Total body fluid-dr aaser m abdelazim

Chemistry of blood and body fluids

Aaser M. Aaser M. Aaser M. Aaser M. AbdelazimAbdelazimAbdelazimAbdelazim, , , , PhDAaser M. Aaser M. Aaser M. Aaser M. AbdelazimAbdelazimAbdelazimAbdelazim, , , , PhDLecturer of medical Biochemistry and Molecular Biology

Zagazig Vet. Medicine

PhD studies in Niigata college of Medicine, Niigata University, Niigata, JAPAN

[email protected]

1Chemistry of blood and body fluids

Dr Aaser Abdelazim17-11-2011

What do you want to

know about body fluids?fluids?



CSF

BloodPericardial

Milk

Vetrous humor

Pleural fluids

Different body fluids

Amniotic fluids

SemenFemale discharge

Urine

LymphGastric fluids

Bile

Intestinal fluids



BLOOD

Pointes of the lecture:

1. Definition

2. Functions of blood

3. Blood composition

4. Plasma proteins

Lecture 14



Blood

Blood is a tissue which circulating inside

closed vessels, It is a liquid which contains

plasma in which red blood cells, white cells and

platelets are suspended.



Functions of blood







BLOOD COMPOSITION

Blood plasma (55%) Cellular elements (45%)

Solids (10%)Water (90%)

Inorganic componentsOrganic components

•Cl

•Na

•K

•Ca

•CO2

•Sugars

•Lipids

•Proteins

•NPN•hormones



e



Blood composition



Cellular elements



Erythrocytes

4.7-6.1 million/mm313



Leukocytes

7,000 mm3

(5-7,000/mm3)



Thrombocytes

250,000/mm3



Plasma proteins



Globulins

Plasma proteins

Albumin



Plasma proteins



Functions of plasma proteins

Albumin





ɣ-globulins functions



Synthesis of plasma proteins

Liver

Non immune proteinsImmunoglobulins

Liver

endocrine glands

lymphoid tissues

Protein hormones



All plasma proteins are glycoproteins except albumin



Protein Neuraminidase

Sialic acid

Galactose

Protein

Recognized by hepatocytes

asialoglycoproteins

Taken by endocytosis

glycoprotein

Protein degradation

Taken by endocytosis

Degraded protein24



Hyper proteimemia

1. Dehydration (diarrhea,

Hypoproteinemia

1. Loss (blood, Urine, GIT)

Normal serum levels= 6-8.2 g/dl

Dysproteinemias


Dr Aaser Abdelazim25

vomiting)

2. Increase antibody

production

Acute hepatitis, typhus, malaria

2. Dec. synthesis (liver

diseases, immun. Diff)

3. Dec. intake(mal-nutrition,

mal-absorption)

4. Incr. catabolism(trauma,

burns) 17-11-2011

Albumin/ globulins ratio (A/G ratio)

It is about 1.6/1 this ratio is inverted in

Liver disease

Kidney diseases

Decrease protein biosynthesis

Loss of more albumins due to its low molecular weight.



Methods used for determination of plasma proteins

Chemical method

Separation techniques

Protein activity method techniques activity

Physical determination



Protein electrophoresis



Protein electrophoresis graph



Plasma enzymes and their role in clinical diagnosis



Plasma enzymes

Functional enzymes Nonfunctional enzymes

1. Lipoprotein lipase

2. Clotting enzymes

�Plasma not their usual site

�Only inside the tissues

3. Cholinesterase 1. Lipases

2. Transaminases

3. Amylases

4. Alkaline phospahtases

5. Acid phosphatases

6.31



Cell Tissue destruction

Marker of organ disease

Infection Diseases

How enzymes used in diagnosis


Dr Aaser Abdelazim

Enzyme

Blood

Enzyme escape

Elevated level

Marker of organ disease

17-11-2011

Enzymes of clinical importance

Transaminases (ALT, AST)

Site:

3-15 IU/L

1

ALT/GPT

Pyruvate Glutamate oxaloacetate

Transamination

ALT


Dr Aaser Abdelazim

Normal level : 3-15 IU/L

1- Acute infectious hepatitis

2- Chronic hepatitis

3- hepatotoxicity

4- Obstructive jaundice

Alanine α- keto glutarate

Aspartate

ALTAST

17-11-2011

AST/GOT

Site:


Diagnose:


Dr Aaser Abdelazim

1- Hepatocellular damage.

2- Myocardial infarction,

it gives its maximum level after 2 days of attack.

3- Neoborn normally

4- Viral hepatitis

5- Circulatory failure

17-11-2011

Alkaline phospahtase (ALP):2

Site:

Normal level : 3-13 U/dL

Diagnose:


Dr Aaser Abdelazim

1- Physiologically, in children and in pregnant women.

2- Rickets, osteomalcia, bone carcinoma and healing phase

of fractures.

3- Hyperparathyroidism

4- Hepatitis, Obstructive jaundice, tumors and hepatic

infiltration.

17-11-2011

3

Site:

Diagnose:

Acid Phophatase

Platelets RBCs

Prostate


Dr Aaser Abdelazim

1. Prostatic cancer

2. Following rectal examination, passage of catheter

3. Constipation

4. Acute urine retention

5. After prostatectomy

17-11-2011

Creatine kinase (CK)/ Creatine phosphokinase (CPK):4

Site:


Diagnose:


Dr Aaser Abdelazim

1. Physiologically, in neoborn.

2. Myocardial infraction

3. Muscle dystrophy

4. Hemolysed samples

5. Muscle injuries

6. After surgery

7. Alcoholism

8. Hypothyroidism

17-11-2011

Lactate dehydrogenase (LDH): 5

Site:


Diagnose:

Tumor


Dr Aaser Abdelazim

1. Marked increase in myocardial infarction.

2. Leukemia

3. Pernicious anemia

4. Circulatory shock

5. Viral hepatitis

6. Skeletal muscle diseases

7. Pulmonary embolism

17-11-2011

Gamma glutamyl transferase (GGT):6

Site:

Diagnose:


Dr Aaser Abdelazim

1. Liver diseases

2. Chronic alcoholism

3. In patient treated with anticonvulsant therapy.

17-11-2011

Amylase 7

Site:

Diagnose:

Fallopian tube Pancreatic juice

Saliva


Dr Aaser Abdelazim

1. Acute pancreatitis

2. Severe diabetic ketoacidosis

3. Severe uremia

4. Perforated peptic ulcer

5. Acute Cholestasis

6. Salivary calculi

7. Ruptured ectopic pregnancy

17-11-2011

Aldolase (ALS):8

Site:

Diagnose:


Dr Aaser Abdelazim

1. Myocardial infraction

2. Muscle trauma

3. Hemolysis

4. Generalized malignancy

17-11-2011

Lipase:9• It produced by pancreas

• Its activity increased in acute pancreatitis and pancreatic carcinoma

Cholinesterase (ChE):10There are two types:

1. Plasma cholinesterase known as pseudocholinesterase.

2. Tissue cholinesterase known as true cholinesterase

Succinyl choline apnea: some patients develop prolonged

apnea after anesthesia continued for hours due to their

plasma is deficient in pseudocholinesterase essential for

hydrolysis of succinyl dicholine used as muscle realant

during anesthesia.



Lipoproteins

Aaser Abdelazim, PhDLecturer of medical biochemistry and molecular biologyLecturer of medical biochemistry and molecular biology

Zagazig university

[email protected]



Structure of lipoproteins: spherical or discoid aggregates of lipids

Core (Polar lipids)


Dr Aaser Abdelazim

Shell 2nm thick (Amphipathic lipids)

17-11-2011

Proteins to lipid contents of lipoproteins:

Chylomicrons

Protein Fat

HDL LDL VLDL ChylomicronsHDL(good)

LDL(bad)

VLDL

High protein, low fat Low protein, high fat



Lipoprotein class

Density (g/ml)

Diameter (nm)

Protein (%) of dry weight

Phospholipids (%)

Triacylglycerol

(%) of dry weight

Chylomicrons

< 0.95 100-500 1-2 7 84

VLDL 0.95-1.006 30-80 10 18 50

Lipoproteins classes: their density, diameter, protein,

phospholipids and triacylglycerol contents.

IDL 1.006-1.019 25-50 18 22 31

LDL 1.019-1.063 18-28 25 21 4

HDL 1.063-1.21 5-15 33-50 29 8



Metabolism of lipoproteins



LDL metabolism



Lipoprotein Main apolipoprotein

Properties and Functions

Chylomicrons (CM)

B48, A-I, C-IIand E

•Largest lipoprotein

•Synthesized in gut after meals

•Not present in normal fasting plasma

•The main carrier of dietary TAGs

Very low density

lipoproteins (VLDL)

B100, C-II and E

•Synthesized in liver •Main carrier of endogenous TAGs

Four main lipoproteins and their functions:

(VLDL)

Low density

lipoproteins (LDL)

B100 •Generated from VLDL in circulation •Main carrier of cholesterol

High density

lipoprotiens(HDL)

A-I and A-II •Smallest but most abundant in plasma

•It has a protective function

•It takes cholesterol from extra hepatic

tissues to liver for excretion.



Apolipoprotein Molecular weight

Site of synthesis Functions

A-I 28,000 Intestine and liver

Activates LCAT

A-II 17,000 Intestine and liver

Unknown

B100 549,000 Liver 1. Transports TAGs and

Cholesterol 2. Binds to LDL receptors

Prosperities of some human Apolipoproteins:

2. Binds to LDL receptors

B48 264,000 Intestine Transports TAGs

C-I 6600 Liver Activates LCAT

C-II 8850 Liver Activates LPL

C-III 8800 Liver Inhibits LPL

E 34,000 Liver, intestine

and macrophage

1. Binds to LDL receptors

2. Binds to another liver receptors 50



Clinical disorders of plasma lipoproteins

(dyslipidemias/ dyslipoproteinemias)

Hyperlipoproteinemias Hypolipoproteinemias


Dr Aaser Abdelazim

Primary hyperlipoproteinemia(Genetic)

Secondary hyperlipoproteinemia

Look to the table (next)

17-11-2011

Disease Genetic defect/effect Fredrickson Risk

Familial Lipoprotein lipase deficiency

1.Reduced functional LPL

2.CM and VLDL high elevated

I Pancreatitis

Apo C-II deficiency Inability to synthesize apo

C-II which is the cofactor for LPL

I Pancreatitis

Familial hypercholesterolemia 1.Reduced number of

functional LDL receptors 2. High plasma LDL and C

II (a) or II (b) CHD and atherosclerosis

Hyperlipoproteinemia 1. Low CM, VLDL clearance

2.High plasma CM and

III CHD

Some genetic causes of dyslipidemias:

2.High plasma CM and VLDL

Familial hypertriglyceridemia 1. Single gene defect2.Over production of VLDL

IV CHD, diabetes and obesity

Familial combinedhyperlipidemia

1. Single gene defect

2.Over production of VLDLand CM

V CHD

A betalipoproteinemia Inability to synthesize Apo B (low level of LDL)

Normal Fat soluble vitamin deficiency

and neurological disorders Low plasma VLDL and CM

Analphalipoproteinemia(Tangier disease).

1. Inability to synthesize

Apo A2.Deficiency of LCAT

Normal Neurological disorders and

Cholestrolyester storage in abnormal sites



Disease Unusual dominant lipid abnormality

1. Diabetes mellitus Increase triacylglycerol

2. Alcoholism Increase triacylglycerol

3. Chronic renal failure Increase triacylglycerol

Secondary causes of hyperlipidemia:

3. Chronic renal failure Increase triacylglycerol

4. Hypothyroidism Increased cholesterol

5. Nephrotic syndrome Increased cholesterol

6. Drugs e.g., thiazide

diuretics, nonselective beta blockers

Increase triacylglycerol



Type N I II (a) II (b) III IV V

Sample

Fredrickson (WHO) classification of dyslipidemias:

Lipoprotein /CM

N CM (+) VLDL /LDL (+)

LDL (+) IDL (+) VLDL (+) (+)

Total cholesterol

N N or (+) (+) (+) (+) N or (+) N or (+)

TAGs N (++) N (+) (+) (+) (++)

LDL-C N N or (-) (+) (+) N or (-) N N

HDL-C N N or (-) N or (-) N or (-) N or (-) N or (-) N or (-)

It based on appearance of fasting plasma and analysis of TAGs and Cholesterol after standing for 12

hs at 4ºC ( N = normal (+) = high (-) = low ) 54Chemistry of blood and body fluids


PLASMA CARBOHYDRATES:

It includes:

1. Glucose: its normal fasting level is 70 – 110 mg / dl.

2. Traces of galactose, fructose and pentoses.

3. Lactose in lactation.

HYPOGLYCEMIA/HYPERGLYCEMIA and DIABETES MELLITUS

Hypoglycemia Hyperglycemia Diabetes mellitus

(1): Reactive hypoglycemia: 1. Diabetes mellitus (1): Reactive hypoglycemia:•Sensitive epinephrine release

•Deficiency of glucagon

•Gastric surgery

(2): Fasting hypoglycemia:•Alcoholism

•Critical illness (liver/heart diseases)

•Hormonal deficiency(cortisol,

epinephrine)

•Tumors (B- cells tumore)

•Drugs (salicylates, pentamidines,

quinines)

1. Diabetes mellitus

2. Gestational diabetes

3. Acromegaly

4. Acute stress (heart attack)

5. Chronic renal failure

6. Cushing syndrome (excess

glucocorticoids)

7. Hyperthyroidism

8. Pancreatitis

9. Pancreatic tumors

10. Excess food intake

11. Drugs (corticosteroids,

diuretics, epinephrine,

estrogen, salicylates large

dose).

1. IDDM (juvenile /non

genetic)

2. NIDDM (adult/genetic)





PLASMA

NON PROTEIN NITROGENOUS COMPOUNDS(NPNs)

Aaser Abdelazim, PhDLecturer of medical biochemistry and molecular biologyLecturer of medical biochemistry and molecular biology

Zagazig university

[email protected]



Properties of NPNs:

1.Determined to monitor renal functions.

2.Nitrogen containing compounds that are not

proteins or polypeptides.

3.The NPN fraction comprises about 15

17-11-2011Chemistry of blood and body fluids


3.The NPN fraction comprises about 15

compounds.

4.Mostly arise from catabolism of proteins and

nucleic acids

Compound Approximate plasma

concentration (% of total NPNs)

Urea 45

Amino acids 20

Clinically significant non protein nitrogenous compounds:



Amino acids 20

Uric acid 20

Creatinine 5

Creatine 1-2

Ammonia 0.2

Blood Urea Nitrogen (BUN):

Ammonia + CO2

Protein catabolism

Liver40%

Sources and fates:



UREA

Kidney

40%

GIT

10%

Skin

BUN CONCENTRATION IS AFFEXTED BY:

1. Renal function

2. Dietary intake

3. Protein catabolism rate

MEASUREMENT OF UREA IS USED TO:

1. Evaluate renal function



1. Evaluate renal function

2. Assess hydration status

3. Determine nitrogen balance

4. Aid in the diagnosis of renal disease

5. Verify adequacy of dialysis

Azotemia: high plasma urea

Pre-renal Post-renalRenal

1. Reduced renal blood flow:

•Congestive heart failure.

•Shock.

•Hemorrhage.

1. Acute & Chronic

renal failure

2. Glomerular nephritis

3. Tubular necrosis

Obstruction of

urine flow due to:

1. Renal calculi

2. Tumors of



•Hemorrhage.

•Dehydration.

2. High protein diet

3. Increased protein catabolism

3. Tubular necrosis

4. Other Intrinsic renal

disease

2. Tumors of

bladder or

prostate

3. Severe

infections

Decreased Urea Nitrogen:

1. Low protein dietary intake

2. Liver disease (lack of synthesis)

3. Severe vomiting and/or diarrhea (loss)

4. Increase protein synthesis



4. Increase protein synthesis

Creatinine

Arginine + glycine + methionine

Liver/ kidneys

CREATINE Creatine-PCPK

Metabolism:

Muscles



CREATININE

H2O

PO4

Kidneys

Muscles

Urine

Plasma creatinine concentration is a function of:

1. Relative muscle mass

2. Renal function

3. Rate of creatine turnover

Measurement of creatinine concentration is used to determine:

1. Sufficiency of kidney function

2. Severity of kidney damage

3. Monitor the progression of kidney disease



3. Monitor the progression of kidney disease

Creatine:

Elevated in plasma in

Muscular dystrophy, hyperthyroidism, trauma.

Uric acidPurines

Adenine/Gauanine

Hypoxanthine

Xanthine Uric acidAllantion

High plasma uric acid

Urate crystals in tissues

Xanthine oxidase

Metabolism:



KidneyReturn to plasma

Monosodium urate

Uric acid is measured to:

1. Assess inherited disorders of purine metabolism

2. Confirm diagnosis and monitor treatment of gout.

3. Assist in the diagnosis of renal calculi.

4. Prevent uric acid nephropathy during



4. Prevent uric acid nephropathy during

chemotherapeutic treatment.

5. Detect kidney dysfunction.

Hyperuricemia

Gout

Increased uric

acid catabolism

Chronic renal disease

It is a metabolic disease

characterized by:

Occurs in patients

on chemotherapy

causes elevated

levels of uric acid



characterized by:

1. Pain & inflammation of

joints

2. Increased risk of renal

calculi

3. Hyperuricemia

on chemotherapy

for diseases such

as leukemia & multiple myeloma

levels of uric acid

because filtration

and secretion are hindered.

Hypouricemia:

It is a condition characterized by low plasma level of uric acid.

Causes:

1. Secondary to severe liver disease

2. Defective renal tubular reabsorption

3. Fanconi’s Syndrome



3. Fanconi’s Syndrome

Activities

Group A:Hemoglobin

Group B:Blood indices and their significance

Group C:Anemias and their diagnosis

Group D:Blood sugar: control and disorders

Group E:Semen analysis



Semen analysis

Group F:Stem cells

Group G:Nanotechnology

Group H:Tumor markers

Group I:Endocrine disorders and their diagnosis

Group J:Prenatal diagnosis

Ammonia

Ammonia

Dietary proteins

Amino acids

α-keto acids

Urea

CO2

Bacterial u

rease

Purines and pyrimidines

Amines

Sources and fates:



Ammonia

NH3

α-keto acidsAmines

Urine

Glutamine

ADP+Pi

Glutamate +ATP

Glutamate

H2O

Hyperammonemia (ammonia intoxication)

Acquired hyperammonemia Inherited hyperammonemia

1. Liver diseases:

• Liver cirrhosis due to

� Bilharziasis

� Alcoholism

� Hepatitis

Genetic deficiency of one or

more of urea cycle enzymes

leads to failure of urea

synthesis.



� Hepatitis

� Biliary obstruction.

• Liver cell failure: inability of

liver cells to convert ammonia

to urea

2. Shunt operation between

portal and systemic

circulation.

3. Renal failure.



ACID–BASE BALANCE/ BLOOD BUFFERS:

Aaser Abdelazim, PhDLecturer of medical biochemistry and molecular biology



Lecturer of medical biochemistry and molecular biologyZagazig university

[email protected]

ACID–BASE BALANCE/ BLOOD BUFFERS:



H+

Carbonic acid

CO2

Phosphoric acid

Sulfuric acid

Organic acids

(1): Sources of protons in blood: Carbohydrates oxidation

Phospholipids/phosphoproteins

sulfur containing amino acids.



Organic acids sulfur containing amino acids.

lactic, citric, acetoacetic acids

(2): Sources of alkalis in blood:

1. Sodium bicarbonate (Na2CO3).

2. Ammonia.

Buffer systems in the plasma:

Carbonic anhydrase



(1) Respiratory:

Disturbances in acid base balance:

(1) Respiratory:



(1) Respiratory:

Pneumonia , emphysema, asphyxia, bronchial asthma,and morphine poisoning.(2) Metabolic:

resulted from decrease in acid production or decreasein acid excretion due to:1. Increase acid production

• Severe muscular exercise produce more lactate

• Increase ketone bodies production they are acids

• Increase protein diets contains acids as phosphoric, sulfuric and uric acids

2. Decrease the excretion of acids in renal failure

3. Increase the loss of bases as in severe diarrhea

(1) Respiratory:

Hyperventilation resulted from; fever, salicylatespoisoning, encephalitis, climbing of high altitudes,hysterical(2) Metabolic: increase of blood HCO3 and lossof acids due to:1. Prolonged vomiting as in pyloric stenosis2. Prolonged suction in high surgical operations 3. High dose of alkalis during treatment of

acidosis 4. Hypokalemia5. Excess mineralocorticoids

Hemoglobin





[email protected]

Hemoglobin structure:

Globin

(146 amino acids)



(141 amino acids)

Hemoglobin α2,ᵦ2

Hemoglobin helices:

Are identified from A-------H as in the diagram:



States of hemoglobin (allosteric effect):

T form(for tense)

R form(for relaxed)

Deoxyhempglobin Oxyhemoglobin



Deoxyhempglobin Oxyhemoglobin

BPG

Oxygen

Low affinity to O2



BPG: 2,3-bisphosphoglycerate

Shift to left: (High affinity to O2)

1. Decrease of temperature

2. Dec. BPG

3. Dec. H

4. Dec.CO2

Shift to right: (low affinity to O2 at level of tissues)

Low pH and high CO2 pressure at the level of tissues lead to lower the O2

binding to Hb and enhance O2 release this binding known as Bohr Effect.

Bohr effects:



Shift to right: (low affinity to O2 at level of tissues)

1. Increase of temperature

2. Inc. BPG

3. Inc. H

4. Inc. CO2

Hemoglobin metabolism

(1) Heme biosynthesis:

Site of synthesis: Both mitochondria and cytoplasm are involved in hemesynthesis.

Organs: 85% in bone marrow Low % in liver



2. Formation of prophobilinogen:

+

2H2O

Prophobilinogen synthase

Uroporphyrinogen I, III synthase

4 prophoblinogens are condensed



2 molecules of δ-amniolevulinic acidProphobilinogen (PBG)

Steps of heme synthesis:

1. Synthesis of ALA (5-aminolevulinic acid/δ-amniolevulinic acid):

Occurs in mitochondria

Succinyl-CoA

+Glycine

H



ALA synthase

CoASH

δ-amniolevulinic acid

PLP CO2

A P

A

A

A

P

P P

Uroprophyrinogen III

A P

A

A

A

P

P

P

Uroprophyrinogen I Uroporphyrin III

6H

Light Uroporphyrin I

6H

Light

4CO24CO2

A; acetic acid

P; propionic acid

M; methyle groupV; vinyle CH2=CH2

Cytosol

Uroprophyrinogen decarboxylase

3. Formation of heme:

6H6H 4CO2

M P

M

M

M

P

P P

Coproprophyrinogen III Coproporphyrin III

6H

Light

M P

M

M

M

P

P

P

4CO2

Coproprophyrinogen ICoproporphyrin I

6H

Light

Cytosol



Coproprophyrinogen III

M P

M

M

M

P

P P

I

III

IIIV

Mitochondria Coproprophyrinogen oxidase

M V

M

M

M

P

P V

Protoporphyrin III (IX)



M V

M

M

M

P

P V

Fe+2

Ferrochelatase

M V

M

M

M

P

P VFe+2

Incorporation of iron in prophyrin to form heme:

Prosthetic group of hemoglobin



Heme Protoporphyrin III (IX)

Porphyria Enzyme Deficient Primary Symptom

Erythropoietic Class

(1) Congenital erythropoietic

porphyria (CEP).Uroprophyrinogen III synthase Photosensitivity

(2) Erythropoietic

protoporphyria (EPP).Ferrochelatase Photosensitivity

Hepatic Class

(3) ALA dehydratase deficiency

porphyria, ADPALA dehydratase Neurovisceral

Types and major findings of prophyrias:



(4) Acute intermittent porphyria,

AIPPBG deaminase Neurovisceral

(5) Hereditary coproporphyria,

HCPCoproporphyrinogen oxidase

Neurovisceral, some

photosensitivity

(6) Variegate porphyria, VP Protoporphyrinogen oxidaseNeurovisceral, some

photosensitivity

(7) Porphyria cutanea tarda,

PCT

Uroporphyrinogen

decarboxylasePhotosensitivity

(8) Hepatoerythropoietic

porphyria, HEP

Uroprophyrinogen

decarboxylase

Photosensitivity, some

neurovisceral

Types of hemoglobin:

α α

ᵦ ᵦ

Hb A (α2β2): 95-97%(Major adult hemoglobin)

α α

ᵦ ᵦ

Hb A1c (glycosylated Hb): 5-8%Gives ideas about Glc. level for last 3months

Glucose units



α α

ɣ ɣ

Hb F (α2 γ2): 1% Has high affinity to O2, only in fetuses

α α

δ δ

Hb A2 (α2δ2): 2%(Minor adult hemoglobin)

α α

ᵦ- thalassemiaα- thalassemia

ᵦ ᵦ

Hemoglobinopathies:

Sickle cell anemia Thalassemia

HbS

(2 normal α chains and 2 mutant β-chains)



αα ᵦ ᵦ

Normal cells Sickle cells

Deleted ᵦ-chains gene Deleted α-chains gene

Abnormal derivatives of hemoglobin:

(1) Met-hemoglobin (Met-Hb):

1. Free radicals as H2O2

2. Drugs

3. Endogenous

oxidants



Ferrous hemeFerric heme

Met-Hb

(Induce hypoxia and cyanosis. )

NADH+H+ cytochrome B5 reductase.

(2) Carboxy –hemoglobin (COHb):



Oxyhemoglobin CarboxyhemoglobinConc. Over 40% lead to death

CO has 200 times affinity to Hb more than O2 itself

(3) Sulf – hemoglobin (S-Hb):

Sulfonamides



Sulf – hemoglobinInduce anoxia and cyanosis

(4) Hematin:



Hematin: Hemoglobin without iron Produced during intravascular hemolysis

Hemoglobin catabolism

Reticuloendothelial cells (REC)

Unconjugated bilirubinAlbumin bound

•Non water soluble (not secreted

from kidneys)

•It is neurotoxic

•Can cause permanent brain damage in neonates

Liver Bile duct

Hemoglobin catabolism:

Unconjugated bilirubin Conjugated bilirubin

Conjugated bilirubin



Stercobilinogen

Urobilinogen Orange color of urine on long standing

•Brown coloration of feces

•If not present lead to pale colored feces

Portal vein

kidneys

Large intestine

Bacteria

Conjugated bilirubin

Stercobilinogen

Stercobilinogen

HYPERBILIRUBINEMIA AND JAUNDICE:

Jaundice: is pathological term while Hyperbilirubinemia is lab term

1. 2 mg/dl bilirubin is hyperbilirubinemia; While 3 mg/dl is jaundice

2. The normal plasma bilirubin level up to 1.2 mg/dl (1 mg = 17.1 µmol/L).

HyperbilirubinemiaHyperbilirubinemiaHyperbilirubinemiaHyperbilirubinemia

Neonatal Pathological Congenital



Neonatal Pathological Congenital

1. Deficiency of UDP-

glucuronyltransferase

2. Accelerated hemolysis

of RBCs.

Hemolytic Obstructive

Gilbert disease

Crigler-Najjar syndromeمتQزمة كريغلر نجار

Hepatocellular Dubin-johnson

syndrome

Different types of pathological jaundice:

Feature Hemolytic Cholestasis (obstructive) Hepatocellular (toxic)

Cause Destruction of RBCsdue to toxins orinfections

Closure of bile ducts bystones or tumors

Death of hepatic cells due toviral infections or toxins

Mechanism Produced bilirubin overthe capacity of liverpower for conjugation

There is a regurgitation ofconjugated bilirubin to thecirculation due to closureits way to intestine

Inability of hepatocytes toperforms conjugation verywell

Serum Bilirubin >75 µmol/l Over 3 times than inhemolytic

>75 µmol/l but appears later

Type of bilirubin Unconjugated Conjugated Unconjugated/conjugated



Type of bilirubin Unconjugated Conjugated Unconjugated/conjugated

Bilirubin in urine Not present(Unconjugated is notwater soluble andbound to albumin andnot filtered )

Present Present(high level of conjugatedbilirubin)

Urine Urobilinogen

Increased Decreased /absent Decreased/absent

Stool Normal Clay/pale in color(no bilirubin reaches the

intestine)

Normal

HEMOSTASIS AND BLOOD COAGULATION





[email protected]

Hemostasis: is the stop of bleeding

When blood vessel is injured, bleeding can be stopped by:

Constriction of blood vessel

Formation of temporary platelets plug (white thrombus):

Formation of fibrin mesh or clot



Formation of fibrin mesh or clot (coagulation):

Mechanism of blood coagulation:

Intrinsic pathway Extrinsic pathway

It occurs mainly in the areaswithout tissue injury to:

It occurs mainly in the areas withtissue injury to:



Restrict theblood flow

Response to

abnormal bloodvessel wall

Release of tissuefactor that acts as a

cofactor for activefactor VIIa

Intrinsic pathway:Intrinsic pathway:Intrinsic pathway:Intrinsic pathway:

Stage I: generation of active factor X (Xa):

Prekallikrein Kallikrein

Collagen

Active factor XII (XIIa)

Injured blood vessel

+

01-12-2011 104

Factor XII

High molecular kininogen HMK HMK

Bradykinin

Factor XIFactor XIa

Factor IXFactor IXa

CaCaCaCa2+2+2+2+

Factor XFactor XaPL

CaCaCaCa2+2+2+2+

VIIIa

Stage II: conversion of prothrombin into thrombin:

Factor Xa

Factor II(Prothrombin)

Factor IIa(Thrombin)

CaCaCaCa2+2+2+2+ PL Factor Va

Stage III: conversion of fibrinogen to fibrin:



Fibrinogen Fibrin

Fibrin gel

Factor XIIIa

CaCaCaCa2+2+2+2+

Fibrin clot

Act as trap for more platelets and red

blood cells to form white or red thrombi.

Extrinsic pathway:Extrinsic pathway:Extrinsic pathway:Extrinsic pathway:

Factor VII Factor VIIa

Thrombin Minute amounts

Tissue factor



Factor XFactor Xa

Tissue factor

Proceeds in the final common pathwayas in intrinsic pathway.

Inhibitors of coagulation:

�The concentration of active thrombin should be controlled to prevent

unneeded clotting

�So there are natural inhibitors to limit the clotting only at the level of tissue

injury.

Inhibitor Action on Stimulators

The major inhibitors of coagulation include:



Inhibitor Action on Stimulators

Antithrombin III Thrombin, factors IXa, Xa, XIa, XIIIa Heparin

Heparin co-factor II thrombin Heparin

α2- macroglobulins Thrombin and kallikrein -----

Protein C Factors Va and VIIIa Vitamin K

dependant/ protein C

Protein S Acts as cofactor for activation of

protein C.

-------

Fibrinolysis:

Definition: It is the dissolution of clotted blood after their formation by enzyme

called plasmin.

Tissue/ Plasma activatorsKidneys activators likeurokinase / sterptokinase

PlasminogenPlasminogenPlasminogenPlasminogen



Fibrin thrombusFibrin thrombusFibrin thrombusFibrin thrombus Soluble proteinsSoluble proteinsSoluble proteinsSoluble proteins

PlasminPlasminPlasminPlasmin

α2-antiplasminIn active plasmin

Hemophilia:Hemophilia:Hemophilia:Hemophilia:

Definition: These are a group of inherited diseases at which clotting factors are

deficient

Hemophilia:Hemophilia:Hemophilia:Hemophilia:

Hemophilia A Hemophilia CHemophilia B



Deficiency of factor VIII. Von Willbrand diseaseDeficiency of factor IX.

BLOOD GROUPS:

DonorRecipient

Antigens

Antibodies



Proteins with oligosaccharides

ABO system for blood grouping:

Glycoproteins or glycolipids (Antigens)

RBC

4 types of blood groups according to Antigens



A B AB H

Terminal residueLacks the terminal residue

ABO system:

Blood group A B AB O

Genotypes AA and AO BB and BO AB OO

Antigens A B A and B H

Antibodies Anti-A Anti-B ------ Anti-A and Anti-B

Frequency in central Europe

40% 16% 4% 40%



Compatibility :

Blood group Compatible

Take Give

A From A A

B From B B

AB From A or B or AB (all) Only AB

O Only from O All

Rh system for blood grouping:

RBC

rhesus factors(Antigen D)

Occurs in 84% ofwhite populationsRBC

Rh-positive



Rh-positive

Rh-negativeFetal erythrocytes

Mother circulation

IgG For this child or mother

1st child

Fetal erythroblastosis:


Dr Aaser Abdelazim 114

IgGAgainst antigen D

For this child or mother there is no problem

Rh-positive

2nd child

IgG (anti-D)Against antigen D

Cross placenta

Destructs fetal RBCs fetal erythroblastosis

Urine




Lecturer of medical biochemistry and molecular biology

Zagazig university

[email protected]

Human urinary system:



Structure of nephron:

Glomerulus

Bowman’s capsule

Proximal convoluted tubules

Distal convoluted tubules

Afferent arteriole Efferent arteriole



Loop of henleCollecting duct

Collecting tubules

URINE FORMATION:

(1) Ultra filtration: (2) Resorption:

In PCT:

•Organic

metabolites

As glucose,

lactate, ketone

bodies and amino

acids

•Amino acids

have special

In DCT:

Resorption of Na+ and Cl–

And water By action of hormone Aldosterone and ADH



1. Glomerular Pore size: 2.9 nm

2. Allow passage of all plasma contents of

less than 15 Kda

3. All large proteins are unfilterable with

RBCs and other cells

4. All passed molecules form primary urine 5. Primary urine pass to tubules

have specialtransporters

(3)Secertion:

H+ and K+ ions, urea, and

creatinine, as well as drugs such as penicillin.

PHASES OF URINE FORMATION:



PHYSICAL PROPERTIES OF URINE:

(1): Volume:

Normal collected urine per day is about 1-2 liters; this volume is depending

on many factors included:

1. Fluid intake per day

2. Body temperature

3. Environmental temperature

4. Respiratory rates



4. Respiratory rates

5. Relative humidity

6. Emotional states

Abnormal volumes

Physiological causes Pathological causes

Polyurea 1. Much fluids and water

intake

2. High protein diets

3. Drugs: as calomel,

salicylates, acetates anddigitalis


2. Diabetes insipidus

3. Hypertention4. Chronic renal failure

Oligurea 1. Severe muscular exercise 1. Acute nephritis

Abnormal urine volumes:



Oligurea 1. Severe muscular exercise

2. Hot weather (more sweating)

1. Acute nephritis

2. Acute renal failure

3. Shock

4. Hemorrhage

5. Conditions lead to loss

of water (diarrhea, vomiting and fever).

Anurea Pure pathological case 1. Bilateral renal calculi

2. Urinary tract tumors

3. Severe stages of acute nephritis

(2) Color:

1. Normal observed color of urine is amber yellow or straw yellow, this

color is resulted from urochrome pigment which is a component of

urobilin.

2. Urine also contains traces of urobilinogens and ribofalvins.

Abnormal urine colors:

Abnormal colors Conditions

Dark yellow color

sever exercise due to void of concentrated urine.



color

Light yellow to whitish

All cases that elevate the urine volume, proteinuria,

and presence of phosphates with high concentration in

urine.

Red to red brown

Hematuria, Hemoglobinuria, and high doses of

antibiotics.

Greenish in jaundice when high level of bile salts and pigments present in urine.

Black Alkaptonuria

(3) Odor:

The normal odor of urine called urinefrous odor or aromatic odor and it

mainly due to presence of some volatile fatty acids in urine.

Abnormal urine odors:

Abnormal colors Conditions

Ammonical odor UTI

Rotten apple/ acetone odor

advanced cases of diabetes mellitus due to high

concentration of ketone bodies in urine.



Putrid odor UTI and all conditions associated by pyouria.

Special odor Spices and drugs

(4) Aspect:

1. Normal appearance of the urine is clear showing no turbidity.

2. Turbidity originates from presence of phosphates, urates, albumin,

lipids, and pus in urine.

(5) Sediment:

�In normal conditions, urine shows no deposits.

�Up on centrifugation one or more of the following deposits could be

appeared:

Urine deposits Conditions

Pus cells UTI due to high levels of dead leukocytes

Red cells Hematuria



Epithelial cells From kidney, uerters, urethra due to UTI.

Parasites and Ova As bilharisasis

Casts Mucoproteins formed in DCT and detached in many conditions

Crystals Urate, Oxalate and Phosphate crystals

(6) Urine reaction (pH):

1. The normal pH of urine is around (5.5-6) means it is slightly acidic.

2. Urine acidity originates from presence of sulfuric and phosphoric acids in

urine.

3. In urine basic phosphates (Na2HPO4) changed to acid phosphates (NaH2PO4)

in distal tubules which confirm the urine acidity.

Alkaline tide: is the excretion of alkaline urine after meals due to absorption of

high amount of bicarbonates and excreted in urine associated with HCl formation

from gastric juice.



pH Conditions

High urine acidity 1. Metabolic and respiratory acidosis

2. High protein diets

3. Drugs e.g., salicylates, acetates

4. Ingestion of citrus fruits e.g., lemon and orange.

Low urine acidity 1. Alkalosis

2. Urinary tract infections

3. Treatment with NaHCO3

4. Ingestion of vegetables

(7) Urine specific gravity:

1. It is known as the ratio between concentrations of total urine solids to its

concentration of water.

2. It means when the solids elevated in urine the specific gravity also increased

and vice versa.

3. Normal urine specific gravity is around 1015-1025.

Specific gravity Conditions

High urine specific gravity 1. Nephritis



High urine specific gravity 1. Nephritis

2. Diabetes mellitus 3. Severe muscle exercise.

Low urine specific gravity 1. Diabetes insipidus

2. All conditions that elevate urine volume

URINE CONSTITUENTS:

(1): Organic components:



(2): inorganic components:





Abnormal components of urine:

�Glucose: normally its level is less than 0.1 g/day in urine.

�Fructose: causing fructosuria, galactose in galactosuria, pentoses in

pentosuria and lactose in infants and lactating mothers during lactation period.

(1) Sugars:

Glucosuria



Physiological causes

1. Much intake of carbohydrates

2. Late stage of pregnancy

3. Alimentary glucosuria

4. Lactosuria in lactating females5. Adrenaline glucosuria

Pathological causes


2. Renal glucosuria

3. Experimental diabetes

due to:

� Pancreatomy.

� Alloxan, Streptozotocin, phlorozin injection.

(3) Ketone bodies:Normally its level in urine is less than 18 mg /day

Ketonuria: its causes are:

1. Uncontrolled diabetes mellitus2. Renal glucosuria (diabetes innocence).

3. Much fat intake

4. Starvation for long time5. Low dietary carbohydrates

(4) Bilirubin:



�It present mainly in urine of patients with obstructive jaundice with

less prevalence in ones of toxic jaundice.

�It gives urine characteristic dark greenish color.

(5) Blood:

�Blood present in urine in the form of intact RBCs in a condition called

Hematuria.

�It is mainly due to urinary bilharziasis, glomerulonephritis and malignant

diseases.

(2) Proteins:

Normal amount of proteins in urine is less than 30mg/L

these proteins are:

1. Albumin: Microalbuminemia: is the excretion of proteins (30-200 mg/L). It

indicates: early affection of the kidneys as in diabetes mellitus.

2. Mucoproteins:

3. Other proteins: e.g., Bence Jones proteins, hemoglobin and myoglobin.

Proteinuria



Physiological causes Pathological causes

1. High protein diet

2. Severe muscular

exercise

3. In late stages of

gestation and lactation

4. Standing for long time (Postural proteinuria)

Pre-renal Post-renalRenal

1. Liver diseases

2. Hemolysis

3. Cardiac diseases4. Hypertension

1. Nephrosis

2. Nephritis

3. Renal failure

1. Urothliasis

2. Cystitis3. Prostitis

URINARY STONES:

Composition of urinary stones:

Less common substances Most common substances

Uric acid (4-10%) Calcium oxalates

Cystine stones (less 1%). Calcium phosphates

Xanthine stones (very rare). Calcium carbonates

Triple phosphates

(Magnesium ammonium



(Magnesium ammonium phosphates).

Classes of urinary stone:

1. Simple stone: consisted of one constituent.

2. Mixed stones: formed from one or more constituents

Calcium oxalates stones:



Calcium oxalates crystalsCalcium oxalates stones

Calcium phosphates stones:



Calcium phosphates crystals Calcium phosphates stones

Triple phosphates stones:



Triple phosphates crystals

Calcium carbonates stones:



Calcium carbonates crystals

Uric acid stones:



Uric acid crystals

Uric acid stones

Cystine stones:



Cystine stone

Xanthine stones:



Causes of urinary stones:

1. Change in urine pH: alkalinity of urine due to bacterial infections lead to

precipitation of crystals and so stone formation.

2. Disturbances in vitamins:

� Excess vitamin D: lead to absorption of more calcium and formation of

calcium stones.

� Excess vitamin C: converted to oxalates and so increase oxalates stones.

� Vitamin A deficiency: lead to roughness of urinary epithelium and make it a



� Vitamin A deficiency: lead to roughness of urinary epithelium and make it a

suitable media for crystals precipitation.

3. Disturbances in hormones: as in hyperparathyroidism; leads to high urinary

excretion of calcium and predispose for calcium stones.

4. High uric acid excretion: leads to uric acid stones.

5. High cystine in urine: as in a metabolic disorder known as cystinuria.

6. High amount of mucoproteins in urine: mucoproteins act as cement

materials for stone formation.

Aaser Abdelazim, PhD




Zagazig university

[email protected]

DEFINITION:

It is the secretion of mammary glands in human and animals which is essential for

newborn feeding up to the age of weaning.

PHYSICAL PROPERTIES:

Properties Human milk Cow milk

Color White due to

presence of fat

Creamy yellow as it

contains excess



presence of fat

globules and

calcium

phosphates.

contains excess

amount of carotenes.

pH 6 - 7.7 6 - 7.7

Specificgravity

1032 1082

COMPOSITION OF MILK

(1) Milk proteins: 1.2 g/dl:

Milk proteins are less in human milk than in animal milk

Protein Properties and Functions

Albumin and globulins (75%)

�Soluble proteins

�Easily digested �Globulins give immunity to babies.

Casein (25%) �It is very important to babies as it shares in



Casein (25%) �It is very important to babies as it shares in

the formation of milk clot.

�Ca paracasinate (milk clot)

Enzymes �Proteinase

� Amylase

� Peroxidase

� Catalase

�Alkaline phosphatase

� Aldehyde oxidase

(2) Milk carbohydrates (lactose) 7 g/dl:

Lactose

More in human milk than animal’s milk

Responsible for the sweetness of

milk it less than the sweetness of cane

sugar sucrose, this enable babies to

take large quantities of milk without



take large quantities of milk withoutdeveloping nausea

After its hydrolysis it gives glucose;

which is a potent source of energy

and galactose; which is used tosynthesize glycolipids.

(3) Milk fats 3.7 g/dl:

Fatty acids: (48% saturated) (52% unsaturated) human contains more unsaturated fatty acids than animals

Little amounts of phospholipids and cholesterol

(4) Milk minerals:

Minerals Contents

Iron �It does not supply the babies need �It is more in human milk than in animal milk.



�It is more in human milk than in animal milk.

Calcium and phosphorus �Milk is one of the richest sources of Calcium

and Phosphorus

�They present in milk with optimal ratio

needed for absorption 2/1.

Sodium and potassium They more in animal milk than human milk

(5) Milk vitamins:

�Milk contains most of vitamins; it is very rich in vitaminsA and B2�Milk is poor in vitamins C, D, K.

Advantages of human milk over animal milk:

1) Breast milk is supplied at best suitable temperature.

2) It is sterile and not liable to be contaminated.

3) Cheaper than animal milk.

4) Not liable to adulteration.

5) Psychological effect on both child and mother.

Differences between human’s milk and cow’s milk

Contents Human milk Cow’s milk

Proteins 1.2 g/dl 3.3 g/dl



Proteins 1.2 g/dl 3.3 g/dl

Casein 0.3 g/dl 2.7 g/dl

Albumin and globulins 0.9 g/dl 0.6 g/dl

Lipids 3.7 g/dl 3.7 g/dl

Saturated fatty acids 48% 58%

Unsaturated fatty acids 52% 42%

Minerals Less More

Vitamins More Less

IMMUNE BENEFITS OF BREAST MILK:

Components Role

Secretory IgA class Protects the babies epithelium lining of digestive tract and prevents subsequent passage of microbes to other tissues

B12 binding protein Reduce amount of B12 vitamin needed for bacterial growth

Bifidus factor Promotes the growth of Lactobacillus bifidus

Fatty acids Disrupt membranes that surround certain viruses and bacteria

Fibronectin �Increases the antimicrobial activity of macrophages

�Helps in repair tissues that damaged by immune reaction in

baby’s gut.



baby’s gut.

Hormones and growth factors

Stimulate the quick maturation of infants gut

Interferon (IFN-γ) Enhances the antimicrobial activities of immune cells.

Lactofferin Binds to iron metal which is needed to the growth of many bacteria.

Lysozymes Kill bacteria by disrupting their walls

Mucin Adheres to Bactria and viruses preventing their attachment to the gut mucosa.

Oligosaccharides Bind to different microorganisms preventing them to attach to mucosa.

HUMANIZATION OF COW’S MILK

It is the process by which cow’s milk is changed to be as near as possible

the human milk, and this to suit the need of babies.

Aim:

Decrease the level of casein in cow’s milk

(casein present in high concentration in cow’s milk which forms dense clot in

stomach when infants drink it leads to vomiting).

Steps of milk humanization

1. Pasteurization of milk: by heating the milk to 60ºC for 30 minutes or to 70 ºC



1. Pasteurization of milk: by heating the milk to 60ºC for 30 minutes or to 70 ºC

for 15 minutes followed by rapid cooling. Then milk left in cool place for a time to

allow fat to concentrate at the surface.

2. Dilution: milk is halved diluted with boiled water to reduce its contents of

proteins and minerals.

3. Addition of lactose: lactose is added to elevate carbohydrates contents.

4. Iron, vitamin C and D may also be added.

TYPES OF MILK

Colostrum

Milk of 1st week

1. Excess carotenes

2. High gamma

globulins

3. More minerals and

Intermediate milk

Milk of 1st month after Colostrum

Mature milk

Milk of 1st year

Late milk

Milk after 1st year

1. Less proteins

2. Less lipids

3. Less vitamins

4. More minerals



3. More minerals and

vitamins

4. More carbohydrates

5. Less fats

6. Stimulates intestinal

movement 7. Has laxative effect

less sweaty

and help on

weaning.



SEMEN/SEMINAL FLUIDS


Zagazig university



Zagazig university

[email protected]



Semen:

Milky mixture of spermatozoa and secretions of epididymis, seminalvesicles and prostate

Spermatozoa:

Produced in testes by a process called spermatogenesis; it requires FSH for stimulation and testosterone for maintenance.

Contains enzymes needed

to penetrate ova, peptidase and hayalouronidase

Head

Acrosome

Nucleus



Oval shape, length; 5-

6microns, width; 2-3 microns

and hayalouronidase

Contains haploid # of chromosomes

Contains

mitochondria

needed to give energy

Contains myosin

like protein aid in movement

Vacuole

Head

Neck/middle piece

Tail

Nucleus

Sheath

surrounding mitochondria

CHARACTERS OF SEMINAL FLUIDS:

Characters Normal Associated abnormal conditions

(1) Volume 2 ml or more

(65% from seminal vesicle, 30-35% from

prostate and 5% from vas deferens

Low or absence of seminal

fluids1. absence of seminal vesicle

2. complete or partial obstruction of

ejaculatory ducts3. Retrograde ejaculation

(2) Semen pH

7777....2222----8888....0000

1. Prostatic secretion is acidic, while

Seminal vesicle fluid is alkaline

1. Acidic ejaculates: blockage of

seminal vesicle

2. Alkaline: infections



Seminal vesicle fluid is alkaline

2. An abnormally high or low semen

pH can kill sperm or affect their

ability to move or to penetrate anegg

2. Alkaline: infections

(3) Sperm

count

(Sperm numbers):

1. Average normal: 60-120

millions/ml2. Low normal: 10 millions/ml

1. Oligospermia: < 10 millions/ml

2. Azospermia: semen containsno sperms at all

(4) Shape Normal shapes >80% Teratospermia: > 50% abnormal

Abnormal headsNormal sperm

Sperm shape:



Abnormal tails

Rough head

Sperm other abnormal shapes:



Giant sperm

Micro-sperm

Double head

Double body

Long head

Rough head

Abnormalmiddle piece

(5) Sperm motility:

Speed: 3mm/minute Reach oviduct within 30 minutes

Normal motile sperms: 70-90% Low normal > 40%

Pattern of motility: Forward or swim



> 50% forward progression> 25% rapid progression

Motility scale:(0:4)

Scale Pattern

0 No movement

1 Movement, none forward

1+ Occasional movement of a few sperm

2 Slow, undirected

2+ Slow directly forward movement



2+ Slow directly forward movement

3- Fast, but undirected movement

3 Fast directed forward movement

3+ Very fast forward movement

4 Extremely fast forward movement

Asthenospermia:

A sperm total motility of less than 50% or less than 25 % with rapid progressive motility.

Causes of asthenospermia

1. Exposure of sperm to rubber (particularly condoms).

2. Spermicides.

3. Extremes of temperature.

4. Long delays between collection and examination of samples



(6) Liquefaction time :

1. Semen initially is liquid then rapidly coagulate by action of protein kinase

secreted from seminal vesicles

2. Prostate proteolytic enzymes liquefy it within 20-25 minutes.

3. Normal LT should be < 60 minutes

4. Long LT indicates: infection, prostate affections

5. Abnormal LT affects sperm motility

SEMEN CONSTITUENTS:

Constituent Properties

Carbohydrates 1. Main sugar is fructose for nutrition and energy supply

2. Normal level 300 mg/dl

3. Should be determined in azoospermia or in patients with < 1

ml semen

4. Low /absence: obstruction, atria, low testosterone 5. Other CHO like, citric acid (52 mmol/ej) and vitamin C

Proteins and

polyamines

1. Fibrinogen: semen clotting

2. Fibrinolysin: semen liqifaction after 20-25 minutes



polyamines 2. Fibrinolysin: semen liqifaction after 20-25 minutes

3. Spermine and spermidines: semen odor

4. Enzymes: hyaluronidase , acid phsphatase, ATPase and protein Kinase

Lipids 1. Prostaglandins: increase semen uptake by increasing

uterine contraction 2. Phospholipids and cholesterol

Minerals 1. Many minerals; Zn, K, Ca, Mg

2. Zinc is the main mineral (> 2.4 mmol/ej)3. Its deficiency associated with hypogonadism and sterility

SPERMOGRAM

Spermatozoa parameters

Immunological analysis

Seminal fluid parameters

1. The number

2. The viability

Mixed-agglutination reaction (MAR)

Assess functions of

prostate, seminal

vesicles and other



3. The motility

4. The morphology Identify antibodies

classes associated

with sperm like IgG,A,M

vesicles and otheraccessory glands

Anti-sperm antibodies



Date post:	22-Nov-2014
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