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Blood Module > Physiology > Flashcards

Physiology Flashcards

1
Q

what is the blood volume in men vs. women?

A

5 liters in woman and 5.5 liters in men

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2
Q

specific gravity of different blood components

A

whole blood is 1.060, for
plasma 1.030 and for blood cells 1.090

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3
Q

blood and plasma viscosity

A

The blood viscosity: 5 times
that of water, while viscosity
of plasma is 2 times that of
water

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4
Q

what are the components of blood?

A

55% - plasma
45% - cellular components - RBCs, WBCs and platelets (<1%)

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5
Q

functions of blood

A
  • Blood maintains internal environment constant (i.e.
    Homeostasis) as water, pH, electrolytes concentration, temperature
  • Transport function:
    O2 and CO2 - respiratory function
    From GIT to liver - nutritive function
    To kidneys - excretory function
    Hormone transport
  • Hemostatic function - blood clot formation to close injury and prevent blood loss
  • Immunologic function - phagocytosis
    WBCs attack foreign bodies
    Antibody formation against invading organisms
  • Body temperature regulation
    plasma is a heat distributor
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6
Q

Describe plasma

A

➢ It is the fluid portion of blood.
➢ Volume: 3,500 ml in a 70 Kg man
(about 5% of body weight).
➢ Color: Yellow.
➢ Specific gravity: 1.030
➢ pH: 7.4
➢ Viscosity: 2 times that of water.
➢ Osmotic pressure:
Crystalloid OP=
5000mmHg.
Colloid OP (proteins) = 25
mmHg.

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7
Q

Plasma composition

A

1- water: 90% of the plasma - body heat regulation and transport medium

2- plasma proteins; 6-8 % of plasma

3- inorganic constituents:1% as (Na+, Cl, HCO3, K+, Ca2+, Mg+ and others).

Remaining 2%:
4-Nutrients e.g. glucose, amino acids, lipids and
vitamins.
5-Dissolved gases (O2 and CO2)
6-Hormones.
7-Waste products e.g. creatinine, bilirubin and
nitrogenous substances as urea

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8
Q

what is serum?

A

It is the fluid remaining after removal of blood clots

Serum is the plasma minus fibrinogen and
clotting factors II, V and VIII

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9
Q

describe plasma proteins

A

-Total plasma proteins 6-8 g/dl
- All proteins are synthesized in liver (4 gm/h)
except γ globulins in B lymphocytes
- include albumin, globulin, fibrinogen, prothrombin, hormones

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10
Q

How is the concentration of plasma proteins kept constant?

A

Rate of breakdown = rate of formation

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11
Q

where are y globulins produced?

A

Lymphocytes

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12
Q

Describe Albumin

A

concentration: 4-4.5 gm/dl
size: Very small (69,000 Da)
function: Osmotic pressure

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13
Q

Describe Globulin

A

concentration: 2.5 gm/dl
types: α1, α2,β1,β2 and γ globulins
size: large
functions: viscosity and
immunity

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14
Q

Describe fibrinogen

A

concentration: 0.3 gm/dl
size: large (400,000Da)
function: viscosity and clotting factor

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15
Q

what is prothrombin?

A

clotting factor

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16
Q

how do plasma proteins exert osmotic pressure?

A

-Water moves between plasma and
interstitial fluid
-Hydrostatic forces= push water out of vessel
-Osmosis= pull water in vessel
Osmosis is made by Nacl and plasma proteins
2-Nacl is present equally on both sides, so it does not affect water
movement
3-Plasma proteins due to their relatively large
molecular size do not diffuse through the capillary wall.
So, plasma proteins exert osmotic pressure
called the colloid osmotic pressure or the
effective osmotic pressure
- Its value is 25mmHg

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17
Q

describe effective osmotic pressure

A

Caused mainly by albumin
 Value: 25 mmHg
 Importance: absorbing force that pulls water into the blood vessel, to maintain blood volume and interstitial fluid volume constant

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18
Q

Absorption vs. Filtration

A

Absorption
- Venous end
-Hydrostatic pressure is 15mmg
- Osmotic pressure is 25mmg

Filtration
- Arterial end
Hydrostatic pressure is 35mmg
- Osmotic pressure is 25mmg

Hydrostatic pressure=filtering force osmotic pressure=absorbing force

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19
Q

what are the causes of hypoproteinemia?

A

-Starvation - decrease in plasma proteins
-Malabsorption syndrome

-Liver disease - decreased hepatic protein synthesis

-Nephrosis - large amounts of albumin lost in urine

-Congenital absence of plasma protein fraction

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20
Q

what are the effects of hypoprotenemia?

A

 No plasma proteins
 Decreased fluid absorption
 Increased tissue filtration
 Accumulation of fluid
in abdomen= Ascites
 Accumulation of fluid
in lower limb=lower
limb oedema

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21
Q

what is the normal albumin: globulin ratio?

A

1.2-1.6

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22
Q

when does a/g ratio decrease

A

▪ In liver disease due to decreased synthesis.
▪ In kidney disease due to increased loss of albumin in urine.
▪ In infections as in typhoid and T.B due to increased synthesis of γ globulin

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23
Q

when does a/g ratio increase

A

Hypogammaglobulinemia.
▪ Acquired immuno-deficiency syndrome (AIDS)

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24
Q

Importance of viscosity and main plasma protein involved

A

Viscosity determines
peripheral resistance and
affect blood pressure

-Large plasma proteins as
fibrinogen shares by 40%
in viscosity

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25
Q

what are the functions of plasma proteins?

A
  1. production of effective osmotic pressure - by their Colloidal osmotic pressure - 25 mmHg
  2. blood viscosity - Fibrinogen helps maintain peripheral resistance and therefore diastolic blood pressure
    - RBCs are more important for blood viscosity

3- Clotting factor: as fibrinogen, prothrombin

4- Defense as: gamma globulin

5-Buffering function:15% of the buffering capacity of the blood.

6- Carrier: carry lipophilic substances as some
hormones, metals as iron and calcium and other molecules (fatty acids, amino acids..)

7- carry carbon dioxide

8-Protein reserve: Reserve proteins are used by the body in cases of fasting or decreased food intake.

9- Maintain capillary permeability - close the pores of capillaries

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26
Q

how do plasma proteins carry CO2?

A

Plasma proteins form carbamino compounds with CO2

CO2 (10%) + amino group (NH2) of plasma proteins
»carbamino compounds&raquo_space; release CO2 to be expired (CO2 + proteins in lung capillaries)

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27
Q

what are the Physiological properties of RBCs? (source, lifespan, abundance)

A

 Formed in the bone marrow
 Lifespan 120 days
 RBCs are the most abundant cells
in the blood
➢ 4-5 million/mm3 in females
5-6 million/mm3 in males
-Higher in male and newly born

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28
Q

what are the contents of rbc cytoplasm?

A

A-60% water
b- chief cation: k+, chief anion: cl
c- 34% hemoglobin:
D-The average normal hemoglobin
concentration in blood is 15 gm/dl:
15-17 g/dL in men and
13-15 g/dL in women, all of it in red
cells

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29
Q

Functions of RBCs membrane

A

1- Concave to increase surface area available for gas exchange and diffusion

2- Maintain the shape and
flexibility of the
cell membrane:
_The integral proteins
Band 3 (the negative ion
exchanger)
_The linker protein ankyrin
_The cytoskeleton protein spectrin
==Genetic mutations in these proteins leads to hereditary spherocytosis==

3-Plasticity
The ability of the red blood
cells (8 microns) to change their shape to cross through the narrow capillaries (3 microns)

4- Semipermeability
allows anions to pass
easily in or out of the RBC,
but not cations.
- It contains Na-K ATPase
pump to maintain cell
volume

5-Blood grouping
Conatins agglutinogens to determine blood groups

6-Keep Hemoglobin (Hb) inside RBCs and prevents loss in urine

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30
Q

Why it is important to keep Hemoglobin (Hb) inside RBCs?

A

A) To avoid increase in:
➢ Blood viscosity, which may increase work of the
heart
➢ Osmotic pressure, which interfere with filtration at capillaries

B) To avoid Hb loss in urine where it will react with HCL, forming acid haematin that block renal tubules leading to renal failure

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31
Q

What is Hemoglobin?

A

The red, oxygen carrying pigment in human red blood cells. It is composed of four polypeptide chains, each with a heme moiety attached to it.

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32
Q

Hemoglobin functions

A

➢ Hemoglobin binds O2
to form oxyhemoglobin
 O2 attaches to the Fe2+ in the heme leading to hemoglobin oxygenation (not oxidation), iron remains in the ferrous state.
 Each Hb molecule carry 4 O2 molecules
 1 gm of blood Hb carry 1.33 ml of oxygen15 gm Hb in 100 ml blood,

 Each 100 ml blood can carry 15 X 1.33 = 19.95ml which is the oxygen carrying capacity of the blood.

➢Hemoglobin binds CO2
to form carbaminohemoglobin
 CO2 binds to amino group
of hemoglobin

➢Hemoglobin acts as a
buffer in the blood as it
contains many amino acids
eg histidine

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33
Q

Types of hemoglobin in normal adults

A

HbA - 98% a2,B2
HbF - ~1% a2,y2
HbA2 - <3.5%

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34
Q

fetal HB

A

➢ The fetus has
HbF (α2 y2)
➢ Fetal Hb is replaced by adult hemoglobin
2-3 months after birth.
It has a higher oxygen affinity than adult Hb which facilitates O2 transport across the placenta

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35
Q

what are the Requirements for erythropoiesis?

A

1-Normal functioning bone marrow: Bone marrow is
the site where erythropoiesis takes place.
2-Normal functioning kidneys: Kidneys secrete 85%
of erythropoietin hormone.
3-Normal functioning liver: Liver stores iron and
vitamin B12.
It also synthesizes the globin part of hemoglobin and secretes 10 % of erythropoietin.
4-Hormones: Androgens, thyroxine and glucocorticoids stimulate erythropoiesis, while estrogen inhibits it
5-Dietary substances
 Proteins: Proteins of high biological value (especially
animal proteins) to build up the globin part of Hb.
 Iron: It is the principle constituent of Hb molecule.
 Vitamin B12 and folic acid: Vitamin B12 and Folic acid are called “Maturation factors” as they are essential for normal formation of DNA and cell division during red
blood cell maturation.
Deficiency of vitamin B12 and Folic acid results in
megaloblastic or macrocytic anemia.
 Other trace elements as Copper and cobalt: They are
required as cofactors for the formation of Hb

Tissue oxygenation is the most important regulator
of erythropoiesis

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36
Q

What is Erythropoietin?

A

It is a glycoprotein that comes from:
85-90% : kidneys
10-15% : liver

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37
Q

Factors stimulating erythropoietin secretion:

A

1) Hypoxia
2) Hormones: androgens (testosterone), catecholamines,
corticosteroids, growth hormone, and thyroxin increase erythropoietin secretion
3) Alkalosis as in high altitudes

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38
Q

correlation between renal failure and anemia

A

➢ Renal failure is associated with anemia that can
be treated only by erythropoietin.
➢ In aplastic anemia the stem cells do not respond
to erythropoietin.

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39
Q

Iron homeostasis

A

1-Iron intake is 15-20 mg%
➢ Absorbed iron (3-6%of the intake)
➢ iron lost by cells sloughing
2-Iron homeostasis depends on control of iron absorption from the intestine (Duodenum). Iron losses
are generally unregulated.

Absorption is also increased by increasing demand
-Females need more iron absorption because of the periodically loss of iron in
menstrual blood flow
- pregnancy, lactation, growing children and blood loss

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40
Q

Iron functions in the body

A

hemoglobin synthesis
myoglobin synthesis
cytochrome oxidase, peroxidase and catalase

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41
Q

Iron distribution in the body

A

hemoglobin - 65%
stored iron (ferritin and hemosiderin) - 15-30%
myoglobin - 4%
cytochrome oxidase, peroxidase and catalase - 1%
In plasma (transferrin) - 0.1%

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42
Q

Describe Iron absorption in duodenum

A

1- Heme absorption:
 Through the enterocyte Heme carrier protein (HCP-1)
 Iron is released from heme by Heme oxygenase enzyme

2- Non- Heme absorption:
 Diet iron is ferric
 Ferric is reduced by ferric reductase helped by HCL and vitamin C to ferrous iron

 Ferrous iron is transported into the enterocyte with a proton via a divalent metal
transporter (DMT-1).

 Fe2+ is transported out of the enterocyte by the basolateral membrane protein (ferroportin)

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43
Q

what is hepcidin?

A

Hepcidin is a hormone released by the liver when iron levels are high.
It inhibits ferroportin transporter
Its deficiency causes tissue iron overload

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44
Q

Factors affecting iron absorption

A

Factors that increase iron absorption:
 Gastric acidity and vitamin C aid iron reduction
 Increased erythropoietic activity e.g. bleeding, hemolysis, high altitude.
 Increased demand in Infancy and adolescence

Factors that decrease iron absorption:
 Phytic acid, oxalates and phosphates form
insoluble salts
 Iron overload
 Calcium in dairy food

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45
Q

absorption of different types of iron

A

➢Heme iron is absorbed better than inorganic iron.
➢Ferrous iron is absorbed better than ferric iron

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46
Q

Describe iron transport

A

 Iron is transported as transferrin, normally 35% saturated.

  • Fe2+ is changed to Fe3+ and bound to apotransferrin forming transferrin
  • Transferrin is a glycoprotein synthesized in the liver.
    -Binds to receptors in cell membrane of erythroblasts in the bone marrow.
  • Ingested by endocytosis and iron is delivered to the mitochondria where heme is synthesized.
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47
Q

Describe iron storage

A

Iron is stored mostly in hepatocytes and to a lesser extent the reticuloendothelial cells of the bone marrow and skeletal muscle cells.

Ferritin is the predominant storage form. It keeps iron in a soluble and non-toxic form. It is present in most cells especially intestinal mucosa, liver, spleen and bone marrow.

Excess iron is stored as hemosiderin - iron deposition adjacent to ferritin spheres

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48
Q

Ferritin vs. Hemosiderin

A

Ferritin
-Iron binds apoferritin to form ferritin
-It is water soluble
-It represents 2/3 of stored iron
-If plasma iron is decreased, iron in ferritin is transported easily to replenish ferritin in plasma
-It is easily mobilized for Hb synthesis

Hemosiderin
-It is water insoluble
-It represents 1/3 of stored iron
-Excess hemosiderin can be found in iron overload due to frequent blood cell destruction and trnasfusions

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49
Q

effects of iron deficiency

A

Can result in microcytic hypochromic anemia due to decreased hemoglobin synthesis and
RBC size.

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50
Q

describe vitamin B12 in terms of function, sources, minimum requirement and absorption

A

 Both vitamin B12 and folic acid are essential for normal formation of DNA and hence for nuclear maturation.
- VB12 is important in myelin sheath formation
 Vitamin B12 is absent from plant sources, formed exclusively by microorganisms
 The minimum requirement is 1-3
microgram/day
- Liver and yeast are good sources
 Absorbed in terminal ileum by
endocytosis

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51
Q

effects of Vitamin B12 deficiency

A

 Malabsorption (lack of the intrinsic factor) due to
atrophy of gastric mucosa, achlorhydria, or after total
gastrectomy.

 Vegetarian peopleare most likely to be infected. If plants are contaminated with
microorganisms, supply of B12 will be sufficient.

 Deficiency Leads to a condition called pernicious anemia or megaloblastic anemia (macrocytic anemia).
This occurs due to Impaired DNA synthesis and prevention of cell division with the accumulation ofimmature erythrocytes in the circulation.

 Neurological disorders are due to progressive
demyelination of nervous tissue.

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52
Q

describe pernicious/ megaloblastic anemia

A

 Large immature
erythrocytes

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53
Q

Define polycythemia

A

Definition: Polycythemia, or erythrocytosis, refers to an increase in the RBC mass, usually with a corresponding increase in hemoglobin level.

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54
Q

what are the effects of polycythemia

A

Increase in RBCs number → increase in blood viscosity
→ sluggish blood flow → increased Work load on
the heart→ increase peripheral resistance → high
blood pressure

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55
Q

types of polycythemia

A

 Primary polycythemia (Polycythemia rubra vera):
It is considered as a neoplastic disease

 B. Secondary polycythemia:
Hypoxia: as in high altitudes, cyanotic congenital
heart disease and chronic pulmonary disease.
Renal disease: due to secretion of an erythropoietin-like substance.

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56
Q

define anemia

A

 Definition of anemia
 It is a decrease or deficiency of RBCs number or
decrease in Hb concentration or decrease in both
RBCs and Hb. in a unit volume of blood in the
presence of a low or normal total blood volume
 It can be caused either by too rapid loss or too slow
production of RBCs.

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57
Q

classify different types of anemia according to cause

A

1-Aplastic anemia
-Due to Bone marrow failure
-causes: X-ray,chloramphenicol,
chemotherapy, idiopathic (primary)
-Aplastic anemia results in Pancytopenia

2-Deficiency anemia:

A) Iron deficiency
-Due to Less Hb formation -Deficient iron intake
- Causes: Excess demand,
puberty, pregnancy
-Poor iron absorption
-> chronic bleeding

Iron deficiency results in Microcytic hypochromic anemia

B) Vitamin B12 deficiency

-Due to Erythroblast failure to proliferate or mature into RBCs
-Causes: Malabsorption, Atrophic gastritis
- Vitamin B12 deficiency results in Pernicious anemia,
Macrocytic hyperchromic anemia
+ Neurological defects

C- Folic acid deficiency
-Due to Erythroblast failure to
proliferate or mature
into RBCs
-Cause:Nutritional defect
-Folic acid deficiency results in Macrocytic hyperchromic anemia

3- Renal anemia
-due to insufficient RBCs
production
- cause: defect in erythropoeitin
- results in : Normocytic normochromic anemia

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58
Q

Microcytic hypochromic
anemia vs. Macrocytic hyperchromic anemia
(megaloblastic anemia)

A

Microcytic hypochromic
anemia:
 Small size RBCs
 Less Hb

Macrocytic hyperchromic anemia (megaloblastic anemia)
 Large size, immature odd
shaped, fragile RBCs
 Severe number reduction

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59
Q

Haemolytic anemia: types and causes

A

corpuscular:
 Hereditary
spherocytosis
 Sickle cell anemia
 Thalassemia
 Glucose 6 p
dehydrogenase
deficiency

extracorpuscular:
 Incompatible blood
transfusion
 Rh incompatability
 Malaria infection
 Sulfonamide
 Snake venum
 Lead

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60
Q

spectrin deficiency results in…

A

Spherocytes
That rupture
easily
(Haemolysis)

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61
Q

Describe hereditary spherocytosis

A

 Genetic defect in RBCs membrane proteins
 RBCs are spherocytic and hemolyze more readily than normal cells

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62
Q

Describe Sickle cell disease and Hb A vs. Hb S

A

Inherited genetic defect in Hb
formation
 Hb A: 4 polypeptide chains:2
alpha, 2 beta
 Hb S: Normal glutamic acid aa
in position 6 on the chain is substituted by Valine aa.
 Oxygenated: Soluble
 Deoxygenated: insoluble, precipitates into long crystals leading to sickled cells which are fragile and liable to hemolysis

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63
Q

Describe Dactylitis

A

Severe pain that affects the bones of the hands, the
feet, or both.
It’s often the first symptom of sickle cell disease in
babies.
Dactylitis is caused by blocked blood circulation.
Symptoms include extreme pain and tenderness, usually with swelling.

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64
Q

Describe glucose 6 phosphate

A

 Glucose 6 phosphate enzyme is an enzyme that :
➢ Is coded by gene on X chromosome
➢ helps in producing the antioxidants

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65
Q

Describe G6P dehydrogenase deficiency {Favism}

A

-X-linked recessive disorder
-Leads to acute intravascular hemolysis on exposure to oxidizing agents
- The oxidizing agents include: fava beans, sulfonamides

66
Q

Describe thalassemia

A

defect or absence of one or more of the genes responsible for synthesis of α or β chains

67
Q

Describe acute vs. chronic hemorrhagic anemia

A

Acute:
RBCs loss
Cause: Wound bleeding
Results in: Normocytic
normochromic anemia

Chronic:
iron loss
Cause: Bleeding piles,
excessive mensis
Microcytic hypochromic anemia

68
Q

Describe Normocytic
normochromic anemia in terms of RBC size, Hb content per cell and Cause

A

RBCs size: normal
Hb content per cell: normal
Cause :
-Aplastic anemia
-Renal failure
-Acute haemorrhage
-Acute haemolysis

69
Q

Describe Microcytic
hypochromic anemia in terms of RBC size, Hb content per cell and Cause

A

RBCs size: small
Hb content per cell: decreased
Cause :
-Iron Deficiency
anemia
-Thalassemia

70
Q

Describe Macrocytic anemia in terms of RBC size, Hb content per cell and Cause

A

RBCs size: large
Hb content per cell: normal or increased
Cause :
- Vitamin B12, folic
acid deficiency
anemia

71
Q

symptoms of anemia

A

Tiredness.
Weakness.
Shortness of breath.
Pale or yellowish skin, which might be more obvious on white skin than on Black or brown skin.
Irregular heartbeat.
Dizziness or lightheadedness.
Chest pain.
Cold hands and feet.
Headaches
yellowing eyes (hemolytic anemia)

72
Q

effects of anemia

A

1-Decreased tissue oxygenation: especially during exercise.

2-Increased work load on the heart due to:
Decreased blood viscosity due to decrease number of RBCs will decrease the resistance to blood flow so that greater quantities of blood flow through the tissues and then return to the heart

73
Q

What is an antigen?

A

Antigen is any substance recognized by the body as
foreign, causing the body to form antibodies that
specifically react with it.
The antigen must be a complex molecule. The more
the complex the molecule , the more its antigenicity.

74
Q

What are blood groups?

A
  • Everybody has a blood type.
  • Blood groups or types are a classification of blood
    based on the presence or absence of antigens
    (agglutinogens) on the surface of RBCs
  • The most common system blood type classification is
    the ABO system According to the ABO system, there
    are 4 major groups (types):
    1. A
    2. B
    3. AB
    4. O
75
Q

Why are the ABO and Rh systems important?

A

A & B antigens are found on RBC membrane as well
as many other tissues e.g. salivary glands, kidney,
liver lung & pancreas.

76
Q

What are agglutinins

A

Antibodies against red cell agglutinogens are called
agglutinins and they are present in plasma.
Agglutinins against A and B‐agglutinogens [anti‐A ( α)
and anti‐B (β )] occur naturally.
Thus,
types A individuals develop anti‐B antibodies,
type B‐individuals develop antiA antibodies,
type O‐individuals develop both antibodies
type AB‐individuals develop neither antibody.

77
Q

Describe the frequency, agglutinogen and agglutinin of each blood group

A

Blood Group
A:
-41% frequency
-Agglutinogen on RBC membrane: A
-Agglutinin in plasma: B

B:
-10% frequency
-Agglutinogen on RBC membrane: B
-Agglutinin in plasma: A

AB:
-4% frequency
-Agglutinogen on RBC membrane: A & B
-Agglutinin in plasma: None

O:
-45% frequency
-Agglutinogen on RBC membrane: None
-Agglutinin in plasma: A & B

78
Q

what is agglutination?

A

When A or B antigen meet its corresponding antibody agglutination reaction occurs.

In agglutination reaction , RBC clump and stick to each other then hemolyse

A& B antigens are called agglutinogens, while
their corresponding antibodies are called A
and B agglutinins

79
Q

How does the agglutination reaction occur?

A

-Agglutination occurs when antigen and its corresponding antibody come together.

 The agglutinins attach themselves to the RBCs.
 Because agglutinins have many binding sites, a single
agglutinin can attach to different red cells at the same time.
 This causes the cells to clump, then these clumps plug small blood vessels, then destroyed by phagocytic cells and the reticuloendothelial system, releasing Hb.

80
Q

Explain plasma compatibility

A
  • Plasma compatibility is the inverse of red blood cell
    compatibility.
  • Type AB plasma carries neither anti‐A nor anti‐B antibodies and can be transfused to individuals of any blood group
  • but type AB patients can only receive type AB plasma.
  • Type O carries both antibodies, so individuals of blood group O can receive plasma from any blood group,
  • but type O plasma can be used only by type O recipients.
  • In addition to donating to the same blood group; plasma from type AB can be given to A, B and O;
  • plasma from types A, B and AB can be given to O.
81
Q

what is the Rh system?

A
  • The “Rh” factor named for the Rhesus monkey because it was first studied using the blood of this animal.
  • This system has not been found or detected in tissues other than red cells.
  • “D” is the most important antigenic component.
  • The population are divided according to presence of D‐Antigen into Rh‐positive and Rh‐negative

“Rh‐positive” means that the individual has agglutinogen D (function is unknown). Never produce anti‐D antibodies and it was found in 85 90% of population.

“Rh‐negative” means that the individual has no D‐antigen and forms the anti‐D agglutinin when injected with D +ve cells.
* The anti‐D‐antibodies (agglutinin) are not naturally present in Rh‐ negative individuals.

82
Q

ABO system vs. Rh system

A

ABO system:

Antigens:
-A and B
-Present on RBC membrane
and many tissues

Antibodies:
-Naturally occurring
-Mostly IgM
-Can not cross the placenta

Rh system:

Antigens:
-many antigens
-Only restricted to red
blood cells

Antibodies:
-Not naturally occurring
-Mostly IgG
-can cross the placenta and
cause hemolytic disease of
the newborn

83
Q

Explain the importance of blood groups

A
  1. Ensure compatible blood transfusion.
  2. Used in pre‐marriage counseling to avoid Rh
    incompatibility.
84
Q

what is erythroblastosis fetalis?

A

(Hemolytic disease of the New‐born):
-It is a condition due to Rh‐incompatibility between mother and fetus blood.
-It occurs when a Rh‐negative mother carries a Rh‐positive fetus.
-During the labor of the first baby, small amounts of fetal blood pass into the maternal circulation leading to formation of anti‐Rh agglutinins in mother’s circulation during the postpartum period
(mother becomes sensitized).

-The first baby is usually normal because sensitization of Rh‐ negative mother carrying a Rh‐positive fetus generally occurs at
birth.
-If the second fetus blood is Rh‐positive, this results in agglutination and then hemolysis of fetus red cells.

85
Q

what are sysmptoms of erythroblastosis fetalis?

A
  • If hemolysis is severe, the infant may die inside the
    mother uterus (Intrauterine death).
  • Less severe form causes hemolysis of fetus RBCs
    causing anemia and increased bilirubin resulting in severe jaundice, and edema of fetus (Hydrops
    fetalis).
  • If bilirubin concentration is very high it deposited
    in the basal ganglia causing brain damage, a serious condition called Kernicterus.
86
Q

How is erythroblastosis fetalis prevented?

A

To prevent sensitization of a Rh‐negative mother, she is given a single dose of anti‐Rh antibodies
(Anti‐D immune globulin) in the first 48 hours after delivery starting from first delivery.

Also, be careful when giving blood transfusion to females (even very young girls) who may be Rh‐negative and are transfused with Rh‐positive
blood.

87
Q

Treatment of erythroblastosis fetalis

A

Exchange transfusion - replace newborn blood with Rh-ve blood

88
Q

what is blood transfusion?

A

It is the process of transferring blood or blood products from one person into the circulatory system of another.

89
Q

what are the indications of blood transfusion?

A
  1. Hemorrhage: from severe trauma or after surgical operation (to restore blood volume) and bleeding attacks due to disturbances in clotting mechanisms or platelet function (transfusion of clotting factors).
  2. Severe anemia: (to restore Hb level)
    people suffering from hemophilia or sickle-cell disease may require frequent blood transfusions.
  3. Erythroblastosis fetalis.
90
Q

what precautions are taken before a blood transfusion?

A

1- Blood typing: the donor’s blood should be compatible with that of the recipient regarding
ABO system and Rh factor.

2- Cross matching test: should be done
“The donor’s cells are added to the recipient plasma and the donor’s plasma tested with the recipient
cells”
This test is done to avoid incompatibility due to any subgroup, or due to increased
concentration of agglutinins in the donor’s plasma.

3- A healthy donor must be carefully chosen with no history of serious diseases such as: Hepatitis, HIV
(human immunodeficiency virus) or AIDS, Malaria and
Syphilis.

4- Good storage of the blood with the addition of
 acid citrate (to prevent its clotting) and
 glucose (as a nutrient to the RBCs).
 The blood should be kept at a temperature of 4º C in
the blood banks and not frozen, otherwise the RBCs
will be destroyed.
 The blood should not be used after 5 weeks

91
Q

what are transfusion reactions?

A

 Hemolytic transfusion reactions occur when blood
is transfused to an individual with incompatible blood group i.e. when the recipient has agglutinins against the RBCs in the donor’s blood.
 The transfused plasma (donor’s plasma) is
usually so diluted in the recipient that it rarely
causes agglutination.

92
Q

what happens if cells agglutinate?

A
  1. Agglutinated RBCs form clumps which block capillaries leading to pain and tightness of the chest immediately. The clumps are then hemolyzed, releasing Hb into plasma causing jaundice.
  2. The cells hemolyze. Free Hb is liberated into the plasma. The severity of the transfusion reaction may vary from minor asymptomatic rise in plasma bilirubin to severe jaundice (hemolytic jaundice), renal tubular damage and renal failure and may be death.
  3. Histamine release from the hemolyzed RBCs causing
    vasodilatation and resulting in hypotension.
93
Q

what are the causes of acute kidney shutdown in blood transfusion?

A

There are three causes:

a- The antigen-antibodies reaction of the transfusion reaction releases toxic substances from the hemolyzing RBCs and causes powerful renal vasoconstriction with reduction in the glomerular filtration rate.

b- Circulatory shock from the loss of RBCs and the production of toxic substances decreasing the glomerular blood flow and
urine output.

c- Renal tubular blockage due to Precipitation of Hb which passes through the glomeruli by the acidic urine in the form of acid hematin which obstruct the lumen of the tubules decreasing the flow of urine.
Thus, renal vasoconstriction, circulatory shock, and renal tubular blockage together cause acute renal shutdown.
Due to renal failure there is uremia and hyperkalemia. If the shutdown is complete and fails to resolve, the patient dies
within a week to 12 days.

summary:
Acute kidney shut down.due to
a-Ag-Ab reaction -> release of toxic substances from hemolysed RBCs -> renal V.C. -> dec GFR
b- circulatory shock -> toxic substances -> dec GBF and urine output
c- renal tubular blockage by precipitated hemoglobin ( acidic urine + HB -> acid hematin)

94
Q

what are the immediate dangers of blood transfusion?

A
  1. Acute hemolytic (Incompatibility) reactions as
    pain, jaundice and acute renal shut down.
  2. Febrile Reactions: fever is body’s response to the white blood cells in the transfused blood (white cell antibodies in a recipient react with white blood cells in a transfused blood).
  3. Allergic Reactions: They arise from recipient antibody response to donor plasma proteins.
  4. Mechanical overloading of the circulation particularly in patients with cardiac diseases
  5. Hyperkalemia: With storage there is increased amount of K+ in the plasma due to its release from old hemolyzed cells that may lead to ventricular fibrillation and sudden death.
  6. Citrate intoxication with massive transfusion due to
    excessive citrate infusion: this may produce decreased ionized calcium (hypocalcemia) and acidosis.
  7. Bacterial infection: due to contamination of blood by bacteria specially with cold-growing gram-negative bacilli. After a latent period, it produces shock associated with fever.
    N.B. Prolonged storage at room temperature (more than 4 hours) encourages the growth of
    contaminating bacteria
95
Q

what are the delayed dangers of blood transfusion?

A
  1. Transmission of diseases e.g. AIDs, hepatitis, malaria and syphilis.
  2. Iron overload: Most common in patients that receive repeated transfusions due to too much
    iron from donor blood. This can produce damage to organs as liver (developing liver cirrhosis),
    pancreas (diabetes mellitus) and heart
96
Q

what is natural hemostasis

A

It is the spontaneous prevention of blood loss by physiological processes. Effective in stopping bleeding from small blood vessels.

97
Q

Mechanisms of natural hemostasis

A

1) Local vasoconstriction
2) Formation of temporary platelet plug
3) Formation of definitive blood clot
4) Repair of injured blood vessel

98
Q

what causes local vasoconstriction in hemostasis

A

1) Nervous reflexes: induced by pain impulses due to trauma
2) Local myogenic spasm: induced by direct damage to vascular wall
3) Chemicals released by endothelial cells and platelets

99
Q

Formation of platelet plug

A

occurs through:
1) platelet adhesion
2)platelet activation
3)platelet aggregation

1) damage to blood vessel disrubts endothelium exposing underlying collagen.

2) The platelets adhere to the collagen and such adhesion is potentiated by Von Willebrand factor

3) Platelet binding to collagen induces platelet activation

4) The activated platelets swell, become irregular in shape with pseudopods and become sticky.

5) They secrete ADP and thromboxane A2 which act on nearby platelets causing platelet activation.

6) formation of platelet plug effective in preventing blood loss from small blood vessels

100
Q

Role of platelet plug

A

1) physically seals the break in the vessel

2) Actin myosin protein complex contracts to compact and strengthen the originally loose plug

3) Platelets release vasoconstrictors (serotonin, epinephrine, thromboxane A2) - induce constriction

4) Release of other chemical substances to enhance blood coagulation

101
Q

Importance of ADP in platelet aggregation

A

1) causes surface of platelets to become sticky
2) Continuous aggregation of platelets by positive feedback

102
Q

Importance of Von Willebrand Factor

A
  • secreted by endothelial cells
  • forms bridge between the vessel wall and first layer of platelets.
  • binds to collagen facilitating adherence of platelets to damaged vessel walls
103
Q

Importance of thromboxane in platelet aggregation

A

Platelet adhesion causes conversion of arachidonic acid to thromboxane A2.
- stimulates platelet aggregation and secretion of platelet granules.

104
Q

Prostacyclin (PGI2)

A

Inhibits platelet aggregation, avoid spread along endothelium

105
Q

Name all clotting factors

A

Factor I - fibrinogen
Factor II - prothrombin
Factor III - tissue thromboplastin (tissue factor)
Factor IV - ionized calcium ( Ca++ )
Factor V - labile factor or proaccelerin
Factor VI - unassigned
Factor VII - stable factor or proconvertin
Factor VIII - antihemophilic factor
Factor IX - plasma thromboplastin component, Christmas factor
Factor X - Stuart-Prower factor
Factor XI - plasma thromboplastin antecedent
Factor XII - Hageman factor
Factor XIII - fibrin-stabilizing factor

106
Q

Briefly describe blood clot formation

A

Proteolytic enzymes called clotting factors undergo a series of chemical reactions resulting in:

1) Formation of prothrombin activators
2) Catalyze conversion of prothrombin to thrombin
3) converts fibrinogen to fibrin

Fibrin is converted to a dense tight aggregate stabilized by activated factor XIII and requires Ca++

107
Q

Describe extrinsic blood clotting pathway

A

1) Begins with trauma to the vascular wall and surrounding tissues
2) Traumatized tissues release tissue factor (Factor III)
3) Tissue factor activates Factor VII (proconvertin)
4) Tissue Factor + Proconvertin + Ca++ activate Factor X (Stuart Prower factor)
5) Xa + Factor V (proaccelerin) + tissue phospholipids form prothrombin activator
6) Prothrombin activator splits prothrombin into thrombin in the presence of Ca++ and platelet phospholipids and the clotting process proceeds

108
Q

Describe Intrinsic pathway of blood clot formation

A

It begins with:
1)
In vivo with:
a) exposure of blood to collagen from traumatized vascular wall or damaged endothelial cells
b) Trauma to the blood

In vitro with:
c) blood coming in contact with wettable surface such as glass

2) These cause activation of Factor XII (Hageman, glass factor)

3) XIIa activates factor XI - this reaction requires HMW kininogen and is accelerated by prekallikrein

4) XIa activates factor IX in presence of calcium

5) IXa acting with VIIIa, platelet phospholipids and calcium activate factor X

6) Xa combines with Va and phospholipids to form prothrombin activator as the last step of the extrinsic pathway

109
Q

Interaction between intrinsic and extrinsic pathway

A

1) Clotting occurs by both pathways simultaneously

2) The extrinsic pathway is much more rapid than the intrinsic pathway

3) The extrinsic pathway potentiates the intrinsic pathway through:
- The trace amount of thrombin formed by the extrinsic system activates factors V and VII which are involved in the intrinsic system
- Activated factor VII share in the activation of factor IX

110
Q

what is Vitamin K?

A
  • fat-soluble vitamin
  • requires bile for its absorption from the small intestine and absorbed in blood along with the fats
111
Q

sources of vitamin k

A
  • bacteria including human intestinal normal flora
  • diet
112
Q

Role of vitamin K in blood coagulation

A

Necessary for liver formation of prothrombin, factor VII, IX and X and protein C and protein S.
- deficiency leads to bleeding tendency

113
Q

General functions of lymphocytes

A
  1. Engulfing and digesting the foreigner.
  2. Initiation of the immune response.
  3. Removal of injured or dead cells and help healing
  4. Destruction of cancer cells. Tumor cells produce proteins that are not normally produced by normal cells. T lymphocytes can recognize these antigens presented on the surface of tumor cells, thereby mediating cancer regression
114
Q

How do leucocytes achieve their function?

A

1) Diapedesis
2) Ameboid motion
3) chemotaxis
4) phagocytosis

115
Q

What is Diapedesis?

A

-The white blood cell leaves the blood stream to the tissues (i.e. a small portion of the cell is momentarily constricted and slides through the capillary pore).
-This happens by interaction between endothelial cells and leukocytes

116
Q

What is ameboid motion?

A

It is the movement of leucocytes which starts by protrusion of pseudopodium from one end, then movement of the remainder of the cell towards this pseudopodium.

117
Q

What is chemotaxis?

A

It is the attraction of white blood cells towards some chemical substances which include:
A. Some of the bacterial or viral toxins.
B. Degenerative products of the inflamed tissues.
C. Leukotrienes and polypeptides from WBCs (lymphocytes, mast cells and basophils).
D. Several components of the “complement complex (C5a).

118
Q

What is phagocytosis

A

It is the ingestion of foreign particles and microorganisms by white blood cells.

119
Q

Mechanisms of phagocytosis

A

Mechanism of Phagocytosis
1. Opsonization: coating of bacteria or virus by opsonins like Immunoglobulins (IGg) and some components of the complement proteins (C3b) to render them tasty for phagocytes.
2. Binding: of the coated bacteria to receptors on the cell membrane of neutrophil.
3. Pseudopodia from neutrophils protrude around the bacteria and fuse to form a phagosome.
4. Fusion of lysosomes with the phagosome creates phagolysosome to digest bacteria.
5. Expulsion of waste materials

120
Q

Functions of thrombin

A

Functions of thrombin:
1. Causes conversion of fibrinogen to fibrin.

  1. Acts in a positive feedback to facilitate its own formation through the activation of factors VIlI & V.
  2. Enhances platelet aggregation, which is essential to clotting process.
  3. Activates factor XIlI to stabilize the resulting fibrin meshwork.
  4. Activates plasminogen to plasmin (anticlotting).
121
Q

What is clot retraction

A

Within few minutes after the fibrin clot is formed it begins to contract and a clear non coagulable fluid called serum is squeezed out. As the clot retracts it pulls the edges of the broken vessel together.

122
Q

How do platelets facilitate clot retraction

A

-bond the fibrin fibers together
- release fibrin stabilizing factor (XIII) which causes more linking bonds between fibrin fibers.

•activate thrombosthenin, actin and myosin, which are all contractile proteins

123
Q

What is clot dissolution (fibrinolysis)

A

• Clot dissolution (Fibrinolysis):
Few days later, after the clot has stopped the bleeding, clot lysis occurs and allows blood flow to be reestablished and allows tissue repair to take place.

124
Q

Define repair of the injured blood vessel

A

It is the eventual growth of fibrous tissue into the blood clot to close the hole in the vessel permanently.

125
Q

Functions of platelets

A

Functions of platelets:

  1. Formation of a hemostatic plug that seals the injured vessel by aggregated platelets
  2. Platelet plug release chemicals (platelet release reaction), such as:
    -ADP which causes the platelets aggregation.
    - Serotonin, epinephrine and thromboxane A2 which are potent vasoconstrictors which induce profound constriction of the affected vessel to reinforce the initial vascular spasm.
    - • Release platelet factor 3 (PF3) which enhances blood clotting mechanism.
  3. Stabilization of blood clot as platelets have cytoplasmic granules, which contain fibrin stabilizing factor (factor XIII)
  4. Induce clot retraction.
  5. Release of platelet-derived growth factor (PDGF) that stimulates wound healing.
126
Q

What are natural anti-clotting mechanisms

A

Definition:
These are mechanisms that prevent clotting inside blood vessels, breakdown any clots that do form, or both.

Include :
1) Anticoagulation system
2) Fibrinolytic system

127
Q

How does Rapid blood flow support anticoagulation

A

it facilitates the removal of activated clotting factors by the circulating blood and their inactivation by the liver.

128
Q

Endothelial factors supporting anticoagulation

A
  1. Intact smooth endothelium
    It prevents contact activation of the intrinsic clotting system and platelets.
  2. Layer of glycocalyx on endothelium
    It repels clotting factors & platelets.
  3. Balance between prostacyclin (PGI2) and thromboxane A2
    -It keeps clot formation at site of injury only and rest of vessel lumen free of clot.
    -PGI2 is produced by healthy endothelium and inhibits platelet aggregation and phospholipid release that initiate coagulation and thus opposes the aggregating effects of thromboxane A2.
  4. Thrombomodulin
    It is a protein present in the endothelium and binds thrombin to prevent clot formation. Thrombomodulin-thrombin complex activates protein C that act as an anticoagulant.
  5. Tissue factor pathway inhibitor (TFPI)
    - It is made by the endothelial cell.
    It inactivates tissue factor / factor VIla complex and active factor X.
129
Q

What are the Anticoagulant proteins?

A
  1. Protein C (PC)
    -It is a naturally occurring anticoagulant plasma protein.
    -Protein C is activated by thrombomodulin-thrombin complex and the activation is enhanced by protein S which acts as a cofactor.

Activated protein C (APC) causes:
• Inactivation of active factors VIII, V
•Inactivation of inhibitors of plasminogen activators.
•Increase of the formation of plasmin which helps lysis of fibrin.

  1. Protein S
    - It is vitamin K-dependent hemostatic protein, and it is PC cofactor.
  2. Anti-thrombin III (heparin cofactor !)
    It causes inactivation of thrombin and active factors IX, X, XI, XII.
    Its action is facilitated by heparin.
130
Q

Describe Thrombin removal from blood

A

Thrombin removal from blood is mediated by:
1. Fibrin fibers (antithrombin action of fibrin)
2. Antithrombin III
- 85 -90% of thrombin is bound to fibrin, which prevents spread of thrombin.
Remaining amount is bound to antithrombin-Ill.

131
Q

Explain function of Heparin

A

-Heparin is a powerful anticoagulant but is present in small amounts in blood.
-When heparin combines with antithrombin III (Heparin + Antithrombin III complex), the effectiveness of antithrombin III for removing thrombin increases 100-1000 folds, and thus it acts as an anticoagulant.
-Heparin + Antithrombin III complex causes removal of thrombin and active factors XII, XI, X, IX.

132
Q

What is the fibrinolytic system

A

A fibrin clot is a transitory device until permanent repair of the vessel occurs.
The fibrinolytic system is the physiological process for:
-Clot removal.
-Restriction of clotting to a limited area, thereby preventing excessive intravascular coagulation.

133
Q

Mechanism of Fibrinolytic system

A
  1. Plasminogen (profibrinolysin) is an Inactive globulin produced by the liver and circulates in the plasma as a plasma protein.
  2. Plasminogen is converted to plasmin (fibrinolysin) by:
    • Thrombin.
    Tissue plasminogen activator (1-PA), which is released very alowly from damaged tissues and vascular endothelium.
    • Urokinase plasminogen activator (u-PA).
  3. Plasmin is a proteolytic enzyme that digests:
    Fibrin and fibrinogen, with the production of degradation products (FDP) that
    inhibit thrombin.
    • Prothrombin, factor V, factor VIlI and factor XII.
  4. FDP inhibits the interaction between fibrinogen and thrombin and inhibits platelets activation and aggregation.
134
Q

Describe regulation of Fibrinolytic system by protein C

A
  1. Thrombomodulin-thrombin complex activates protein C.
  2. Activated protein C along with its cofactor protein S inactivates:
    Active Factor V and Factor VIII.
    Inhibitors of tissue plasminogen activator, increasing the formation of plasmin.
135
Q

what are bleeding disorders?

A

These are a group of diseases characterized by an increased tendency to bleeding after trauma or spontaneously.

Vessel wall defects and platelet disorders - superficial bleeding

Clotting disorders - deep bleeding

136
Q

Describe bleeding due to defect in the blood vessel and causes

A

It is prolonged bleeding time due to weak fragile vascular wall

Causes:
1) Hereditary
2) Acquired:
- Nutrient deficiency (scurvy)
-Drug induced (steroids)
-Aging
-Certain Infections
-Malignancies

-

137
Q

Describe thrombocytopenia

A

Decreased Platelet count
- Clot retraction is deficient and there is poor vessel constriction
- tendency to bleed from many small capillaries and venules, causing small punctuate hemorrhages.

– Bleeding occurs when platelet count is below 50,000uL
Lethal - <10,000uL

Normal range 150,000 - 410,000

138
Q

Effects of thrombocytopenia

A
  • petechiae - subcutaneous hemorrhages
    small, purplish blotches on skin
  • prolonged bleeding time
139
Q

Causes of thrombocytopenia

A

1) Autoimmune disease in which platelets are destructed by antibodies
(Idiopathic thrombocytopenia purpura)

2) Secondary thrombocytopenia purpura due to :
- Hypersplenism
-Severe bone marrow destruction

140
Q

What is thrombasthenia/ thrombocytopathia

A
  • weak platelet function
    It gives the same picture as thrombocytopenia
141
Q

causes of thrombocytopathia

A

1) Prolonged use of aspirin leads to defective platelet aggregation

2) Renal failure

3) Von WillebrandT factor deficiency

142
Q

Treatment of thrombocytopenia

A
  • Platelet transfusions
  • Fresh whole blood transfusions containing large number of platelets
143
Q

Describe bleeding due to abnormal coagulation

A

Deficient clotting due to lack of any of the clotting factors
-Tendency to bleed from large vessels
- Coagulation tests are prolonged while bleeding time is normal

144
Q

Causes of abnormal coagulation

A

1) Liver diseases - almost all clotting factors are formed by the liver

2) Vitamin K deficiency - insufficiency of clotting factors II, VII, IX and X.

3) Congenital deficiency of clotting factor
- hemophilia congenital deficiency of factor VIII or IX or XI

145
Q

Congenital clotting factor deficiencies

A

1) Parahemophilia - deficiency of factor V
2) Afibrinogenemia - deficiency of fibrinogen
3) Hypothrombinemia - decreased prothrombin synthesis by the liver, usually in Vitamin K deficiency

146
Q

Causes of Vitamin K deficiency

A

1) Liver disease - failure to secrete bile
2) Failure of absorption in case of:
- obstruction of bile ducts so no bile reaches the intestine
- chronic diarrhea
- GIT disease as a result of poor absorption of fats

3) Deficient intestinal bacteria in case of
- prolonged use of antibiotics
- newly born infant

4) Anticoagulant drugs

147
Q

What is hemophilia?

A

Inherited sex-linked anomaly, transmitted by females
-females show no symptoms, males manifest signs of the disease
- symptoms usually begin early in life
-slight injury causes severe hemorrhage

148
Q

Types of hemophilia

A

1) Hemophilia A (classical):
- It is due to deficiency of factor VIII
- represents 85% of hemophilic patients

2) Hemophilia B
- due to factor IX deficiency (Christmas disease)

3) Hemophilia C
- due to factor XI deficiency

149
Q

Pathological findings of hemophilia

A

1) Bleeding either from natural orifices or after injury or incisions

2) Recurrent hemarthrosis - bleeding in joints, preceded by minor injury leading to crippling deformity due to fibrous adhesions

150
Q

Treatment of hemophilia

A

supplying the patient with the deficient clotting factor

151
Q

what is intravascular thrombosis

A

Abnormal clot formation inside the blood vessel is called thrombus

152
Q

Causes of intravascular thrombosis

A
  1. Sluggish blood flow: It allows activated clotting factors to accumulate instead of being washed away.
  2. Damaged or roughened endothelial surface of a vessel as in atherosclerosis.
  3. As a complication of septicemia or extensive tissue damage.
  4. Imbalance between clotting-anticlotting systems.
  5. Factor V Leiden: an inherited disorder which is an abnormal form of factor V caused by mutation in the gene that makes clotting factor V.

Factor V Leiden is resistant to the action of activated protein C (APC), so it leads to increased risk of developing blood clots in legs (DVT) or lungs (PE). These blood clots can be life-threatening.

153
Q

Effect of intravascular thrombosis

A

1) blood vessel occlusion due to thrombus enlargement

2) formation of embolus in distant sites

3) block of vessel prevents blood flow and oxygen to tissues and organs - leads to organ damage and failure

154
Q

Differentiate between Hemophilia and purpura

A

Heredity
Hemophilia: congenital
Purpura: not congenital

Sex
Hemophilia: males
Purpura: males + females

Cause
Hemophilia: lack of clotting factors purpura: diminished platelets

PT
Hemophilia: normal
Purpura: normal

aPTT
Hemophilia: prolonged
Purpura: normal

Bleeding time
Hemophilia: normal
Purpura: prolonged

155
Q

Role of neutrophil in inflammatory reaction

A

1) Neutrophils produced by bone marrow leave bloodstream by diapedesis

2) They are attracted by chemotaxis to:
- C5a
- leukotrienes and polypeptides from lymphocyrtes

3) Neutrophils migrate towards site of inflammation via ameboid movement

4) phagocytosis of bacteria

156
Q

Phagocytosis of bacteria by neutrophils

A
  • a single neutrophil can phagocytize 3-20 bacteria before death
  • contain proteases and antimicrobial molecules that kill ingested organism
  • synthesize toxic oxygen metabolites like superoxide radical and hydrogen peroxide and hypochlorous acid. These are strong oxidants

formation of killing zone that destroys organism

157
Q

Function of eosinophils

A
  • First line of defense against parasites
  • Exhibit diapedesis, chemotaxis, and weak phagocytosis
  • Target certain tissues such as skin, lungs, urinary tract and GIT
  • secrete lysozymes, ROS, interleukins and leukotrienes
158
Q

Function of basophils

A
  • Contain IgE and are involved in allergic reactions

a. release histamine and other mediators to initiate inflammation

b. release heparin which prevents blood coagulation by acting as a cofactor for anti-thrombin II.
Heoarin may also exert anti-inflammatory effects

c. involved in type 1 hypersensitivity which range from mild urticaria to severe anaphylactic shock

159
Q

what is IgE?

A
160
Q

Function of monocytes

A
161
Q

Function of lymphocytes

A
  • form the core of immune system
  • 2% found in peripheral blood and the rest in the lymphoid tissues

functions:
- B lymphocytes are responsible for humoral immunity. Each B-cell produces immunoglobulins with a single antigenic specificity.
- T-lymphocytes are responsible for cell mediated immunity. They attack and kill virus-infected cells as well as malignant cells. They facilitate antibody production by B-cells.

Blood Module (9 decks)

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