Physiology

Physiology

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FUNCTIONS OF BLOOD
NUTRITIVE FUNCTION
 Nutritive substances like glucose, amino acids, lipids and vitamins
derived from digested food are absorbed from gastrointestinal tract
 And carried by blood to different parts of the body for growth and
production of energy.

RESPIRATORY FUNCTION
 Transport of respiratory gases is done by the blood.
 It carries oxygen from lungs to different tissues and carbon dioxide
from tissues to lungs.

EXCRETORY FUNCTION
 Waste products formed in the tissues during various metabolic activities
are removed by blood
 They are carried to the excretory organs like kidney, skin, liver, etc. for
excretion.

TRANSPORT OF HORMONES AND ENZYMES

 Hormones which are secreted by endocrine glands are released directly
into the blood.
 The blood transports these hormones to their target organs/tissues.
 Blood also transports enzymes.

REGULATION OF WATER BALANCE

 Water content of the blood is freely interchangeable with interstitial
fluid.
 This helps in the regulation of water content of the body.

REGULATION OF ACID-BASE BALANCE

 Plasma proteins and hemoglobin act as buffers and help in the
regulation of acid-base balance.

REGULATION OF BODY TEMPERATURE

 It is responsible for maintaining the thermoregulatory mechanism in
the body, i.e. the balance between heat loss and heat gain in the body.

STORAGE FUNCTION

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 Water and some important substances like proteins, glucose, sodium

and potassium are constantly required by the tissues.
 Blood serves as a readymade source for these substances.

DEFENSIVE FUNCTION
 Blood plays an important role in the defense of the body.
 The white blood cells are responsible for this function.
 Neutrophils and monocytes engulf the bacteria by phagocytosis.
 Lymphocytes are involved in development of immunity.
 Eosinophils are responsible for detoxification, disintegration and
removal of foreign Substances.

FUNCTIONS OF RED BLOOD CELLS

Following are the functions of RBCs:

Transport of Oxygen from the Lungs to the Tissues

 Hemoglobin in RBC combines with oxygen to form oxyhemoglobin.
 About 97% of oxygen is transported in blood in the form of
oxyhemoglobin.

Transport of Carbon Dioxide from the Tissues to the Lungs

 Hemoglobin combines with carbon dioxide and form carbhemoglobin.
 About 30% of carbon dioxide is transported in this form.
 RBCs contain a large amount of the carbonic anhydrase.
 This enzyme is necessary for the formation of bicarbonate from water
and carbon dioxide
 Thus, it helps to transport carbon dioxide in the form of bicarbonate
from tissues to lungs. About 63% of carbon dioxide is transported in
this form.

Buffering Action in Blood

 Hemoglobin functions as a good buffer.
 Plays a role in the maintenance of acidbase balance

In Blood Group Determination

 RBCs carry the blood group antigens like A antigen, B antigen and Rh
factor.
 This helps in determination of blood group and enables to prevent
reactions due to incompatible blood transfusion.

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Que. FUNCTIONS OF PLASMA PROTEINS

Plasma proteins are very essential for the body.

ROLE IN COAGULATION OF BLOOD

 Fibrinogen is essential for the coagulation of blood

ROLE IN DEFENSE MECHANISM OF BODY

 Gamma globulins play an important role in the defense mechanism of
the body by acting as antibodies.
 These proteins are also called immunoglobulins
 Antibodies react with antigens of various microorganisms and destroy
them.

ROLE IN TRANSPORT MECHANISM

 Plasma proteins transport various substances in the blood.
 Albumin, alpha globulin and beta globulin transport hormones,
enzymes.

ROLE IN MAINTENANCE OF OSMOTIC PRESSURE IN BLOOD

 Plasma proteins cannot pass through the capillary membrane easily and
remain in the blood.
 In the blood, these proteins exert the colloidal osmotic pressure.
 Osmotic pressure exerted by the plasma proteins plays an important
role in the exchange of various substances between blood and the cells
through capillary membrane.

ROLE IN REGULATION OF ACID-BASE BALANCE

 Plasma proteins, particularly the albumin, play an important role in
regulating the acid base balance working as buffer.

ROLE IN VISCOSITY OF BLOOD

 Plasma proteins provide viscosity to the blood, which is important to
maintain the blood pressure.

ROLE IN ERYTHROCYTE SEDIMENTATION RATE

 Globulin and fibrinogen accelerate the tendency of rouleaux formation
by the red blood cells.
 Rouleaux formation is responsible for ESR

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ROLE IN SUSPENSION STABILITY OF RED BLOOD CELLS

 During circulation, RBC remain suspended uniformly in the blood.
 Globulin and fibrinogen help in the suspension stability of the RBC

ROLE AS RESERVE PROTEINS

 During fasting, the plasma proteins are utilized by the body tissues as
the last source of energy.
 Plasma proteins are split into amino acids
 Amino acids are taken back by blood and distributed throughout the
body to form cellular protein molecules.
 Because of this, the plasma proteins are called the reserve proteins.

Erythropoiesis
 Erythropoiesis is the process of the origin, development and
maturation of erythrocytes.

SITE OF ERYTHROPOIESIS IN FETAL LIFE

 In fetal life, mesenchyme of yolk sac, liver and finally the RBCs are
produced from red bone marrow and liver.

 IN NEWBORN BABIES, CHILDREN AND ADULTS- only from the red bone
marrow.
 Up to the age of 20 years: from red bone marrow of all bones
 After the age of 20 years: from membranous bones like vertebra,
sternum, ribs, scapula, and from the ends of long bones.
 The shaft of the long bones becomes yellow bone marrow because of
fat deposition and looses the erythropoietic function.

CHANGES DURING ERYTHROPOIESIS

 Reduction in size of the cell
 Disappearance of nucleoli and nucleus.
 Appearance of hemoglobin
 Change in the staining properties of the cytoplasm.

STAGES OF ERYTHROPOIESIS
Various stages between CFU-E cells and matured RBCs are
 Proerythroblast
 Early normoblast
 Intermediate normoblast.

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 Late normoblast
 Reticulocyte
 Matured erythrocyte.

FACTORS NECESSARY FOR ERYTHROPOIESIS

1. General factors
2. Maturation factors
3. Factors necessary for hemoglobin formation.

GENERAL FACTORS
Erythropoietin
 Most important factor for erythropoiesis is the hormone called
erythropoietin.
 Erythropoietin is a glycoprotein.
Source of secretion
 Major quantity of erythropoietin is secreted by peritubular capillaries of
kidney.
Stimulant for secretion
 Hypoxia is the stimulant for the secretion of erythropoietin.

Actions of erythropoietin
 Increase Production of proerythroblasts from CFU-E of the bone
marrow
 Development of proerythroblasts into matured RBCs
 Increase Release of matured erythrocytes into blood.

Blood level of erythropoietin increases in anemia.

Thyroxine
 Thyroxine accelerates the process of erythropoiesis at many levels.

Hemopoietic Growth Factors

 Hemopoietic growth factors are the interleukins and stem cell factor
which increase RBC formation.

MATURATION FACTORS
 Vitamin B12, intrinsic factor and folic acid are necessary for the
maturation of RBCs.
Vitamin B12
 Vitamin B12 is essential for synthesis of DNA in RBCs.
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 Its deficiency leads to failure in maturation of the cell and reduction in

the cell division.
 Deficiency of vitamin B12 causes pernicious anemia.

Intrinsic Factor of Castle

 Intrinsic factor of castle is produced in gastric mucosa by the parietal
cells of the gastric glands.
 It is essential for the absorption of vitamin B12 from intestine.

Folic Acid
 Folic acid is also essential for maturation.
 It is required for the synthesis of DNA.
 In the absence of folic acid, the synthesis of DNA decreases causing
failure of maturation.

FUNCTIONS OF HEMOGLOBIN
TRANSPORT OF RESPIRATORY GASES
Main function of hemoglobin is the transport of respiratory gases:
1. Oxygen from the lungs to tissues.
2. Carbon dioxide from tissues to lungs.

1. Transport of Oxygen
 When oxygen binds with hemoglobin and formation of oxyhemoglobin.
 When oxygen is released from oxyhemoglobin, it is called reduced
hemoglobin

2. Transport of Carbon Dioxide

 When carbon dioxide binds with hemoglobin, carbhemoglobin is
formed.
 This Combination is reversible, i.e. the carbon dioxide can be released
from this compound.
 The affinity of hemoglobin for carbon dioxide is 20 times more than that
for oxygen.

BUFFER ACTION
 Hemoglobin acts as a buffer and plays an important role in acid-base
balance.

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Que. Anemia
Anemia is the blood disorder, characterized by reduced oxygen carrying capacity of
blood. Which is due to reduced
 Red blood cell (RBC) count or Hemoglobin content

CLASSIFICATION OF ANEMIA
MORPHOLOGICAL CLASSIFICATION
Morphological classification depends upon the size and color of RBC.
 Size of RBC is determined by mean corpuscular volume (MCV).
 Color is determined by mean corpuscular hemoglobin concentration
(MCHC).
Normocytic Normochromic Anemia
 Size and color of RBCs are normal. But the number of RBC is less.
Macrocytic Normochromic Anemia
 RBCs are larger in size with normal color. RBC count is less.
Macrocytic Hypochromic Anemia
 RBCs are larger in size. color is less, so the cells are pale.
Microcytic Hypochromic Anemia
 RBCs are smaller in size with less color.

ETIOLOGICAL CLASSIFICATION
On the basis of etiology, anemia is divided into five types.
1. Hemorrhagic Anemia
Anemia due to excessive loss of blood is known as hemorrhagic anemia.
 Loss of a large quantity of blood as in the case of accident.
 Loss of blood by internal or external bleeding, over a long period of time
ex. peptic ulcer, menorrhagia.
 The replacement of RBCs does not occur quickly.
 Morphologically the RBCs are normocytic and normochromic.

2. Hemolytic Anemia
 Anemia due to excessive destruction of RBCs.
 Which is not compensated by increased RBC production
Extrinsic hemolytic anemia: It is the type of anemia caused by destruction of RBCs by
external factors. Ex. Hypersplenism

Intrinsic hemolytic anemia: It is the type of anemia caused by destruction of RBCs

because of the defective RBCs. Ex Sickle cell anemia, Thalassemia

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3. Nutrition Deficiency Anemia

Anemia that occurs due to deficiency of a nutritive substance necessary for
erythropoiesis is called nutrition deficiency anemia.
 The substances which are necessary for erythropoiesis are iron and
vitamins like B12 and folic acid.
 Iron deficiency anemia- RBCs are microcytic and hypochromic.
 Pernicious anemia- due to deficiency of vitamin B12. Cells are macrocytic
and normochromic/hypochromic.
 Megaloblastic anemia- due to the deficiency of folic acid. The RBCs are
megaloblastic and hypochromic.

4. Aplastic Anemia
Aplastic anemia is due to the disorder of red bone marrow.
 Red bone marrow is reduced and replaced by fatty tissues.
 Bone marrow disorder occurs in Repeated exposure to Xray ,
Tuberculosis, Viral infections like hepatitis
 RBCs are normocytic and normochromic.

5. Anemia of Chronic Diseases

Anemia develops after few months of sustained disease.
 RBCs are normocytic and normochromic.
 Occurs in Chronic infections like tuberculosis, Chronic renal failure, in
which the erythropoietin secretion decreases, Cancer disorders.

SIGNS AND SYMPTOMS OF ANEMIA

 SKIN AND MUCOUS MEMBRANE - Color of the skin and mucous
membrane becomes pale.
 CARDIOVASCULAR SYSTEM There is an increase in heart rate and
cardiac output
 RESPIRATION- There is an increase in rate and force of respiration.
Sometimes, it leads to breathlessness and dyspnea
 DIGESTION - Anorexia, nausea, vomiting, abdominal discomfort.
 KIDNEY- Renal function is disturbed.
 REPRODUCTIVE SYSTEM In females, the menstrual cycle is disturbed.

 NEUROMUSCULAR SYSTEM headache, lack of concentration,

restlessness, irritability, vertigo
 Muscles become weak and the patient feels lack of energy and fatigued
quite often and quite easily.

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FUNCTIONS OF WHITE BLOOD CELLS

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FUNCTIONS OF PLATELETS
Normally, platelets are inactive and execute their actions only when activated.
 Activated platelets immediately release many substances.
 Functions of platelets are carried out by these substances.
Functions of platelets are:
ROLE IN BLOOD CLOTTING
 Platelets are responsible for the formation of intrinsic prothrombin
activator.
 This substance is responsible for the onset of blood clotting.

ROLE IN CLOT RETRACTION

 In the blood clot, blood cells including platelets are entrapped in
between the fibrin threads.
 Cytoplasm of platelets contains the contractile proteins, namely actin &
myosin which are responsible for clot retraction.

ROLE IN PREVENTION OF BLOOD LOSS (HEMOSTASIS)

Platelets accelerate the hemostasis by three ways:
 Platelets secrete 5-HT, which causes the constriction of blood vessels.
 Due to the adhesive property, the platelets seal the damage in blood
vessels like capillaries.
 By formation of temporary plug, the platelets seal the damage in blood
vessels.

ROLE IN REPAIR OF RUPTURED BLOOD VESSEL

 Platelet-derived growth factor (PDGF) formed in cytoplasm of platelets
is useful for the repair of the endothelium and other structures of the
ruptured blood vessels.

ROLE IN DEFENSE MECHANISM

 By the property of agglutination, platelets encircle the foreign bodies
and destroy them.
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Que. ANTICOAGULANTS
Substances which prevent coagulation of blood are called anticoagulants.
 Anticoagulants used to prevent blood clotting inside the body, i.e. in
vivo.
 Anticoagulants used to prevent clotting of blood that is collected from
the body, i.e. in vitro.

1. HEPARIN
Heparin is a naturally produced anticoagulant in the body.
 It is produced by mast cells and Basophils
 Heparin is a conjugated polysaccharide.
It Prevents blood clotting by its antithrombin activity.
 It Combines with antithrombin III and removes thrombin from
circulation
 Inactivates the active form of other clotting factors like IX, X, XI and XII.
Heparin is used as an anticoagulant both in vivo and in vitro.
 In vivo - In clinics it is used to prevent intravascular blood clotting.
 In vitro - In the laboratory Heparin is also used as anticoagulant while
collecting blood for various investigations.

2. COUMARIN DERIVATIVES
Warfarin and dicoumoral are the derivatives of coumarin.
 Coumarin derivatives prevent blood clotting by inhibiting the action of
vitamin K.
 Vitamin K is essential for the formation of various clotting factors,
namely II, VII, IX and X.
Dicoumoral and warfarin are the commonly used as oral anticoagulants

3. EDTA
Ethylenediaminetetraacetic acid (EDTA) is a strong anticoagulant.
 These substances prevent blood clotting by removing calcium from
blood.
EDTA is used as an anticoagulant both in vivo and in vitro.
 Used intravenously, in cases of lead poisoning.
 Used as an anticoagulant in the laboratory

4. OXALATE COMPOUNDS
 Oxalate combines with calcium and forms insoluble calcium oxalate.

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 Thus, oxalate removes calcium from blood and lack of calcium prevents
coagulation.
 Oxalate compounds are used only as in vitro anticoagulants

5. CITRATES
 Citrate combines with calcium in blood to form insoluble calcium citrate.
Citrate removes calcium from blood and lack of calcium prevents
coagulation.
 Citrate is used as in vitro anticoagulant.

TRANSFUSION REACTIONS
DUE TO ABO INCOMPATIBILITY
Transfusion reactions are the adverse reactions in the body, which occur due to
transfusion of incompatible (mismatched) blood.
 In mismatched transfusion, the transfusion reactions occur between
donor’s RBC and recipient’s plasma.
 If the donor’s plasma contains antibody against recipient’s RBC,
agglutination does not occur because these antibodies are diluted in
the recipient’s blood.
 But, if recipient’s plasma contains antibody against donor’s RBCs, the
immune system launches a response against the new blood cells.
 The recipient’s antibodies (IgG or IgM) adhere to the donor RBCs, which
are agglutinated and destroyed.
 Large amount of free hemoglobin is liberated into plasma.
 This leads to transfusion reactions.

Signs and Symptoms of Transfusion Reactions

Non-hemolytic transfusion reaction
 It develops within a few minutes to hours after blood transfusion.
 Common symptoms are fever, difficulty in breathing and itching.
Hemolytic transfusion reaction
 Hemolytic transfusion reaction may be acute or delayed.
The acute hemolytic reaction occurs within few minutes of transfusion.
 It develops because of rapid hemolysis of donor’s RBCs.
 Symptoms include fever, chills, increased heart rate, low blood pressure,
breathlessness, nausea, vomiting, red urine, chest pain, back pain and
rigor.

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 Some patients may develop pulmonary edema and congestive cardiac

failure.
Delayed hemolytic reaction occurs from 1 to 5 days
 The hemolysis of RBCs results in release of large amount of hemoglobin
into the plasma.
 This leads to the following complications.
Jaundice
 Hemoglobin is degraded and bilirubin is formed from it.
 When the serum bilirubin level increases jaundice occurs

Cardiac Shock
 Hb increases the viscosity of blood.
 This increases the workload on the heart leading to heart failure.

Renal Shutdown
 The toxic substances from hemolyzed cells cause constriction of blood
vessels in kidney.
 Free hemoglobin is filtered through glomerular membrane and enter
renal tubules. It damages the kidney.

TRANSFUSION REACTIONS DUE TO Rh INCOMPATIBILITY

 When a Rh negative person receives Rh positive blood for the first time,
he is not affected much, since the reactions do not occur immediately.
 But, the Rh antibodies develop within one month.
 The transfused RBCs, which are still present in the recipient’s blood, are
agglutinated.
 So, a delayed transfusion reaction occurs. But, it is usually mild and
does not affect the recipient.
 However, antibodies developed in the recipient remain in the body
forever.
 So, when this person receives Rh positive blood for the second time,
the donor RBCs are agglutinated and severe transfusion reactions
occur immediately
These reactions are similar to the reactions of ABO incompatibility.

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HEMOLYTIC DISEASE OF FETUS AND NEWBORN –

ERYTHROBLASTOSIS FETALIS
It is due to Rh incompatibility, i.e. the difference between the Rh blood group of
the mother and baby.
 Hemolytic disease leads to erythroblastosis fetalis.

When a mother is Rh negative and fetus is Rh positive.

 Usually the first child escapes the complications of Rh incompatibility.
 This is because the Rh antigen cannot pass from fetal blood into the
mother’s blood through the placental barrier.
 However, at the time of delivery of the child, the Rh antigen from fetal
blood may leak into mother’s blood because of placental detachment.
 Within a month after delivery, the mother develops Rh antibody in her
blood.

When the mother conceives for the second time and if the fetus happens to be Rh
positive again
 The Rh antibody from mother’s blood crosses placental barrier and
enters the fetal blood.
 Thus, the Rh antigen cannot cross the placental barrier, whereas Rh
antibody can cross it.
 Rh antibody causes agglutination of fetal RBCs resulting in hemolysis.
 To compensate the hemolysis of more and more number of RBCs, there
is rapid production of RBCs, not only from bone marrow, but also from
spleen and liver.
 Now, many large and immature cells in proerythroblastic stage are
released into circulation.
 Because of this, the disease is called erythroblastosis fetalis.

Ultimately due to excessive hemolysis severe complications develop, viz.

Severe Anemia
 Excessive hemolysis results in anemia and the infant dies when anemia
becomes severe.

Hydrops Fetalis
 Hydrops fetails is a serious condition in fetus, characterized by edema.
 When this condition becomes more severe, it may lead to intrauterine
death of fetus.
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Kernicterus
 Kernicterus is the form of brain damage in infants caused by severe
jaundice.
 Kernicterus develops because of high bilirubin content.
 The blood-brain barrier is not well developed in infants as in the adults
 So, the bilirubin enters the brain and causes permanent brain damage.

Prevention or treatment for erythroblastosis fetalis

 Anti D should be administered to the mother at 28th and 34th weeks of
gestation, as prophylactic measure.
 If Rh negative mother delivers Rh positive baby, then anti D should be
administered to the mother within 48 hours of delivery.
 This prevents the formation of Rh antibodies in mother’s blood.
 If the baby is born with erythroblastosis fetalis, the treatment is given
by means of exchange transfusion Rh negative blood

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NON-RESPIRATORY FUNCTIONS OF RESPIRATORY

TRACT
Besides primary function of gaseous exchange, the respiratory tract is involved
in several non respiratory functions of the body.

1. OLFACTION
 Olfactory receptors present in the mucous membrane of nostril are
responsible for olfactory sensation.

2. VOCALIZATION
 Along with other structures, larynx forms the speech apparatus.
 larynx plays major role in the process of vocalization. Therefore, it is
called sound box.

3. PREVENTION OF DUST PARTICLES

 Dust particles, which enter the nostrils from air, are prevented from
reaching the lungs by filtration action of the hairs in nasal mucous
membrane.
 Particles are thrown out by cough reflex and sneezing reflex

4. DEFENSE MECHANISM
Lungs play important role in the immunological defense system of the body.
Defense functions of the lungs are performed by
 Their own defenses and by the presence of various types of cells in
mucous membrane lining the alveoli of lungs.
 These cells are leukocytes, macrophages, mast cells, natural killer cells
and dendritic cells.

5. MAINTENANCE OF WATER BALANCE

 Respiratory tract plays a role in water loss mechanism.
 During expiration, water evaporates through the expired air and some
amount of body water is lost by this process.

6. REGULATION OF BODY TEMPERATURE

 During expiration, along with water, heat is also lost from the body.
 Thus, respiratory tract plays a role in heat loss mechanism.

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7. REGULATION OF ACID-BASE BALANCE

Lungs play a role in maintenance of acidbase balance of the body by
regulating the carbon dioxide content
 When metabolic activities are accelerated, more amount of carbon
dioxide is produced in the tissues.
 So, Concentration of hydrogen ion is increased and reduction in pH.
 Increased hydrogen ion concentration causes increased pulmonary
ventilation (hyperventilation)
 Due to hyperventilation, excess of carbon dioxide is removed from
body fluids and the pH is brought back to normal.

8. ANTICOAGULANT FUNCTION
 Mast cells in lungs secrete heparin. Heparin is an anticoagulant and it
prevents the intravascular clotting.

9. SECRETION OF ANGIOTENSINCONVERTING ENZYME

 Endothelial cells of the pulmonary capillaries secrete the angiotensin
converting enzyme (ACE).
 It converts the angiotensin I into active angiotensin II.

10. SYNTHESIS OF HORMONAL SUBSTANCES

 Lung tissues are also known to synthesize the hormonal substances,
prostaglandins, acetylcholine.

Surfactant
Surfactant is a surface acting material or agent that is responsible for lowering
the surface tension of a fluid.

Source of secretion of pulmonary surfactant

Pulmonary surfactant is secreted by two types of cells:
1. Type II alveolar epithelial cells in the
2. Clara cells, which are situated in the bronchioles.

Chemistry of surfactant
 Surfactant is a lipoprotein complex formed by lipids especially
phospholipids, proteins and ions.

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 Phospholipids: mostly dipalmitoylphosphatidylcholine (DPPC).

 Other lipids: Triglycerides and phosphatidylglycerol (PG).
 Proteins: surfactant proteins.
 Ions: mostly calcium ions.

Functions of surfactant
1. Surfactant reduces the surface tension in the alveoli of lungs and prevents
collapsing tendency of lungs.

Surfactant acts by the following mechanism:

 Phospholipid molecule in the surfactant has two portions.
 One portion of the molecule is hydrophilic. This portion dissolves in
water and lines the alveoli.
 Other portion is hydrophobic and it is directed towards the alveolar air.
 This surface of the phospholipid along with other portion spreads over
the alveoli and reduces the surface tension.

2. Surfactant is responsible for stabilization of the alveoli, which is necessary

to withstand the collapsing tendency.

3. It plays an important role in the inflation of lungs after birth.

 Until birth, the lungs are solid and not expanded.
 Soon after birth, the first breath starts because of the stimulation of
respiratory centers by hypoxia and hypercapnea.
 Lungs tend to collapse repeatedly.
 But, the presence of surfactant in the alveoli prevents the lungs from
collapsing.

4. Role in defense within the lungs against infection and inflammation.

 It destroys the bacteria and viruses by means of opsonization.

Effect of deficiency of surfactant –

Respiratory distress syndrome
 Absence of surfactant in infants, causes collapse of lungs and the
condition is called respiratory distress syndrome
 Deficiency of surfactant occurs in adults also and it is called adult
respiratory distress syndrome (ARDS).
 Increases the susceptibility for bacterial and viral infections.

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RESPIRATORY PRESSURES
Two types of pressures are exerted in the thoracic cavity and lungs during
process of respiration:
1. Intra pleural pressure or intrathoracic pressure
2. Intra alveolar pressure or intrapulmonary pressure.

Que. INTRAPLEURAL PRESSURE

Intrapleural pressure is the pressure existing in pleural cavity
 It is also called intrathoracic pressure since it is exerted in the whole of
thoracic cavity.

Normal Values
 Respiratory pressures are always expressed in relation to atmospheric
pressure, which is 760 mm Hg.
 Under physiological conditions, the intrapleural pressure is always
negative.
Normal values are:
1. At the end of normal inspiration: –6 mm Hg (760 – 6 = 754 mm Hg)
2. At the end of normal expiration: –2 mm Hg (760 – 2 = 758 mm Hg)
3. At the end of forced inspiration: –30 mm Hg

Cause for Negativity of Intrapleural Pressure

 Pleural cavity is always lined by a thin layer of fluid that is secreted by
the visceral layer of pleura.
 This fluid is constantly pumped from the pleural cavity into the
lymphatic vessels.
 Pumping of fluid creates the negative pressure in the pleural cavity.

Intrapleural pressure becomes positive in some pathological conditions

 such as pneumothorax, hydrothorax, hemothorax and pyothorax.

Measurement
Intrapleural pressure is measured by direct method and indirect method.
In the direct method
 Introducing a needle into the pleural cavity and connecting the needle
to a mercury manometer.
In indirect method

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 Introducing the esophageal balloon, which is connected to a

manometer.
 Intrapleural pressure is considered as equivalent to the pressure
existing in the esophagus.

Significance of Intrapleural Pressure

Intrapleural pressure has two important functions:
1. It prevents the collapsing tendency of lungs
2. Because of the negative pressure in thoracic region, larger veins and vena
cava are enlarged.
 Negative pressure acts like suction pump.
 It is responsible for venous return.
 So, it is called the respiratory pump for venous return

INTRA-ALVEOLAR PRESSURE
Intra alveolar pressure is the pressure existing in the alveoli of the lungs.
 It is also known as intrapulmonary pressure.

Significance of Intra-alveolar Pressure

 Intraalveolar pressure causes flow of air in and out of alveoli.
 During inspiration, the intraalveolar pressure becomes negative, so the
atmospheric air enters the alveoli.
 During expiration, intra alveolar pressure becomes positive. So, air is
expelled out of alveoli.

Transpulmonary Pressure
Transpulmonary pressure is the pressure difference between intraalveolar
pressure and intrapleural pressure.
 It is the measure of elastic forces in lungs, which is responsible for
collapsing tendency of lungs.

QUE. COMPLIANCE
Compliance is the ability of the lungs and thorax to expand.
 it is the expansibility of lungs and thorax.

It is defined as the change in volume per unit change in the pressure.

Significance of Determining Compliance

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Determination of compliance is useful as it is the measure of stiffness of lungs.

Stiffer the lungs, less is the compliance.

NORMAL VALUES
Compliance is expressed by two ways
1. Compliance in Relation to Intra-alveolar Pressure
Compliance is the volume change in lungs per unit change in the intraalveolar
pressure.
 Compliance of lungs and thorax together: 130 mL/1 cm H2O pressure
 Compliance of lungs alone: 220 mL/1 cm H2O pressure.

2. Compliance in Relation to Intrapleural Pressure

Compliance is the volume change in lungs per unit change in the intrapleural
pressure.
 Compliance of lungs and thorax together: 100 mL/1 cm H2O pressure
 Compliance of lungs alone: 200 mL/1 cm H2O pressure.

Thus, if lungs could be removed from thorax, the expansibility (compliance)

of lungs alone will be doubled.
 It is because of the absence of inertia and restriction exerted by the
structures of thoracic cage.

TYPES OF COMPLIANCE
1. Static Compliance
Static compliance is the compliance measured under static conditions
 by measuring pressure and volume when breathing does not take place
2. Dynamic Compliance
 Dynamic compliance is the compliance measured during dynamic
conditions, i.e. during breathing.
APPLIED PHYSIOLOGY
Increase in Compliance
 Compliance increases due to loss of elastic property of lung tissues.
o Physiological condition: Old age
o Pathological condition: Emphysema
Decrease in Compliance
 Compliance decreases in several pathological conditions such as:
o Paralysis of respiratory muscles
o Pleural effusion
o Abnormal thorax such as pneumothorax, hydrothorax,
hemothorax and pyothorax
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QUE. WORK OF BREATHING

Work of breathing is the work done by respiratory muscles during breathing
to overcome the resistance in thorax and respiratory tract.

WORK DONE BY RESPIRATORY MUSCLES

 During respiratory processes, inspiration is active process and the
expiration is a passive process.
 So, during quiet breathing, respiratory muscles perform the work only
during inspiration and not during expiration.

UTILIZATION OF ENERGY
During the work of breathing, the energy is utilized to overcome three types
of resistance.
1. Airway Resistance
 Airway resistance is the resistance offered to the passage of air through
respiratory tract.
 Work done to overcome the airway resistance is called airway
resistance work.

2. Elastic Resistance of Lungs and Thorax

 Energy is required to expand lungs and thorax against the elastic force.
 Work done to overcome this elastic resistance is called compliance
work.

3. Non-elastic Viscous Resistance

 Energy is also required to overcome the viscosity of lung tissues and
tissues of thoracic cage.
 Work done to overcome this viscous resistance is called tissue
resistance work.

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VITAL CAPACITY
Vital capacity is the maximum volume of air that can be expelled out of lungs
forcefully after a maximal or deep inspiration.

LUNG VOLUMES INCLUDED IN VITAL CAPACITY

 Vital capacity includes inspiratory reserve volume, tidal volume and
expiratory reserve volume.

NORMAL VALUE
VC = IRV + TV + ERV
VC = 3,300 + 500 + 1,000 = 4,800 mL.

VARIATIONS OF VITAL CAPACITY

Physiological Variations
 Sex: In females, vital capacity is less than in males
 Body built: Vital capacity is slightly more in heavily built persons
 Posture: Vital capacity is more in standing position and less in lying
position
 Athletes: Vital capacity is more in athletes
 Occupation: Vital capacity is decreased in people with sedentary jobs. It
is increased in persons who play musical wind instruments such as
bugle and flute.

Pathological Variations
Vital capacity is decreased in the following respiratory diseases:
 Asthma, Emphysema
 Weakness or paralysis of respiratory muscle
 Pneumonia
 Pneumothorax, Hemothorax, Pyothorax, Hydrothorax

Measurement
Vital capacity is measured by spirometry.
 The subject is asked to take a deep inspiration and expire forcefully.

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DEAD SPACE
Dead space is defined as the part of the respiratory tract, where gaseous
exchange does not take place.
 Air present in the dead space is called dead space air.

TYPES OF DEAD SPACE

Anatomical Dead Space
 Anatomical dead space extends from nose up to terminal bronchiole.
 It includes nose, pharynx, trachea, bronchi and branches of bronchi up
to terminal bronchioles.
 These structures serve only as the passage for air movement.
 Gaseous exchange does not take place in these structures.

Physiological Dead Space

Physiological dead space includes anatomical dead space plus two additional
volumes.
Additional volumes included in physiological dead space are:
 Air in the alveoli, which are non-functioning.
o In some respiratory diseases, alveoli do not function because of
dysfunction or destruction of alveolar membrane.
 Air in the alveoli, which do not receive adequate blood flow.
o Gaseous exchange does not take place during inadequate blood
supply.

These two additional volumes are generally considered as wasted ventilation.

 Wasted air refers to air that is not utilized for gaseous exchange.
 Dead space air is generally considered as wasted air.

NORMAL VALUE OF DEAD SPACE

Volume of normal dead space is 150 mL.
 Under normal conditions, physiological dead space is equal to
anatomical dead space.
 It is because, all the alveoli are functioning and all the alveoli receive
adequate blood flow in normal conditions.
 Physiological dead space increases during respiratory diseases, which
affect the pulmonary blood flow or the alveoli.

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Que-OXYGEN-HEMOGLOBIN DISSOCIATION
CURVE
Oxygen-hemoglobin dissociation curve demonstrates the relationship between
partial pressure of oxygen and the percentage saturation of hemoglobin with
oxygen.

 It explains hemoglobin’s affinity for oxygen.

 Saturation of haemoglobin with oxygen depends upon the partial
pressure of oxygen.
Normal Oxygen-hemoglobin Dissociation Curve
Under normal conditions, oxygen-hemoglobin dissociation curve is ‘S’ shaped
or sigmoid shaped.
Why?
 Initially as the po2 rises, the saturation of haemoglobin with oxygen
increase slowly
 But once the process picks up, the saturation increases vary fast
between 15 to 40 mm of hg [20% to 75%]
 Beyond 40 mm of hg further rise in po2 dose not change saturation
much.
 Because the saturation cannot go beyond 100%

Molecular basis of sigmoid shaped curve

Out of four molecules of oxygen The first molecule of oxygen combines with
himoglobin with great difficulty. Binding of an oxygen molecule to Hb
increases affinity for next o2 molecule to Hb.

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P50
 P50 is the partial pressure of oxygen at which haemoglobin saturation
with oxygen is 50%.
 When the partial pressure of oxygen is 25 to 27 mm Hg, the hemoglobin
is
saturated to about 50%.
 At 40mm of hg its 75%, at 60 mm of hg its 90%, at 100mm of hg its
97.5%
Factors Affecting Oxygen-hemoglobin Dissociation Curve
Oxygen-hemoglobin dissociation curve is shifted to left or right by various
factors:
Shift to right – Means decreasing affinity
Oxygen-hemoglobin dissociation curve is shifted to right in the following
conditions:
 Decrease in partial pressure of oxygen
 Increase in partial pressure of carbon dioxide (Bohr effect)
 Acidic ph.
 Increased body temperature
 Excess of 2,3-Bisphosphoglycerate (BPG) in RBC.

Shift to left – Means increasing affinity.

Oxygen-hemoglobin dissociation curve is shifted to
left in the following conditions:
 High affinity for oxygen to himoglobin. Ex. in fetal blood,fetal
hemoglobin has more affinity for oxygen than the adult haemoglobin.
 Alkaline Ph
What is Bohr Effect?
Increase in Pco2 , decrease the O2 affinity to haemoglobin and shifts the
oxygen haemoglobin dissociation curve to right is; it is called Bohr effect.
 In the tissues, the partial pressure of carbon dioxide is very high and
the partial pressure of oxygen is low.
 Due to this pressure gradient, carbon dioxide enters the blood
 Co2 increase H+ ion concentration in the RBC and it binds to Hb and
release more O2.
 So, oxygen-HB dissociation curve is shifted to right.

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Que.TRANSPORT OF CARBON DIOXIDE

Carbon dioxide is transported by the blood from cells to the alveoli.
Carbon dioxide is transported in the blood in four ways:
1. As dissolved form (7%)
2. As carbonic acid (negligible)
3. As bicarbonate (63%)
4. As carbamino compounds (30%).
AS DISSOLVED FORM
 Carbon dioxide diffuses into blood and dissolves in the
fluid of plasma forming a simple solution.
 It is about 7% of total carbon dioxide in the blood.
AS CARBONIC ACID
 Part of dissolved carbon dioxide in plasma combines
with the water to form carbonic acid.
 Transport of carbon dioxide in this form is negligible.
AS BICARBONATE
About 63% of carbon dioxide is transported as bicarbonate.

 From plasma, carbon dioxide enters the RBCs. In the RBCs, carbon
dioxide combines with water to form carbonic acid.
 The reaction inside RBCs is very rapid because of the presence of
carbonic anhydrase.
 Carbonic acid in rbc, dissociates into bicarbonate and hydrogen ions.
 Concentration of bicarbonate ions in the cell increases.
 Due to high concentration, bicarbonate ions diffuse through the cell
membrane into plasma.
 Thus, carbon dioxide is transported as bicarbonate.

Chloride Shift or Hamburger Phenomenon

Chloride shift or Hamburger phenomenon is the exchange of a chloride ion

for a bicarbonate ion across RBC membrane.
 It When carbon dioxide enters the blood it forms Carbonic acid in rbc,
dissociates into bicarbonate and hydrogen ions.
 In plasma, plenty of sodium chloride is present. It dissociates into
sodium and chloride ions

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 Concentration of bicarbonate ions in the cell increases.

 Due to high concentration, bicarbonate ions diffuse through the cell
membrane into plasma.
 When the negatively charged bicarbonate ions move out of RBC into the
plasma, the negatively charged chloride ions present in plasma move
into the RBC.
 This occurs in order to maintain the electrolyte equilibrium (ionic
balance).

Anion exchanger 1 (band 3 protein), which acts like antiport pump in RBC
membrane is responsible for the exchange of bicarbonate ions and chloride
ions.

AS CARBAMINO COMPOUNDS
About 30% of carbon dioxide is transported as carbamino compounds.
 Carbon dioxide is transported in blood in combination with hemoglobin
and plasma proteins in the form of carbamino haemoglobin and
carbamino proteins.
 They together called carbamino compounds.

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Que-Regulation of Respiration
Normally,quiet regular breathing occurs because of two regulatory
mechanisms:
1. Nervous or neural mechanism
2. Chemical mechanism
NERVOUS MECHANISM
 RESPIRATORY CENTERS
 Depending upon the situation in brainstem, the respiratory centres are
classified into two groups:
MEDULLARY CENTERS

1. Dorsal Respiratory Group of Neurons

Situation
 Dorsal respiratory group of neurons are situated in the nucleus of
tractus solitarius
Function
 Dorsal group of neurons are responsible for basic rhythm of respiration.
 Innervating primary muscles of inspiration.

2. Ventral Respiratory Group of Neurons

Situation
 Ventral respiratory group of neurons are present in nucleus ambiguous .
 Ventral respiratory group has both inspiratory and expiratory neurons.

Function
 Normally, ventral group neurons are inactive during quiet breathing and
 It becomes active during forced breathing.
During forced breathing, these neurons stimulate both inspiratory muscles
and expiratory muscles.
PONTINE CENTERS

3. Apneustic Center
Situation
 Apneustic center is situated in the reticular formation of lower pons.
Function

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 Apneustic center produce prolonged inspiratory drive by acting directly

on dorsal group neurons.
4. Pneumotaxic Center
Situation
Pneumotaxic center is situated reticular formation in upper pons.

Function
 pneumotaxic center control the switch off point of the inspiratory
ramp.
 Thus controlling the depth of inspiration.
 Pneumotaxic center also inhibits the apneustic center so that the dorsal
group neurons are inhibited.
 Because of this, inspiration stops and expiration starts

CHEMICAL MECHANISM of Regulation of Respiration

Changes in Chemical Constituents of Blood which Stimulate Chemoreceptors

1. Hypoxia (decreased pO2)
2. Hypercapnea (increased pCO2)
3. Increased hydrogen ion concentration.

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Que. HYPOXIA
 Hypoxia is defined as reduced availability of oxygen to the tissues.
Hypoxia is classified into four types:
1. Hypoxic Hypoxia
Hypoxic hypoxia means decreased oxygen content in blood.

Causes for hypoxic hypoxia

Low oxygen tension in inspired (atmospheric) air, which does not provide
enough oxygen
 High altitude, While breathing air in closed space
Respiratory disorders associated with decreased pulmonary ventilation,
 Asthma, Depression of respiratory centers, pneumothorax

2. Anemic Hypoxia
Anemic hypoxia is the condition characterized by the inability of blood to carry
enough amount of oxygen.
Causes for anemic hypoxia
 Decreased number of RBCs
 RBC decreases in conditions like bone marrow diseases, Hemorrhage.
 Decreased hemoglobin content in the blood-
 Formation of altered haemoglobin ex- Methemoglobin

3. Stagnant Hypoxia
Stagnant hypoxia is the hypoxia caused by decreased velocity of blood flow.
Causes for stagnant hypoxia
 Congestive cardiac failure, Hemorrhage
 Thrombosis, Embolism.

4. Histotoxic Hypoxia
Histotoxic hypoxia is the type of hypoxia produced by the inability of tissues to
utilize oxygen.
Causes for histotoxic hypoxia
 Histotoxic hypoxia occurs due to cyanide or sulphide poisoning.
 These poisonous substances destroy the cellular oxidative enzymes

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EFFECTS OF HYPOXIA
Effects on blood
 Hypoxia induces secretion of erythropoietin from kidney.
 Erythropoietin increases production of RBC. This in turn, increases the
oxygen carrying capacity of blood.

Effects on cardiovascular system

 increase in rate and force of contraction of heart, cardiac output and
blood pressure.

Effects on respiration
 Initially, respiratory rate increases due to chemoreceptor reflex.
 Later, the respiration tends to be shallow and periodic. Finally, the rate
and force of breathing are reduced.

Effects on digestive system

 Hypoxia is associated with loss of appetite, nausea and vomiting. Mouth
becomes dry and there is a feeling of thirst.

Effects on kidneys
 Hypoxia causes increased secretion of erythropoietin from the kidneys.

Effects on central nervous system

 Individual is depressed
 fatigue of muscles are common in hypoxia.
 Sudden loss of consciousness.
 If not treated immediately, coma occurs, which leads to death.

TREATMENT FOR HYPOXIA –

OXYGEN THERAPY
 In hypoxic hypoxia, the oxygen therapy is 100% useful.
 In anemic hypoxia, oxygen therapy is moderately effective to about 70%.
 In stagnant hypoxia, the effectiveness of oxygen therapy is less than 50%.
 In histotoxic hypoxia, the oxygen therapy is not useful at all. It is because,
even if oxygen is delivered, the cells cannot utilize oxygen
So, treating the underlying cause behind the hypoxia is the definitive
treatment

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CYANOSIS
Cyanosis is defined as the diffused bluish coloration of skin and mucus
membrane.
 It is due to the presence of large amount of reduced hemoglobin in the
blood.
 Quantity of reduced hemoglobin should be at least 5 to 7 g/dL in the
blood to cause cyanosis.

DISTRIBUTION OF CYANOSIS
 Cyanosis is distributed all over the body.
 But, it is more marked in certain regions where the skin is thin.
 These areas are lips, cheeks, ear lobes, nose and fingertips above the
base of the nail.

CONDITIONS WHEN CYANOSIS OCCURS

 Any condition which leads to arterial hypoxia and stagnant hypoxia.
 Cyanosis does not occur in anemic hypoxia because the hemoglobin
content is less.
 It does not occur in histotoxic hypoxia because of tissue damage.

 Cyanosis occurs when altered hemoglobin is formed. Ex. Due to

poisoning, hemoglobin is altered into methemoglobin or sulfhemoglobin

 During polycythemia,
o because of increased RBC count, the viscosity of blood is increase
o It leads to sluggishness of blood flow.
o So the quantity of deoxygenated blood increases, which causes
bluish discoloration of skin.

CYANOSIS AND ANEMIA

 Cyanosis usually occurs only when the quantity of reduced hemoglobin
is about 5 g/dL to 7 g/dL.
 But, in anemia, the hemoglobin content itself is less. So, cyanosis cannot
occur in anemia.

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MOUNTAIN SICKNESS
Mountain sickness is the condition characterized by adverse effects of
hypoxia at high altitude.

 It is commonly developed in persons going to high altitude for the first

time.
 It occurs within a day before person gets acclimatized to the altitude.

SYMPTOMS
1. Digestive System
 Loss of appetite, nausea and vomiting occur because of expansion of
gases in GI tract.

2. Cardiovascular System
 Heart rate and force of contraction of heart increases.

3. Respiratory System
 Pulmonary blood pressure increases
 Increased pulmonary blood pressure results in pulmonary edema, which
casus breathlessness.

4. Nervous System
 Headache, depression, irritability, lack of sleep, weakness and fatigue.
 These symptoms are developed because of cerebral edema.
 Sudden exposure to hypoxia in high altitude causes vasodilatation in
brain.
 Autoregulation mechanism of cerebral blood flow fails to cope with
hypoxia.
 It leads to an increased capillary pressure and leakage of fluid from
capillaries into the brain tissues.

TREATMENT
 Oxygen therapy

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DECOMPRESSION SICKNESS
Decompression sickness is the disorder that occurs when a person returns
rapidly to normal surroundings (atmospheric pressure) from the area of high
atmospheric pressure like deep sea.
 It is also known as caisson disease or diver’s palsy.

CAUSE
 High barometric pressure at deep sea leads to compression of gases in
the body. Compression reduces the volume of gases.
 Nitrogen, which is present in high concentration, i.e. 80% is an inert gas.
 When nitrogen is compressed by high atmospheric pressure in deep
sea, it escapes from blood vessels and enters the organs.
 As it is fat soluble, it gets dissolved in the fat of the tissues and tissue
fluids.

As long as the person remains in deep sea, nitrogen remains in solution and
does not cause any problem.
 But, if the person ascends rapidly and returns to atmospheric pressure
 Due to sudden return to atmospheric pressure, the nitrogen is
decompressed and escapes from the tissues at a faster rate.
 Being a gas, it forms bubbles
 Bubbles obstruct the blood flow and produce air embolism, leading to
decompression sickness.

SYMPTOMS
Symptoms of decompression sickness are mainly due to the escape of
nitrogen from tissues in the form of bubbles.
1. Severe pain in tissues, particularly the joints, produced by nitrogen bubbles
in the myelin sheath of sensory nerve fibers
2. Sensation of numbness, tingling and itching
3. Temporary paralysis due to nitrogen bubbles in the myelin sheath of motor
nerve fibers
5. Occlusion of coronary arteries caused by bubbles in the blood
6. Occlusion of blood vessels in brain and spinal cord
8. Shortness of breath
9. Finally, fatigue, unconsciousness and death.
PREVENTION
Decompression sickness is prevented by proper precautionary measures.

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 While returning to mean sea level, the ascent should be very slow with
short stay at regular intervals.
 Stepwise ascent allows nitrogen to come back to the blood, without
forming bubbles.

TREATMENT
 If a person is affected by decompression sickness, first recompression
should be done.
 It is done by keeping the person in a recompression chamber.
 Then, he is brought back to atmospheric pressure by reducing the
pressure slowly.
 Hyperbaric oxygen therapy may be useful.

SCUBA
Selfcontained Underwater Breathing Apparatus
 It is used by the deep sea divers and the underwater tunnel workers
 It contains air cylinders, valve system and a mask.
 By using this instrument, it is possible to breathe air or gas mixture
without high pressure.
 Also, because of the valve system, only the amount of air necessary
during inspiration enters the mask and the expired air is expelled out of
the mask.

Disadvantage
 Person using this can remain in the sea or tunnel only for a short
period.
 Especially, beyond the depth of 150 feet, the person can stay only
for few minutes.

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FUNCTIONS OF KIDNEY
Kidneys perform several vital functions besides formation of urine.
The functions of kidney are:

ROLE IN HOMEOSTASIS
Primary function of kidneys is homeostasis. It is accomplished by the formation of
urine.
Kidneys regulate various activities in the body, which are related with homeostasis
such as:

Excretion of Waste Products

 Kidneys excrete the unwanted waste products, which are formed during
metabolic activities:
 Urea, Uric acid, Creatinine, Bilirubin, Products of metabolism of other
substances.
 Kidneys also excrete harmful foreign chemical substances such as toxins,
drugs, heavy metals pesticides, etc.

Maintenance of Water Balance

 Kidneys maintain the water balance in the body by conserving water
when it is decreased and excreting water when it is excess in the body.

Maintenance of Electrolyte Balance

 Maintenance of electrolyte especially sodium is in relation to water
balance.
 Kidneys retain sodium if the osmolarity of body water decreases and
eliminate sodium when osmolarity increases.

Maintenance of Acid–Base Balance

The pH of the blood and body fluids are maintained by kidneys
 Body is under constant threat to develop acidosis, because of
production of lot of acids during metabolic activities.
 It is prevented by kidneys, lungs and blood buffers, which eliminate
these acids.
 Kidneys are capable of eliminating metabolic acids.

HEMOPOIETIC FUNCTION
 Kidney stimulate production of erythrocytes by secreting erythropoietin
 Erythropoietin is the important stimulating factor for erythropoiesis

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ENDOCRINE FUNCTION
Kidneys secrete many hormonal substances
 Erythropoietin
 Thrombopoietin
 Renin
 1,25-dihydroxycholecalciferol (calcitriol)
 Prostaglandins.

REGULATION OF BLOOD PRESSURE

Kidneys play an important role in the long-term regulation of arterial blood
pressure by two ways:
 By regulating the volume of extracellular fluid
 Through renin-angiotensin mechanism.

REGULATION OF BLOOD CALCIUM LEVEL

 Kidneys play a role in the regulation of blood calcium level by activating
vitamin D.
 Vitamin D is necessary for the regulation of calcium metabolism.

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Que. Nephron
Nephron is defined as the structural and functional unit of kidney.
 Each kidney consists of 1 to 1.3 millions of nephrons.
Each nephron is formed by two parts.
 A blind end called renal corpuscle or Malpighian corpuscle
 A tubular portion called renal tubule.

RENAL CORPUSCLE
 Function of the renal corpuscle is to do filtration of blood which forms
the first phase of urine formation.

SITUATION OF RENAL CORPUSCLE AND TYPES OF NEPHRON

 Renal corpuscle is situated in the cortex of the kidney either near the
periphery or near the medulla.

Classification of Nephrons
Based on the situation of renal corpuscle, the nephrons are classified into two types:
 Cortical nephrons or superficial nephrons- Nephrons having the
corpuscles in outer cortex of the kidney near the periphery
 In human kidneys, 85% nephrons are cortical nephrons.
 Juxtamedullary nephrons- Nephrons having the corpuscles in inner
cortex near medulla or corticomedullary junction.

STRUCTURE OF RENAL CORPUSCLE

Renal corpuscle is formed by two portions:

Glomerulus
 Glomerulus is a tuft of capillaries enclosed by Bowman capsule.
 It consists of glomerular capillaries interposed between afferent
arteriole on one end and efferent arteriole on the other end.
 Thus, the vascular system in the glomerulus is purely arterial.
 Glomerular capillaries arise from the afferent arteriole. After entering
the Bowman capsule, the afferent arteriole divides into 4 or 5 large
capillaries.
 Each large capillary subdivides into many small capillaries. These small
capillaries are arranged in irregular loops and form anastomosis.
 All the smaller capillaries finally reunite to form the efferent arteriole.
 Diameter of the efferent arteriole is less than that of afferent arteriole.
Bowman Capsule

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Bowman capsule is a capsular structure, which encloses the glomerulus.

It is formed by two layers: Inner visceral layer and Outer parietal layer.
 Visceral layer covers the glomerular capillaries. It is continued as the
parietal layer.
 Parietal layer is continued with the wall of the tubular portion of
nephron.
 The cleftlike space between the visceral and parietal layers is continued
as the lumen of the tubular portion.

TUBULAR PORTION OF NEPHRON

Tubular portion of nephron is the continuation of Bowman capsule.
It is made up of three parts:

PROXIMAL CONVOLUTED TUBULE

 Proximal convoluted tubule is the coiled portion arising from Bowman
capsule. It is situated in the cortex.
 It is continued as descending limb of loop of Henle.

LOOP OF HENLE - Loop of Henle consists of:

Descending Limb
 Descending limb of loop of Henle is the direct continuation of the
proximal convoluted tubule.
 It descends down into medulla.
Hairpin Bend
 Descending limb is continued as hairpin bend
 Hairpin bend is continued as the ascending limb of loop of Henle.
Ascending Limb- has two parts:
 Thin ascending segment- is the continuation of hairpin bend.
 Thin ascending segment is continued as thick ascending segment.
 Thick ascending segment-ascends to the cortex and continues as distal
convoluted tubule.

DISTAL CONVOLUTED TUBULE

 Distal convoluted tubule is the continuation of thick ascending segment
and occupies the cortex of kidney.
 It is continued as collecting duct.
COLLECTING DUCT
 The lower part of the collecting duct lies in medulla.

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Juxtaglomerular apparatus
Juxtaglomerular apparatus is a specialized organ situated near the glomerulus of
each nephron (juxta = near).

STRUCTURE OF JUXTAGLOMERULAR APPARATUS

Juxtaglomerular apparatus is formed by three different structures.
MACULA DENSA
 Macula densa is at the end portion of
thick ascending segment before it opens
into distal convoluted tubule.
 It is situated between afferent and
efferent arterioles of the same nephron.

EXTRAGLOMERULAR MESANGIAL CELLS

 Extraglomerular mesangial cells are
situated in the triangular region
bound by afferent arteriole,
efferent arteriole and macula densa.
 mesangial cells support the glomerular
capillary loops

JUXTAGLOMERULAR CELLS
 Juxtaglomerular cells are specialized cells situated in the wall of afferent
arteriole just before it enters the Bowman capsule.

FUNCTIONS OF JUXTAGLOMERULAR APPARATUS

Primary function of juxtaglomerular apparatus is the secretion of hormones.
 It also regulates the glomerular blood flow and glomerular filtration
rate.

SECRETION OF HORMONES
1. Renin
Juxtaglomerular cells secrete renin. Renin is a peptide.
Secretion of renin is stimulated by four factors:
 Fall in arterial blood pressure
 Reduction in the ECF volume
 Increased sympathetic activity
 Decreased load of sodium and chloride in macula densa.
Renin-angiotensin system
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 Renin acts on a specific plasma protein called angiotensinogen.

angiotensinogen is converted into angiotensin I.
 Angiotensin I is converted into angiotensin II by the activity of
angiotensin-converting enzyme (ACE) secreted from lungs.
Actions of Angiotensins
 Angiotensin II increases arterial blood pressure
 It is a potent constrictor of arterioles.
 It increases blood pressure indirectly by increasing the release of
noradrenaline
 It stimulates aldosterone secetion.
 Aldosterone increases retention of sodium, which is also responsible for
elevation of blood pressure.

2. Prostaglandin
 Extraglomerular mesangial cells of juxtaglomerular apparatus secrete
prostaglandin.

SECRETION OF OTHER SUBSTANCES

 Extraglomerular mesangial cells of juxtaglomerular apparatus secrete
cytokines like interleukin-2 and tumor necrosis factor

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FUNCTIONS OF SALIVA
Saliva is a very essential digestive juice. It has many functions.

PREPARATION OF FOOD FOR SWALLOWING

 Food is moistened and dissolved by saliva.
 The mucus membrane of mouth is also moistened by saliva.
 Mucin of saliva lubricates the bolus and facilitates swallowing.

APPRECIATION OF TASTE
 saliva dissolves the solid food substances, so that the dissolved
substances can stimulate the taste buds.
DIGESTIVE FUNCTION
 Saliva has three digestive enzymes, namely salivary amylase, maltase
and lingual lipase
Salivary Amylase
 Salivary amylase is a carbohydrate-digesting (amylolytic) enzyme.
 It acts on starch and converts it into dextrin and maltose.
Maltase
 Maltase is present only in traces in human saliva and it converts maltose
into glucose.
Lingual Lipase
 Lingual lipase is a lipid-digesting (lipolytic) enzyme
 It digests milk fats (pre-emulsified fats).
 It hydrolyzes triglycerides into fatty acids and diacylglycerol.
CLEANSING AND PROTECTIVE FUNCTIONS
 The mouth and teeth are rinsed and kept free off food debris by saliva.
 In this way, saliva prevents bacterial growth by removing materials,
 Enzyme lysozyme of saliva kills some bacteria
 Immunoglobulin IgA in saliva also has antibacterial and antiviral actions.

ROLE IN SPEECH
 By moistening and lubricating soft parts of mouth and lips, saliva helps in
speech.
EXCRETORY FUNCTION
 Many substances are excreted in saliva.
 It excretes substances like mercury, potassium iodide, lead
 Glucose and urea in abnormal conditions.

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QUE. REGULATION OF SALIVARY SECRETION

Salivary secretion is regulated only by nervous mechanism.
Autonomic nervous system is involved in the regulation of salivary secretion.

PARASYMPATHETIC FIBERS
Parasympathetic Fibers to Submandibular and Sublingual Glands
 Arise from the superior salivatory nucleus, situated in pons.
Parasympathetic Fibers to Parotid Gland- Arise from inferior salivatory nucleus
Function of Parasympathetic Fibers
 Stimulation of parasympathetic fibers of salivary glands causes secretion
of saliva with large quantity of water.
 It is because the parasympathetic fibers activate the acinar cells and
dilate the blood vessels of salivary glands.

SYMPATHETIC FIBERS
 Sympathetic fibers to salivary glands arise from the first and second
thoracic segments of spinal cord.
Function of Sympathetic Fibers
 Stimulation of sympathetic fibers causes secretion of saliva, which is
thick and rich in organic constituents such as mucus.
 These fibers activate the acinar cells and cause vasoconstriction.

REFLEX REGULATION OF SALIVARY SECRETION

1. Unconditioned Reflex
 Unconditioned reflex is the inborn reflex that is present since birth.
 This reflex induces salivary secretion when any substance is placed in
the mouth.
 It is due to the stimulation of nerve endings in the mucus membrane of
the oral cavity.
2. Conditioned Reflex
 Conditioned reflex is the one that is acquired by experience and it needs
previous experience
 Sight, smell, hearing or thought of food generate reflex and salivation
starts
APPLIED PHYSIOLOGY
HYPOSALIVATION- Reduction in the secretion of saliva is called hyposalivation.
HYPERSALIVATION- Excess secretion of saliva is known as hypersalivation.

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Que. FUNCTIONS OF STOMACH

MECHANICAL FUNCTION + FUNCTION OF GASTRIC JUICE

MECHANICAL FUNCTION
1.Storage Function
 Food is stored in the stomach for a long period, i.e. for 3 to 4 hours and
emptied into the intestine slowly.
 Slow emptying of stomach provides enough time for proper digestion
and absorption of food substances.
Formation of Chyme
 Peristaltic movements of stomach mix the bolus with gastric juice and
convert it into the semisolid material known as chyme.

2.EXCRETORY FUNCTION
 Many substances like toxins, alkaloids and metals are excreted through
gastric juice.

FUNCTIONS OF GASTRIC JUICE

1. DIGESTIVE FUNCTION
 Gastric juice acts mainly on proteins.
 Proteolytic enzymes of the gastric juice are pepsin and rennin.
 Gastric juice also contains some other enzymes like gastric lipase,
gelatinase, urase and gastric amylase.
Pepsin
 Pepsin is secreted as inactive pepsinogen.
 Pepsinogen is converted into pepsin by hydrochloric acid.
 Optimum pH for activation of pepsinogen is below 6.
Action of pepsin
 Pepsin converts proteins into proteoses, peptones and polypeptides.
 Pepsin also causes curdling and digestion of milk (casein).
Gastric Lipase
 Gastric lipase is a weak lipolytic enzyme
 Gastric lipase hydrolyzes butter fat into fatty acids and glycerols.

Actions of Other Enzymes of Gastric Juice

 Gelatinase: Degrades gelatin, collagen
 Urase: Acts on urea and produces ammonia
 Gastric amylase: Degrades starch (but its action is insignificant)

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 Rennin: Curdles milk (present in animals only).

2. HEMOPOIETIC FUNCTION
 Intrinsic factor of Castle, secreted by parietal cells of gastric glands plays
an important role in erythropoiesis.
 It is necessary for the absorption of vitamin B12. (which is called
extrinsic factor)
 Vit-B12 is necessary for erythropoiesis.
 Absence of intrinsic factor in gastric juice causes deficiency of vitamin
B12, leading to pernicious anemia.

3. PROTECTIVE FUNCTION – FUNCTION OF MUCUS

Mucus is a mucoprotein, secreted by mucus cells of the gastric glands
 It Protects the stomach wall from irritation or mechanical injury
 It Prevents the digestive action of pepsin on the wall of the stomach
 Protects the gastric mucosa from hydrochloric acid

4. FUNCTIONS OF HYDROCHLORIC ACID

 Activates pepsinogen into pepsin
 Bacteriolytic action – HCL Kills some of the bacteria entering the
stomach along with food substances.
 Provides acid medium, which is necessary for the action of Enzymes.

Que. PROPERTIES AND COMPOSITION OF GASTRIC JUICE

 Gastric juice is a mixture of secretions from different gastric glands.
PROPERTIES OF GASTRIC JUICE
 Volume : 1200 mL/day to 1500 mL/day.
 Reaction : Gastric juice is highly acidic with a pH of 0.9 to 1.2. Acidity of
gastric juice is due to the presence of hydrochloric acid.
 Specific gravity : 1.002 to 1.004

COMPOSITION OF GASTRIC JUICE

Gastric juice contains 99.5% of water and 0.5% solids.

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Que. PHASES OF GASTRIC SECRETION

Secretion of gastric juice is a continuous process.
 But the quantity varies, depending upon time and stimulus
 There are three phases of gastric secretion – Cephalic phase, Gastric
phase and Intestinal phase.

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QUE. PEPTIC ULCER

Ulcer means discontinuation of skin or mucous membrane followed by necrosis
of surrounding cells.
 Peptic ulcer means an ulcer in the wall of stomach or duodenum,
caused by digestive action of gastric juice.
 If peptic ulcer is found in stomach, it is called gastric ulcer
 If it is found in duodenum, it is called duodenal ulcer.
Causes
 Increased secretion of pepsin in gastric juice
 Hyperacidity of gastric juice
 Reduced alkalinity of duodenal content
 Decreased mucin content in gastric juice or decreased protective activity
in stomach or duodenum
 Constant physical or emotional stress
 Food with excess spices or smoking (classical causes of ulcers)
 Long term use of NSAIDs (see above) such as Aspirin, Ibuprofen
 Chronic inflammation due to Helicobacter pylori.

Features
Most common feature of peptic ulcer is severe burning pain in epigastric region
In gastric ulcer
 Pain occurs while eating or drinking.
 Nausea, Vomiting
 Hematemesis (vomiting blood)
 Heartburn (burning pain in chest due to regurgitation of acid from
stomach into esophagus)
 Anorexia (loss of appetite), Loss of weight.

In duodenal ulcer
 pain is felt 1 or 2 hours after food intake and during night.
 Increased habit of taking food so weight gain occurs.

SQ. ZOLLINGER-ELLISON SYNDROME

It is characterized by secretion of excess hydrochloric acid in the stomach.
 Caused by Tumor of pancreas which produces gastrin in large amount
 Gastrin increases the hydrochloric acid secretion in stomach by
stimulating the parietal cells of gastric glands.

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FUNCTIONS OF PANCREATIC JUICE

Pancreatic juice has digestive functions and neutralizing action.
DIGESTIVE FUNCTIONS OF PANCREATIC JUICE
 Pancreatic juice plays an important role in the digestion of proteins and
lipids.
 It also has mild digestive action on carbohydrates.

DIGESTION OF PROTEINS
Major proteolytic enzymes of pancreatic juice are trypsin and chymotrypsin.
 Other proteolytic enzymes are carboxypeptidases, nuclease, elastase
and collagenase.

Trypsin
It is secreted as inactive trypsinogen,
 It is converted into active trypsin by enterokinase.
 Enterokinase is secreted by cells of duodenal mucus membrane.
Once formed, trypsin itself activates trypsinogen

Actions of trypsin
Digestion of proteins: Trypsin is the most powerful proteolytic enzyme.
 It breaks the interior bonds of the protein molecules and converts
proteins into proteoses and polypeptides
 Curdling of milk: It converts caseinogen in the milk into casein
 It activates the other enzymes of pancreatic juice, viz.
 Chymotrypsinogen into chymotrypsin
 Procarboxypeptidases into carboxypeptidases
 Proelastase into elastase
 Trypsin also activates collagenase, phospholipase A, phospholipase
B.

Chymotrypsin
 Digestion of proteins: Chymotrypsin also converts proteins into
polypeptides
Carboxypeptidases
 Carboxypeptidases are exopeptidases and break the terminal bond of
protein
 Convert some proteins into amino acids.
Nucleases
 Nucleases of pancreatic juice are ribonuclease and deoxyribonuclease,
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 These enzymes convert the RNA and DNA into mononucleotides.

Elastase- Elastase digests the elastic fibers.
Collagenase- It digests collagen.

DIGESTION OF LIPIDS
Lipolytic enzymes present in pancreatic juice are…

Pancreatic lipase
 Pancreatic lipase is a powerful lipolytic enzyme.
 It digests triglycerides into monoglycerides and fatty acids.
 Activity of pancreatic lipase is accelerated in the presence of bile.
 Optimum pH required for activity of this enzyme is 7 to 9.

Cholesterol ester hydrolase

 It converts cholesterol ester into free cholesterol and fatty acid.

Phospholipase A and Phospholipase B

 Both are activated by trypsin.
 Phospholipase A and Phospholipase B digests phospholipids
Colipase
 Colipase facilitates digestive action of pancreatic lipase on fats.
Bile-salt-activated lipase
 Bilesaltactivated lipase is the lipolytic enzyme activated by bile salt.
 This enzyme has a weak lipolytic action

DIGESTION OF CARBOHYDRATES
Pancreatic amylase is the amylolytic enzyme present in pancreatic juice.
 Pancreatic amylase converts starch into dextrin and maltose.

NEUTRALIZING ACTION OF PANCREATIC JUICE

 When acid chyme enters intestine from stomach, pancreatic juice with
large quantity of bicarbonate is released into intestine.
 It is highly alkaline and neutralizes acidity of chyme.
 It protects the intestine from the destructive action of acid in the
chyme.
 Provide alkaline medium for functioning of Enzymes.

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Que. FUNCTIONS OF SUCCUS ENTERICUS

1. DIGESTIVE FUNCTION
 Enzymes of succus entericus act on the partially digested food and
convert them into final digestive products.
 Enzymes are produced and released into succus entericus by
enterocytes of the villi.
Proteolytic Enzymes
 Proteolytic enzymes present in succus entericus are the peptidases
 Peptidases convert peptides into amino acids.

Amylolytic Enzymes
 Dextrinase digest dextrin
 Lactase, sucrase and maltase- They convert the disaccharides (lactose,
sucrose and maltose) into two molecules of monosaccharides
 Trehalase causes hydrolysis of trehalose and converts it into glucose.

Lipolytic Enzyme
 Intestinal lipase acts on triglycerides and converts them into fatty acids.

2. PROTECTIVE FUNCTION
 Mucus present in the succus entericus protects the intestinal wall from
the acid chime
 Defensins secreted by intestinal glands and they kill bacteria.

3. ACTIVATOR FUNCTION
 Enterokinase present in intestinal juice activates trypsinogen into
trypsin. Trypsin, in turn activates other enzymes.

4. HEMOPOIETIC FUNCTION
 Intrinsic factor of Castle present in the intestine plays an important role
in erythropoiesis
 It is necessary for the absorption of vitamin B12.

5. HYDROLYTIC PROCESS
 Intestinal juice helps in all the enzymatic reactions of digestion.

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FUNCTIONS OF SMALL INTESTINE

MECHANICAL FUNCTION
 Mixing movements of small intestine help in the mixing of chyme with
the digestive juices.
SECRETORY FUNCTION
 Small intestine secretes succusentericus, enterokinase and the GI
hormones.

Write down the function of FUNCTIONS OF SUCCUS ENTERICUS as described in

previous question

HORMONAL FUNCTION
 Small intestine secretes many GI hormones such as secretin,
cholecystokinin, etc.
 These hormones regulate the movement of GI tract and secretory
activities of small intestine and pancreas

ABSORPTIVE FUNCTIONS
 Presence of villi and microvilli in small intestinal mucosa increases the
surface area of mucosa.
 This facilitates the absorptive function of intestine.
o Absorption of Carbohydrates
o Absorption of Proteins
o Absorption of Fats
o Absorption of Water and Minerals
o Absorption of Vitamins
 From the lumen of intestine, these substances pass through villi, cross
the mucosa
 They enter the blood directly or through lymphatics.

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DEGLUTITION
Deglutition or swallowing is the process by which food moves from mouth into
stomach.

Stages of Deglutition
Deglutition occurs in three stages:

ORAL STAGE OR FIRST STAGE- food moves from mouth to pharynx

 Oral stage of deglutition is a voluntary stage.
In this stage, the bolus from mouth passes into pharynx by means of series of actions.
 Bolus is placed over postero-dorsal surface of the tongue.
 Anterior part of tongue is depressed and Posterior part of tongue is
elevated and retracted against the hard palate.
 Forceful contraction of tongue against the palate produces a positive
pressure in the posterior part of oral cavity.
 This pushes the food into pharynx

PHARYNGEAL STAGE OR SECOND STAGE- food moves from pharynx to esophagus.

Pharyngeal stage is an involuntary stage.
 during this stage of deglutition, bolus from the pharynx can enter into
four paths:
Back into Mouth
 It is prevented by: Position of tongue against the soft palate
Upward into Nasopharynx
 It is prevented by elevation of soft palate
Forward into Larynx
 It is prevented by Approximation of the vocal cords
 Forward and upward movement of larynx
 Backward movement of epiglottis to seal the opening of the larynx
 All these movements stop respiration for a few seconds. It is called
deglutition apnea.
Entrance of Bolus into Esophagus
 The bolus has to pass only through the esophagus.
 This part of esophagus is formed by the cricopharyngeal muscle and it is
called upper esophageal sphincter which is relaxed.
ESOPHAGEAL STAGE OR THIRD STAGE-
 food moves from esophagus to stomach.
 Esophageal stage is also an involuntary stage.
Food is pushed down by peristaltic waves.

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 Peristalsis means a wave of contraction, followed by the wave of

relaxation of muscle fibers of GI tract, which travel in aboral direction
(away from mouth).
 By this type of movement, the contents are propelled down along the
GI tract.
 When bolus reaches the esophagus, the peristaltic waves are initiated.

Role of Lower Esophageal Sphincter

 Distal 2 to 5 cm of esophagus acts like a sphincter and it is called lower
esophageal sphincter.
 It is constricted always.
 When bolus enters this part of the esophagus, this sphincter relaxes so
that the contents enter the stomach.
 After the entry of bolus into the stomach, the sphincter constricts and
closes the lower end of esophagus.

MOVEMENTS OF SMALL INTESTINE

Movements of small intestine are essential for mixing the chyme with digestive
juices, propulsion of food and absorption.

1. MIXING MOVEMENTS
 Mixing movements of small intestine are responsible for proper mixing
of chyme with digestive juices such as pancreatic juice, bile and
intestinal juice.
The mixing movements of small intestine are
Segmentation Contractions
 The contractions occur at regularly spaced intervals along a section of
intestine.
 The segments of intestine in between the contracted segments are
relaxed.
 After sometime, the contracted segments are relaxed and the relaxed
segments are contracted
 Therefore, the segmentation contractions chop the chyme many times.
 This helps in mixing of chime with digestive juices.

Pendular Movement
 Pendular movement is the sweeping movement of small intestine,
resembling the movements of pendulum of clock.

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 Small portions of intestine (loops) sweep forward and backward or

upward and downward.
 This helps in mixing of chime with digestive juices.

2. PROPULSIVE MOVEMENTS
These movement push the chyme in the aboral direction through intestine.
The propulsive movements are
Peristaltic Movements
 Peristalsis is defined as the wave of contraction followed by wave of
relaxation of muscle fibers.
 Under normal conditions, the progress of contraction in an oral
direction is inhibited quickly and the contractions disappear.
 Only the contraction that travels in an aboral direction persists.
 Peristaltic contractions start at any part of the intestine and travel
towards anal end
Peristaltic Rush
 Sometimes, the small intestine shows a powerful peristaltic contraction.
 It is caused by excessive irritation of intestinal mucosa or extreme
distention of the intestine.
 This type of powerful contraction begins in duodenum and passes
through entire length of small intestine and reaches the ileocecal valve
within few minutes. This is called peristaltic rush or rush waves.
 Peristaltic rush sweeps the contents of intestine into the colon.

3. PERISTALSIS IN FASTING –
MIGRATING MOTOR COMPLEX
 It is a type of peristaltic contraction, which occurs in stomach and small
intestine during the periods of fasting for several hours.
 It is different from the regular peristalsis because, a large portion of
stomach or intestine is involved in the contraction.
 It takes about few minutes to reach the colon after taking origin from
the stomach.

Significance of Peristalsis in Fasting

 Migrating motor complex sweeps the excess digestive secretions into
the colon
 It prevents the accumulation of the secretions in stomach and
intestine.
 It also sweeps the residual indigested materials into colon.

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4. MOVEMENTS OF VILLI
 Intestinal villi also show movements simultaneously along with intestinal
movements.
 This helps in absorption of digested food particles from the lumen of
intestine.

QUE. PERISTALSIS
Peristalsis means a wave of contraction, followed by the wave of relaxation of
muscle fibers of GI tract
 It travel in aboral direction (away from mouth).
 By this type of movement, the contents are propelled down along
the GI tract.

PERISTALSIS IN OESOPHAGUS
 When bolus reaches the esophagus, the peristaltic waves are initiated.
 Food moves from esophagus to stomach by these waves

PERISTALSIS IN STOMACH
 When food enters the stomach, the peristaltic contraction or peristaltic
wave appears
 It starts from the lower part of the body of stomach, passes through the
pylorus till the pyloric sphincter.
 This type of peristaltic contraction is called digestive peristalsis because
it is responsible for the grinding of food particles and mixing them with
gastric juice for digestive activities.

PERISTALSIS IN SMALL INTESTINE

Peristaltic Movements
 Peristaltic contractions start at any part of the intestine and travel
towards Colon.
Peristaltic Rush
 Sometimes, the small intestine shows a powerful peristaltic contraction.
 This type of powerful contraction begins in duodenum and passes
through entire length of small intestine and reaches the ileocecal valve
within few minutes. This is called peristaltic rush or rush waves.
 Peristaltic rush sweeps the contents of intestine into the colon.

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MASS PERISTALSIS OF LARGE INTESTINE

 Mass peristalsis propels the feces from colon towards anus.
 Usually, this movement occurs only a few times every day.
 Neurogenic factors like gastrocolic reflex and parasympathetic
stimulation is responsible for this movement

GASTRIN
Gastrin is a peptide with 34 amino acid residues.
It is secreted
 Mainly by the G cells of pyloric glands of stomach, duodenum and
jejunum.
Duration of secretion of gastrin
 From stomach during (second) phase of gastric secretion
 From small intestine during the intestinal (third) phase of gastric
secretion.

Stimulant for Secretion of gastrin are-

 Presence of food in the stomach.
 Stimulation of local nervous plexus in stomach and small intestine.
 Vagovagal reflex during the gastric phase of gastric secretion:
o Gastrin-releasing polypeptide is released at the vagal nerve
ending.
o It causes the secretion of gastrin by stimulating the G cells
Actions
 Stimulates gastric glands to secrete gastric juice with more pepsin and
hydrochloric acid.
 Accelerates gastric motility.
 Promotes growth of gastric mucosa.
 Stimulates secretion of pancreatic juice, which is rich in enzymes.
 Stimulates islets of Langerhans in pancreas to release pancreatic
hormones.

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Classification of Nerve Fibers

 Nerve fibers are classified by six different methods.
 The basis of classification differs in each method.

1. DEPENDING UPON STRUCTURE

Based on structure, nerve fibers are classified into two types:
i. Myelinated Nerve Fibers
 Myelinated nerve fibers are the nerve fibers that are covered by myelin
sheath.
ii. Non-myelinated Nerve Fibers
 Nonmyelinated nerve fibers are the nerve fibers which are not covered
by myelin sheath.„

2. DEPENDING UPON DISTRIBUTION

Nerve fibers are classified into two types, on the basis of distribution:
i. Somatic Nerve Fibers
 Somatic nerve fibers supply the skeletal muscles of the body.
ii. Visceral or Autonomic Nerve Fibers
 Autonomic nerve fibers supply the various internal organs of the body.

3. DEPENDING UPON ORIGIN

On the basis of origin, nerve fibers are divided into two types:
i. Cranial Nerve Fibers
 Nerve fibersarising from brain are called cranial nerve fibers.
ii. Spinal Nerve Fibers
 Nerve fibers arising from spinal cord are called spinal nerve fibers.
4. DEPENDING UPON FUNCTION
 Functionally, nerve fibers are classified into two types:

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 Physiology

i. Sensory Nerve Fibers

 Sensory nerve fibers carry sensory impulses from different parts of the
body to the central nervous system.
 These nerve fibers are also known as afferent nerve fibers.

ii. Motor Nerve Fibers

 Motor nerve fibers carry motor impulses from central nervous system to
different parts of the body.
 These nerve fibers are also called efferent nerve fibers.

5. DEPENDING UPON SECRETIONOF NEUROTRANSMITTER

Depending upon the neurotransmitter substance secreted, nerve fibers are
divided into two types:
i. Adrenergic Nerve Fibers
 Adrenergic nerve fibers secrete noradrenaline.
ii. Cholinergic Nerve Fibers
 Cholinergic nerve fibers secrete acetylcholine.

6. DEPENDING UPON DIAMETER ANDCONDUCTION OF IMPULSE

 Erlanger and Gasser classified the nerve fibers intothree major types, on
the basis of diameter (thickness)of the fibers and velocity of conduction
of impulses
 Type A nerve fibers
 Type B nerve fibers
 Type C nerve fibers

 Among these fibers, type A nerve fibers are the thickest fibers and
 type C nerve fibers are the thinnest fibers.
 Type A nerve fibers are divided into four types:

 Type A alpha or Type I nerve fibers

 Type A beta or Type II nerve fibers
 Type A gamma nerve fibers
 Type A delta nerve fibers.

Velocity of Impulse
 Velocity of impulse through a nerve fiber is directly proportional to the
thickness of the fiber

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 Physiology

Que. DEGENERATIVE CHANGESIN THE NEURON

Degeneration refers to deterioration or impairment or pathological changes
of an injured tissue.
 When a peripheral nerve fiber is injured, the degenerative changes
occur in the nerve cell body and the nerve fiber of same neuron and
the adjoining neuron.
Accordingly, degenerative changes are classified into three types:
1. Wallerian degeneration
2. Retrograde degeneration
3. Transneuronal degeneration.

Que.WALLERIAN DEGENERATIONOR ORTHOGRADE

DEGENERATION
 Wallerian degeneration is the pathological change that occurs in the
distal cut end of nerve fiber (axon).
 It is named after the discoverer Waller.
 It is also called orthograde degeneration.
 Wallerian degeneration starts within 24 hours of injury.
Changes in Nerve
 Axis cylinder swells and breaks up into small pieces.

 Myelin sheath is slowly disintegrated into fatdroplets.

 The changes in myelin sheath occur from 8th to 35th day.

 Neurilemmal sheath is unaffected, but the Schwanncells multiply

rapidly.
 Macrophages invade from outside and remove the debris of axis
cylinder and fat droplets of disintegrated myelin sheath.
 So,the neurilemmal tube becomes empty.
 Later it is filled by the cytoplasm of Schwann cell.
 All these changes take place for about 2 months from the day of injury.

RETROGRADE DEGENERATION
Retrograde degeneration is the pathological changes, which occur in the nerve
cell body and proximalaxon to the cut end.

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 Physiology

Changes in Nerve Cell Body

Changes in the nerve cell body commence within 48 hours after the section of
nerve.
The changes are:
 First, the Nissel granules disintegrate into fragments by chromatolysis
 Golgi apparatus is disintegrated
 Nerve cell body swells due to accumulation of fluid and becomes round
 Neurofibrils disappear followed by displacement of the nucleus towards
the periphery
 Sometimes, the nucleus is extruded out of the cell.
In this case, death of the neuron occurs and regeneration of the injured nerve
is not possible.

Changes in Axon Proximal to Cut End

 In the axon, changes occur only up to first node ofRanvier from the site
of injury.
 Degenerative changesthat occur in proximal cut end of axon are similar
tothose changes occurring in distal cut end of the nervefiber.

TRANSNEURONAL DEGENERATION
 If an afferent nerve fiber is cut, the degenerative changesoccur in the
neuron with which the afferent nervefiber synapses.
 It is called transneuronal degeneration.
Examples:
i. Chromatolysis in the cells of lateral geniculate body occurs due to sectioning
of optic nerve
ii. Degeneration of cells in dorsal horn of spinal cord occurs when the
posterior nerve root is cut.

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 Physiology

FUNCTIONS OF
SYNAPSE
Main function of the synapse is to
transmit the impulses
 , i.e. action potential from one
neuron to
another.
 some of the synapses inhibit these
impulses. So the impulses are not
transmitted to thepostsynaptic
neuron.

On the basis of functions, synapses are

divided into
two types:
1. Excitatory synapses, which transmit
the impulses(excitatory function)
2. Inhibitory synapses, which inhibit the
transmissionof impulses (inhibitory
function).

Que.Epsp [Exitatory
postsynaptic potential]
EXCITATORY FUNCTION
See the chart...

Properties of EPSP
 EPSP is confined only to the
synapse. It is a graded potential
 It is similar to receptor
potentialand endplate potential.
EPSP has two properties:
1. It is nonpropagated
2. It does not obey all or none law.

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 Physiology

FUNCTIONS OF HYPOTHALAMUS
It regulates many vital functions of the body like endocrine functions, visceral
functions, metabolic activities, hunger, thirst, sleep, wakefulness,
emotion, sexual functions, etc.
SECRETION OF POSTERIOR PITUITARY HORMONES
 Hypothalamus is the site of secretion for the posterior pituitary
hormones.
 Antidiuretic hormone (ADH) and oxytocin are secreted by supraoptic
and paraventricular nuclei.

CONTROL OF ANTERIOR PITUITARY

Hypothalamus controls the secretions of anterior pituitary gland by secreting
releasing hormones and inhibitory hormones.
 Growth hormone-releasing hormone (GHRH)
 Growth hormone-releasing polypeptide (GHRP)
 Growth hormone-inhibiting hormone (GHIH) or somatostatin
 Thyrotropin-releasing hormone (TRH)
 Corticotropin-releasing hormone (CRH)
 Gonadotropin-releasing hormone (GnRH)
 Prolactin-inhibiting hormone (PIH).

REGULATION OF AUTONOMIC NERVOUS SYSTEM

 Hypothalamus controls autonomic nervous system (ANS).
 Sympathetic division of ANS is regulated by posterior and lateral nuclei
of hypothalamus.
 Parasympathetic division of ANS is controlled by anterior group of
nuclei.
REGULATION OF HEART RATE and BLOOD PRESSURE
 Hypothalamus regulates heart rate through vasomotor center in the
medulla oblongata.
 Stimulation of posterior and lateral nuclei of hypothalamus increases the
 heart rate.
 Stimulation of anterior nuclei decreases the heart rate.
„
REGULATION OF BODY TEMPERATURE
Body temperature is regulated by hypothalamus, which sets the normal range
of body temperature.
 The set point, under normal physiological conditions is 37°C.

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 Physiology

Hypothalamus has two centers which regulate the body temperature:

 Heat loss center that is present in anterior hypothalamus
 Heat gain center that is situated in posterior hypothalamic nucleus.

REGULATION OF HUNGER AND FOOD INTAKE

Food intake is regulated by two centers present in hypothalamus:
Feeding Center
 Feeding center is in the lateral hypothalamic nucleus. It stimulate
hunger.
Satiety Center
 Satiety center is in the ventromedial nucleus of the hypothalamus.

REGULATION OF WATER BALANCE

Hypothalamus regulates water content of the body by two mechanisms:
Thirst Mechanism
 Thirst center is in the lateral nucleus of hypothalamus.
 There are some osmoreceptors in the areas adjacent to thirst center.
 Osmoreceptors activate the thirst center and thirst sensation is initiated.

ADH Mechanism
 When the volume of ECF decreases, supraoptic nucleus is stimulated and
ADH is released.

REGULATION OF SLEEP AND WAKEFULNESS

 Mamillary body in the posterior hypothalamus is considered as the
wakefulness center.

ROLE IN BEHAVIOR AND EMOTIONAL CHANGES

Reward Center
 Reward center is situated near ventromedial nucleus of hypothalamus.
Stimulation of these areas in animals pleases or satisfies the animals.
Punishment Center
 Punishment center is situated in posterior and lateral nuclei of
hypothalamus. Stimulation of these nuclei leads to pain, fear.
REGULATION OF SEXUAL FUNCTION
 hypothalamus regulates the sexual functions by secreting gonadotropin
releasing hormone.
ROLE IN CIRCADIAN RHYTHM
 Suprachiasmatic nucleus of hypothalamus plays an important role in
setting the biological clock
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 Physiology

FUNCTIONS OF BASAL GANGLIA

Basal ganglia form the part of extrapyramidal system, which is concerned with
integration and regulation motor activities.
Various functions of basal ganglia are:
CONTROL OF MUSCLE TONE
Basal ganglia control the muscle tone.
 Basal ganglia decrease the muscle tone by inhibiting gamma motor
neurons

CONTROL OF MOTOR ACTIVITY

Regulation of Voluntary Movements
 Movements during voluntary motor activity are initiated by cerebral
cortex.
 However, these movements are controlled by basal ganglia,
 Basal ganglia control the motor activities because of the nervous
(neuronal) circuits between basal ganglia and other parts of the brain
involved in motor activity.

Regulation of Conscious Movements

This function of basal ganglia is also known as the cognitive control of activity.
 For example, when a stray dog barks at a man, immediately the person,
understands the situation, turns away and starts running.

Regulation of Subconscious Movements

 It regulates skilled activities such as writing the learnt alphabet, paper
cutting.

CONTROL OF REFLEX MUSCULAR ACTIVITY

 Basal ganglia are responsible for the coordination and integration of
impulses.

CONTROL OF AUTOMATIC ASSOCIATED MOVEMENTS

 Automatic associated movements are the movements in the body,
which take place along with some motor activities.
 Examples are the swing of the arms while walking, appropriate facial
expressions while talking or doing any work.
 Basal ganglia are responsible for the automatic associated movements.
ROLE IN AROUSAL MECHANISM
 Connections with reticular formation help in arousal mechanism.

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 Physiology

APPLIED PHYSIOLOGY or DISORDERS OF BASAL GANGLIA

PARKINSON DISEASE
Parkinson disease is a slowly progressive degenerative disease of nervous
system
 It is named after the discoverer James Parkinson. It is also called
parkinsonism or paralysis agitans.

Causes of Parkinson Disease

Parkinson disease occurs due to lack of dopamine caused by damage of basal
ganglia.
It is mostly due to
 the destruction of substantia nigra
 Viral infection of brain
 Injury to basal ganglia
Parkinsonism due to the drugs is known as drug-induced parkinsonism.

Signs and Symptoms of Parkinson Disease

Tremor
 In Parkinson disease, the tremor occurs during rest.
 But it disappears while doing any work. So, it is called resting tremor.
 Thumb moves rhythmically over the index and middle fingers.
 These movements are called pill-rolling movements.

Slowness of movements
 Over the time, movements start slowing down (bradykinesia)
 Voluntary movements are reduced (hypokinesia).
Poverty of movements
 Loss of all automatic associated movements.
 The body becomes statue-like.
 The face becomes mask-like, due to absence of appropriate expressions
like blinking and smiling.
Rigidity
 Stiffness of muscles occurs in limbs resulting in rigidity of limbs.
 The muscular stiffness occurs because of increased muscle tone
 So, the limbs become more rigid like pillars. The condition is called
lead-pipe rigidity.
Gait
 The patient looses the normal gait.

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 Physiology

 The patient walks quickly in short steps by bending forward

Speech problems
 Many patients develop speech problems.
 They may speak very softly or sometimes rapidly.

Emotional changes
 The persons affected by Parkinson disease are often upset emotionally.
Dementia
 Loss of memory occurs in some patient.

Treatment for Parkinson Disease

Dopamine does not cross the bloodbrain barrier.
 Levodopa (Ldopa) which crosses the bloodbrain barrier is given.
 another substance called carbidopa is administered to increase
levodopa action on brain.

WILSON DISEASE
 Copper deposits cause damage to basal ganglia.

CHOREA
 Chorea is an abnormal involuntary movement. Chorea means rapid jerky
movements.
 It occurs due to damage to basal ganglia.
Que.Functions of cerebellum
Cerebellum having three functional devision
1]Vestibulocerebellum
 Regulates tone, posture and equilibrium by receiving impulses from
vestibular apparatus.

2] Spinocerebellum
 Rregulates tone, posture and equilibrium by receiving sensory impulses
form tactile receptors, proprioceptors, visual receptors and auditory
receptors.

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 Physiology

3]Corticocerebellum
Control of ballistic movements
 Ballistic movements are the rapid alternate movements.
 EX. typing, cycling, dancing, etc.
 Corticocerebellum plays an important role in preplanning the ballistic
movements during learning process.
Cerebellum is like inspector which
receives command from
Comparator function cortex and see whether its
 On one side, cerebellum receives the informationdonefromproperly
cerebralor not
cortex,
regarding the cortical impulses which are sent to the muscles.
 On the other side, it receives the feedback information (proprioceptive
impulses) from muscles, regarding their actions under the instruction of
cerebral cortex.
 By receiving the messages from both ends, corticocerebellum compares
the cortical commands for muscular activity and the actual movements
carried out by the muscles.
 If any correction is to be done, then, corticocerebellum sends
instructions (impulses) to the motor cortex.
 Accordingly, cerebral cortex corrects or modifies the signals to
muscles,so that the movements become accurate, precise and smooth..
Damping action
 Damping action refers to prevention of exaggeratedmuscular activity.
 This helps in making the voluntary movements smooth and accurate.
Servomechanism
 Servomechanism is the correction of any disturbance or interference
while performing skilled work.
 Once the skilled works are learnt, the sequential movements are
executed without any interruption.
Timing and programming the movements
 Corticocerebellum plays an important role in timing and programming
the movements, particularly during learning process.
 Ex. While using a typewriter

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 Physiology

FASCICULUS GRACILIS(TRACT OF GOLL)

ANDFASCICULUS CUNEATUS(TRACT OF
BURDACH)
 Fasciculus gracilis and fasciculus cuneatus aretogether called
ascending posterior column tracts.
 These tracts are formed by the fibers from posterior root ganglia.
Situation
 Tracts of Goll and Burdach are situated in
posteriorwhite column of spinal cord
hence the nameposteriorcolumn tracts.
 the posterior white column isdivided by
posterior intermediate septum into
 medialfasciculus gracilis and
 lateral fasciculus cuneatus.

Origin
Fibers of these two tracts are the axons of
first orderneurons.
Cell body of these neurons is in the posterior
root ganglia
Course
 After entering spinal cord, the fibers ascend
Throughthe posterior white column.
 These fibers do notsynapse in the
spinal cord.
 Fasciculus gracilis contains the fibers from
lowerextremitiesand lower parts of
the body, i.e. fromsacral, lumbar and
lower thoracic ganglia of posteriornerve
root.

 Fasciculus cuneatus contains fibers from

upper part of the body, i.e. from upper
thoracic andcervical ganglia of posterior
nerve root.

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Termination
 Tracts of Goll and Burdach terminate in the medullaoblongata.
 Fibers of fasciculus gracilis terminate in Thenucleus gracilis
 The fibers of fasciculus cuneatusterminate in the nucleus cuneatus.

 Neurons of thesemedullary nuclei form the second order neurons.

 Axons of second order neurons form the internalarcuate fibers.
 Internal arcuate fibers from both sidescross the midline
formingsensory decussation
 ascend through pons and midbrain as mediallemniscus.
 Fibers of medial lemniscus terminate inventral posterolateral nucleus of
thalamus.
 Fromhere, fibers of the third order neurons relay to sensoryarea of
cerebral cortex.
Functions
Tracts of the posterior white column convey impulsesof
following sensations:
 Finetactile sensation
 Tactile localization
 Tactile discrimination
 Sensation of vibration
 Conscious kinesthetic sensation
 Stereognosis
Effect of Lesion
Lesion of nerve fibers in tracts of Goll and Burdach or
lesion in the posterior white column leads to the following
symptoms on the same side below the lesion:
 Loss of fine tactile sensation; however, crude
touch sensation is normal
 Loss of tactile localization
 Loss of two point discrimination
 Loss of sensation of vibration
 Astereognosis
 Loss of proprioception

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 Physiology

Que.PHYSIOLOGICAL CHANGES DURING SLEEP

During sleep, most of the body functions are reduced to basal level.
Following are important changes in thebody during sleep:
1. PLASMA VOLUME
Plasma volume decreases by about 10% during sleep.

2. CARDIOVASCULAR SYSTEM
Heart Rate
 During sleep, the heart rate reduces. It varies between 45 and 60 beats
per minute.
Blood Pressure
 Systolic pressure falls to about 90 to 110 mm Hg.
 Lowest level is reached about 4th hour of sleep

3. RESPIRATORY SYSTEM
 Rate and force of respiration are decreased. 9. REFLEXES
 Certain reflexes
4. GASTROINTESTINAL TRACT particularly knee jerk,
 Salivary secretion decreases during sleep. are abolished.
 Gastricsecretion is not altered or may be  Babinski sign
increased slightly. becomes positive
 Contraction of empty stomach is more vigorous. during deep sleep.
„  Threshold for most of
5. EXCRETORY SYSTEM the reflexes increases.
Formation of urine decreases and specific gravity of 10. BRAIN
urine increases Brain is active during sleep.
There is a characteristic
6. SWEAT SECRETION
 cycle of brain wave
 Sweat secretion increases during sleep. activity varies during
sleep withirregular
7. LACRIMAL SECRETION intervals of dreams.
Lacrimal secretion decreases during sleep.
 Electrical activity in
the
8. MUSCLE TONE
brain varies with stages of sleep
 Tone in all the muscles of body except ocular muscles decreases very
much during sleep. It is called sleep paralysis.

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 Physiology

TYPES OF SLEEP
Sleep is of two types:
1. Rapid eye movement sleep or REM sleep
2. Non-rapid eye movement sleep, NREM sleep ornon-REM sleep.

1. RAPID EYE MOVEMENT SLEEP –REM SLEEP

 Rapid eye movement sleep is the type of sleep associated with rapid
conjugate movements of the eyeballs, which occurs frequently.
 Though the eyeballs move, the sleep is deep.
 So, it is also called para-doxical sleep.
 It occupies about 20% to 30% of sleeping period.
 Functionally, REM sleep is very important because, it plays an important
role in consolidation of memory.
 Dreams occur during this period.

2. NON-RAPID EYE MOVEMENT SLEEP –NREM OR NON-REM SLEEP

 Non-rapid eye movement (NREM) sleep is the type of sleep without the
movements of eyeballs.
 It is also called slow-wave sleep.
 Dreams do not occur in this type of sleep and it occupies about 70% to
80% of total sleeping period.
 Non-REM sleep is followed by REM sleep.
Differences between the two types of sleep are given in below table

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 Physiology

STAGES OF SLEEP AND EEG PATTERN

RAPID EYE MOVEMENT SLEEP
 During REM sleep, electroencephalogram (EEG)shows irregular waves
with high frequency and low amplitude.
 These waves are desynchronized waves.
NON-RAPID EYE MOVEMENT SLEEP
 The NREM sleep is divided into four stages,
based onthe EEG pattern.
 During the stage of wakefulness, i.e.
while lying down with closed eyes and
relaxed mind, thealpha waves of
EEG appear.
Stage I: Stage of Drowsiness
 It is transition from wakefulness to sleep.
 It charecterised by disappearance of
alpha wave and appearance of
theta activity
Stage II: Stage of Light Sleep
 Stage II is characterized by
sleep spindles in EEG.

Stage III: Stage of Medium Sleep

 During this stage, the spindle spindles
disappear.
 Frequencyof delta waves decreases
to 1 or 2 per secondand amplitude
increases to about 100 μV.
State IV: Stage of Deep Sleep
Delta waves become more prominent with
lowfrequency and high amplitude

Que.EEG [Electroencephalography ]
 Electroencephalography is the study of electrical activities of brain.
 Electroencephalogram (EEG) is thegraphical recording of electrical
activities of brain.

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 Physiology

Also known as Berger waves.

SIGNIFICANCE OF EEG
 Electroencephalogram is useful in the diagnosis of neurological
disorders and sleep disorders.
 EEG patternis altered in the following neurological
disorders:Epilepsy,Disorders of midbrain , Subdural hematoma

METHOD OF RECORDING EEG

 Electroencephalograph is the instrument used to record EEG.
 The electrodes called scalp electrodes.
 Electrodes are of two types, unipolar and bipolar electrodes.

WAVES OF EEG
 Electrical activity recorded by EEG may have synchronized or
desynchronized waves.
Synchronized waves
are the regular and invariant waves, whereas
Desynchronizedwaves
are irregular and variant.

In normalpersons, EEG has four frequency bands.

1. Alpha rhythm
2. Beta rhythm
3. Theta rhythm
4. Delta rhythm.

ALPHA RHYTHM
 Alpha rhythm consists of rhythmical waves
 It appears at a frequency of 8 to 12 waves/second withthe amplitude of
50 μV.
 Alpha waves are synchronized waves.
 Alpha rhythm is associated with decreased level of attention. Person is
awake but has decreased attention[relaxed] person is thinking but
decreased attention
 It is diminished when eyes are opened.
 Waves of alpha rhythm are most marked in parieto-occipital area

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 Physiology

BETA RHYTHM
 Beta rhythm includes high frequency waves of 15 to 30per second but,
the amplitude is low, i.e. 5 to 10 μV.
 It is mostly marked on frontal lobe
 It occurs when person is fully awake and alert.
 Replacement of beta wave for alpha wave is called arousal or alerting
response or alpha block. It can be produced by sensory stimulation or
increasing concentration like solving arithmetic problem.
 Person is thinking with maximum concentration or conscious thinking
produce beta wave.

Theta wave
 When person with alpha rhythm becomes slightly more relaxed itoccurs
 Alpha rhythm is replaced with theta rhythm during stage 1 NREM.
 Frequency 4-7 per second.

DELTA RHYTHM
 Delta rhythm includes waves with low frequency and high amplitude.
 These waves have the frequency of 1to 5 per second with the amplitude
of 20 to 200 μV.
 Itis common in early childhood during waking hours.
 Inadults, it appears mostly during deep sleep.
 No thinking stage. NREM Stage 3 and 4.

 Presence of delta waves in adults during conditionsother than sleep

indicates the pathological process in brain like
o tumor,
o epilepsy,
o increased intracranial pressure and
o mental deficiency or depression.

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 Physiology

Que. LEARNING
DEFINITION
Learning is defined as the process by which new information is acquired.

CLASSIFICATION OF LEARNING
Learning is classified into two types:
1. Non-associative learning
2. Associative learning.
1. Non-associative Learning
Non-associative learning involves response of a person to only one type of
stimulus. It is based on two factors:
Habituation
 Habituation means getting used to something, to which a person is
constantly exposed
 During first experience, the event (stimulus) evokes a response.
However, it evokes less response when it is repeated.
 Finally, the person is habituated to the event (stimulus) and ignores it.

Sensitization
 Sensitization is a process by which the body is made to become more
sensitive to a stimulus. It is called amplification of response.
 if the same stimulus is combined with another type of stimulus, which
may be pleasant or unpleasant, the person becomes more sensitive to
original stimulus.
 For example, a woman is sensitized to crying sound of her baby.
 She gets habituated to different sounds around her and sleep is not
disturbed by these sounds.
 However, she suddenly wakes up when her baby cries because of
sensitization to crying sound of the baby.

2. Associative Learning
 Associative learning is a complex process.
 It involves learning about relations between two or more stimuliat a
time.
 Classic example of associative learning is the conditioned reflex

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 Physiology

Que. MEMORY
Memory is defined as the ability to recall past experience or information.

ANATOMICAL BASIS OF MEMORY

 Anatomical basis of memory is the synapse in brain.
 One terminal is primary presynaptic terminal, which ends on
postsynaptic neuron
 Sensations are transmitted to the postsynaptic neuron through this
terminal
 Other presynaptic terminal ends on the primary presyneptic terminal.
This terminal is called facilitator terminal.

PHYSIOLOGICAL BASIS OF MEMORY

Memory is stored in brain by the alteration of synaptic transmission between the
neurons involved in memory.

Facilitation
 Facilitation is the process by which memory storage is enhanced.
 It involves increase in synaptic transmission and increased postsynaptic
activity. Often, facilitation is referred as positive memory.

Habituation
 Habituation is the process by which memory storage is decreased in
strength
 It involves reduction in synaptic transmission and slowdown or
stoppage of postsynaptic activity.
 Sometimes, habituation is referred as negative memory.

CLASSIFICATION OF MEMORY
Memory is classified by different methods
Short-term Memories and Long-term Memories
1. Short-term memory
 Short-term memory is the recalling events that happened very recently,
i.e. within hours or days.
 It is also known as recent memory.
 For example, telephone number that is known today may be
remembered till tomorrow. But if it is not recalled repeatedly, it may be
forgotten.
2. Long-term memory
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 Long-term memory is the recalling of events of weeks, months, years or

sometimes lifetime.
 It is otherwise called the remote memory.
 Examples are, recalling first day of schooling, birthday celebration of
previous year
 Long-term memory is more resistant and is not disrupted easily.

Explicit and Implicit Memories

Physiologically, memory is classified into two types, namely explicit memory and
implicit memory.
Explicit memory
 Explicit memory is defined as the memory that involves conscious
recollection of past experience.
 It consists of memories regarding events
 Examples of explicit memory are recollection of a birthday party
celebrated few days ago

Implicit memory
 Implicit memory is defined as the memory in which past experience is
utilized without conscious awareness.
 It helps to perform various skilled activities properly.
 Implicit memory is otherwise known as skilled memory.
 Examples of implicit memory are cycling, driving, playing tennis, dancing,
typing, etc.

APPLIED PHYSIOLOGY – ABNORMALITIES OF MEMORY

1. Amnesia
Loss of memory is known as amnesia. Amnesia is classified into two types:
 Anterograde amnesia: Failure to establish new long-term memories.
 Retrograde amnesia: Failure to recall past remote long-term memory.
2. Dementia
 Dementia is the progressive deterioration of emotional control, social
behavior and associated with loss of memory.
 It is an age-related disorder. Usually, it occurs above the age of 65 years.
3. Alzheimer Disease
 Alzheimer disease is a progressive neurodegenerative disease.
 It is due to degeneration, loss of function and death of neurons in
many parts of brain

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Que. SPEECH
Speech is defined as the expression of thoughts by production of articulate
sound, bearing a definite meaning.
 If it is expressed by visual symbols, it is known as writing.
 If visual symbols or written words are expressed verbally, that becomes
reading.

MECHANISM OF SPEECH
Speech depends upon coordinated activities of central speech apparatus and
peripheral speech apparatus.
 Central speech apparatus consists of higher centers, i.e. the cortical and
subcortical centers.
 Peripheral speech apparatus includes larynx or sound box, pharynx,
mouth, nasal cavities, tongue and lips.
 All the structures of peripheral speech apparatus function in
coordination with respiratory system
DEVELOPMENT OF SPEECH
First Stage
First stage in the development of speech is the association of certain words with
visual, tactile, auditory and other sensations
 Association of words with other sensations is stored as memory.

Second Stage
 New neuronal circuits are established during the development of
speech.
 When a definite meaning has been attached to certain words, pathway
between the auditory area and motor area for the muscles of
articulation, which helps in speech

Role of Cortical Areas in the Development of Speech

Development of speech involves integration of three important areas of cerebral
cortex:
1. Wernicke area 2. Broca area 3. Motor area.
Role of Wernicke area – Speech understanding
 Wernicke area is responsible for understanding the visual and auditory
information required for the production of words.
 After understanding the words, it sends the information to Broca area.

Role of Broca area – Speech synthesis

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 By receiving information required for production of words from

Wernicke area, the Brocas area develops the pattern of motor activities
required to verbalize the words.
 The pattern of motor activities is sent to motor area.

Role of motor area – Activation of peripheral speech apparatus

 By receiving the pattern of activities from Broca area, motor area
activates the peripheral speech apparatus.
 It results in initiation of movements of tongue, lips and larynx required
for speech.

APPLIED PHYSIOLOGY – DISORDERS OF SPEECH

Speech disorder is a communication disorder
APHASIA
 Aphasia is defined as the loss or impairment of speech due to brain
 Aphasia is not due to paralysis of muscles of articulation. It is due to
damage of speech centers.
DYSARTHRIA OR ANARTHRIA
 The term dysarthria refers to disturbed articulation.
 Anarthria means inability to speak. Dysarthria or anarthria is defined as
the difficulty or inability to speak because of paralysis of muscles
involved in articulation.
DYSPHONIA
 Dysphonia is a voice disorder. Often, it is characterized by hoarseness
and a sore or a dry throat. voice may be weak or husky.

STAMMERING
 Stammering or shuttering is a speech disorder characterized by
hesitations and involuntary repetitions of certain words.

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ORGAN OF CORTI
 Organ of Corti is the receptor organ for hearing.
 It is the neuroepithelial structure in cochlea
Situation and Extent
 Organ of corti rests upon the basilar membrane.
 It extends throughout the cochlear duct, except for a short distance on
either end.
 Roof of the organ of Corti is formed by tectorial membrane.

Structure
Organ of Corti is made up of sensory elements called hair cells and various
supporting cells.
Cells of organ of Corti:
1. Border Cells
2. Inner Hair Cells
 Inner hair cells are flaskshaped cells
 Surface of the inner hair cell bears number of short stiff hairs, which are
called stereocilia.
 Each hair cell has about 100 sterocilia.
 One of the sterocilia is larger and it is called kinocilium.
 Stereocilia are in contact with the tectorial membrane.
 Inner hair cells and outer hair cells together form the receptor cells.
And Connected with Nerve.

3. Inner Phalangeal Cells

Inner phalangeal cells are the supporting cells of inner hair cells.

4 and 5. Inner and Outer Pillar Cells – Rods of Corti

They enclose a triangular tunnel called inner tunnel or tunnel of Corti.

6. Outer Phalangeal Cells

Outer phalangeal cells are the supporting cells of outer hair cells.

7. Outer Hair Cells

Their bases are supported by outer phalangeal cells.
 Structure of outer hair cells is similar to that of inner hair cells.

8. Cells of Hensen
9. Cells of Claudius

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10. Tectorial Membrane and Lamina Reticularis

 It forms the roof of organ of Corti.
 It is in contact with the processes of hair cells.
 It is assumed that the processes of hair cells are stimulated by the
movements of tectorial membrane, in relation to vibrations in
endolymph.

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