Blood
Gases and pH
|
Regulation of Acid-Base balance
|
Lungs and Kidneys
CO2 + H2O <--(Carbonic
anhydrase)--> H2CO3
H2CO3 <-------(Carbonic
anhydrase)--> H+ + HCO3-
|
20:1
|
HCO3-: H2CO3
ratio
|
4:1
|
HPO4: H2PO4
ratio
|
Expanded Henderson-Hasselbalch equation
|
pH = 6.1 + log [Total CO2 –
(pCO2 x 0.03)]
pCO2
x 0.03
|
Chloride-isohydric shift
|
Buffering effect of hemoglobin
|
pCO2
|
Index of efficiency of gas exchange
Increased: Barbiturates, morphine, alcohol,
heparin (á12-15%)
|
pO2
|
Reflects the availability of the gas in
blood but not its content
Excessive O2 supply à acidosis
|
Metabolic Acidosis
|
Causes:
-Bicarbonate deficiency
-DKA (normochloremic acidosis)
-Renal failure
-Diarrhea (âHCO3-)
Compensation: Hyperventilation
Compensated: â HCO3- + âpCO2 + pH
<7.4
|
Metabolic Alkalosis
|
Causes:
-Bicarbonate excess
-Vomiting (âCl-)
-Hypochloremia
-Hypokalemia
Compensation: Hypoventilation
Compensated: á HCO3- + ápCO2 + pH >7.4
|
Respiratory Acidosis
|
Causes:
-CO2 excess (Hypoventilation)
-COPD
-Drug overdose (morphine, barbiturates,
opiates)
Compensation: Bicarbonate retention
Compensated: á HCO3- + â pCO2 + pH <7.4
|
Respiratory Alkalosis
|
Causes
-CO2 loss (Hyperventilation)
Compensation: Bicarbonate excretion
Compensated: â HCO3- + â pCO2 + pH >7.4
|
Full compensation
|
pH Ã normal range
|
Partial compensation
|
pH Ã near normal
|
Buffer base
|
All forms of base that will titrate
hydrogen ions
|
Methods for Blood Gases and pH
|
Specimen: Arterial blood
Blood gas analyzers: meas. pH, pCO2,
pO2
|
Factors affecting Blood gases & pH
measurements
|
For every á1OC above 37OC:
â pH by 0.015
â pO2 by 7%
á pCO2 by 3%
Bacterial contamination: consume O2 (âpO2)
Excess heparin (acid MPS) = âpH
Air exposure (bubbles):
ápO2 = 4 mmHg/2mins
âpCO2 = 4 mmHg/2mins
|
Methods
(Blood gases & pH)
|
1. Gasometer
a. Van Slyke
b. Natelson
-Mercury: produce vacuum
-Caprylic alcohol: anti-foam reagent
-Lactic acid
-NaOH
-NaHSO3
2. Electrodes
a. pH = potentiometry
-Silver-silver chloride electrode
(Reference electrode)
-Calomel electrode [Hg2Cl2]
(Reference electrode)
b. pCO2 = Severinghaus electrode
(potentiometry)
c. pO2 = Clark electrode
(polarography-amperometry)
|
Whole blood total CO2
|
Dissolved CO2 + H2CO3
+ HCO3-
|
Transcutaneous electrodes
|
Continuous monitoring of pO2
Directly placed on the skin
|
Blood gas QC
|
Min. requirement:
-1 sample every 8 hours
-3 levels of control (acidosis, normal,
alkalosis) every 24 hours
|
Normal Values
(Blood gases and pH)
|
pH = 7.35-7.45
pCO2 = 35-45 mmHg
Total CO2:
WB arterial = 19-24 mmol/L
WB venous = 22-26 mmol/L
HCO3- = 21-28 mEq/L
pO2 = 81-100 mmHg
[Hypoxemia:]
-Mild (61-80 mmHg)
-Moderate (41-60 mmHg)
-Severe (40 mmHg or less)
O2 saturation = 94-100%
|
Endocrinology
|
Endocrine
|
Hormone à blood circulation à specific receptor
|
Paracrine
|
Hormone à interstitial space à adjacent cell
|
Autocrine
|
Hormone à self-regulation
|
Juxtacrine
|
Hormone à direct cell-to-cell contact
|
Exocrine
|
Hormone à gut
|
Neurocrine
|
Hormone à neurons à extracellular space
|
Neuroendocrine
|
Hormone à neurons à nerve endings
|
Glycoproteins
|
FSH, hCG, TSH, LH
|
Polypeptides
|
ACTH, ADH, GH, angiotensin, calcitonin,
CCK, gastrin, glucagons, insulin, MSH, oxytocin, PTH, PRL, somatostatin
|
Steroids
|
Precursor: cholesterol
Aldosterone, cortisol, estrogen,
progesterone, testosterone, vitamin D
|
Amines
|
Derived from amino acids
Catecholamines, T3, T4
|
Hypothalamus
|
Connected to the posterior pituitary by the
infundibulum stalk
Hypophyseal hormones: TRH, GnRH, GH-IH,
GH-RH, PIF
|
Pineal gland
|
Melatonin: decreases pigmentation of the
skin
|
Pituitary gland
|
Master Gland
Located in the sella turcica or Turkish
saddle
|
Anterior Pituitary
(Adenohypophysis)
|
True endocrine gland
Hormones: PRL, GH, FSH, LH, TSH, MSH, ACTH
|
GH (Somatotropin)
|
Most abundant of all pituitary hormones
Structurally similar to PRL and HPL
Markedly elevated during deep sleep
|
Dwarfism
|
Decreased GH
|
Acromegaly
|
Increased GH
|
GH deficiency tests
|
1. Insulin tolerance test = Gold standard
(Confirmatory test)
2. Arginine stimulation test = 2nd
confirmatory test
|
Tests for Acromegaly
|
1. Somatomedin C or insulin-like growth
factor I (Screening)
-Increased: Acromegaly
-Decreased: GH deficiency
2. OGTT (Confirmatory)
-75g glucose
|
FSH
|
Spermatogenesis
|
LH
|
Helps Leydig cells to produce testosterone
(male)
Ovulation (female)
Synthesis of androgens, estrogens, and
progesterone
|
TSH (Thyrotropin)
|
Stimulates thyroid gland to produce T3 and
T4
Increased: 1’ hypothyroidism, 2’
hyperthyroidism
Decreased: 1’ hyperthyroidism, 2’
hypothyroidism, 3’ hypothyroidism
|
ACTH
(Corticotropin)
|
Highest: 6-8 AM
Lowest: 6-11 PM
Not allowed to have contact with glass
because it adheres to glass surface
Collect blood in plastic tubes
|
Prolactin
|
Initiation and maintenance of lactation
Inhibited by Dopamine
Highest: 4AM and 8AM, and 8PM and 10PM
Increased: Menstrual irregularity,
infertility, amenorrhea, galactorrhea
|
Panhypopituitarism
|
From pituitary tumor (adenoma) or Ischemia
|
Pituitary ischemia
(Shechan’s)
|
Hemorrhage or shock in a pregnant female at
the time of deliver
|
Posterior pituitary
(Neurohypophysis)
|
Release but not produce oxytocin and
vasopressin
|
Oxytocin
|
Uterine contraction and milk ejection
|
ADH/AVP (Arginine vasopressin)
|
H2O reabsorption (DCT and CD)
Stimulus: Increased plasma osmolality
(>295 mOsm/kg), decreased blood vol.
Promotes factor VII and vWF release
|
Overnight water deprivation test (Conc. test)
|
Diagnostic test for ADH
|
Neurogenic DI
|
True Diabetes Insipidus
Failure of the pituitary gland to secrete
ADH
|
Nephrogenic DI
|
Failure of the kidneys to respond to normal
or elevated ADH
|
SIADH
|
Syndrome of inappropriate ADH
Sustained production of ADH
Decreased urine volume
Low plasma osmolality
Low serum electrolytes
|
Thyroid Gland
|
Butterfly-shaped
2 lobes = connected by the isthmus
|
Follicle
|
Fundamental structural unit of the thyroid
gland
|
Follicular cells
|
Secrete T3 and T4
|
Parafollicular or C cells
|
Secrete calcitonin
|
Thyroglobulin
|
Preformed matrix containing tyrosyl groups
Stored in the follicular colloid of the
thyroid gland
|
Thyroid hormone Biosynthesis
|
1. Trapping of Iodine
2. Iodination: I2 à Tyrosine ring à MIT and DIT
3. Condensation: MIT+DIT=T3 / DIT+DIT=T4
4. Release: T3/T4 Ã Blood circulation
5.
Transport of T3/T4 by proteins
|
Protein-bound hormones
|
Metabolically inactive
Biologically inert
Do not enter cells
Storage sites
|
Free hormones (FT3/FT4)
|
Physiologically active
Readily enters cells
|
Reverse T3 (rT3)
|
From removal of one iodine from T4 (product
of T4 metabolism)
Metabolically inactive
|
I2 intake <50 μg/day
|
Deficiency of hormone secretion
|
T3
|
3,5,3’-Triiodothyronine
Most active thyroid hormonal activity
75-80% is produced from the tissue
deiodination of T4
Diagnosis of T3 thyrotoxicosis
|
T4
|
3,5,3’5’-Tetraiodothyronine
Principal secretory product
All originated in the thyroid gland
|
TBG
|
Transports 70-75 of TT4, and majority of T3
|
TBPA (Transthyretin)
|
Transports 15-20% of TT4
No affinity for T3
|
TBA
|
Transports T3 and 10% of T4
|
Thyroid autoantigens
|
TPO
Tg
TSHR
|
Thyroid disorders
|
Screening is recommended when a person
reaches 35 yrs old and every 5 yrs thereafter
|
Primary hyperthyroidism
|
á T3 and T4
â TSH
|
Secondary hyperthyroidism
|
á T3 and T4
á TSH
|
T3 Thyrotoxicosis (Plummer’s disease)
|
á T3
N-T4
â TSH
|
Graves’ disease
(Diffuse toxic goiter)
|
1’ Hyperthyroidism
Most common cause of thyrotoxicosis (autoimmune)
Women > Men
Anti-TSH receptor
|
Riedel’s thyroiditis
|
Thyroid à woody or stony-hard mass
|
Subclinical hyperthyroidism
|
No symptoms
N-T3 and T4
â TSH
|
Subacute granulomatous/ Subacute
nonsuppurative/ De Quervain’s thyroditis
|
Hyperthyroidism
Painful thyroiditis
Neck pain, low-grade fever
(-) anti-TPO, á ESR and Tg
|
Hypothyroidism
|
Treatment: Levothyroxine
|
Primary hypothyroidism
|
â T3 and T4
á TSH
|
Hashimoto’s disease (Chronic autoimmune
thyroiditis)
|
Most common cause of 1’ hypothyroidism
Thyroid is replaced by a nest of lymphoid
tissue (T cells)
Goiter
(+) anti-TPO
á TSH
|
Myxedema coma
|
Severe form of 1’ hypothyroidism
Peculiar nonpitting swelling of the skin
Skin is infiltrated by mucopolysaccharides
“Puffy” face, thin eyebrows
|
Secondary hypothyroidism
|
â T3 and T4
â TSH
|
Tertiary hypothyroidism
|
â T3 and T4
â TSH
â TRH
|
Congenital hypothyroidism
(Cretinism)
|
Mental retardation (child)
Screening: âT4
Confirmatory: áTSH
|
Subclinical hypothyroidism
|
N-T3 and T4
á TSH
|
TRH stimulation test
|
Most specific and sensitive test for
diagnosing thyroid disease
Confirm borderline cases and euthyroid
Graves’ disease
á: 1’ hypothyroidism
â: Hyperthyroidism
|
Radioactive Iodine Uptake (RAIU)
|
Measure the ability of the thyroid gland to
trap iodine
|
Thyroglobulin (Tg) assay
|
Postoperative marker of thyroid cancer
á: Untreated and metastatic
differentiated thyroid cancer, hyperthyroidism
â: Hypothyroidism,
thyrotoxicosis factitia
|
rT3
|
Assess borderline or conflicting
laboratory results
|
Free Thyroxine Index (FT4I)
|
Indirectly assesses the level of FT4 in
blood
Equilibrium relationship of bound T4 and
FT4
Reference method: Equilibrium dialysis
FT4I = TT4 x T3U(%) or TT4 x THBR
100
|
TT3, FT3, FT4
|
FT4 test: differentiates drug induced TSH
elevation and hypothyroidism
TT3 or FT3: confirm hyperthyroidism
Reference method (FT4): Equilibrium
dialysis
|
T3 Uptake test
|
Measures the number of available binding
sites of the thyroxine binding proteins (TBG)
á TBG = â T3U
â TBG = á T3U
|
TBG test
|
Confirm results of FT3 or FT4 or
abnormalities in the relationship of TT4 and THBR test
Estrogen: áTBG
Androgen: âTBG
|
Fine-needle aspiration
|
Most accurate tool in the evaluation of
thyroid nodules
|
Recombinant Human TSH
|
Test patients w/ thyroid cancers for the
presence of residual or recurrent dis.
|
Tanned Erythrocyte Hemagglutination method
|
Test for anti-Tg disorders
|
Serum calcitonin test
|
Marker for familial medullary thyroid
carcinoma
|
FT4 and TSH
|
Best indicators of thyroid status
|
FT3 and FT4
|
More specific indicators of thyroid
function than meas. of total hormone
Not affected by TBG
|
Euthyroid sick syndrome
|
Acutely ill but without thyroid disease
â T3 and T4
N/á TSH
á rT3
|
Parathyroid gland
|
4 parathyroid glands
Smalles endocrine gland
|
PTH
|
Hypercalcemic hormone
á Ca2+ (bone
resorption and renal reabsorption) and Mg2+
â iPO4
|
1’ hyperparathyroidism
|
Defective: Parathyroid gland
Most common cause of hypercalcemia
Parathyroid adenoma
á PTH and iCa2+
Hypercalciuria
Phosphaturia à Hypophosphatemia
If goes undetected à severe demineralization
(osteitis fibrosa cystica)
|
2’ hyperparathyroidism
|
In response to âCa2+
Hyperplasia of all 4 glands
Causes: Vit. D deficiency and chronic renal
failure
á PTH
â Ca2+
|
3’ hyperparathyroidism
|
Occurs w/ 2’ hyperparathyroidism (â Ca2+)
Autonomous function of hyperplastic PT
glands or PT adenoma
á PO4
Calcium phosphates precipitate in soft
tissues
|
Hypoparathyroidism
|
Accidental injury of the PT glands (neck)
during surgery
Autoimmune parathyroid destruction
â PTH = â Ca2+
|
Hyperparathyroidism
|
Acidosis
|
Hypoparathyroidism
|
Alkalosis
|
Adrenal glands
|
Pyramid-shaped
Above the kidneys
Adrenal cortex = outer (yellow)
Adrenal medulla = inner (dark mahogany)
Has prime effects on blood pressure
|
Adrenal cortex
|
Major site of steroid hormone production
G cells: convert cholesterol à pregnenolone
|
CPPP ring
|
17-carbon skeleton derived from cholesterol
|
3 layers (Adrenal cortex)
|
1. Zona Glomerulosa = Mineralocorticoids
(Aldosterone)
2. Zona Fasciculata = Glucocorticoids (Cortisol)
3. Zona Reticularis = Weak androgens
(androstenedione, DHEA)
|
Cortisol
|
Gluconeogenesis à hyperglycemia
The only adrenal hormone that inhibit the
secretion of ACTH
Anti-inflammatory and immunosuppressive
Diurnal: á 6-8AM / â 10PM-12AM
Urinary metabolites: 17-OHCS and 17-KGS
|
Porter-Silber method
|
Meas. 17-OHCS
Rgt: DNPH in H2SO4 +
Alcohol
(+) Yellow
|
Zimmerman reaction
|
Meas. 17-KGS
Rgt: m-dinitrobenzene
(+) Reddish purple
Oxidation procedure: Norymberski (Na+
bismuthate)
|
Pisano method
|
For quantitating metanephrines and
normetanephrines
|
Kober reaction
|
For estrogen
Rgt: H2SO4 +
hydroquinone
(+) Reddish brown color
|
Cushing’s syndrome
(Hypercortisolism)
|
Excessive production of cortisol and ACTH
Overuse of corticosteroids
Buffalo hump
Hyperglycemia
Hypertension
Hypercholesterolemia
â Lymphocytes
|
Screening tests (Cushing’s)
|
1. 24-hour urine free cortisol test
2. Overnight dexamethasone suppression
tests = Most widely used (1mg)
3. Salivary cortisol test
|
Confirmatory tests (Cushing’s)
|
1. Low-dose dexamethasone suppression test
(0.5mg)
2. Midnight plasma cortisol
3. CRH stimulation test
|
Addison’s disease
(1’ Hypocorticolism)
|
Primary adrenal insufficiency
â Cortisol and aldosterone
á ACTH
(+) Hyperpigmentation
Screen: ACTH Stimulation Test
|
2’ Hypocorticolism
|
Secondary adrenal insufficiency
Hypothalamic-pituitary insufficiency
â ACTH
Test: ACTH Stimulation test
|
ACTH Stimulation test
(Corsyntropin stimulation test)
|
Corsyntropin: synthetic coritsol and aldosterone
stimulator
Differentiates:
2’ adrenal insufficiency (âACTH) from
3’ adrenal insufficiency (á ACTH)
|
Metyrapone test
|
Metyrapone: inhibitor of 11 β-hydroxylase
Measures the ability of the pituitary gland
to respond to declining levels of circulating cortisol, thereby secrete ACTH
Alternative diagnostic or confirmatory test
for 2’ or 3’ adrenal insufficiency
(+): âACTH
|
24-hour urine free cortisol
|
Most sensitive and specific screening test
for excess cortisol production because plasma cortisol is affected by diurnal
variation
Methods: HPLC or GC-MS
|
HPLC-MS
|
Reference method for measuring urinary free
cortisol
|
ITT (Insulin tolerance test)
|
Gold standard for 2’ and 3’ hypocorticolism
Confirms borderline response to ACTH
stimulation test
|
Serum ACTH
|
Differentiates:
Cushing’s disease (áACTH)
Cushing’s syndrome (0-ACTH)
|
áACTH
|
á17-OHCS and 17-KS
|
Congenital Adrenal Hyperplasia
|
Enzyme deficiencies:
1.) 21-hydroxylase = most common
2.) 11 β-hydroxylase = 2nd most
common
3.) 3β-hydroxysteroid dehydrogenase-isomerase
4.) C-17,20-lyase/17α-hydroxylase
â Cortisol
á ACTH
á Androgens (hirsutism,
virilization, amenorrhea, pseudohermaphroditism)
|
Aldosterone (Aldo)
|
Electro-regulating hormone
á Na+ and Cl-
â K+ and H+
â at night
18-hydroxysteroid dehydrogenase: enzyme
needed for aldosterone synthesis
|
Conn’s disease
(1’ hyperaldosteronism)
|
Aldosterone-secreting adrenal adenoma
Screen: Plasma Aldo conc./Plasma renin
activity ratio (PAC/PRA ratio)
-(+): >50 ratio
Confirm: Saline suppression test
-(+): >5 ng/dL aldosterone
|
2’ Hyperaldosteronism
|
Excessive production of renin
|
Liddle’s syndrome
|
Pseudohyperaldosteronism
Resembles 1’ aldosteronism clinically
â Aldosterone
(-) Hypertension
|
Bartter’s syndrome
|
Bumetanide-sensitive chloride channel mutation
á Aldosterone and Renin
|
Gitelman’s syndrome
|
Thiazide-sensitive transporter mutation
á Aldosterone
|
Hypoaldosteronism
|
Destruction of the adrenal glands
Glucocorticoid deficiency
21-hydroxylase deficiency
|
Postural stimulation test
|
Test for aldosterone
|
Florinef
|
Synthetic mineralocorticoid
|
Weak androgens
|
Precursors for the production of more
potent androgens and estrogens
Precursors: Pregnenolone and 17-OH
pregnenolone
Examples: DHEA and androstenedione
Bound to steroid hormone binding globulin
(SHBG)
á: Virilization
(pseudohermaphroditism)
|
DHEA (Dehydroepiandrosterone)
|
Principal adrenal androgen
Converted to estrone
|
Adrenal medulla
|
Chromaffin cells: secrete catecholamines
Precursor: L-tyrosine
Norepinephrine/Epinephrine ---(Monoamine oxidase
and Catechol-0-methyl-transferase)---> Metanephrines and VMA
|
9:1
|
Norepinephrine: Epinephrine ratio
|
Norepinephrine
|
Primary amine
á in CNS
Metabolites:
-3-methoxy-4-hydroxyphenylglycol (MHPG) =
Major metabolite
-VMA
|
Epinephrine
|
Secondary amine
Most abundant medullary hormone
“Flight or fight hormone”
Metabolites:
-Vanillylmandelic acid (VMA) = Major
metabolite
-Metanephrines
-Normetanephrines
-HVA
|
Dopamine
|
Primary amine
From the decarboxylation of
3,4-Dihydroxyphenylalanine (DOPA)
Major metabolite: Homovanillic acid (HVA)
|
Pheochromocytoma
|
Tumors of the adrenal medulla
áCatecholamines
Classic “Spells”: tachycardia, headache,
chest tightness, sweating, hypertension
|
Clonidine test
|
Differentiates:
Pheochromocytoma (Catecholamines not
suppressed) from
Neurogenic hypertension (50% decreased in
catecholamines)
|
Neuroblastoma
|
áNorepinephrine (Children)
á urinary HVA, VMA or both and
dopamine
|
Methods (Catecholamines)
|
Specimen: 24-hr urine and plasma
1. Chromatography: HPLC or GC-MS
2. RIA: sensitive screening test
->2000pg/mL = diagnostic for
pheochromocytoma
|
Estrogens
|
Estrone = áPostmenopausal women
Estradiol = áPremenopausal women (most
potent, secreted by the ovary)
Estriol = áPregnancy (placenta)
|
Markers for Down Syndrome
|
âAFP
âUnconjugated Estriol
áhCG
áInhibin A
|
Karyotyping or FISH typing
|
Test for Down syndrome (amniotic fluid)
|
Progesterone
|
Produced mainly by the corpus luteum
Det. whether ovulation has occurred
áLuteal phase
|
Tests for menstrual cycle dysfunction and
anovulation
|
Estrogen
Progesterone
FSH
LH
|
Tests for female infertility
|
hCG
PRL
FT4
TSH
FSH
LH
Estradiol
Progesterone
|
Pancreas (Exocrine)
|
Digestive enzymes (AMS, LPS)
Acinus: functional secretory unit
|
Pancreas (Endocrine)
|
Hormones:
Alpha cells (20-30%) = glucagon
Beta cells (60-70%) = insulin
Delta cells (2-8%) = somatostatin
|
hCG
|
Produced by the syncytiotrophoblasts
(placenta)
Maintain progesterone production by the
corpus luteum
|
Human placental lactogen (HPL)
|
Stimulates development of mammary gland
Increases maternal plasma glucose levels
Diagnosis of intrauterine growth
retardation
|
Gastrin
|
Secreted by G cells (stomach)
Stimulates parietal cells to secrete HCl
Stimulus: Amino acid
áZollinger-Ellison syndrome
âPernicious anemia
|
Serotonin
(5-hydroxytryptamine)
|
Synthesized by argentaffin cells (GIT)
Metabolite: 5-HIAA
|
5-HIAA
|
Diagnostic marker for carcinoid syndrome
Test: Ehrlich’s aldehyde test = (+) purple
color
|
Somatostatin
|
A.k.a. GH-IH
Inhibitor of GH, glucagon and insulin
|
1’ amenorrhea
|
Menstruation having never occurred
|
2’ amenorrhea
|
Absence of menses for 6 months
|
Cushing’s disease
|
Abnormal increased secretion of ACTH
|
Cushing’s syndrome
|
Chronic excessive production of cortisol by
the adrenal cortex
-Large doses of glucocorticoids
-Pituitary tumor (áACTH) = most common cause
|
Gynecomastia
|
Development of breast tissue in males
|
Hirsutism
|
Excessive hair growth w/ a male
distribution pattern in a female
Most common endocrine disorder in women
|
Mullerian agenesis
|
Congenital malformation or absence of the
fallopian tubes, uterus or vagina
N-FSH, LH and testosterone
|
Nonthyroidal illness
|
Illness that do not directly involve the
thyroid gland
|
Sipples syndrome (MEN II)
|
Medullary carcinoma of the thyroid
Pheochromocytoma
Parathyroid adenoma
|
Stein-Leventhal syndrome
|
Mild hirsutism w/ normal menses to
excessive hirsutism w/ amenorrhea
|
Thyroid stones
|
A.k.a. thyroid crisis
Life-threatening
Uncontrolled thyrotoxicosis
|
Normal Values
(Endocrinology)
|
T3:
Adult = 80-200 ng/dL
Children 1-14 y.o. = 105-215 ng/dL
T4:
Adult = 5.5-12.5 μg/dL
Neonate = 11.8-22.6 μg/dL
T3U = 25-35%
|
|
