in response to ACTH -Single determination neither specific or sensitive -90-97% is bound to CBG or transcortin - Elevated in adrenal hyperfunction (Cushing’s Sx) - Decreased in adrenal hypofunction (Addison’s) - Diurnal rhythm of cortisol secretion is lost in Cushing Sx
and patients under stress
2. Urine Free Cortisol (UFC): **Glucocorticoids:
Degraded in the liver and excreted in the urine as Hydroxycorticosteroid (17-OHCS).
Urine 17 OHCS is an indirect measurement of excessive plasma Glucorticosteroid -indirect measure of the cortisol production rate
-Normal: <90ug/24hr - UFC> 250mg/24 hr is almost always due
to Cushing Sx
3. Dexamethasone Suppression Test• Dexamethasone: cortisol analoque that should
suppress ACTH in normal person and reduce cortisol.
Rapid DST for screening (low Dose DST) Administer 1 mg dexamethasone at 11pm; measure
8am the following day: Normal: Suppressed cortisol <5ug/dl No suppression in Cushing’s Sx: useful for screening
Dexamethasone Suppression Test
Normal person: dexamethasone will suppress ACTH secretion (feedback) and cortisol production is consequently reduced.
In pituitary- dependent Cushings only high doses may suppress ACTH secretion
Ectopic ACTH Syndrome: no suppression even to HDST
No suppression to low dose: Cushing Syndrome
Adrenal Function Test
1. Plasma ACTH level Increased : pituitary tumors ectopic ACTH producing tumors Decreased: cortisol producing tumors in
adrenals exogenous hormones
Adrenal Function Test
2. Overnight HIGH DOSE DST:
Procedure: Administer 8mg at 11pm measure serum cortisol 8am before and on the morning following dexamethasone
ACTH producing adenoma : Suppression of cortisol to 50% of basal
Adrenal neoplasm or ACTH syndrome: No suppression of cortisol
Primary Adrenal Insufficiency (Addison’s Disease) Deficiency of all adrenal steroids Relatively rare Results from progressive destruction of
adrenals by local disease or systemic disorder
Adrenal Function Test for Adrenal Insufficiency
3. Metyrapone test
Metapyrone: Blocks 11 beta-hydroxylase in ad. cortex which reduces synthesis of cortisol hence stimulate synthesis of ACTH with proximal buildup of deoxycortisol in adrenal
Procedure: 1. Administer 3.0 mg metyrapone at midnight. 2. Measure cortisol and 11 deoxycortisol at 8am baseline and post-metyrapone
Metapyrone: Blocks 11 beta-hydroxylase in ad. cortex which reduces synthesis of cortisol hence stimulate synthesis of ACTH with proximal buildup of deoxycortisol in adrenal
deoxycortisol
11-β Hydroxylase
Cortisol
Metapyrone
Metyrapone Test: Normal response: fall in cortisol to <5ug/dl and
increase in ACTH, 11 deoxycortisol and urinary 17-OHCS
Cushing’s Dse: Increase in 11-deoxycortisol levels
Adrenal tumors/Ectopic ACTH: 11-deoxycortisol fails to increase
Failure of cortisol to fall invalidates the test Not routinely used, although maybe better than
High dose DST
Adrenal Function Test Cortisone Stimulation (Cosyntropin); ACTH
Stimulation Screening test; less time consuming; can be
done on OPD basis Cortrosyn (synthetic subunit of ACTH) have full
stimulating effect of ACTH in healthy individuals
- failure to respond : adrenal insufficiency
Procedure: 1. Get 4ml fasting blood venous sample at 8am 2. Administer cosyntropin IM/IV 3. Get 4ml samples at 30 and 60 mins after
Mineralocorticoid (Aldosterone)
Regulation: ALDOSTERONE (predominant mineralocorticoid) is
secreted by cells in the zona glomerulosa in response to ANGIOTENSIN (mainly); and by ACTH (not significant)
Clinical effects Retains Na and H20 accompanied by K
depletion leads to excess intravascular volume HPN
Aldosterone Elevated levels (primary aldosteronism)
Conn’s disease ( aldosterone producing adenoma) Elevated levels (secondary aldosteronism)
because of extenal stimuli or greater activity in the RAS: Salt depletion Potassium loading Cardiac Failure Nephrotic syndrom Diuretic abuse
Aldosterone Decreased levels of aldosterone:
Aldosterone deficiency Addison’s disease
Tests for hyperaldosteronism:
1. Basal level of plasma aldosterone *limited diagnostic value 2. Urinary Aldosterone 3. Captopril Suppression Test
Angiotensin- converting enzyme inhibitor: decrease the renin-stimulated aldosterone production secondary aldosteronism; no response in primary aldosteronism
Test for hyperaldosteronism:
5. Aldosterone Suppression test (Isotonic Saline infusion)
Normal response suppress aldosterone release by decreasing renin
Primary aldosteronism lack of aldosterone suppression
6. Aldosterone Stimulation Test ( Sodium restricted from diet) Normal response renin level increasedPrimary aldosteronism slight or no response in renin level
Adrenal Insufficiency:
1. Serum cortisol decreased 2. Rapid ACTH stimulation test 3. Long ACTH stimulation test 4. Serum ACTH
Elevated in primary adrenal insufficiency Decreased in secondary and tertiary
5. Metapyrone test
PHEOCHROMOCYTOMA: Cathecolamine Excess
1. Increased cathecolamines at all times. Cathecolamines: either epinephrine or
norepinephrine is increased and should be assayed separately.
Plasma norepinephrine >750pg/ml or Epinephrine >100pg/ml are found in 90-95% of
patients 2. Urine test
Vanyllmandelic acid Total metanephrine Fractionated cathecholamines
PHEOCHROMOCYTOMA: Cathecolamine Excess
3. Clonidine Suppression test: Clonidine (alpha agonist) decrease
efferent symphathetic flow Normal: Norepinephrine level within N range Pheochromocytoma: exaggerated response
PHEOCHROMOCYTOMA: Patient Preparation
Blood should be drawn through a previously inserted catheter from a patient who is fasting, resting quietly and non-stressed.
If patient is to kept on antiHPN meds during resting The least interfering agents shld be used:
diuretics. Vasodilators, and alpha or Beta adrenergic blockers.
THYROID DISORDERS
Thyroid function
Hormone Regulation TRH TSH
iodine uptake, organification synthesis & release of thyroid hormone
T4/T3 Regulate: basal metabolism, thermogenesis,
lipogenesis fetal CNS development
Regulation of thyroid hormone secretion
>99% of thyroid hormones are carried in plasma bound to protein <1% is free & active
Thyroxin-binding protein (TBG) binds most of the T4 and T3 TBG is synthesed by liver, severe liver disease TBG
TT4 due to protein-bound T4 Estrogen (ex. Pregnancy) synthesis of TBG total T4
due to protein-bound T4 Albumin and pre-albumin also carry T4 and T3 in plasma
Thyroid Hormones
Thyroxine (T4) Thyroid gland t1/2: 8 days
Triiodothyronine (T3) 80% in Periphery
Liver/kidney remove iodine from T4 t1/2: 1-1.5 days
Binding Proteins T4/T3 99% protein bound
Prevents excess tissue uptake Maintains accessible reserve
T4
T320%
80%
Protein* binding + 0.03% free T4
Protein* binding + 0.3% free T3
(10-20x less than T4)
Total T4 60-155 nMTotal T3 0.7-2.1 nMT3RU/THBI 0.77-1.23
*TBG 75% TBPA 15% Albumin 10%
Thyroid Function Tests : TSH T3 T4 FTI ( free thyroxine index ), FT4 ( free
thyroxine ) TRH TBG ( Thyroid binding globulin )
More T4 in serum (5.5 to 12.5 ug/dl) T3 in serum 9(100 to 200ng/dl)
T3 exerts the major hormone effects thus more phyiologically significant
T4 converted by peripheral nonthyroidal tissues to T3
T4 may have no direct effect until converted to T3
THYROID FUNCTION TESTS
THYROID STIMULATING HORMONE (TSH) Stimulated by TRH (from hypothalamus) Serum TSH is single best screening test for
thyroid fxn followed by FT4 Useful for evaluating both thyroid and pituitary
function Elevated serum level:
sensitive and specific indicator of primary HYPOTHYROIDISM
Normal or decreased level: secondary or tertiary hypothyroidism
Clinical Uses of TSH
Screening for euthyroidism Initial screening and diagnosis for
hyperthyroidism (dec. to undetectable levels except in rare TSH-secreting pituitary adenoma) and hypothyroidism
Useful in early or subclinical hypothyroidism before the patient develops clinical findings
Clinical uses of TSH
Differentiate primary (increased levels) from central [pituitary or hypothalamic] hypothyroidism (decreased levels)
Monitor adequate thyroid hormone replacement therapy in primary hypothyroidism
TSH increased in :
Primary untreated hypothyroidism Hypothyroidism receiving insufficient
thyroid hormone replacement therapy Hashimoto thyroiditis
THYROID FUNCTION TESTS: Total T4 and T3
1. TOTAL THYROXINE(T4) ANDTRIIODOTHYRONINE(T3) LEVELS
Total thyroxine (T4) is a good index of thyroid fxn when TBG are normal
T3 level- in cases of hyperthyroidisn with normal or low T4: T4; useful in monitoring therapy
THYROID FUNCTION TESTS:Total Thyroxine ( T4)
High: hyperthyroidism and acute thyroiditis
Low: hypothyroidism and chronic thyroiditis
Affected by concentration of binding proteins (TBG)
THYROID FUNCTION TESTS:Total Serum T3 ( Triiodothyronine )
Elevated proportionately to T4 in hyperthyroidism
Decreased in hypothyroidism T3 thyrotoxicosis ( 5% of ind.) T3
elevated while T4 is normal Not routinely measured except to
monitor tx of T3 thyrotoxicosis
THYROID FUNCTION TESTS: Thyroxine Binding Globulin
A glycoprotein: synthesized in the liver Principal serum carrier for T4 ( 75% ) and T3 Less than 1% of T3 and T4 are in the free form
which determines function Estrogen influences thyroxin binding Phenytoin, coumarin, heparin clofibrate and aspirin
compete with T3 & T4 for TBG binding sites Measurement is rarely indicated
T3 Uptake Indirect measurement of unsaturated
TBG in blood Determination is expressed in arbitrary
terms is inversely proportional to the TBG Low T3U is indicative of conditions where
there is elevated levels of TBG uptake
T3 Uptake Hypothyroidism: insufficient T4 to saturate
TBG unbound TBG is elevated and T3U values are low
Pregnant patients: TBG are increased proportionately more than T4 levels high levels of unbound TBG reflected in low T3U values
Useful only when T4 is done Used to calculate FTI or F7
T3 Uptake Procedure:
Known amount of radiolabeled T3 is added to test serum
Available binding sites in test serum combine with labeled T3 inversely proportional to the amount of endogenous T4 already bound
Low endogenous T4 (hypothyroid) many TBG sites free to react with labeled T3—measured residual radiocativity is low
High endogenous T4 (hyperthyroid) few TBG sites free to react with labeled T3 measured residual radioactivity is high
Resin is used to measure residual radioctivity Low residual activity—numerous binding sites
unoccupied( low endogenous T4) High residual activity—few binding sites
unoccupied( high endogenous T4)
Results are expressed as % radioactivity left unbound Hyperthyroidism: both T4 and T3U high values Hypothyroidism: both T4 and T3U have low values
THYROID FUNCTION TESTS: FREE THYROXINE INDEX Correlates better with clinical status in the presence of abnormalities in TBG Calculated as the product of absolute thyroid
hormone and the binding capacity of TBG FTI= Measured FT4 (T4 x Value of T3 Uptake)
(Reference Interval=1-4.2) Normal in pregnancy; low in hypothyroidism; high in hyperthyroidism
Thyroid Function TestsHyperthyroidismHyperthyroidism HypothyroidismHypothyroidism
Total T3 & T4 in serumTotal T3 & T4 in serum IncreasedIncreased DecreasedDecreased
Free thyroxine indexFree thyroxine index IncreasedIncreased DecreasedDecreased
Serum TSHSerum TSH DecreasedDecreased IncreasedIncreased
Interpreting Thyroid Function Tests
Clinical patterns of thyroid disease
Hyperthyroidism- Lab: excessive levels of TH ( T3 , T4 ) ; S/sx: heat intolerance, palpitation, weight loss,
tachycardia tremors Causes: Graves Ds, toxic adenoma, toxic
goiter , TSH secreting pituitary adenoma
Hypothyroidism – Lab: decrease levels of TH S/sx: Bradycardia, cold sensitivity, dry
skin, muscle weakness , myxedema, cretinism
Causes : TG ablation and destruction ( primary ) ; pituitary hypofuncytion of TSH (secondary )
Laboratory Diagnosis of Thyroid Disease
1 thyroid dis. is abnormality in the thyroid gland TRH and TSH level just reflect N feedback response
2 thyroid dis. is really an abnormality in pituitary gland which cause error in amount of TSH produced T4 and T3 conc’n just reflect N feedback response
3 thyroid dis. is abnormality in hypothalamus causing error of TRH produced Both TSH and T4 & T3 levels just reflect N feedback response
Measuring trophic hormones and hormones of the peripheral endocrine gland
High TSH - Low T3/T4 1o
Hypothyroidism
Low TSH - High T3/T4 1o
Hyperthyroidism
Low TSH - Low T3/T4 2o
Hypothyroidism
“Euthyroid Sick Syndrome” Severe illness often results in low serum
levels of T3 and T4 Causes:
1. Decreased in serum pre albumin in severe illness decrease in hormone binding capacity
2. Fall in amount of T4 deiodinatd to T3 with increase in the metabolic pathways leadig to the inactive product reverse T3
Diagnosis: demonstrating normal TSH level.