Clinical chemistry

Presented by
Alyazeed Hussein, BSc
 Outline
• Sample collection and handling.
• Carbohydrates.
• Acid-base.
• Proteins.
• Enzymes.
• Lipids and lipoproteins.
• Endocrinology and Tumor markers.
Sample collection and handling
 Serum (red top) for most chemistry tests, then heparinized blood.
 Blood (on ice): ammonia and lactic acid.
 For glucose (sodium fluoride is used as anticoagulant) prevent glycolysis(10 mg/dl/1hr) in whole blood!
 Pseudohyperkalemia: caused by tightening the tourniquet too much during venipuncture, storing the tube
too long before testing, or hemolyzed sample.
 Falsely decreased bilirubin : leaving a specimen tube exposed to light. Falsely increased bilirubin:
hemolysis.
 Drawing blood from an arm with an IV: sample dilution (low results).
 Carbohydrates and Glucose Metabolism
1. During a fast, the blood glucose level is kept constant by mobilizing the glycogen stores in the liver.
2. During long fasts, gluconeogenesis is required to maintain blood glucose levels because glycogen stores
are used up in about 24-48 hours.
 glucose is the only source of energy for brain.
 Fructose utilized by sperms.
 Fructose-2-6-bi phosphate: gluconeogenesis and glycolysis.
 Hereditary fructose intolerance: deficiency of aldolase >accumulation of fructose-1-phosphate.
 Glucose methods:
1. Glucose oxidase(enzymatic): used in urine dipsticks.
2. Hexokinase method: reference method.
Use sodium fluoride tube!
 Glycated/glycosylated hemoglobin
 Hemoglobin A is composed of three forms, Hb A I a, Hb A I b, and Hb A I c, which are referred to
as glycated or glycosylated hemoglobin.
 Glycated hemoglobin is formed by attachment of glucose to hemoglobin A.
 Measurement of glycated hemoglobin reflects blood glucose levels for the past 2-3 months. It
is useful in monitoring effectiveness of treatment and compliance of diabetic individual to
treatment protocol.
 Specimen collection: blood drawn in EDTA tubes.
 Reference range: 4-6% Hb A 1 c; effective treatment range <7% Hb A 1c.
 Fructosamine
 Ketoamine linkage forms between glucose and protein, mainly represented by albumin.
 Clinical significance: Measurement of fructosamine reflects blood glucose levels for 2-3
weeks.
 Reference range: 205-285 μmol/L.
 Lactate: The normal end product of glucose metabolism is pyruvate; however, lactate is produced under
conditions of oxygen deficit (anaerobic metabolism) also in RBCs. The production and accumulation of
lactate in the blood and its measurement aid in assessing the degree of oxygen deprivation that is
occurring. Change in the blood lactate level precedes a change in blood pH. Lactate is metabolized by
the liver via gluconeogenesis.
Clinical significance: (lactic acidosis)
 acute myocardial infarction, congestive heart failure, shock, pulmonary edema, and so on.
 diabetes mellitus, renal disorders, liver disease, ingestion of toxins.
 Special specimen handling : Avoid using a tourniquet because venous stasis(hemoconcentration) will
falsely raise blood lactate levels; place the specimen on ice and immediately transport to the laboratory
(NaF) tube. Reference range : 0.5-1.3 mmol/L.
Acid-base balance: (Lungs and kidneys): The pH of plasma is a function of two independent variables:
the (PC02), which is regulated by the lungs or (respiratory mechanism), and the concentration of
bicarbonate (HC03), which is regulated by the kidneys (renal mechanism).
 Reference ranges for arterial blood gas analysis: pH: 7.35-7.45, PC02: 35-45 mm Hg,

HC03: 22-28 mm Hg.

 Electroplytes: Electrolytes: Charged ions found in intracellular fluid, extracellular fluid, and
interstitial fluid.
 Cations are positively charged ions. The major cations in the body are sodium, potassium,
calcium, and magnesium.
 Anions are negatively charged ions. The major anions in the body are chloride, bicarbonate,
phosphate, sulfate, and protein.
 The serum concentration of these four electrolytes is quantified using ion-selective electrodes
(ISEs).
 Sodium (Na+): Major cation of extracellular fluid,
 Reference range: 136-145 mmol/L. Changes in sodium result in changes in plasma volume.
 Largest constituent of plasma osmolality.

Clinical significance:
 Hyponatremia occurs when serum sodium level is <135 mmol/L.
Hypoaldosteronism (Addison disease), syndrome of inappropriate antidiuretic hormone (SIADH),
diarrhea, or vomiting.
 Hypernatremia occurs when serum sodium level is> 150 mmol/L.
Usually occurs when water is lost as through diarrhea, excessive sweating, or diabetes insipidus &
hyperaldosteronism.
 Potassium (K +): Major intracellular cation
 Reference range: 3.4-5.0 mmol/L.

Note that!!!
Because the concentration of potassium in red blood cells is higher than in serum, any level of
hemolysis will falsely increase serum potassium results.
 Clinical significance
 1) Hypokalemia occurs when serum potassium level is <3.0 mmol/L.
 Results from decreased dietary intake, hyperaldosteronism, diuretics, vomiting, diarrhea and
excess insulin which causes increased cellular uptake of potassium.
 2) Hyperkalemia occurs when serum potassium level is >5.0 mmol/L.
 Results from increased intake, renal failure, hypoaldosteronism, metabolic acidosis,
increased red blood cell lysis, leukemia, chemotherapy.
 Calcium: Regulation: Serum calcium is controlled by parathyroid hormone, vitamin D and
calcitonin:
 Parathyroid hormone (PTH)
1/ A decrease in free (ionized) calcium stimulates the release of PTH by the parathyroid gland,
and a rise in free calcium terminates PTH release.
2/ In bone, PTH activates osteoclasts to break down bone with the release of calcium.
3/ In the kidneys, PTH increases tubular reabsorption of calcium and stimulates hydroxylation of
vitamin D to the active form,
(1,25-dihydroxycholecalciferol).
 Calcitonin: 1) Released by the parafollicular cells of the thyroid gland when serum calcium level
increases
 2) Inhibits vitamin D and parathyroid hormone activity, thus decreasing serrm calcium.
 3) Medullary carcinoma of the thyroid gland is a neoplasm of the parafollicular cells, resulting in elevated
serum levels of calcitonin.
Clinical significance: Hypercalcemia is caused by primary hyperparathyroidism, other endocrine
disorders such as hypothyroidism and acute adrenal insufficiency, malignancy involving bone, and renal
failure.
 Hypocalcemia is caused by hypoparathyroidism, hypoalbuminemia, chronic renal failure, magnesium
deficiency, and vitamin D deficiency.
 Reference ranges: Total calcium (adults): 8.6-10.3 mg/dL, Free calcium (adults): 4.6-5.3 mg/dL.
 Facts:

• Na is the major cation in the ECF.

• K is the major cation in the ICF.
• Cl is the major anion in the ECF.
• PO4 (from phosphorus) is the major anion in the
ICF.
• Anion gap: the difference between the cations
and anions, in the ECF, main cation is Na, main
anions are CL & HCO3.
Anion gap= Na – (Cl + HCO3) or
(Na + K) – (Cl + HCO3), normal range: 10 ±2
mEq/L, affected by metabolic acidosis,
Urine anion gap= (Na + K) – (Cl) (excess ammonia,
acid!): high.
proteins
 Proteins are macromolecules made of amino acids, with each amino acid linked to another via a
peptide bond.
 Peptide bond is formed when the carboxyl (-COOH) group of one amino acid links to the amino

(-NH2) group of another amino acid.

 Electrophoresis is the migration of charged particles in some medium (either liquid or solid) when
an electrical field is applied. Depending on the charge of the molecules, negatively charged particles
migrate toward the positive electrode (anode), and positively charged particles migrate toward the
negative electrode (cathode).
 Protein electrophoresis: principle:
 proteins can have positive or negative charge because of their acidic and basic side
chains(amphoteric).
 Isoelectric point of protein is the pH at which a protein has no net charge.
 At pH 8.6, proteins are negatively charged and migrate toward the anode.
 medium (agarose gel or cellulose acetate) is put in contact with the buffer (stain used are: ponceau
S, amido black), while ethidium bromide used for DNA.
Monoclonal gammopathy : Multiple
myeloma and Waldenström's
macroglobulinemia.
 Serum Iron and Total Iron-Binding Capacity:
 Iron is found in several locations in the body, including: component of hemoglobin and myoglobin,
stored form (ferritin and hemosiderin), Serum iron: 45-160 μg/dL.
 Iron is transported in the blood by transferrin.
 Ferritin reflects iron stores(confirmatory for IDA), F: 20-250 ng/mL, M: 10-120 ng/mL.
 Total iron-binding capacity (TIBC): Measures the quantity of iron bound to transferrin, 250-425
μg/dL.
 Decreased serum iron is associated with iron-deficiency anemia, malnutrition, blood loss, and
chronic infection.
 Increased serum iron is associated with iron overdose, sideroblastic anemia, viral hepatitis, and
hemochromatosis.
 Ammonia:
 Ammonia produced from deamination of amino acids, and transported via blood to the liver in form
of alanine and glutamine.
 Hepatocytes convert ammonia to urea for excretion.
 With severe liver cell malfunction, blood levels of ammonia increase.
 Ammonia is neurotoxic.
 Clinical significance: Increased plasma ammonia levels seen in hepatic failure.
 Urea and creatinine
 Urea
 Urea results from protein catabolism and is synthesized in the liver from the deamination of amino
acids. Urea is excreted by the kidneys.
 Clinical significance: Abnormal serum urea levels may be due to prerenal, renal, or postrenal
disorders.
 a. Increased serum urea: Renal failure, glomerular nephritis, urinary tract obstruction,.
 b. Decreased serum urea: Severe liver disease, vomiting, diarrhea, malnutrition.
 Creatinine: 1. Regulation: Creatinine is a waste product of muscle contraction that is formed from
phosphocreatine, a high-energy compound. Creatinine levels are regulated by kidney excretion.
Measurements of creatinine in serum and urine (creatinine clearance) are used to assess the
glomerular filtration rate (GFR). Creatinine levels are not changed by diet or rate of urine flow.
 Creatinine is not reabsorbed by renal tubules.
 2. Clinical significance
 a. Increased serum creatinine: Renal disease, renal failure.
 Test methodology: Jaffe method /

Creatinine + picric acid ( alkaline solution) > creatinine picrate(red).

 0.6-1.1 mg/dL.
 Uric acid
 Regulation: Uric acid, the major waste product of purine (adenosine and guanine) catabolism, is
synthesized in the liver. Uric acid elimination from the blood is regulated by the kidneys through
glomerular filtration, and some uric acid is excreted through the GI tract.
 Clinical significance: a. Increased serum uric acid: Gout, renal disorders, treatment of
myeloproliferative disorders, lead poisoning,.
 b. Decreased serum uric acid: Severe liver disease, tubular reabsorption disorders.
 Reference ranges: Male, 3.5-7.2 mg/dL; female, 2.6-6.0 mg/dL.
 Liver functions:
 Liver synthesizes proteins, coagulation factors, ammonia, carbohydrates, fat, ketones, vitamin A,
enzymes.
 Bilirubin: Principal pigment in bile that is derived from hemoglobin breakdown:

A. Bilirubin is produced in the reticuloendothelial system from the breakdown of hemoglobin from
aged red blood cells (RBCs). Bilirubin forms a complex with albumin for transport to the liver. In this
form, bilirubin is unconjugated and not water soluble.
B. Bilirubin is conjugated in the hepatocyte with glucuronic acid to form bilirubin diglucuronide
(conjugated bilirubin). The reaction is catalyzed by uridine diphosphate (UDP)
glycuronyltransferase.
Conjugated bilirubin is water soluble.
Conjugated bilirubin is excreted into the
bile then secreted into the duodenum and
reduced by intestinal bacteria to
urobilinogen.
Some intestinal urobilinogen (10%) is
reabsorbed; a portion (5%) returns to the
liver then secreted to bile and other (5%)
enters the kidney and excreted in the
urine(urobilin). (90%) of the intestinal
urobilinogen is again oxidized by the
intestinal bacteria to stercobilin: (brown
pigment) that gives stool its characteristic
color.
Jaundice (icterus) is a yellow discoloration that occurs when
the bilirubin concentration in the blood rises (>2-3 mg/dL)
and the bilirubin is deposited in the skin and sclera of the
eyes.

Kernicterus: Elevated bilirubin deposits in brain tissue of

infants, affecting the central nervous system and resulting in
mental retardation.
Classification of Causes of Jaundice

A. Prehepatic jaundice (hemolytic jaundice).

B. Hepatic jaundice.
C. Posthepatic jaundice(obstructive jaundice).
A. Pre-hepatic jaundice occurs when there is excessive erythrocyte destruction, as seen
in hemolytic anemias, spherocytosis, hemolytic disease of the newborn caused by Rh or
ABO incompatibility.
In these cases, the rate of hemolysis exceeds the liver's ability to take up the bilirubin for
conjugation. Prehepatic jaundice is characterized by an increased level of unconjugated
bilirubin (indirect bilirubin) in the sernm.
B. Hepatic jaundice(liver problems):
 occurs when the liver cells malfunction and cannot take up, conjugate, or secrete bilirubin:

1. Gilbert syndrome: transport problem, mild increased in unconjugated bilirubin.

2. Crigler-Najjar disease: Partial or complete deficiency of UDPglycuronyltransferase; little,
if any, conjugated bilirubin formed with moderate to extremely elevated unconjugated
bilirubin.
3. Dubin-Johnson syndrome: excretion defect, high conjugated bilirubin.
4. Neonatal jaundice(physiological): at birth, low level UDP-glycuronyltransferase cause
high indirect bilirubin.
C. Post-hepatic jaundice: obstruction blocks the flow of bile into the intestines.
May be caused by gallstones obstructing the common bile duct, neoplasms and acute
cholangitis or acute pancreatitis.
Posthepatic jaundice is characterized by a significantly increased level of conjugated
bilirubin and enzyme called Alkaline phosphatase(ALP), deceased urobilinogen in
urine and pale stool color due to absence of stool pigment (stercobilin).
Note that!!! When test bilirubin: avoid the Hemolyzed, lipemic and sample exposed
to light.
 Normal range: Total bilirubin 0.2-1.0 mg/dL

Indirect bilirubin 0.2-0.8 mg/dL

Direct bilirubin 0.0-0.2 mg/dL
 Clinical significance of Urine urobilinogen:
 Increased: urine urobilinogen is associated with hemolytic disease and
hepatocellular disease, such as hepatitis.
 Decreased: In posthepatic obstruction, This is evidenced by a clay-colored (partial
biliary obstruction) or chalky white stool (complete biliary obstruction).
 Normal range: 0.1-1.0 Ehrlich units/2 hr.
 Liver disease test
Hepatic jaundice High: ALT, AST and
total bilirubin
Post hepatic or biliary High: total and direct
obstructive jaundice bilirubin, no
urobilinogen and pale
color stool
Chronic hepatitis(viral High liver enzymes
hepatitis) and high ALP, bilirubin

Pre hepatic or High liver enzymes

hemolytic jaundice and high urobilinogen
Enzymes
 ENZYMES
 Enzymes are proteins that function as biological catalysts and are neither consumed nor
permanently altered during a chemical reaction. Enzymes circulate as zymogens.
 In healthy individuals, these enzymes exhibit very low levels in serum. They appear in the serum in
increased amounts after cellular injury or tissue damage.
 Enzymes are reported in activity units because they are measured based on their activity instead of
their concentration(IU or U).
1-Lactate dehydrogenase (LD), oxidoreductase enzyme: (high concentration) in: Liver, heart, skeletal
muscle, kidney and erythrocytes.
 Elevated in cardiac disorders (acute myocardial infarction), hepatic diseases, skeletal muscle diseases
and hemolytic disorders.
 Sources of error: Hemolysis! Reference range: I 00-225 U/L.

2-Creatine kinase (CK) and CK isoenzymes:

 Highest concentrations: Skeletal muscle, heart muscle, brain tissue.
 CK isoenzymes: CK-MM, CK-MB and CK-BB.
 CK-MB+ troponin increase in: heart muscle damage, and elevations are indicative of AMI.
 CK-MM increases are associated with skeletal muscle and heart muscle disorders.
 CK-BB is elevated in central nervous system disorders and tumors.
 Acute myocardial infarction:

Troponin > CK-MB > LDH > Myoglobin>AST.

 CK isoenzymes are measured by electrophoresis, ion-exchange chromatography, and several types of
immunoassays. Reference ranges: Total CK: male, 15-160 U/L; female, 15-130 U/L. CK-MB: <6% of
total CK.
3-Aspartate aminotransferase (AST): Highest concentrations in heart, liver, and skeletal muscle. Less
amount in RBCs. Clinical significance: hepatocellular disorders, AMI. Note that!!! AST is not used to
diagnose AMI, it is useful when ruling out other disorders, including liver damage.
 Sources of error: Hemolysis, Reference range: 5-30 U/L.

4-Alanine aminotransferase (ALT): Highest concentrations in liver, with lesser amounts in other tissues.
 Clinical significance: Hepatocellular disorders (hepatitis), ALT is more specific for liver disease than
AST. Reference range: 6-37 U/L, measured by end point enzymatic.
5-Alkaline phosphatase (ALP): Highest concentrations are found in liver, bone, intestines, spleen,
kidney, and placenta.
 Clinical significance: Increased serum ALP levels are seen in hepatobiliary disease and bone
disorders. Acid phosphatase (ACP), in prostate, + prostate specific antigen (PSA) (carcinoma).
 In obstructive disease the ALP levels are increased more significantly than ALT and AST.
 Sources of error: Hemolysis, Reference ranges: Adults: 50-115 U/L, Children aged 4-15 years: 54
-369 U/L.
 6-Gamma-glutamyltransferase (GGT): kidneys, pancreas, intestine but not found in skeletal muscle
tissue or bone.
 Clinical significance: Increased levels in all hepatobiliary diseases (viral hepatitis, alcoholic cirrhosis)
very sensitive indicator for these conditions. Reference ranges: Male, up to 55 U/L; female, up to 38U/L.
7-Amylase (AMS): Found in pancreas, salivary glands and small intestine. It is responsible of
carbohydrates digestion.
 Clinical significance: Increase in acute pancreatitis. Reference range: 28-100 U/L.

8-Lipase (LPS): Found in pancreas, lipolysis. Clinical significance: Increase in acute pancreatitis.
 Sources of error: Hemolysis because hemoglobin inhibits LPS activity. Reference range: Up to 38
U/L. Note that!! AMS & LPS are affected by meals.
 Myoglobin: Found in skeletal and cardiac muscles.
 Clinical significance: Increased in skeletal muscle injuries and AMI.
 Reference ranges: Male, 30-90 ng/mL; female, <50 ng/mL
 Troponin: Tissue location: Troponins T, I, and C form a complex of three protein that bind to filaments of
skeletal muscle and cardiac muscle to regulate muscle contraction.
 Clinical significance: (cardiac troponin T or cardiac troponin I) is used as an AMI indicator(specific).
 Reference ranges: cTnT <0.03 ng/mL, cTnI <0.40 ng/mL.
 Brain natriuretic peptide (BNP) marker for congestive heart failure (CHF).
Lipids and lipoproteins
 Lipids and lipoproteins
 Cholesterol: Precursor for synthesis of bile acids, steroid hormones, and vitamin D.
 Low-density lipoprotein (LDL) is the primary carrier of cholesterol.
 Triglyceride: Triglycerides comprise 95% of all fats stored in adipose tissue.
 Triglycerides are transported through the body by chylomicrons and VLDL (very-low-density
lipoprotein).
 Lipase, lipoprotein lipase, epinephrine, and cortisol break down triglycerides.
 Lipoproteins are molecules that combine water insoluble dietary lipids and water-soluble proteins
(apolipoproteins) so that lipids can be transported throughout the body.
 Chylomicrons are the largest lipoproteins and have the lowest density. They are formed in the intestines
and transport triglycerides after a meal, giving serum a turbid appearance. Because of their low density,
chylomicrons will float to the top and form a creamy layer when plasma is stored overnight.
 Very-low-density lipoprotein carries endogenous triglycerides synthesized in the liver.
 Low-density lipoprotein is the body's major cholesterol carrier and transports a large amount of
endogenous cholesterol. Known as "bad cholesterol," LDL is easily taken up by cells, so elevated levels
are associated with increased risk for atherosclerosis. LDLs are composed of 50% cholesterol.
• LDL= (cholesterol – HDL – TG/5)
 High-density lipoprotein (HDL) is also known as
"good cholesterol." HDL is synthesized in the intestine
and liver cells(antiatherogenic).
 Normal ranges:
 Total Cholesterol: < 200 (mg/dl),
 HDL Cholesterol: ≥ 60 (mg/dl),
 LDL Cholesterol:< 100 (mg/dl),
 Triglyceride: <150 (mg/dl).
Clinical significance: Abnormal lipid metabolism is associated with risk of
coronary heart disease(LDL:HDL).
 Note that!!! LDL (Apo B-100) is directly associated with
artherosclerosis and coronary heart disease.
 Familial hyper cholesterolemia caused by deficiency of LDL-R.
 Apolipoproteins measured by immunoturbidimetric and
Endocrinology
Hormones
 Hormones are chemical compounds secreted into the blood that affect
target tissues generally at a site distant from original production.
 Hormone synthesis is regulated through negative feedback by another
hormone (e.g., cortisol/ACTH).
A. Steroid hormones: Synthesized from cholesterol: include cortisol,
aldosterone, testosterone, estrogen, and progesterone.
B. Protein hormones: include glycoproteins: follicle-stimulating hormone
(FSH), luteinizing hormone (LH), thyroid-stimulating hormone (TSH), human
chorionic gonadotrophin (hCG).
peptide: insulin, glucagon, parathyroid hormone, growth hormone, and
prolactin.
C. Amine hormones: include epinephrine, norepinephrine, thyroxine, and
triiodothyronine.
 Methods for quantifying hormones:
 Fluorescent immunoassay (FIA),
 Chemiluminescent immunoassay (CUA).
 Thyroid gland
 Follicular cells: Make and secrete thyroid T4 T3 TSH condition
hormones: Thyroxine(T4) and low low increase Primary
riiodothyronine(T3). d hypothyroidism
 Hypothalamic-pituitary-thyroid axis:
Thyrotropin-releasing hormone (TRH) is
low low low Secondary
released by hypothalamus and stimulates
hypothyroidism
anterior pituitary to secrete thyroid-stimulating
hormone.
 TSH regulates synthesis and release of the increase increase Normal Primary
thyroid hormones. d d or low hyperthyroidism
 Secretion of TSH is regulated by TRH, T 3 &
T4. increase increase increase Secondary
 Thyroid hormones circulate in blood bound d d d hyperthyroidism
to thyroxine-binding globulin (TBG).
 Parathyroid Glands: Chief cells synthesize, store, and secrete parathyroid hormone (PTH).
 PTH aids in the regulation of calcium and phosphate, having direct action on bone and kidney and
indirect action on the intestines through vitamin D. PTH increases the serum calcium level by increasing
calcium resorption from bone, increasing calcium reabsorption in the renal tubules, and increasing
intestinal absorption of calcium by stimulating production of vitamin D.
 Note that!!! If Calcium increased, phosphate reduced.
 High PTH: cause hypercalcemia. Reference range: 15-65 pg/mL.
 Pancreas:
 Islets of Langerhans secrete insulin(beta cells) and glucagon (alpha cells).
 Secrete digestive enzymes include lipase and amylase.

1- Insulin: (hypoglycemic), lowers blood glucose by binding to cell membrane receptors,which increases
membrane permeability in the liver, muscle, and adipose tissue(glycogenesis and lipogenesis while
inhibiting glycogenolysis).
 Clinical significance:

1) Hyperinsulinemia: May be caused by insulinomas (insulin-producing

tumors of the, which result in hypoglycemia.
2) Hypoinsulinemia: Lack of insulin or ineffective insulin, which results
in diabetes mellitus.
 Glucagon is secreted when the blood glucose level is low.
 Glucagon increases blood glucose by promoting glycogenolysis in the liver and gluconeogenesis.
 The secretion of glucagon is promoted by exercise, stress, and amino acids.
 Secretion is inhibited by insulin.
 Clinical significance
 Hyperglucagonemia is associated with glucagon-secreting tumors of the pancreas(sugar appear in
urine).
 Adrenal Glands: (adrenal coretx):

1. cortisol: stimulates glycogenolysis, lipolysis, and gluconeogenesis.

 Increased cortisol levels turn off secretion of ACTH and CRH.
 Decreased cortisol levels stimulate secretion of ACTH through negative feedback, which promotes
cortisol synthesis. High ACTH and cortisol called (Cushing syndrome).
2. aldosterone: controls the retention of Na + , Cl-, and H20, the excretion of K+ and H+ and, therefore,
the amount of fluid in the body.
3. Epinephrine and norepinephrine(catecholamines), adrenal medulla: ( AKA adrenaline and
noradrenaline). Final metbolism product is Vanillylmandelic acid.
Fight and flight hormone(release free fatty acid from adipose tissue).
 Posterior pituitary
1. Antidiuretic hormone(ADH): AKA vasopressin, produced by Posterior pituitary and control the
water reabsorption.
 Clinical significance: Increased ADH level (hyperfunction): The syndrome of inappropriate ADH
secretion (SIADH):
hyperglycemia and hyponatremia.
Decreased ADH level (hypofunction): Results in polyuria, causing diabetes insipidus and polydipsia.
2. oxytocin: uterine contractions during childbirth and ejection of breast milk, (prolactin).
 Placenta:
Human chorionic gonadotropin: (HCG), synthesizes progesterone and estrogens.
 Ovaries: LH triggers ovulation and progesteron production, FSH: stimulates growth of the ovarian
follicles and increases the plasma estrogen level(female sex hormones).
 Testes: FSH > spermatogenesis,

LH > production of testosterone(male sex hormone).

 Tumor markers:
1. Alpha fetoprotein: increased levels of AFP can be indicative of
hepatocellular carcinoma and gonadal tumors(testicular and ovarian).
2. Prostate specific antigen (PSA): Prostate cancer detection.
3. Carcinoembryonic antigen (CEA): adenocarcinoma of digestive
tract and colorectal carcinoma.
4. Human chorionic gonadotropin (hCG): trophoblastic tumors,
testicular and ovarian tumors.
5. CA 15-3: Breast cancer.
6. CA 125: ovarian and endometrial cancers.
7. Thyroglobulin: thyroid cancer.
Thanks