৪৮তম বিশেষ বিসিএস [স্বাস্থ্য] ⎯ মেডিকেল অংশ [Archived]

Decreased blood volume stimulates the secretion of renin
(because of decreased renal perfusion pressure) and initiates the renin–angiotensin–
aldosterone cascade. Angiotensin-converting enzyme (ACE) inhibitors block the cascade
by decreasing the production of angiotensin II. Hyperosmolarity stimulates antidiuretic
hormone (ADH) [not aldosterone] secretion. Hyperkalemia, not hypokalemia, directly
stimulates aldosterone secretion by the adrenal cortex.

„ ACCOMMODATION
„ DEFINITION
Accommodation is the adjustment of eye to see either
near or distant objects clearly. It is the process by
which light rays from near objects or distant objects
are brought to a focus on sensitive part of retina. It is
achieved by various adjustments made in the eyeball.
„ MECHANISM OF ACCOMMODATION
Light rays from distant objects are approximately parallel
and are less refracted while getting focused on retina.
But, the light rays from near objects are divergent. So,
to be focused on retina, these light rays should be
refracted (converged) to a greater extent. There are
three possible ways by which, accommodation occurs:
1. Retina must be moved towards or away from the
lens. It is done by shortening or elongation of eyeball.
So, the divergent, parallel or convergent rays are
focused accurately. This mechanism is present only
in some molluscs and not in human beings.
2. Lens must be moved towards or away from the
retina. It is done in photography. This mechanism
exists in some fishes.
3. Convexity of lens must be altered, so that the
refractory power of lens is altered according to the
need. This mechanism is present in human eye and
it was first suggested by Young and later supported
by Helmholtz (Fig. 169.2).„ ACCOMMODATION REFLEX
Accommodation is a reflex action. When a person
looks at a near object after seeing a far object, three
adjustments are made in the eyeballs:
1. Convergence of the eyeballs due to contraction of
the medial recti
2. Constriction of the pupil due to the contraction of
constrictor pupillae of iris
3. Increase in the anterior curvature of the lens due to
contraction of the ciliary muscle.
Thus, the accommodation reflex involves both
skeletal muscle (medial recti) and smooth muscle
(ciliary muscle and sphincter pupillae).
During accommodation, all the adjustments are
carried out simultaneously. Although accommodation
is a reflex action, it can be controlled by willpower to
a certain extent.
„ PATHWAY FOR ACCOMMODATION REFLEX
Afferent Pathway
Visual impulses from retina pass through the optic
nerve, optic chiasma, optic tract, lateral geniculate
body and optic radiation to visual cortex (area 17) of
occipital lobe. From here, the association fibers carry
the impulses to frontal lobe (Fig. 169.4).
Center
The center for accommodation lies in frontal eye field
(area 8) that is situated in the frontal lobe of cerebral
cortexEfferent Pathway
1. Efferent fibers to ciliary muscle
and sphincter pupillae
From area 8, the corticonuclear fibers pass via
internal capsule to the Edinger-Westphal nucleus of
third cranial nerve. From here, the preganglionic fibers
pass through the third cranial nerve to ciliary ganglion.
Postganglionic fibers from ciliary ganglion pass via the
short ciliary nerves and supply the ciliary muscle and
the constrictor pupillae.
2. Efferent fibers to medial rectus
Some of the fibers from frontal eye field terminate in
the somatic motor nucleus of oculomotor nerve. The
fibers from motor nucleus supply medial rectus.

BODY FLUIDS
Water is the medium of the internal environment and
constitutes a large percentage of the body weight. Discussion in this section includes the distribution of
water in various compartments of the body; the methods
of measuring volumes of the body fluid compartments;
the differences in concentrations of major cations and
anions among the compartments; and the shifts of
water that occur between the body fluid compartments
when a physiologic disturbance occursDistribution of Water among the Body Fluids
Total Body Water
Water accounts for 50% to 70% of body weight, with
an average value of 60% (Fig. 6-4). The percentage of
total body water varies, depending on gender and the
amount of adipose tissue in the body. Water content of
the body correlates inversely with fat content. Women
have lower percentages of water than men (because
women have the higher percentage of adipose tissue).
For these reasons, thin men have the highest percentage of body weight as water (≈70%) and obese women
have the lowest percentage (≈50%).
The relationship between water content and body
weight is clinically important because changes in bodyweight can be used to estimate changes in body water
content. For example, in the absence of other explanations, a sudden weight loss of 3 kg reflects a loss of
3 kg (≈3 L) of total body water.
The distribution of water among the body fluid compartments is shown in Figure 6-4. Total body water is
distributed between two major compartments: intracellular fluid (ICF) and extracellular fluid (ECF).
Approximately two thirds of total body water is in the
ICF, and about one third is in the ECF. When expressed
as percentage of body weight, 40% of body weight is
in ICF (two thirds of 60%), and 20% of body weight
is in ECF (one third of 60%). (The 60-40-20 rule is
useful to know: 60% of body weight is water, 40% is
ICF, and 20% is ECF.) ECF is further divided among two minor compartments: the interstitial fluid and the
plasma. Approximately three fourths of the ECF is
found in the interstitial compartment, and the remaining one fourth is found in the plasma. A third body
fluid compartment, the transcellular compartment
(not shown in Fig. 6-4), is quantitatively small and
includes the cerebrospinal, pleural, peritoneal, and
digestive fluids.
Intracellular Fluid
ICF is the water inside the cells in which all intracellular solutes are dissolved. It constitutes two thirds
of total body water or 40% of body weight. The composition of ICF is discussed in Chapter 1. Briefly, the
major cations are potassium (K+
) and magnesium (Mg2+
), and the major anions are proteins and organic
phosphates such as adenosine triphosphate (ATP),
adenosine diphosphate (ADP), and adenosine monophosphate (AMP).
Extracellular Fluid
ECF is the water outside the cells. It constitutes one
third of total body water or 20% of body weight. ECF
is divided among two subcompartments: plasma and
interstitial fluid. Plasma is the fluid that circulates in
the blood vessels, and interstitial fluid bathes the
cells. The composition of ECF differs substantially from
ICF: The major cation of ECF is sodium (Na+
), and
the major anions are chloride (Cl−
) and bicarbonate
(HCO3
−
).Plasma is the aqueous component of blood. It is
the fluid in which the blood cells are suspended. On a
volume basis, plasma constitutes 55% of blood volume
and blood cells (i.e., red blood cells, white blood cells,
and platelets) constitute the remaining 45% of blood
volume. The percent of blood volume occupied by red
blood cells is called the hematocrit, which averages
0.45 or 45% and is higher in males (0.48) than in
females (0.42). Plasma proteins constitute about 7%
of plasma by volume; thus, only 93% of plasma
volume is plasma water, a correction that usually is
ignored.
Interstitial fluid is an ultrafiltrate of plasma: It
has nearly the same composition as plasma, excluding
plasma proteins and blood cells. To understand why
interstitial fluid contains little protein and no blood
cells, simply remember that it is formed by filtration
across capillary walls (see Chapter 4). Pores in the
capillary wall permit free passage of water and small
solutes, but these pores are not large enough to permit
passage of large protein molecules or cells. There are
also small differences in the concentrations of smallcations and anions between interstitial fluid and plasma, explained by the Gibbs-Donnan effect of the negatively charged plasma proteins (see Chapter 1). The
Gibbs-Donnan effect predicts that plasma will have a
slightly higher concentration of small cations (e.g.,
Na+
) than interstitial fluid and a slightly lower concentration of small anions (e.g., Cl−
)

Renal circulation

The renal blood flow exhibits a number of characteristics:

1. It has two cap. beds, separated by the efferent arterioles that help to regulate the hydrostatic pressures in both sets of capillaries. Glomerular cap. are high pressure 60 mmHg causes rapid filtration. Peritubular cap. are low pressure. 13mmHg causes rapid reabsorption. It is an arterial portal system (unique).

2. The rate of blood flow is very high 400 ml/min/100 gm. It is about 1100-1200 ml/min about 22% of cardiac output ( renal fraction)

3. Blood flow within the kidney is not homogenous. The cortex (80%) is better perfused than medulla (20%).

4. The arteriovenous oxygen difference for the whole kidney is only 1.4 ml/dl of blood. (5 ml/dl for whole body)

5. The kidneys are unique in that changes in blood flow are accompanied by parallel changes in O2 consumption, with the A-V O2 difference remaining the same. Renal O2 consumption is proportional to amount of Na+ reabsorption.

6. The metabolic demand of the kidney is determined by blood flow, whereas the opposite is true for other organs with significant metabolic regulation.

7. In medula blood flow is very low 60ml/100gm/min, but Na+ reabsorbed in TAL of LOH is high.

8. The PO2 of the cortex is about 50mmHg. The PO2 of the medulla is about 15mmHg. Relatively large amounts of O2 are extracted from the blood in the medulla. This makes the medulla vulnerable to hypoxia if flow is reduced further.

9. The renal circulation shows a remarkable constancy in face of B.P. changes – Autoregulation of renal blood flow- It is produced by a direct contractile response of the smooth muscle of the afferent arteriole to stretch (NO may also be involved). Myogenic mechanism stretch entry of Ca++ from ECF causing them to contract.


SPECIAL FEATURES OF RENAL CIRCULATION Renal circulation has some special features to cope up with the functions of the kidneys. Such special features are: 1. Renal arteries arise directly from the aorta. So, the high pressure in aorta facilitates the high blood flow to the kidneys. 2. Both the kidneys receive about 1,300 mL of blood per minute, i.e. about 26% of cardiac output. Kidneys are the second organs to receive maximum blood flow, the first organ being the liver, which receives 1,500 mL per minute, i.e. about 30% of cardiac output. 3. Whole amount of blood, which flows to kidney has to pass through the glomerular capillaries before entering the venous system. Because of this, the blood is completely filtered at the renal glomeruli. 4. Renal circulation has a portal system, i.e. a double network of capillaries, the glomerular capillaries and peritubular capillaries. 5. Renal glomerular capillaries form high pressure bed with a pressure of 60 mm Hg to 70 mm Hg. It is much greater than the capillary pressure elsewhere in the body, which is only about 25 mm Hg to 30 mm Hg. High pressure is maintained in the glomerular capillaries because the diameter of afferent arteriole is more than that of efferent arteriole. The high capillary pressure augments glomerular filtration. 6. Peritubular capillaries form a low pressure bed with a pressure of 8 mm Hg to 10 mm Hg. This low pressure helps tubular reabsorption. 7. Autoregulation of renal blood flow is well established.

Water reabsorption :
Facultative water reabsorption is the regulated reabsorption of water in the distal convoluted tubule (DCT) and collecting ducts of the kidney, influenced by the antidiuretic hormone (ADH). This process helps the body conserve or excrete water based on hydration status, and it's distinct from obligatory reabsorption, which occurs regardless of ADH levels. 

DEFENSE OF VOLUME The volume of the ECF is determined primarily by the total amount of osmotically active solute in the ECF. The composition of the ECF is discussed in Chapter 1. Because Na+ and Cl− are by far the most abundant osmotically active solutes in ECF, and because changes in Cl− are to a great extent secondary to changes in Na+, the amount of Na+ in the ECF is the most important determinant of ECF volume. Therefore, the mechanisms that control Na+ balance are the major mechanisms defending ECF volume. However, there is volume control of water excretion as well; a rise in ECF volume inhibits vasopressin secretion, and a decline in ECF volume produces an increase in the secretion of this hormone. Volume stimuli override the osmotic regulation of vasopressin secretion. Angiotensin II stimulates aldosterone and vasopressin secretion. It also causes thirst and constricts blood vessels, which help maintain blood pressure. Thus, angiotensin II plays a key role in the body’s response to hypovolemia (Figure 38–5). In addition, expansion of the ECF volume increases the secretion of atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) by the heart, andIn disease states, loss of water from the body (dehydration) causes a moderate decrease in ECF volume, because water is lost from both the intracellular and ECF compartments; but excessive loss of Na+ in the stools (diarrhea), urine (severe acidosis, adrenal insufficiency), or sweat (heat prostration) decreases ECF volume markedly and eventually leads to shock. The immediate compensations in shock operate principally to maintain intravascular volume, but they also affect Na+ balance. In adrenal insufficiency, the decline in ECF volume is not only due to loss of Na+ in the urine but also to its movement into cells. Because of the key position of Na+ in volume homeostasis, it is not surprising that more than one mechanism has evolved to control the excretion of this ion. The filtration and reabsorption of Na+ in the kidneys and the effects of these processes on Na+ excretion are discussed in Chapter 37. When ECF volume is decreased, blood pressure falls, glomerular capillary pressure declines, and the glomerular filtration rate (GFR) therefore falls, reducing the amount of Na+ filtered. Tubular reabsorption of Na+ is increased, in part because the secretion of aldosterone is increased. Aldosterone secretion is controlled in part by a feedback system in which the change that initiates increased secretion is a decline in mean intravascular pressure. Other changes in Na+ excretion occur too rapidly to be solely due to changes in aldosterone secretion. For example, rising from the supine to the standing position increases aldosterone secretion. However, Na+ excretion is decreased within a few minutes, and this rapid change in Na+ excretion occurs in adrenalectomized subjects. It is probably due to hemodynamic changes and possibly to decreased ANP secretion. The kidneys produce three hormones: 1,25-dihydroxycholecalciferol (see Chapter 21), renin, and erythropoietin. Natriuretic peptides, substances secreted by the heart and other tissues, increase excretion of sodium by the kidneys, and an additional natriuretic hormone (endogenous ouabain) inhibits Na, K ATPase.

PHYSICAL EXAMINATION

1. Volume Increase in urine volume indicates increase in protein catabolism and renal disorders such as chronic renal failure, diabetes insipidus and glycosuria.

2. Color Normally urine is straw colored. Abnormal coloration of urine is due to several causes such as jaundice, hema turia, hemoglobinuria, medications, excess urobili no gen, ingestion of beetroot or color added to food.

3. Appearance Normally urine is clear. It becomes turbid in both physiological and pathological conditions. Physiological conditions causing turbidity of urine are precipitation of crystals, presence of mucus or vaginal discharge. Pathological conditions causing turbidity are presence of blood cells, bacteria or yeast.

4. Specific Gravity Specific gravity of urine is the measure of dissolved solutes (particles) in urine. It is low in diabetes insipidus and high in diabetes mellitus, acute renal failure and excess medications

. 5. Osmolarity Osmolarity of urine decreases in diabetes insipidus.

6. pH and Reaction Measurement of pH is useful in determining the metabolic or respiratory acidosis or alkalosis. The pH decreases in renal diseases. In normal conditions, pH of urine depends upon diet. It is slightly alkaline in vegetarians and acidic in non-vegetarians.

UPPER MOTOR NEURON AND
LOWER MOTOR NEURON
Neurons of the motor system are divided into upper
motor neurons and lower motor neurons, depending
upon their location and termination.
Upper Motor Neuron
Upper motor neurons are the neurons in higher centers
of brain, which control the lower motor neurons.
Upper motor neurons are of three types:
1. Motor neurons in cerebral cortex. Fibers of these
neurons form corticospinal (pyramidal) and
corticobulbar tracts.
2. Neurons in basal ganglia and brainstem nuclei
3. Neurons in cerebellum.
Motor neurons in cerebral cortex, which give origin
to pyramidal tracts belong to the pyramidal system and
the remaining motor neurons belong to extrapyramidal
system.
Some controversy exists in including the neurons
of extrapyramidal system under the category of upper
motor neurons. However, considering in terms of the
definition, neurons other than lower motor neurons are
to be named as upper motor neurons.
Lower Motor Neuron
Lower motor neurons are the anterior gray horn cells in
spinal cord and motor neurons of cranial nerve nuclei,
situated in brainstem, which innervate the muscles
directly.
Thus, the lower motor neurons constitute ‘final
common pathway’ of motor system. Lower motor neurons
are under the influence of upper motor neurons

6. DEPENDING UPON CLINICAL BASIS
Depending upon the clinical basis, reflexes are classified
into four types:
i. Superficial reflexes
ii. Deep reflexes
iii. Visceral reflexes
iv. Pathological reflexes.
„ SUPERFICIAL REFLEXES
Superficial reflexes are the reflexes, which are elicited
from the surface of the body. Superficial reflexes are
of two types: mucus membrane reflexes and skin
reflexes.
„ 1. MUCOUS MEMBRANE REFLEXES
Mucous membrane reflexes arise from the mucus
membrane. Details of mucus membrane reflexes are
listed in Table 142.1.
„ 2. CUTANEOUS REFLEXES OR
SKIN REFLEXES
Cutaneous reflexes are elicited from skin by the
stimulation of cutaneous receptors. Details of these
reflexes are given in Table 142.2.
„ DEEP REFLEXES
Deep reflexes are elicited from deeper structures
beneath the skin like tendon. These reflexes are
otherwise known as tendon reflexes. Details of these
are given in Table 142.3.
„ VISCERAL REFLEXES
Visceral reflexes are the reflexes arising from pupil
and visceral organs. Other details of visceral reflexes
are already given above.

1.Glucocorticoids prevent the inflammatory changes by:

i. Inhibiting the release of chemical substances from damaged tissues and thereby preventing vasodilatation and erythema in the affected area
ii. Causing vasoconstriction through the permissive action on catecholamines. This also prevents rushing of blood to the injured area
iii. Decreasing the permeability of capillaries and preventing loss of fluid from plasma into the affected tissue
iv. Inhibiting the migration of leukocytes into the affected area
v. Suppressing T cells and other leukocytes, so that there is reduction in the reactions of tissues which enhance the inflammatory process.

2.Anti-allergic Actions:

Corticosteroids prevent various reactions in allergic conditions as in the case of inflammation.

3.Immunosuppressive Effects:

Glucocorticoids suppress the immune system of the body by decreasing the number of circulating T lymphocytes. It is done by suppressing proliferation of T cells and the lymphoid tissues (lymph nodes and thymus). Glucocorticoids also prevent the release of interleukin-2 by T cells.

REGULATION OF UTERINE CHANGES:

Uterine changes during menstrual cycle are influenced by estrogen and progesterone.

Proliferative Phase:

During proliferative stage, the repair of the damaged endometrium occurs mainly by estrogen. Estrogen stimulates: 1. Proliferation of cells in endometrial stroma 2.Development of uterine glands and appearance of blood vessels in the endometrial stroma.

Secretory Phase:

Secretory phase of uterine changes, coincides with luteal phase of ovarian cycle. Under the influence of FSH and LH from anterior pituitary, the corpus luteum secretes large amount of progesterone and small amount of estrogen. Progesterone is responsible for endometrial changes along with estrogen during this phase.

Progesterone stimulates: 1. Growth of endometrial glands and makes them more tortuous 2. Growth of blood vessels and makes them also tortuous, leading to increase in blood flow to endometrium 3. Secretory activities of endometrial glands. Thus, during the secretory phase, the structure, blood flow and secretory functions of uterus are influenced by estrogen and progesterone secreted by corpus luteum.

Menstrual Phase:

If pregnancy does not occur, menstrual phase occurs: 1. During the last two days of secretory phase, i.e. two days prior to onset of menstruation, the secretion of large quantity of progesterone and estrogen from corpus luteum inhibits the secretion of FSH and LH from anterior pituitary, by negative feedback 2. In the absence of LH and FSH, the corpus luteum becomes inactive and starts regressing 3. Sudden withdrawal (absence) of ovarian hormones progesterone and estrogen occurs 4. It leads to menstrual bleeding. Lack of ovarian hormones causes the release of gonadotropins once again from anterior pituitary. It results in the onset of development of new follicles in ovary and the cycle repeats.


REGULATION OF OVARIAN CHANGES:

Follicular Phase:

1. The biological clock responsible to trigger the cyclic events is the pulsatile secretion of GnRH, at about every 2 hours (due to some mechanism that is not understood clearly)

2. Pulsatile release of GnRH stimulates the secretion of FSH and LH from anterior pituitary

3. LH induces the synthesis of androgens from theca cells of growing follicle

4. FSH promotes aromatase activity in granulosa cells of the follicle, resulting in the conversion of androgens into estrogen. It also promotes follicular development

5. Estrogen is responsible for development and growth of graafian follicle. It also stimulates the secretory activities of theca cells

6. Estrogen also exerts a double feedback control on GnRH i. Initially, when estrogen secretion is moderate, it exerts a negative feedback control on GnRH so that GnRH secretion is inhibited. This leads to decrease in secretion of FSH and LH (negative feedback) ii. During later period of follicular phase, when a large amount of estrogen is secreted by the maturing follicle, it exerts a positive feedback effect on GnRH secretion. Now, GnRH secretion is increased, resulting in secretion of large quantity of FSH and LH. This in turn, facilitates the growth of graafian follicle

7. In addition, estrogen shows the following actions: i. Increases the number of FSH and LH receptors on the granulosa cells of follicles and increases the sensitivity of these cells for FSH and LH ii. Facilitates the faster growth of graafian follicle

8. LH is necessary to provide the final touches for the growth of graafian follicle. It stimulates the secretion of estrogen. At the same time, it stimulates the theca cells to secrete progesterone.

Ovulation:LH is important for ovulation. Without LH, ovulation does not occur even with a large quantity of FSH. The need for excessive secretion of LH for ovulation is known as ovulatory surge for LH or luteal surge. Prior to ovulation, a large quantity of LH is secreted due to positive feedback effect of estrogen on GnRH, as mentioned above.

Luteal Phase:

Role of LH:

Ovarian changes during luteal phase depend mainly on LH.
Luteinizing hormone:
1. Induces development of corpus luteum from the follicle (devoid of ovum) by converting the granulosa cells into lutein cells
2. Stimulates corpus luteum to secrete progesterone and estrogen
3.Necessary for the maintenance of corpus luteum.

Role of FSH:

FSH also plays a role during luteal phase.

Follicle-stimulating hormone: 1.Maintains the secretory activity of corpus luteum 2. Stimulates lutein cells to secrete inhibin, which in turn inhibits FSH secretion. If the ovum is not fertilized or if implantation of ovum does not take place, the changes in the level of the hormones produce some effects on corpus luteum which are: 1. Progesterone and estrogen secreted from corpus luteum, inhibit the secretion of FSH and LH from anterior pituitary by negative feedback 2.Granulosa lutein cells secrete another hormone called inhibin (which is also secreted by Sertoli cells of testes in males: Chapter 74). Inhibin also inhibits the secretion of FSH and LH by negative feedback 3. In the absence of FSH and LH, the corpus luteum becomes inactive 4. Finally, the corpus luteum regresses by means of luteolysis; so progesterone and estrogen are not available 5. Absence of progesterone and estrogen induces the secretion of GnRH from hypothalamus 6.GnRH stimulates the secretion of FSH and LH from anterior pituitary 7. FSH and LH stimulate the new immature follicles, resulting in the commencement of next cycle.

Interstitial Cells of Leydig Interstitial cells of Leydig are the hormone secreting cells of testis, lying in between the seminiferous tubules.

Sertoli Cells Sertoli cells are the supporting cells for spermatogenic cells in seminiferous tubules. These cells are also called sustentacular cells or nurse cells. Sertoli cells are the large and tall irregular columnar cells, extending from basement membrane to lumen of the seminiferous tubule. Germ cells present in seminiferous tubule are attached to Sertoli cells by means of cytoplasmic connection. This attachment between germ cells and Sertoli cells exists till the matured spermatozoa are released into the lumen of seminiferous tubules. Functions of Sertoli cells Sertoli cells provide support, protection and nourishment for the spermatogenic cells present in seminiferous tubules. Sertoli cells: 1. Support and nourish the spermatogenic cells till the spermatozoa are released from them 2. Secrete the enzyme aromatase, which converts androgens into estrogen 3. Secrete androgen-binding protein (ABP), which is essential for testosterone activity, especially during spermatogenesis 4. Secrete estrogen-binding protein (EBP) 5. Secrete inhibin, which inhibits FSH release from anterior pituitary 6. Secrete activin, which has opposite action of inhibin (increases FSH release) 7. Secrete müllerian regression factor (MRF) in fetal testes. MRF is also called müllerian inhibiting substance (MIS). MRF is responsible for the regression of müllerian duct during sex differentiation in fetus. Blood-testes Barrier Blood-testes barrier is a mechanical barrier that separates blood from seminiferous tubules of the testes. It is formed by tight junctions between the adjacent Sertoli cells, near the basal membrane of seminiferous tubule. Functions of blood-testes barrier 1. Protection of seminiferous tubules Blood-testes barrier protects the seminiferous tubules and spermatogenic cells by preventing the entry of toxic substances from blood and fluid of the surrounding tissues into the lumen of seminiferous tubules. However, blood-testes barrier permits substances essential for spermatogenic cells. Substances prevented by blood-testes barrier: i. Large molecules including proteins, polysaccharides and cytotoxic substances ii. Medium-sized molecules like galactose. Substances permitted by blood-testes barrier: i. Nutritive substances essential for spermatogenic cells ii. Hormones necessary for spermatogenesis iii. Water. 2. Prevention of autoimmune disorders Blood-testes barrier also prevents the development of autoimmune disorders by inhibiting the movement of antigenic products of spermatogenesis, from testis into blood. Damage of blood-testes barrier Blood-testes barrier is commonly damaged by trauma or viral infection like mumps. Whenever, the bloodtestes barrier is damaged the sperms enter the blood. The immune system of the body is activated, resulting in the production of autoantibodies against sperms. The antibodies destroy the germ cells, leading to consequent sterility. FUNCTIONS OF TESTES Testes performs two functions: 1. Gametogenic function: Spermatogenesis 2. Endocrine function: Secretion of hormones.

ENDOCRINE FUNCTIONS OF TESTES HORMONES SECRETED BY TESTES Testes secrete male sex hormones, which are collectively called the androgens. Androgens secreted by testes are: 1. Testosterone 2. Dihydrotestosterone 3. Androstenedione. Among these three androgens, testosterone is secreted in large quantities. However, dihydrotestosterone is more active. Female sex hormones, namely estrogen and progesterone are also found in testes. Two more hormones activin and inhibin are also secreted in testes. However, these two hormones do not have androgenic action.


OVARIAN HORMONES Ovary secretes the female sex hormones estrogen and progesterone. Ovary also secretes few more hormones, namely inhibin (Chapter 80), relaxin (Chapter 84) and small quantities of androgens. ESTROGEN Source of Secretion In a normal non-pregnant woman, estrogen is secreted in large quantity by theca interna cells of ovarian follicles and in small quantity by corpus luteum of the ovaries. Estrogen secretion is predominant at the later stage of follicular phase before ovulation (Chapter 80). Estrogen is derived from androgens, particularly androstenedione, which is secreted in theca interna cells. Androstenedione migrates from theca cells to granulosa cells, where it is converted into estrogen by the activity of the enzyme aromatase. A small quantity of estrogen is also secreted by adrenal cortex. In pregnant woman, a large amount of estrogen is secreted by the placenta.

„ PHYSIOLOGICAL OR
FUNCTIONAL DIVISIONS
Based on functions, the cerebellum is divided into three
divisions:
1. Vestibulocerebellum
2. Spinocerebellum
3. Corticocerebellum.
1. Vestibulocerebellum
Vestibulocerebellum includes flocculonodular lobe that
forms the archicerebellum.
2. Spinocerebellum
Spinocerebellum includes lingula, central lobe, culmen,
lobulus simplex, declive, tuber, pyramid, uvula and
paraflocculi and medial portions of lobulus ansiformis
and lobulus paramedianus.
3. Corticocerebellum
Corticocerebellum includes lateral portions of lobulus
ansiformis and lobulus paramedianusAPPLIED PHYSIOLOGY –
CEREBELLAR LESIONS
Cerebellar lesions may be due to tumor, abscess or an
injury. Excess alcohol ingestion also leads to cerebellar
lesions. Loss of functions of cerebellum also occurs due
to degenerative changes in cerebellar cortex, cerebellar
nuclei, cerebellar peduncles and spinocerebellar tracts.
In general, during cerebellar lesions, there are
disturbances in posture, equilibrium and movements. In
unilateral lesion, symptoms appear on the affected side
because cerebellum controls the same (ipsilateral) side
of the body.
Most of the disturbances are due to the damage to
corticocerebellum (neocerebellum) because in human
beings, it is larger than other divisions.
„ DISTURBANCES IN TONE AND POSTURE
1. Atonia or Hypotonia
Atonia is the loss of tone and hypotonia is reduction in
tone of the muscle. Cerebellar lesion causes atonia or
hypotonia, depending upon the severity of the lesion.
Atonia or hypotonia due to cerebellar lesion causes
disturbances in the postural reflexes.
Cause for atonia or hypotonia during cerebellar
lesion is the loss of facilitatory impulses to gamma motor
neurons in the spinal cord via cerebello-vestibulospinal
and cerebello-reticulospinal fibers.
2. Attitude
Attitude of the body changes in unilateral lesion of the
cerebellum. Changes in the attitude are:
i. Rotation of head towards the opposite side
(unaffected side)
ii. Lowering of shoulder on the same side
iii. Abduction of leg on the affected side. Leg is
rotated outward.
iv. Weight of the body is thrown on leg of unaffected
side. So, trunk is bent with concavity towards
the affected side.
3. Deviation Movement
Deviation movement is the lateral deviation of arms
when both the arms are stretched and held in front of
the body, with closed eyes. In bilateral lesion, both the
arms deviate and in unilateral lesion, arm of the affected
side deviates.
4. Effect on Deep Reflexes
Pendular movements (Chapter 142) occur while
eliciting a tendon jerk. These movements are very
common while eliciting the knee jerk or patellar tendon
reflex in the patients affected by cerebellar lesion.
A tap on the patellar tendon when leg is hanging
freely causes a brisk extension of leg due to the
contraction of quadriceps muscle. In normal conditions,
after extension, the leg returns back to resting position
immediately. In cerebellar lesion, the leg shows
pendular movements.
„ DISTURBANCES IN EQUILIBRIUM
While Standing
While standing, the legs are spread to provide a broad
base and the body sways side-to-side with oscillations
of the head.While Moving – Gait
Gait means manner of walking. In cerebellar lesion, a
staggering, reeling and drunken-like gait is observed.
„ DISTURBANCES IN MOVEMENTS
1. Ataxia: Lack of coordination of movements.
2. Asynergia: Lack of coordination between different
groups of muscles such as protagonists, antagonists
and synergists.
3. Asthenia: Weakness, easy fatigability and slowness
of muscles.
4. Dysmetria: Inability to check exact strength and
duration of muscular contractions required for any
voluntary act. While reaching for an object, the arm
may overshoot (past pointing) or it may fall short of
the object. Overshooting is called hypermetria and
falling short is known as hypometria.
5. Intention tremor: Tremor that occurs while attempting to do any voluntary act. Refer Chapter 147 for
details of tremor.
6. Astasia: Unsteady voluntary movements.
7. Nystagmus: To and fro movement of eyeball is
called nystagmus. Details of nystagmus are given
in Chapter 158.
8. Rebound phenomenon: When the patient attempts
to do a movement against resistance and if the
resis tance is suddenly removed, the limb moves
forcibly in the direction in which the attempt was
made. It is called rebound phenomenon. It is due
to the absence of breaking action of antagonistic
muscle.
9. Dysarthria: Disturbance in speech. It is due to the
incoordination of various muscles and structures
involved in speech.
10. Adiadochokinesis: Ability to do rapid alter nate
successive movements such as supination and
pronation of arm is called diadochokinesis. Inability
to do rapid alternate successive movements is called
adiadochokinesis. It is a common feature of cerebellar
lesion. It is also called dysdiadochokinesia.

G. Taste
1. Taste pathways
a. Taste receptor cells line the taste buds that are located on specialized papillae. The
receptor cells are covered with microvilli, which increase the surface area for binding
taste chemicals. In contrast to olfactory receptor cells, taste receptors are not neurons.
b. The anterior two-thirds of the tongue
■ has fungiform papillae.
■ detects salty, sweet, and umami sensations.
■ is innervated by CN VII (chorda tympani).
c. The posterior one-third of the tongue
■ has circumvallate and foliate papillae.
■ detects sour and bitter sensations■ is innervated by CN IX (glossopharyngeal).
■ The back of the throat and the epiglottis are innervated by CN X.
d. CN VII, CN IX, and CN X enter the medulla, ascend in the solitary tract, and terminate on
second-order taste neurons in the solitary nucleus. They project, primarily ipsilaterally,
to the ventral posteromedial nucleus of the thalamus and, finally, to the taste cortex.
2. Steps in taste transduction
■ Taste chemicals (sour, sweet, salty, bitter, and umami) bind to taste receptors on the
microvilli and produce a depolarizing receptor potential in the receptor cell.



„ PATHWAY FOR TASTE
„ RECEPTORS
Receptors for taste sensation are the type III cells of
taste buds. Each taste bud is innervated by about 50
sensory nerve fibers and each nerve fiber supplies at
least five taste buds through its terminals.
„ FIRST ORDER NEURON
First order neurons of taste pathway are in the nuclei
of three different cranial nerves, situated in medulla
oblongata. Dendrites of the neurons are distributed to
the taste buds. After arising from taste buds, the fibers
reach the cranial nerve nuclei by running along the
following nerves (Fig. 176.2):
1. Chorda tympani fibers of facial nerve, which run
from anterior two third of tongue
2. Glossopharyngeal nerve fibers, which run from
posterior one third of the tongue
3. Vagal fibers, which run from taste buds in other
regions.
Axons from first order neurons in the nuclei of these
nerves run together in medulla oblongata and terminate
in the nucleus of tractus solitarius„ SECOND ORDER NEURON
Second order neurons are in the nucleus of tractus
solitarius. Axons of second order neurons run through
medial lemniscus and terminate in posteroventral
nucleus of thalamus.
„ THIRD ORDER NEURON
Third order neurons are in the posteroventral nucleus
of thalamus. Axons from third order neurons project
into parietal lobe of the cerebral cortex.
„ TASTE CENTER
Center for taste sensation is in opercular insular cortex,
i.e. in the lower part of postcentral gyrus, which receives
cutaneous sensations from face. Thus, the taste fibers
do not have an independent cortical projection

The semicircular canals are involved in angular acceleration or rotation. Hair cells of the right semicircular canal are excited (depolarized) when
there is rotation to the right. This rotation causes bending of the stereocilia toward the
kinocilia, and this bending produces depolarization of the hair cell. Ascent in an elevator
would activate the saccules, which detect linear acceleration.


E. Vestibular system
■ detects angular and linear acceleration of the head.
■ Reflex adjustments of the head, eyes, and postural muscles provide a stable visual image
and steady posture.
1. Structure of the vestibular organ
a. It is a membranous labyrinth consisting of three perpendicular semicircular canals, a
utricle, and a saccule. The semicircular canals detect angular acceleration or rotation.
The utricle and saccule detect linear accelerationb. The canals are filled with endolymph and are bathed in perilymph.
c. The receptors are hair cells located at the end of each semicircular canal. Cilia on the
hair cells are embedded in a gelatinous structure called the cupula. A single long cilium
is called the kinocilium; smaller cilia are called stereocilia (Figure 2-7).
2. Steps in vestibular transduction—angular acceleration (see Figure 2-7)
a. During counterclockwise (left) rotation of the head, the horizontal semicircular canal
and its attached cupula also rotate to the left. Initially, the cupula moves more quickly
than the endolymph fluid. Thus, the cupula is dragged through the endolymph; as a
result, the cilia on the hair cells bend.
b. If the stereocilia are bent toward the kinocilium, the hair cell depolarizes (excitation). If
the stereocilia are bent away from the kinocilium, the hair cell hyperpolarizes (inhibition). Therefore, during the initial counterclockwise (left) rotation, the left horizontal
canal is excited and the right horizontal canal is inhibited.
c. After several seconds, the endolymph “catches up” with the movement of the head and
the cupula. The cilia return to their upright position and are no longer depolarized or
hyperpolarized.
d. When the head suddenly stops moving, the endolymph continues to move counterclockwise (left), dragging the cilia in the opposite direction. Therefore, if the hair cell
was depolarized with the initial rotation, it now will hyperpolarize. If it was hyperpolarized initially, it now will depolarize. Therefore, when the head stops moving, the left
horizontal canal will be inhibited and the right horizontal canal will be excited.

„ INTRODUCTION
Pupillary reflexes are the visceral reflexes, which alter
the size of pupil. Pupillary reflexes are classified into
three types:
1. Light reflex
2. Ciliospinal reflex
3. Accommodation reflex.
„ LIGHT REFLEX
Light reflex is the reflex in which pupil constricts when
light is flashed into the eyes. It is also called pupillary
light reflex. Light reflex is of two types:
1. Direct light reflex
2. Indirect light reflex.
„ DIRECT LIGHT REFLEX
Direct light reflex is the reflex in which there is
constriction of pupil in an eye when light is thrown into
that eye. It is also called the direct pupillary light reflex
or the direct reaction to light.
„ INDIRECT LIGHT REFLEX
Indirect light reflex is the reflex that involves constriction
of pupil in both eyes when light is thrown into one eye.
If light is flashed into one eye, the constriction of pupil
occurs in the opposite eye, even though no light rays
falls on that eye. It is otherwise called consensual light
reflex.
„ PATHWAY FOR LIGHT REFLEX
Pathway for light reflex is slightly deviated from visual
pathway. Fibers of light reflex pathway and the fibers of
visual pathway are the same up to optic tract. Beyond
that, these two sets of fibers are separated.
When light falls on the eye, the visual receptors
are stimulated. Afferent (sensory) impulses from the
receptors pass through the optic nerve, optic chiasma
and optic tract. At the midbrain level, few fibers get separated from optic tract and synapse on the neurons
of pretectal nucleus, which lies close to the superior
colli culus. Pretectal nucleus of midbrain forms the center
for light reflexes. Efferent (motor) impulses from this
nucleus are carried by short fibers to Edinger-Westphal
nucleus (parasympathetic nucleus) of oculomotor nerve
(third cranial nerve). From Edinger-Westphal nucleus,
preganglionic fibers pass through oculomotor nerve and
reach the ciliary ganglion. Postganglionic fibers arising
from ciliary ganglion pass through short ciliary nerves
and reach the eyeball. These fibers cause contraction of
constrictor pupillae muscle of iris (Fig. 169.1).
Reason for consensual light reflex is that, some
of the fibers from pretectal nucleus of one side cross
to the opposite side and end on opposite EdingerWestphal nucleus.

„ APPLIED PHYSIOLOGY
„ ARGYLL ROBERTSON PUPIL
Argyll Robertson pupil is a clinical condition in which
the light reflex is lost but the accommodation reflex is
present. It is common in tertiary syphilis. It also occurs
because of lesion in Edinger-Westphal nucleus,
diabetes and alcoholic neuropathy.
„ HORNER SYNDROME
Horner syndrome is an eye disorder caused by damage
to cervical sympathetic nerve. It is also called BernardHorner syndrome, Claude Bernard-Horner syndrome or
oculosympathetic palsy.
Symptoms of Horner syndrome appear on the
affected side. The symptoms are:
1. Ptosis (drooping of upper eyelid)
2. Swelling of lower eyelid
3. Miosis (abnormal constriction of pupil)
4. Enophthalmos (sinking of eyeball into its cavity)
5. Absence of sweating on affected side of the face.
„ PRESBYOPIA
In old age, the amplitude of accommodation is decreased and the near point is away from the eye. This
condition is called presbyopia. Details are given in
Chapter 171

Cutting the optic nerve from the left eye causes blindness in the
left eye because the fibers have not yet crossed at the optic chiasm.