Download Zagazig University

‫جامعة بنها‬
‫كلية الطب البيطرى‬
‫قسم وظائف األعضاء‬
Benha University
Faculty of Veterinary Medicine
Dept. Physiology
First Grade
ANSWER MODEL
First question
Functions of thrombocytes:
1-The primary function of platelets is to maintain of hemostasis by interacting with endothelial cells.
They strengthen the endothelium of blood vessels. They can maintain vascular integrity .
Thrombocytopenia causes petechiae, ecchymosis and bleeding from body surface.
2- They have an important role in blood coagulation by providing platelet factors 3 and by carrying
several coagulation factors on their surface . Also, platelets surface membrane provides the reaction
site for such an in vivo interaction .
3- They are essential for clot retraction, which depends on their contractile protein system.
4- They have role in the inflammatory response through the activation of chemotactic substances and
the release cationic protein and vasoactive amines and other substances such as prostaglandins,
histamine, collagenase, elastase, that initiate or contribute to persistence of an inflammatory response
.
5- They have phagocytic function. They phagocytize small particles and bacteria in human.
6- They stimulate mitogenesis and vessel repair by releasing platelet derived growth factor (PDGF).
7- β-thromboglobulin rleased from α-granules acts as chemotactic agents for granulocytes .
Functions of the red cell membrane
1- It encloses the cellular components and is vital to the survival and function of the red cell.
2- It gives the red cell with its normal deformability to survive during its passage through minute
capillaries of body tissues.
3- It has transport functions and selective permeability to cations regulate the red cell contents and ionic
gradient between the intracellular and extracellular environments.The normal red cell membrane is
nearly impermeable to monovalent (Na+ , K+) and divalent cations ( Ca++ ) thereby maintaining a
high potassium ,low sodium and very low calcium content .In contrast , the red cell is highly
permeable to water and anions ( Cl- , HCO3- ) which are readily exchanged and as a result
erythrocytes behave as perfect osmometers .Glucose is transported without
energy utilization , while larger molecules such as ATP and related compounds do not cross
the red cell membrane although phosphoenol-pyruvate can pass through the red cell membrane
.Complement-mediated hemolysis can disrupt the red cell permeability barrier. Therefore , activation
of complement on the red cell surface causing increase in intracellular monovalent cations and water
that followed by cell swelling leading to colloid osmotic hemolysis .
4-Membrane properties are important in regulation of interaction of the red cell with other cells
(macrophages) or surrounding medium .
5- Several enzymes important to normal red cell function
and survival are found in the membrane.
3-macrophages:
1- Antigen processing and professional phagocytes and can intentialized particle much more rapidly
than other cell phagocytes involving recognition of an antigen by macrophage cell surface
2- Secration of cytokines ,chemokines and growth factors
3- Secration of proteolytic enzymes as proteinase
4- Tissue healing
4-lysosmes
The main function of these microbodies is digestion
Beakdown cellular waste product into simple compound
Second question
Function of albumin
Albumin is important in the regulation and maintenance of colloidal osmotic pressure of
the blood. It responsible for nearly 75% of osmotic pressure of plasma because it is more
numerous and smaller molecules than other types of plasma proteins. Osmotic pressure of
plasma proteins is about 25 mmHg across the capillary wall. Osmotic pressure produced by
plasma proteins is opposed by capillary hydrostatic pressure, thus prevent excessive passage of
fluid to tissues .
Albumin has also an important transport function . It binds reversibly with a large
number of anions and cations . Albumin transports free fatty acids, bile acid, bilirubin and
porphyrins and many drugs such as penicillin, aspirin, burbiturates, histamine and cations such
as calcium and trace elements (copper and Zinc).
Second question
Folic acid is necessary for direct synthesis of DNA, while vitamin B12 is essential for allowing
the cells to utilize folic acid.
Defective nucleoprotein synthesis in vitamin B12 and folate deficiencies leads to
prolonged cell division and maturation stops at the prorubricyte and basophilic rubricyte stages
causing these cells to be larger and more numerous in the bone marrow. Although mitosis is
delayed or slowed due to lack of nucleoprotein synthesis while Hb synthesis occurs normally
leading to extrusion of the nucleus and production of large (macrocytic) erythrocytes .The large
rubricytes are then called megaloblasts and the marrow is called megaloblastic. As a result of
slow rate of erythroid proliferation and moderate decrease in the life span of RBCs, the number
of the RBC count is greatly reduced .
Vitamin K
Vit K needs for their synthesis in liver for factor II,VII,IX,XIII they are stable compounds that are well
preserved in stored plasma
Importance of lung surfactact
1) Lung surfactant decreases the surface tension of the fluids lining the alveoli. Thus it prevents the
collapse of small alveoli. In fact, the surface tension at the air-liquid interface causing collapse of
an alveolus and this effect becomes very much greater as the diameter of the alveolus decrease.
Therefore, the lung surfactant decreases the tension especially in small alveoli, thus decreasing
the pressure required for its expansion. Thereby in the absence of surfactant, lung expansion is
extremely difficult, often requiring intera-pleural pressure from - 20 to - 30 mmHg to overcome
the collapse tendency of the alveoli.
2) Maintaining proper humidity of the alveolar wall.
3) It provides a constant essential factor for easier pulmonary elastic recoil and reducing the work of
breathing during passive expiration.
4) It resisting infiltration of capillary and interstitial fluids into the alveoli because the surface
tension tends to pull fluid into the alveoli from the alveolar wall, thereby absence of surfactant
causing sever pulmonary edema due to accumulation of edema fluid in the alveoli.
5) It emulsifying very small inhaled particles that may have reached the alveoli and thus facilitating
their phagocytosis by macrophages.
Effect of 2,3- diphosphoglycerate (DPG)
DPG is present in large amounts in RBCs, which is a
product of glycolysis. It binds to -chains of deoxyhemoglobin. Binding DPG with Hb shifts the
reaction to the right causing more O2 to be liberated from HbO2.
Formation of carbamino compounds: The formation of carbamino compound is the second form in
which CO2 is transported in the blood. In plasma, CO2 combines will terminal amino groups of
plasma proteins to form carbamino compounds as following:
R – NH2 + CO2  R.NH.COOH
Formation of carbamino compound is also formed by binding reversibly CO2 to amino groups of Hb
to form carbaminohemoglobin as following:
CO2 + Hb.NH2  Hb.NH.COOH
3- Formation of Bicarbonate: About 2.5 ml of tidal CO2 added to the tissues is transported in form
bicarbonate. In plasma small amounts of CO2 are slowly hydrated to H2CO3 because of absence
of carbonic anhydrase . Then H2CO3 is dissociated to HCO3 + H+, then it is buffered by plasma
proteins. A great amounts of CO2 diffuse into RBCs, where it rapidly hydrated to H2CO3 due to
presence of carbonic anhydrase. The carbonic acid that is formed ionizes to produce hydrogen
and bicarbonate ions. The produced hydrogen ions are buffered by Hb and bicarbonate ions
diffuse from RBCs to plasma, therefore reversible reaction is kept moving to the right as
following:
H2O + CO2  H2CO3  HCO3 + H+
DeoyHb binds more H+ than oxyHb, therefore, release of O2 from Hb at tissues increases the
buffering capacity of Hb. Since oxyhemoglobin is a stronger acid than deoxy Hb. Thus oxyHb
holds K+ ions to from KHbO2. Binding of H+ with oxyHb, displacing K+ which combines with
HCO3.
Iron deficiency anemia
Pernicious anemia
It is caused by iron deficiency
It is caused bv failure of Vit.B12
RBCs,Hb conc.and PCV are reduced
absorption due to deficiency of
intrinsic factor .
MCV,MCH and MCHC are reduced
RBCs,Hb conc.and PCV are reduced
RBCs are microcytic hypochromic
MCV,MCH are increased
Not Associated with pancytopenia
wheareas,MCHC is normal
RBCs are macrocytic normochromic
Associated with pancytopenia
Hemoglobin
Myoglobin
Hemoglobin (Hb) is the red
Myoglobin is an iron-containing pigment
Oxygen-carrying pigment in RBCs
present in skeletal muscles. It is consists
one heme and one globin. When this
of vertebrates. Hb is a complex
monomeric molecule is exposed to high
iron-containing, conjugated protein
O2 tension, it binds to one O2 molecules.
composed of pigment and simple
This O2 molecule will remain attached to
the myolglobin as long as the O2 tension
protein. It consists of 4 heme and
remains high and O2 release from
globin. It contains 4 ferrous iron so
myoglobin occurs at very low O2 tension
it can bind to 4 O2 molecules
.On other word, myoglobin remains fully
.Oxygen-dissociation curve is Sshaped.
saturated with O2 until very low O2
tension, it becomes desaturated and O2
release from myoglobin to the muscles.
So, O2 dissociation curve is extremely
shifted to the left of Hb curve to be
hyperbolic curve (rectangular hyperbola).
It takes up O2 from blood Hb and
becomes fully saturated at low PO2
(about 40 mmHg). Thus it acts as O2
store in skeletal muscles which become
available to active muscles during
exercise when O2 tension is markedly
decreased
Resting volume of the lung
Residual volume
4- Residual volume (RV) is the volume
It also called functional residual
of air that remains in the lungs after
capacity (FRC). Is the volume of air that
maximal expiration. It is normally about
remaining in the lung at the end of
1200 ml in humans.
normal expiration about 40% of TLC.
Importance of RV:
FRC = RV + ERV
A- It provides air in the alveoli to
aireate the blood between
breathes that prevents
fluctuation (changes) in
alveolar and arterial oxygen
during breathing.
B- It increases in some respiratory
diseases such as bronchial asthma and
emphysema
Oxygen content
- This is the amount of O2 present in 100
Oxygen capacity
it is the amount of O2 that is present in
ml blood in chemical combination 100 ml blood in chemical combination
with Hb it depends on the O2 tension with Hb when Hb is fully saturated with
and Hb content of blood.Arterial O2 and depends on Hb content only. It
blood; under normal condition the can be calculated as following:
PO2 is about 100 mmHg and the
percent saturation of Hb is about
- If the concentration of Hb in blood is 15
g/dl.
97.5%, the O2 content is about 19.5
ml/dl .
- Each gram of Hb can combine with 1.34
ml O2, therefore capacity of blood
- Venous blood: under normal condition,
the PO2 is about 40 mmHg and
percent of saturation is about 70 %,
the O2 content is about 14 ml/dl .
equals 20 ml/dl when Hb is fully
saturated with O2 (O2 tension is high
enough causing full saturation of
hemoglobin with O2 ) .
active transport
Pumping of ions or other substance
across the membrane in combination with
protein carrier (need sourse of energy)but
additional against concentrationgradient
such as from low concentration to high
states conc
.
aneamic hypoxia
Secondary active transport
It is called facilitated diffusionThe
molecules cobine with a carrier in the cell
membrane. The diffusion can move only
from a higher conc. Toward a low conc.It
depends on amount of carrier, temp., and
conc. Gradient.`For example Na-glucose
or Na-amino acid carriers at intestine and
kidney.
Hypoxic hypoxia
Caused by decrease in the
Decrease in O2 at tissue level in which
amount of functioning Hb
the arterial PO2 is abnormal low
Caused by
1- co poising
1- decrease PO@ in inspired air as
2-decrease of Hb or
breathing O2 poor gas mixture at high
erythrocyte production
altitudes
3-formation of MetHb
2- hypoventilation caused by paralysis of
respiratory muscle or air way obstruction
3- impairment of alveolar capillary
diffusion
4- shunting of venous blood into arterial
circulation
Hormonal factors :
1- Multi-colony stimulating factor, This nonspecific growth factor is also known as
interleukin 3 (IL3) . Multi-CSF only acts early in the level stem cells, but certainly at the
level of myeloid progenitor cells . It is produced by T lymphocytes.It is essential for
providing the bone marrow with cells that are responsive to erythropoietin.
2- Erythropoietin: It is a glycoprotein hormone that stimulates erythropoeisis by acting on bone
marrow stem cells. It is synthesized primary in the kidney (90%) and in the liver (10%) in
response to hypoxia .
Actions of erythropoietin :
-Stimulates the differentiation of stem cells into pronormoblasts .
- Stimulates the rate of maturation of normoblasts .
- Stimulates the rate of Hb synthesis .
- Stimultes premature release of reticulocytes from bone marrow.
Factors increase level of erythropoietin
Generally, low O2 tension or hypoxia stimulates renal tissue to increase erythropoietin
synthesis, while increased O2 tension reduces the erythropouetin release .
- All types of anemia except anemia due to renal diseases (uremia).
- High altitude .
- Hypoventilation .
- Cardiovascular diseases .
- Chronic obstructive plumonary disease .
- Hemoglobinopathies with high O2 affinity.
Factors decrease erythropoietin :
- Renal failure .
- Polycythemia vera .
- Endocrine deficiencies, hypothyroidism, hypocorticism, hypogonadism and hypopituitarism
because, hormones of these endocrine glands stimulate erythropoietin production.
3- Corticosteroids and prostaglandins have stimulatory effects on erythropoisis by increasing
the production of erythropoietin hormone as well as activation of erythropoietin - responsive
cells .
4- Thyroid hormones have a definite effect on proliferation of erythroid precursors .
5- Anderogens stimulate erythropoiesis in animals and humans by increasing the production of
erythropoietin hormone .
6- Estrogen inhibits erythropoiesis .
Neural control of respiration
Ordinary respiration occurs involuntary produced by rhythmic discharge of impulses from
respiratory centers to respiratory muscles. However, involuntary respiration may be changed to
voluntary respiration. The voluntary conrol system is located in the cerebral cortex and it controls the
activity of respiratory neurons through corticospinal tracts and bypassing the medullary neurons.
Respiratory centers
Two separate neural mechanisms regulate respiration. One is responsible for voluntary control
and the other for automatic or involuntary control. The automatic system is located in the pons and
medulla and the motor outflow from this system to the spinal respiratory motor neurons that is located in
the lateral and ventral portions of the spinal cord. The respiratory centers in pons and medulla control
the activity of respiratory spinal motor neurons through continuous discharge of impulses through the
descending tracts to the ventral and lateral portions of spinal cord.
Meduallry centers
Rhythmic discharge of neurons in medulla oblongata produce automatic respiration. The area in
the medulla that is concerned with respiration is called respiratory center. There are two groups of
respiratory neurons. The dorsal group of neurons near to the nucleus tractus solitarius and the ventral
respiratory groups is located in the nucleus ambiguus and the nucleus retroambigualis .
A) Dorsal group: These neurons are associated with inspiration. Axons of these neurons pass
through bulbospinal tracts to inspiratory spinal motor neurons that supply the inspiratory
muscles (phrenic motor neurons). These neurons also project to ventral group and
pneumotaxic center .
B) Ventral Respiratory group : This group is composed of two separate nuclei. The cranial one
(nucleus ambiguus), that innervate the accessory muscles of respiration via vagus nerve. The
caudal nucleus (retroambigualis) that provide the inspiratory and expiratory drive to the
motor neurons in the spinal cord to expiratory muscles (intercostal muscles and abdominal
muscles).
There is a reciprocal innervation between DRG and VRG i.e, the motor neurons to expiratory
muscles are inhibited when the inspiratory muscles are activated and vice versa .
Pontine centers :
The rhythmic discharge of the neurons in the respiratory center is spontaneous, but it is modified
by centers in the pons and by afferent in vagus nerves from receptors in the lungs .
Pneumotaxic center :
This center is a group of neurons that are located in the cranial pons, that transmits impulses to
inspiratory center. Destruction of the pneumotaxic center produces a slower, deeper pattern of breathing
in anesthetized animals. With bilateral vegotomy, the breathing becomes apnueustic (arrest of
respiration in the inspiration). It has been thought that pneumotaxic center can affect the rate of
respiration by switching off inspiration to initiate expiration, therefore it limiting the duration of
inspiration or shortening the entire respiratory cycle.
Apneustic center :
This is a group of neurons present in the caudal pons. The precise physiological role of the
pontine respiratory areas is uncertain, but they apparently make the rhythmic discharge of the medullary
neurons smooth and regular. It appears that there are tonically discharging neurons in the apneustic
center which drive inspiratory neurons in the modulla and these neurons inhibited by impulses from
pneumotaxic center and vagal afferents. It is believed that apneustic center is associated with prolonged
deep inspirations (apneusis) .
I- Lung receptors :
A- Pulmonary stretch receptors :
( Hering-Breuer Reflex)
Inflation reflex : Inflation of the lungs leads to inhibition of the inspiration due to inhibition of
inspiratory center and probably the apneustic center . The receptors of this reflex are pulmonary stretch
receptors located in the smooth muscle layer of bronchi and bronchioles. Activation of these receptors
occurs by lung inflation during inspiration. Afferent impulses from the activated receptors are carried in
large myelinted fibers passing through the vagus to the inspireatory neurons to reflexly shorten the
duration of inspiration time and promote expiration. This reflex increases the rate of respiration because
it shortens the period of inspiration.
This reflex has little importance during eupnea, but it was found that this reflex is not activated
unless the tidal volume is more than 1000 ml in human. Therefore, this reflex seems to play important
protective reflex of the lungs by termination of inspiration during hyperpnea (during exercise) to
increase the rate of respiration (tachypnea). Therefore when the vagus nerves are cut, the amplitude of
inspiration is increased and the frequency of breathing is decreased.
Deflation reflex: Sever deflation of the lungs leads to stimulation of the inspiratory center. The
receptors of this reflex is called deflation receptors. These receptors when activated discharge impulses
through vagus nerve to terminate expiration and initiate inspiration. These receptors are located
juxtcapillary (J- receptors).
B- Pulmonary irritant receptors: These receptors located between epithelial cells of the
airways and are inactive drung eupnea (resting breathing). When activated chemically or mechanically
send impulses through vagus nerve to inspiratory center causing rapid shallow breathing by reflex
stimulation of inspiratory center and constriction of airways. These receptors limit penetration of
dangerous agents into the lungs and prevent damage to gas-exchanging surfaces. These receptors are
activated mechanically by lung inflation, sold particles, dusts inhalation of noxious gases or endogenous
substances such as histamine and brady kinin.
at lungs, the high PO2 and the low PCO2 at the alveoli drives the reaction in reverse
direction as following:
O2 + Deoxy Hb + HCO3  CO2 + OxyHb + H2O
at which the CO2 is removed via lungs to outside . The H+ released in the conversion of
deoxyHb to OxyHb is taken up by the conversion of HCO3 to CO2 .
deoxy Hb + O2  oxyHb + H+
H+ + HCO3  H2CO3  CO2 + H2O
In the lungs, where the PCO2 is low, the CO2 is released from carbamino Hb as following :
CO2 + HbNH2  HbNHCOOH
Erythrocyte deformability:
1- Maintenance of biconcave shape
2- Normal internal or Hbfluidity
3- Intrinsic membrane deformability