Physiology Notes: From B Lymphocytes to the Auditory Cortex

Posted on Aug 24, 2024 in Biology

Activation of B lymphocytes

2. Describe the absorption, function and effect of deficiency of vitamin B12

Absorption: It is absorbed in the lower ileum. Its absorption needs intrinsic factor secreted by the stomach. The intrinsic factor binds the vitamin and together they bind to specific receptorsthe the vitamin is absorbed by endocytosis. It is stored in the liver.Function: It is essential for the synthesis of DNA and maturation of RBCs. It is important for the formation of myelin sheath.
Deficiency: Failure of nuclear maturation and division of erythroblasts in the bone marrow. The erythroblasts increase in size (megaloblasts) with shorter life span. The cells become large in size with decreased number thus producing macrocytic anemia. It is accompanied by neurological symptoms. Deficiency of intrinsic factor produces macrocytic anemia called pernicious anemia which is treated by vitamin B12 injections.

3. Explain the functions of interferons

1- The α and β replication in other non infected cells. 2- The gamma interferons are released from lymphocytes exposed to malignant cells and they function to protect the body against cancer by inhibiting cell division, inhibition of protein synthesis and activation of natural killer cells.

B- Describe three characteristics of the graded potential. 1. Depolarization or hyperpolarization

With stimulation, certain gated channels are activated & opened, resulting in influx or efflux of ions for which the channel is specific:* Opening of Na⁺ channels ® influx of Na⁺ into nerve fiber ® ¯ negativity in this area = depolarization.* Opening of K⁺ channels ® efflux of K⁺ out of nerve fiber ® ­ negativity in this area = hyperpolarization.

2. Graded

The magnitude of the local response is proportional to the intensity of the stimulus. The stronger the stimulus, the greater the number of opened channels.

3. Summation:

If additional subthreshold stimuli occur before the local response dies away, they are added to the depolarization created by the first stimulus. There are 2 types:a.

Temporal Summation

where several successive stimuli are applied rapidly after each other.b.

Spatial Summation

where several simultaneous stimuli are applied in close proximity to each other.

The phases of the cardiac cycle
:
1-

Isovolumetric ventricular contraction phase:

The ventricles contract while the AV and the semilunar valves are closed. The ventricular volume is constant because blood is not compressible. The tension in the ventricular walls increases and the ventricular pressure increases. 2-

Ventricular ejection phase

Once the raising ventricular pressure exceeds the pressure in the aorta and pulmonary arteries the semilunar valves open. The blood is ejected into the arteries and the contracting ventricles shorten. The pressure in the ventricles decreases as the blood passes from the ventricles to the arteries.
The stroke volume (SV) is the amount of blood ejected by each ventricle per stroke (beat). It equals 70 ml.3-

Isovolumetric ventricular relaxation phase:

When the ventricular pressure falls below the pressure in the arteries the semilunar valves close. The ventricles relax without change in their volume and the pressure decreases more.4-

Ventricular filling phase:

When the atrial pressure exceeds the ventricular pressure the AV valves open permitting the ventricles to fill. This phase is divided into 3 parts: 1-

Rapid filling

Where the flow of the blood from atria to ventricles is very rapid. 2-

Reduced filling

The flow of the blood from the atria to the ventricles slows down, and when the inflow is almost at a standstill it is called diastasis.
3-

Atrial systole:

which occurs at the end of diastole to propel additional amount of blood to the ventricles. About 70% of ventricular filling occurs in the early diastole before atrial contraction.

6. Describe the glial cells of the central nervous system and their different functions

A. Astrocytes = Astroglia:

Have small cell bodies & extensively branching processes.
Functions:1. Help regulate composition of extracellular fluid (ECF) in CNS.2. Some of their processes form “end-feet”, which are close to cerebral blood capillaries → form a barrier around capillaries (blood-brain barrier) → prevents toxins & other substances from entering brain.

B. Microglia

Scavenger cells (= phagocytic cells) of CNS.Activated by injury or inflammatory processes: On activation, they migrate to area of injury to become macrophages & clean cellular debris.

C. Oligodendrocytes = Oligodendroglia

They cover axons in central nervous system (CNS).Unlike Schwann cells, they may branch to form myelin on up to 40 axons.

4. Draw the action potential. Describe the ionic bases of each phase of the action potential (10 marks)

5. Describe the structure of the sarcotubular system and its role in excitation-contraction coupling in the skeletal muscle.

Sarcotubular System: It is composed of:

1. Transverse (T) Tubules

– They are an extensive network of tubules. – They surround each myofibril at the junction between A & I bands.- They eventually join the plasma membrane, where their lumina open to ECF.- They carry depolarization from surface of muscle fiber to the interior.- They contain a voltage sensitive protein called the dihydropyridine (DHP2. Sarcoplasmic Reticulum (S.R.):–
It forms a series of sleeve-like segments around each myofibril.- At the end of each segment there are 2 enlarged parts known as “lateral sacs”.- It is a modified endoplasmic reticulum, as it is the site of storage of Ca2+. Ca2+ is released following membrane excitation.- It contains a Ca2+ release channel called the ryanodine receptor.
– Its membrane contains Ca2+-ATPase (Ca2+ pump) which transports Ca2+ from I.C. Fluid back into S.R., keeping Ca2+ concentration in the sarcoplasm low.

Its role in excitation-contraction coupling

Action potentials are propagated from the plasma membrane of the ms. Fiber into its interior via the lumen of the T-tubules.→ AP activates the voltage sensor in the DHP receptor→ triggers unlocking of the ryanodine receptor Ca2+ channel in SR→ Ca2+ is released from lateral sacs of SR into sarcoplasm → activates contraction by attaching to troponin.- A contraction continues until Ca2+ is removed from sarcoplasm byCa2+-ATPase, which pumps Ca2+ back into SR.

a- Describe the complement system. Explain how it is activated and what is its function? A- The Complement system:1- They are family of plasma proteins that are inactive enzymes.2- They circulate in the blood in an inactive form.3- They are identified by numbers e.G. C1, C2, C3, …They are activated by 2 ways:a- Antigen-Antibody reaction (Classic pathway).B- Alternative pathway:In this pathway complement system is activated by repetitive sugar structures such as the polyfructose and polyglucose structures present in bacterial and viral cell membranes.5- The complement system is activated in a cascade manner.Functions of activated complement system:a- Lysis of foreign organisms:Active complement enzymes C5-C9 are inserted in the microbial cell membrane like a circle forming a pore in the center which allows the passage of water and lysis of cells (membrane attack complex).B- Opsonization:Active C3 attaches the organism to the phagocyte thus promoting phagocytosis.C- Chemotaxis: They attract phagocytes to the site of the infection.

b- Describe the ventricular filling phase of the cardiac cycle.
Define the end diastolic volume (EDV) 2b- Ventricular filling phase: When the atrial pressure exceeds the ventricular pressure the AV valves open permitting the ventricles to fill. This phase is divided into 3 divisions.1- Rapid filling: during it 70% of the blood passes from the atria to ventricles by pressure gradient.2- Reduced filling: during it the flow of the blood to the ventricles is very slow (almost stops), so it is called diastasis.3- Atrial systole: it occurs at the end of diastole to propel additional blood to the ventricles. End diastolic volume (EDV): is the amount of blood present in each ventricle at the end of diastole. It equals 135 ml. 

a- Describe the cross-bridge cycle in skeletal muscles. 1. Binding of actin to myosin:  For the myosin head to bind to actin, it must contain ADP & P_i. This activates or “energizes” the head, i.E., it stands in a “cocked” position (upright) allowing it to bind to actin & form a cross-bridge. 2. Bending of cross-bridge & sliding of actin over myosin:  – Once a myosin head binds to actin, it undergoes a conformational change: it bends in a forward direction ® it pulls the thin filament toward the center of the sarcomere in a power stroke (= sliding of actin over myosin) ® tension is produced in the thin filament. – The energy used for bending is obtained from ATP.  ADP & P_i are now released.3. Release of cross-bridge from actin: ATP binds to myosin. This weakens the binding of myosin head to actin ® the head is released from actin.  If no ATP is available, thick & thin filaments cannot separate.4. Return of cross-bridge to energized state: ATP is split into ADP & P_i, which remain attached to myosin. They cause the head to become energized (“cocked”) again for a new cycle, and the energy is stored for the next power stroke.

A- Discuss monocyte-tissue macrophage system. Monocytes:

1- They are formed in the bone marrow.2- They have kidney shaped nucleus. They circulate in the blood for 72 hours then pass through capillaries to the tissue spaces. They require 8 hours to swell, increase in size, develop large number of lysosomes and become tissue macrophages.
They do not return back to circulation. The monocytes and tissue macrophages are phagocytic cells. So they are the precursors of tissue macrophages and together they constitute the monocyte-macrophage system. 

A- Discuss presynaptic and postsynaptic mechanisms involved in synaptic plasticity. 1. Calcium concentration

With high frequency stimulation of presynaptic neuron, Ca²⁺ removal is not fast enough ® ­ Ca²⁺ conc. ® ­ NT release ® ­ number of ion channels opened in postsynaptic neuron ® ­ amplitude of EPSPs & IPSPs. It is the basis of immediate memory.

2. Presynaptic receptors:

A 3^rd neuron ends on a presynaptic knob & acts on presynaptic receptors → it influences the activity of the presyn. Neuron.A.

Presynaptic facilitation

3^rd neuron releases an excitatory NT, e.G., serotonin ® ­ release of NT by presynaptic neuron. Its effect lasts for up to 3 weeks ® basis for memory & learning.B.

Presynaptic inhibition

3^rd neuron releases an inhibitory NT, e.G., GABA ® ¯ release of NT by presynaptic neuron. Neighbouring neurons can inhibit each other, thereby accentuating the stimulation of specific postsynaptic neurons.

3. Autoreceptors

They are present in presynaptic neuron. They are activated by NT released from the same presynaptic neuron. Their stimulation results in inhibition of release of more NT (= negative feedback inhibition).

B. Postsynaptic Mechanisms Affecting Synaptic Strength: 1. Up- and down-regulation of receptors:

The number of receptors is not constant.  It increases­ with up- & ¯ with down-regulation ® ­ or ¯ sensitivity of synapse.

2. Receptor desensitization:

(In some conditions, receptors respond once & then temporarily fail to respond, despite continued presence of NT.

3. Effect of co-transmitters and neuromodulators:

They may be secreted together with NTs from presynaptic neuron & modify the response of the postsynaptic neuron to a specific NT.

B- Discuss the mechanism of hearing

1. Propagation of sound to inner ear

  Air waves strike ear drum ® It vibrates back & forth ® Ossicles in middle ear vibrate & transmit sound waves to cochlea by moving oval window in & out.  

2

Movement of organ of Corti

In & out movement of oval window by ossicles creates pressure waves in the fluid of scala vestibuli called “travelling waves”.  Pressure wave is transmitted through Reissner’s membrane into scala media to basilar membrane into scala tympani. Pressure is relieved by bulging of round window.  Vibration of basilar membrane causes up & down movement of organ of Corti.

3. Stimulation of hair cells:

  The basilar membrane is more elastic than the tectorial membrane ® Vibration of the basilar membrane causes the stereocilia of hair cells to bend by a shearing force as they push against the tectorial membrane.   Bending of stereocilia of hair cells ® opens K⁺channels ® depolarization ® opens V-gated Ca²⁺ channels ® release of the NT glutamate.

4. Stimulation of auditory nerve (part of VIII cranial nerve)

b-Define rhythmicity. Describe (with the help of a diagram) the different phases of the pace maker action potential explaining the cause of each phase–

Definition of Rhythmicity

It is the ability of the cardiac muscle to initiate its own impulses regularly independent of any nerve supply.
The pace maker action potentialThe SAN has unstable membrane potential which is called diastolic prepotential The cause of the diastolic prepotential is:
a- Decreased K⁺ efflux (end of repolarization of previous action potential so K⁺ channels gradually close)b-Activation of unusual channel called funny (f) channel this channel is called funny for 2 causes: 1- It is activated (turned on) by the repolarization from the preceding action potential. Thus ensuring that each action potential in the SAN will be followed by another action potential 2- It can pass both Na⁺ and K⁺.The opening of f- channels produces inward current and the membrane begins to depolarize forming the first part of the membrane prepotential.C- Opening of the T-type Ca²⁺ channels (T for transient).Once the firing level is reached (about -40 mV) the action potential is produced.The depolarization is due to the opening of L–type Ca²⁺ channels.The repolarization is due to the opening of K⁺ channels.

A- Describe the steps of the systole (contraction) of the cardiac muscle.1-

The action potential spreads into the interior of the cardiac muscle via T-tubules.
2- The action potential in the T-tubule opens voltage-gated Ca²⁺ channels in the T-tubule membrane itself (the L-type Ca²⁺ channels)
3- The T-tubules are continuous with the extracellular fluid so Ca²⁺ diffuses from extracellular fluid through these channels to the cells causing increase in the cytosolic Ca²⁺ concentration.
4- Ca²⁺ binds to calcium-receptors on the external surface of the sarcoplasmic reticulum (SR) membranes. These receptors contain intrinsic Ca²⁺ channels

. 5-

This binding opens these Ca²⁺ channels allowing diffusion of Ca²⁺ from SR to the cytosol (Calcium-induced calcium release).

B- steps of diastole of the cardiac muscle

Diastole begins at the end of plateau due to: 1- Closure of L-type Ca²⁺ channels. 2- Active transport of Ca²⁺ back into SR (Ca²⁺ATPase pump).3- Small amount of Ca²⁺ (equal to the amount entered from outside) is transported out of the cell by Ca²⁺ ATPase pump and Ca²⁺/Na⁺ exchanger which exchanges intracellular Ca²⁺ for extracellular Na⁺. The rate of this exchange is proportional to the concentration gradient.

B- The role of the arterial baroreceptors in the regulation of the arterial blood pressure. If ABP rises

:

1- The rate of discharge of impulses from baroreceptors increases and the CVC is more stimulated. This leads to decreased sympathetic and increased parasympathetic activity.   2- Decreased sympathetic supply to the heart will decrease HR and SV thus decreasing COP. Decreased sympathetic supply to the arterioles decreases VC and thus decreases the TPR. Decreased sympathetic supply to the veins decreases venoconstriction and increases the venous capacity thus decreases the venous return and EDV and as a result decreases the COP.3- The increased parasympathetic stimulation will decrease HR thus decreasing the COP. 4- The decrease in COP and TPR will decrease the ABP back to normal.

If the ABP drops:

1- The rate of discharge of impulses from baroreceptors decreases and the CVC is less stimulated.2- This leads to increased sympathetic and decreased parasympathetic stimulation which produces increased COP and TPR thus elevating the ABP back to normal.

A. Describe the mechanism of synaptic transmission

1.
Action potential arrives at presynaptic knob. 2.
Opening of voltage-gated Ca²⁺ channels by depolarization ® influx of Ca²⁺ according to concentration gradient.

N.B

I.C. [Ca²⁺] is kept low by a Ca²⁺ pump which extrudes Ca²⁺.3.
Movement of vesicles toward their docking sites in the active zone when Ca²⁺ binds to their membrane. 4.
Fusion of vesicles to active zone by formation of complexes between  the SNARE proteins on the vesicles & those on presynaptic membrane. 5.
Release of NT by exocytosis into synaptic cleft. 6.
Diffusion of NT across synaptic cleft. 7.
Binding of NT to its receptor in postsynaptic membrane. 8.
Opening of ligand-gated ion channels.
9.
Removal of NT from synaptic cleft terminates action of NT by: a. Active reuptake b. Enzymatic destruction c. Passive diffusion  d. Removal by glial cells.

B. Discuss autonomic cholinergic receptors (definition, types, sites)

They are receptors activated by acetylcholine.There are 2 different types of cholinergic receptors:
A.

Nicotinic Receptors

Are found in1. Autonomic ganglia, i.E., in membrane of postganglionic neurons2. At adrenal medullaB.

Muscarinic Receptors

Are found in 1. All effectors stimulated by postganglionic parasympathetic NS. 2. At sweat glands (receiving sympathetic cholinergic fibers).

A. How is sound frequency determined by the auditory cortex?

1. Place Principle:

The ear can distinguish between various frequencies because of the structure of the basilar membrane:

A

Narrow & stiff part at the base vibrates maximally with high frequencies.

B

Broad & flexible part at the apex vibrates maximally with low frequencies.

C

Rest of the membrane responds to a wide variety of intermediate frequencies.

D

 The traveling wave causes maximum deflection of the basilar membrane at a specific distance from the oval window (“place”) that is characteristic for a given frequency.  The hair cells stimulated in that place send impulses to auditory cortex in brain, which interprets them as a specific pitch.

2. Tonotopic Organization:

– Each region of the organ of Corti sends impulses to a specific part of the auditory cortex.  – Fibers & nuclei of the auditory pathway show spatial organization, e.G.,neurons responding to low frequency are located on one side of nuclei &  tracts, while those responding to high frequency are located on the other side

4. Name the types of receptors in pre- & postsynaptic neurons that cause and/or influence synaptic transmission.
Describe in details the effect of stimulation of each of these receptors.

 I. 

Types of Receptors in Postsynaptic Neuron

1.

Ionotropic Receptors

Formed of a binding protein that unites with the NT and a ligand-gated ion channel, which may be a Na⁺, K⁺ or Cl^– channel. Their stimulation may result in:

A. Excitatory Postsynaptic Potential (EPSP):

If an excitatory NT (e.G., ACh) binds to its specific receptors, a state of partial depolarization of postsynaptic membrane (= graded potential)
Will occur, as it causes opening of Na⁺ channels.  Na⁺ enters according to its concentration and electric gradients. The inside becomes less negative than at rest, i.E., closer to the firing level and the membrane is said to be “facilitated”.

B. Inhibitory Postsynaptic Potential (IPSP):

If an inhibitory NT (e.G., GABA) binds to its specific receptors, a state of hyperpolarization of postsynaptic membrane will occur, as it causes opening of Cl^– (mainly) or K⁺ channels. Cl^– enters (or K⁺ leaves) according to concentration gradient.  The inside becomes more negative than at rest, i.E., away from firing level. The membrane is said to be “inhibited”. 2.

Metabotropic Receptors

Are receptors linked to G-proteins.  They activate a 2^nd messenger, which has one of the following effects on postsynaptic neuron: a) opens ion channels  b) influences metabolic activities c) binds to the nucleus & influences synthesis of new proteins.  

II.

Types of Receptors in Presynaptic Neuron

1.

Presynaptic receptors

A 3^rd neuron ends on a presynaptic knob and acts on presynaptic receptors. It influences the activity of the presynaptic neuron. Its stimulation may cause:a. Presynaptic facilitation:3^rd neuron releases an excitatory NT, e.G., serotonin.  It increases the release of NT by presynaptic neuron. Its effect lasts for up to 3 weeks and is the basis for memory & learning.B. Presynaptic inhibition:3^rd neuron releases an inhibitory NT, e.G., GABA. It causes decreased release of NT by presynaptic neuron. Neighbouring neurons can inhibit each other, thereby accentuating the stimulation of specific postsynaptic neurons.  2.

Autoreceptors

They are activated by NT released from the same presynaptic neuron. Their stimulation results in inhibition of release of more NT (= negative feedback inhibition).

Concerning Erythropoiesis:

1- Definition: It is the process of the formation of red blood cells. Site: It occurs in the liver and spleen during fetal life. After birth it occurs in the bone marrow of all bones. By the age of 20 the bone marrow of long bones is replaced by fatty tissue thus after the age of 20 erythropoiesis takes place in the bone marrow of membranous bones e.G. The ribs, sternum, vertebrae, pelvis and skull. 2- Iron: Function: Formation of Hemoglobin.Absorption: 1- Most dietary iron is in the Fe³⁺ form.2- It must be reduced to the Fe²⁺ form to be absorbed. This occurs by gastric HCl and vitamin C in the diet.3- Iron absorption occurs in the upper part of the small intestine by an active process. 4- It is transported into mucosal cells by an intra cellular iron carrier. Then it is transported to the blood by an active transport. After absorption it is oxidized to Fe³⁺ form.5- Intestinal cells regulate the amount of iron absorbed. If there is excess amount of iron in the body the active transport mechanism stops .

A-role of erythropoetin hormone:

Erythropoietin hormone is produced by the kidney 85% and the liver 15%.It acts on the colony forming unit-erythrocyte cells, it prevents DNA cleavage and inhibits apoptosis of this cells. Hypoxia stimulates erythropoiesis due to the stimulation of the release of the erythropoietin hormone

4a- Aqueous Humour: Site:

It is the clear transparent fluid in front & to the sides of the lens.

Synthesis:

It is constantly being synthesized and reabsorbed by ciliary processes.Rate of formation: 2-3 ml/s .

Drainage:

From ciliary processes ® pupil ® anterior chamber of eye ® iridocorneal angle ® network of trabeculae (= spaces of Fontana) ® canal of Schlemm ® extraocular veins Functions:
1. Supplies nutrients to avascular structures in the eye, e.G., lens & cornea, & carries away waste products.2. It maintains the intraocular pressure (I.O.P.).

Glaucoma:

Glaucoma is one of the most common causes of blindness.  It is a disease in which IOP rises above 21 mmHg.  It is usually due to ­ resistance to outflow through spaces of Fontanta.

It leads to

– Disturbance of focusing mechanism during near vision- Pressure on axons of optic nerve & retinal artery ® retinal atrophy, severe pain, blindness.

Treatment

1. Eye drops to ¯ secretion of aq. Humour or to ­ reabsorption 2. Surgical: to open the spaces of Fontana

b. Describe the somatosensory cortex.–
It lies behind behind 1^ry motor area (postcentral gyrus)
In the parietal lobe.
– It receives somatic sensations, i.E., from skin and muscles: e.G., touch, pain, pressure, temperature, ms. Position from different parts of body.- The arrangement of cortical neurons is upside-down & crossed.
– Large areas are devoted to hands & lips as they transmit more sensory information than the rest of body

a. Describe (using a diagram) the different phases of the ventricular action potential. Explain the ionic causes of each phase. 1- Initial rapid depolarization and the overshoot (phase 0):
It forms the rapid ascending limb of the action potential. It is due to the opening of voltage-gated Na+ channels. It lasts about 2 ms.

2- Initial rapid repolarization (phase 1): It is due to:

 1- The closure of Na⁺ channels. 2- The opening of transient outward K⁺ channels. These channels produce transient, early outward current (ITO).

3-The prolonged plateau (phase 2):

1- Repolarization slows down forming a plateau, during which the membrane potential is near 0 mv. It is due to the slow but prolonged opening of the voltage gated L-type Ca²⁺ channels. 2-The voltage gated Ca²⁺ channels (L-type) produce inward current so they maintain a prolonged period of depolarization causing a plateau in the action potential. Slow Ca²⁺ channel is activated at membrane potential -30 to -40 mV. 3-The flow of  Ca²⁺ ions into the cell just balances  the outflow of K⁺ out of the cell and keeps the membrane at the plateau level. 4- The second one of potassium channels in the heart is the inwardly rectifying K⁺ channel. This channel at the membrane potential 0 mV (the plateau potential) allows K⁺ influx (entry) but resists K⁺ efflux (outflow), and only at a lower membrane potential than the plateau potential it permits K⁺ efflux.  5- The third type of K⁺ channels is slowly activating K⁺ channel which is activated slowly and is not fully opened until the end of plateau. It allows K⁺ efflux (I Ks). The sum of K⁺ flow by the 2 K⁺ channels is a small net outward current that balances the Ca²⁺ entry & maintains the plateau. This current increases by time.

4- Late rapid repolarization (phase 3) to the resting membrane potential (phase 4): It is due to:

1- The closure of Ca²⁺ channels.  2- K⁺ efflux (outflow) through K⁺ channels:a- Slowly activating channel: It is fully opened now thus allowing large K⁺ efflux.B- The Inwardly rectifying channel: The potential now is lower than 0 mV so the channel permits K⁺ efflux (outflow). So the net current of these 2 K⁺ channels is a big outward K⁺ current which produces rapid repolarization.

B

1. Definition

   
   Accommodation is the process by which the lens increases its curvature for viewing near objects (< 6=””>)
   By becoming more spherical (= ­ diopteric power of lens).
2. The lens possesses an elastic capsule, which tends to make it assume a more spherical shape.
3. 
   

   Under resting conditions (= far vision)

   In the resting eye, light rays from an object at a distance of ³
   6 m are focused on the retina while the lens is flat.  The lens is kept flat because its tendency to become more spherical is opposed by the constant tension of the suspensory ligaments on the lens. The suspensory ligaments are attached to both ring-shaped ciliary body & lens. Thus, they stretch the lens and flatten it.
4. 
   

   During near vision

   The lens becomes more spherical so that the image of the near object falls on the retina.
   

   Mechanism:

    firing of parasympathetic nerves to ciliary muscle ® contraction of ciliary muscle, producing a sphincter-like action ® relaxation of ligaments holding the lens, resulting in ¯ pull on lens® relaxation of lens capsule, so that lens becomes more spherical ® near objects are brought into focus on retina.
   

   N.B

   Changes in curvature of lens during accommodation affect mainly the anterior surface of the lens!!
5. 
   

   Power of accommodation

   It is the difference between the power of lens during far vision (20 D) & near vision (34 D).

2. Define the cardiac output, mention its equation and discuss the factors which control it.Definition:

It is the volume of the blood pumped by each ventricle per minute.
The COP= Heart rate (HR) x The Stroke volume (SV).

Control of COP:  A- Control of heart rate (HR):

1-

Parasympathetic stimulation

It inhibits the heart rate 2-

Sympathetic stimulation

It increases the heart rate 3-

Epinephrine hormone:

It is released from the adrenal medulla .It acts on the same receptors as norepinephrine thus producing the same effect.

B- Control of Stroke volume (SV):

1-

Changes in EDV (Preload):

The ventricles contract more forcefully during systole when they have been filled to a greater extent during diastole. This means that stretch of the cardiac muscle fibers produces stronger contraction. Frank Starling’ law states that the force of contraction is directly proportional to the initial length of cardiac muscle fiber. In the heart the initial length of the muscle fiber is equivalent to EDV. Thus the greater the EDV the greater the stretch of the cardiac muscle fibers and the more forceful the contraction produced which increases the stroke volume. It is the mechanism that matches COP to venous return.2-

Factors affecting ventricular contraction

The amount of the increase in the intracellular calcium is the major determinant of the strength of cardiac muscle contraction. More intracellular Ca²⁺ means stronger contraction.A- Sympathetic stimulation:It increases the force of ventricular contraction (positive inotropic effect). Norepinephrine acts on ß₁ receptors thus increasing the level of cAMP and facilitating the opening of L- type Ca²⁺ channels. This leads to the increase of Ca²⁺ level inside the muscle fibers thus increasing the force of contraction and consequently the SV.B- Parasympathetic stimulation: It has no effect on ventricular contraction as the parasympathetic supply to the ventricles is negligible.C- Digitalis

:

It increases the force of ventricular contraction. It inhibits Na⁺ K⁺ pump thus increasing the intracellular Na⁺ and decreasing the Na⁺ gradient across cell membrane. This prevents the Na⁺ /Ca²⁺ exchanger from pumping Ca²⁺ to the extra cellular fluid in exchange with Na⁺. This leads to increased intracellular Ca²⁺ and increased force of contraction.D- Epinephrine hormone: It increases the force of ventricular contraction by the same mechanism as norepinephrine.3

– The Afterload

:

It is the resistance against which the blood is expelled. It is equivalent to the arterial blood pressure. The greater the afterload, the less the cardiac muscle can shorten.

Functions of the lymphatic system:

1-Removal of the proteins of the interstitial spaces and return them back to blood. The amount of protein returned is 20-50% of circulating plasma proteins/day.2-Return of excess tissue fluid which is not absorbed at the venous end of the capillary to the circulation. The amount filtered exceeds the amount absorbed by 4 liters/day. Obstruction of lymphatic system leads to accumulation of excessive interstitial fluid (edema) and massive swelling of the involved area (as in the disease Elephantiasis)
.3-Transport of absorbed long chain fatty acids and cholesterol from the intestine to circulation. 4-Important in specific immunity.

2. Discuss the factors which help the venous return against gravity. Explain how increased venous return affects the cardiac output.
Sympathetic stimulation: Veins contain muscle fibers innervated by sympathetic nerves. Sympathetic stimulation produces venoconstriction thus decreasing diameter and capacity of veins leading to increased venous pressure and increased driving force of the blood to the heart. 1-Muscular activity and venous valves:  Contraction of lower limb muscles leads to compression of veins forcing more blood back to the heart. During relaxation the valves close preventing backflow of blood. 2-Respiratory pump: During inspiration the abdominal pressure is increased and this increase is transmitted to the abdominal veins. Also the intra thoracic pressure becomes more negative thus decreasing the pressure in intra thoracic veins. This leads to an increase in the pressure difference and consequently an increase the venous return. The increase in venous return will lead to an increase in the end diastolic volume. This will increase the force of contraction as stated by starling law (The force of contraction is directly proportional to the initial length of cardiac muscle fibers) thus the stroke volume increase increasing the cardiac output.

A. Neuropeptides:

1. Name the receptors stimulated in the inner ear when a dancer is rotating or tilting his head backwards.  Describe the mechanism of action of the receptors under these two conditions.
These receptors include

:

a. Crista ampullaris in the semicircular canals are stimulated during angular acceleration b. Maculae in utricle & saccule are stimulated with bending of the head backwards MECHANISM OF STIMULATION OF CRISTA AMPULLARIS: 1- At rest:
The receptors constantly release neurotransmitters, i.E., there are tonic impulses arising from receptors of SCC to vestibular nerves (VIII cr. Nerve).
2-

With beginning of rotation

:

In the plane of rotation, the bony SCCs & the attached hair cells rotate with the head, while the endolymph lags behind due to its inertia. Thus, the endolymph pushes against cupula and the stereocilia bend in the direction opposite of that of rotation

.

If stereocilia are bent toward kinocilium, the hair cell depolarizes (excitation). If they are bent away from kinocilium, the hair cell hyperpolarizes (inhibition).
3-

With continued rotation

:

After several seconds, the endolymph “catches up” with the movement of the SCC, the cilia return to their upright position and are no longer depolarized or hyperpolarized. 4-

With cessation of rotation

:

The endolymph continues to flow in the same direction of previous rotation due to its own momentum although the bones of SCC are no longer rotating. Thus, there is a false sensation of rotation (= vertigo).

MECHANISM OF STIMULATION OF MACULAE:  At rest:

Otoliths exert uniform pressure on cilia of hair cells. Thus, there is continuous tonic discharge of impulses in vestibular fibers.

With tilting of head

:

The gelatinous otolith material moves according to gravity against hair cells, resulting in bending of the stereocilia & the receptor is either depolarized or hyperpolarized: Bending towards kinocilium causes depolorarization & bending away from kinocilium causes hyperpolarization

.

B- The myelin sheath is formed by the following cells

1. In the peripheral NS (PNS): by Schwann cells 2. In the central NS (CNS): by oligodendrocytes. 

Functions of myelin sheath

1. Myelin sheath helps to insulate axons & prevents cross-stimulation of adjacent axons.2. Myelin sheath allows nerve impulses to travel with great speed down the axons, “jumping” from one node of Ranvier to the next.

A- Explain how the neutrophils perform their function

1- Margination: It is the sticking of the neutrophils to the capillary wall.2- Diapedesis: The cells squeeze themselves through the pores of the capillaries and migrate to the tissue spaces.3- Amoeboid movement: It is the movement by which the cells can reach the invading organisms.4- Chemotaxis: The breakdown products of inflammed tissues and bacterial toxins attract neutrophils to the infected area.5- Phagocytosis: It is the ability of the neutrophil to ingest bacteria forming a phagocytic vacuole byendocytosis. The neutrophil granules: lysosomes (which contain proteolytic enzymes) and the vacuole fuse together forming the phagolysosome. Inside the vacuole the bacteria is destroyed by the lysosomal proteolytic enzymes.

 b- Innumerate different types of plasma proteins and mention their sites of formation. Describe 3 functions of plasma proteins.
 The plasma proteins include:
Albumin, Prothrombin, Fibrinogen all formed completely in liver and Globulins which are divided into α, β formed in liver and γ formed by plasma cells of the lymphoid tissue in the liver, spleen, lymph nodes and bone marrow.

1- Osmotic function:

1-The osmotic pressure of plasma is 5000 mmHg.  2-The osmotic pressure of plasma proteins (colloidal osmotic P or oncotic P) is only 25-28 mmHg, it is mainly due to albumin. 3-This oncotic pressure is very important in the determination of the flow of fluids across the capillary membrane as plasma proteins cannot pass across the capillary membrane because of their large size so they pull water to inside the capillary. 4- The remaining of the 5000 is due to crystalloids (e.G. Sodium, chloride, and glucose) and is called crystalloid P but it is not important because these substances have small size and move freely across the capillary membrane, thus they cause no significant difference in water concentration as the net osmotic effect equals zero. 2-

Transport function

1-It is the function of albumin, α & β globulins.2-They transport many substances e.G. Hormones, vitamins and lipids. 3-

Importance

A- They help in the distribution of these materials.B- They prevent their loss in urine. C- They act as a reservoir of these materials.3-

Defensive function:

 It is the function of gamma globulins

2- The Renin-Angiotensin System:

1-Decreased ABP will decrease the renal pressure and renal blood flow. 2-This will stimulate the kidney to secrete the proteolytic enzyme renin which acts on the plasma globulin angiotensinogen formed by the liverchanging it to angiotensin I.3- Angiotensin I is converted by the angiotensin converting enzyme (ACE)to Angiotensin II. Angiotensin II causes elevation of the ABP by 2 mechanisms:1- It produces powerful VC of the arterioles thus increasing TPR and ABP.2- It stimulates the release of aldosterone hormone from the adrenal gland which results in salt and water retention by the kidney. This leads to increased plasma volume and venous return thus increasing COP and ABPACE inhibitors (e.G., captopril) block the conversion of angiotensin I to angiotensin II and, therefore, decrease the arterial blood pressure.

A- Neuromuscular transmission:

1. The AP in the motor axon reaches the nerve terminal and depolarizes it. 2. This depolarization opens V-gated Ca²⁺ channels in the terminal membrane ® Ca²⁺ ions flow into the axon terminal down their electrochemical gradient.3. This leads to a local rise in free calcium within the axon terminal, which triggers the fusion of ACh-containing vesicles with the plasma membrane of the terminal 4. The ACh contained within the vesicles is released into the synaptic cleft by exocytosis 5. ACh molecules diffuse across the cleft and bind to the nicotinic receptors in the MEP.6. When the receptors bind Ach, non-selective cation channels open.  The  amount of Na⁺ entering the muscle fiber is more than the amount of K⁺ leaving it, resulting in local depolarization of the muscle membrane in the MEP region.  This depolarization is called the endplate potential (EPP)
.7. When the MEP is depolarized, local currents cause depolarization of the  adjacent muscle membrane.  When the threshold is reached, an AP is  initiated.  The AP is propagated in the muscle plasma membrane and triggers the contraction of the muscle fiber. 8. The EPP is transient because ACh is degraded rapidly. This prevents ACh from causing multiple muscle contractions.

Breakdown of ACh

 a- Discuss the presentation of antigens and the activation of cytotoxic T lymphocytes during viral infections.1-Presentation of antigens to cytotoxic T cells:
The cytotoxic T cell cannot bind free antigens. The cytotoxic T cells can only bind antigens presented to them as peptide fragments coupled with MHC protein class Ι. So any nucleated body cell can present the antigen for a cytotoxic T cell if it contains endogenous antigens. This occurs in case of body cells infected with viruses. The virus nucleic acid causes the host cell to produce viral proteins inside the cell that are foreign to the cell (endogenous antigens) so they are partially digested into peptide fragments by the proteolytic enzymes (in the proteasomes) and then presented on the cell membrane coupled with MHC protein class Ι.

2- Activation Of cytotoxic T lymphocytes:

The cytotoxic T lymphocytes are activated when their T cell receptor binds to its specific antigen presented to it as peptide fragments coupled to MHC protein class Ι. After the activation of the cytotoxic T lymphocytes they proliferate and differentiate into clone of cells. These cells include 2 types:a-

Activated cytotoxic T lymphocytes

They destroy the antigen directly by lysis due to the insertion of pore forming proteins (perforins).  b

– Memory cells:

They remain dormant inside the body and on second exposure to the same antigen they proliferate rapidly producing more rapid and powerful response.   

B.Parasympathetic function in: A. In Head & Neck: 1. Oculomotor Nerve = III Cranial Nerve:

a. Contraction of constrictor pupillae ms. ® makes pupil smaller b. Contraction of ciliary ms. ® allows lens to become more convex for near vision 2. Facial Nerve = VII Cranial Nerve:
a. Secretion of lacrimal, nasal and salivary glande  b. VD of the blood vessels of the same glands 3. Glossopharyngeal Nerve = IX Cranial Nerve:
a. Secretion of parotid gland (another salivary glande b. VD of  the blood vessels of parotid gland B. In Thorax & Abdomen:1. Heart:
  a. ¯ all atrial properties (vagus does not supply the ventricles) b. VC of coronary arterioles 2. Lungs:
a. Contraction of bronchial muscles b. VD of pulmonary arterioles.

3. GIT:

a. ­ motility of oesophagus, stomach, small intestine, proximal part of large intestine b. Relaxation of sphincters c. VD of blood vessels 4. Gall Bladder:
 Contraction of gall bladder & relaxation of its sphincter C. In Pelvis:  1. Defecation:
 Contraction of wall of rectum & relaxation of internal anal sphincter 2. Micturition: 
Contraction of bladder wall & relaxation of internal urethralsphincter 3. Male Genital System:
 Erection due to VD of blood vessels in penis 4. Female Genital System:
 VD.

B. The functions of sympathetic nervous system in the head & neck and in the pelvis

In Head & Neck

: 1.

Eye

A. Contraction of dilator pupillae ms. ® widens pupil (= mydriasis)  b. Relaxation of ciliary ms. ® makes lens flat for far vision 2.

Skin

A. Secretory fibers to sweat glands b. Vasoconstriction (VC) to cutaneous blood vessels c. Contraction of piloerector ms. ® erection of hair  In Pelvis:
1.
Lower GIT (distal part of large intestestine & rectum): → retention of stools a. Relaxation of wall b. Contraction of internal anal sphincter 2.

Urinary Bladder

→ retention of urine a. Relaxation of bladder wall b. Contraction of internal urethral sphincter 3.

Male Genital System

Ejaculation

b- Functions of sympathetic nervous system in the abdomen 1. Upper GIT (stomach, small intestine & proximal part of large intestine): a. Relaxation of walls b. Contraction of sphinctersc. VC of arterioles of stomach, intestine, kidney, liver & pancreas2. Liver:–
Stimulation of glycogenolysis & gluconeogenesis ® ­ blood glucose level3. Adrenal Gland:–
Preganglionic fibers to adrenal medulla stimulate secretion of catecholamines (E & NE) directly into blood.

B. Functions of sympathetic nervous system in thorax

In Thorax:

1. Heart:

a.­ all cardiac properties (heart rate, contractility, excitability & conductivity) b. Vasodilation (VD) of coronary arterioles 2. Lungs:
 a. Relaxation of bronchial muscles ® opening of airways b. VC of pulmonary arterioles

A- The role of the skin in body temperature regulation. – When the body temperature rises:

1. Perspiration (sweating) helps to remove excess heat from the body, since evaporation of sweat from the skin surface has a tremendous cooling effect (heat of vaporization of water is about 580 Calories/liter). 2. Dilation of cutaneous blood vessels causes more blood to course closer to the body surface, thus allowing excess heat to be lost from the skin surface to surrounding environment by convection.

– When the body temperature drops:

1. Sweat glands constrict. 2. Cutaneous blood vessels constrict, thus conserving heat

Errors of refraction:

 (1)

Emmetropia – normal

Light focuses on retina during distant & near vision.

(2)

Myopia – nearsighted

Light focuses in front of the retina during distant vision & is corrected by a concave lens.

(3)

Hypermetropia – farsighted

Light focuses behind the retina during near vision & is corrected by a convex lens.

(4)

Presbyopia

Is the result of loss of accomodation power of the lens that occurs with aging.  The near point (closest point on which one can focus by accomodation of lens) moves farther from the eye and is corrected with a convex lens.

The iris:The iris pigment restricts the passage of light rays to the pupil. The amount of light entering the eye is proportional to the diameter of the pupil, which is controlled by 2 muscles:A.

Dilator pupillae muscle

It dilates the pupil producing mydriasis:–
It is a radial ms. – Nerve supply: sympathetic – Mydriasis can be induced by:  sympathomimetic drugs, e.G., adrenaline, or parasympatholytic drugs, e.G., atropine.B.

Constrictor pupillae

It constricts the pupil producing miosis.
– It is a circular ms.- Nerve supply: parasympathetic – Miosis can be induced by:  parasympathomimetic drugs, e.G., pilocarpine.