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Sneeze Reflex

The sneeze reflex is very much like the cough reflex,
except that it applies to the nasal passageways instead
of the lower respiratory passages. The initiating stimulus
of the sneeze reflex is irritation in the nasal passageways;
the afferent impulses pass in the fifth cranial
nerve to the medulla, where the reflex is triggered. A
series of reactions similar to those for the cough reflex
takes place; however, the uvula is depressed, so that
large amounts of air pass rapidly through the nose, thus
helping to clear the nasal passages of foreign matter.

Cough Reflex

The bronchi and trachea are so sensitive to light touch
that very slight amounts of foreign matter or other
causes of irritation initiate the cough reflex. The larynx
and carina (the point where the trachea divides into the
bronchi) are especially sensitive, and the terminal bronchioles
and even the alveoli are sensitive to corrosive
chemical stimuli such as sulfur dioxide gas or chlorine
gas. Afferent nerve impulses pass from the respiratory
passages mainly through the vagus nerves to the
medulla of the brain. There, an automatic sequence of
events is triggered by the neuronal circuits of the
medulla, causing the following effect.
First, up to 2.5 liters of air are rapidly inspired.
Second, the epiglottis closes, and the vocal cords shut
tightly to entrap the air within the lungs. Third, the
abdominal muscles contract forcefully, pushing against
the diaphragm while other expiratory muscles, such as
the internal intercostals, also contract forcefully. Consequently,
the pressure in the lungs rises rapidly to as
much as 100 mm Hg or more. Fourth, the vocal cords
and the epiglottis suddenly open widely, so that air
under this high pressure in the lungs explodes outward.
Indeed, sometimes this air is expelled at velocities
ranging from 75 to 100 miles per hour. Importantly, the
strong compression of the lungs collapses the bronchi
and trachea by causing their noncartilaginous parts to
invaginate inward, so that the exploding air actually
passes through bronchial and tracheal slits. The rapidly
moving air usually carries with it any foreign matter that
is present in the bronchi or trachea.

Scratch Reflex

An especially important cord reflex in some animals is
the scratch reflex, which is initiated by itch or tickle sensation.
It involves two functions: (1) a position sense that
allows the paw to find the exact point of irritation on
the surface of the body, and (2) a to-and-fro scratching
The position sense of the scratch reflex is a highly
developed function. If a flea is crawling as far forward
as the shoulder of a spinal animal, the hind paw can still
find its position, even though 19 muscles in the limb
must be contracted simultaneously in a precise pattern
to bring the paw to the position of the crawling flea. To
make the reflex even more complicated, when the flea
crosses the midline, the first paw stops scratching and
the opposite paw begins the to-and-fro motion and
eventually finds the flea.
The to-and-fro movement, like the stepping movements
of locomotion, involves reciprocal innervation
circuits that cause oscillation.
Galloping Reflex. Another type of reflex that occasionally
develops in a spinal animal is the galloping reflex,
in which both forelimbs move backward in unison
while both hindlimbs move forward.This often occurs
when almost equal stretch or pressure stimuli are
applied to the limbs on both sides of the body at the
same time; unequal stimulation elicits the diagonal
walking reflex. This is in keeping with the normal patterns
of walking and galloping, because in walking,
only one forelimb and one hindlimb at a time are stimulated,
which would predispose the animal to continue
walking. Conversely, when the animal strikes the
ground during galloping, both forelimbs and both
hindlimbs are stimulated about equally; this predisposes
the animal to keep galloping and, therefore, continues
this pattern of motion.

Autonomic Reflexes

Many visceral functions of the body are regulated by
autonomic reflexes. Throughout this text, the functions
of these reflexes are discussed in relation to individual
organ systems; to illustrate their importance, a few are
presented here briefly.
Cardiovascular Autonomic Reflexes. Several reflexes in the
cardiovascular system help to control especially the
arterial blood pressure and the heart rate. One of these
is the baroreceptor reflex, which is described in Chapter
18 along with other cardiovascular reflexes. Briefly,
stretch receptors called baroreceptors are located in the
walls of several major arteries, including especially the
internal carotid arteries and the arch of the aorta.When
these become stretched by high pressure, signals are
transmitted to the brain stem, where they inhibit the
sympathetic impulses to the heart and blood vessels and
excite the parasympathetics; this allows the arterial
pressure to fall back toward normal.
Gastrointestinal Autonomic Reflexes. The uppermost part of
the gastrointestinal tract and the rectum are controlled
principally by autonomic reflexes. For instance, the
smell of appetizing food or the presence of food in
the mouth initiates signals from the nose and mouth
to the vagal, glossopharyngeal, and salivatory nuclei
of the brain stem.These in turn transmit signals through
the parasympathetic nerves to the secretory glands of
the mouth and stomach, causing secretion of digestive
juices sometimes even before food enters the mouth.
When fecal matter fills the rectum at the other end
of the alimentary canal, sensory impulses initiated by
stretching the rectum are sent to the sacral portion of
the spinal cord, and a reflex signal is transmitted back
through the sacral parasympathetics to the distal parts
of the colon; these result in strong peristaltic contractions
that cause defecation.
Other Autonomic Reflexes. Emptying of the urinary bladder
is controlled in the same way as emptying the rectum;
stretching of the bladder sends impulses to the sacral
cord, and this in turn causes reflex contraction of the
bladder and relaxation of the urinary sphincters,
thereby promoting micturition.
Also important are the sexual reflexes, which are initiated
both by psychic stimuli from the brain and by
stimuli from the sexual organs. Impulses from these
sources converge on the sacral cord and, in the male,
result first in erection, mainly a parasympathetic function,
and then ejaculation, partially a sympathetic
Other autonomic control functions include reflex
contributions to the regulation of pancreatic secretion,
gallbladder emptying, kidney excretion of urine, sweating,
blood glucose concentration, and many other visceral
functions, all of which are discussed in detail at
other points in this text.

(ANS) Autonomic Effects on Various Organs of the Body

Autonomic Effects on Various Organs of the Body
Organ Effect of Sympathetic Stimulation Effect of Parasympathetic Stimulation
Pupil Dilated Constricted
Ciliary muscle Slight relaxation (far vision) Constricted (near vision)
Glands Vasoconstriction and slight secretion Stimulation of copious secretion (containing many enzymes for Nasal enzyme-secreting glands)
Sweat glands Copious sweating (cholinergic) Sweating on palms of hands
Apocrine glands Thick, odoriferous secretion None
Blood vessels Most often constricted Most often little or no effect
Muscle Increased rate Slowed rate
Increased force of contraction Decreased force of contraction(especially of atria)
Coronaries Dilated (b2); constricted (a) Dilated
Bronchi Dilated Constricted
Blood vessels Mildly constricted ?Dilated
Lumen Decreased peristalsis and tone Increased peristalsis and tone
Sphincter Increased tone (most times) Relaxed (most times)
Liver Glucose released Slight glycogen synthesis
Gallbladder and bile ducts Relaxed Contracted
Kidney Decreased output and renin secretion None
Detrusor Relaxed (slight) Contracted
Trigone Contracted Relaxed
Penis Ejaculation Erection
Systemic arterioles
Abdominal viscera Constricted None
Muscle Constricted (adrenergic a) None
Dilated (adrenergic b2)
Dilated (cholinergic)
Skin Constricted None
Coagulation Increased None
Glucose Increased None
Lipids Increased None
Basal metabolism Increased up to 100% None
Adrenal medullary secretion Increased None
Mental activity Increased None
Piloerector muscles Contracted None
Skeletal muscle Increased glycogenolysis None
Increased strength
Fat cells Lipolysis None

Abnormalities of Secretion by the Ovaries

Amenorrhea is the lack of menstrual flow and can be a normal occurrence or a sign of malfunction or disease. In primary amenorrhea, menstruation does not begin when expected (by the age of 16). Secondary amenorrhea occurs when the normal established menstrual cycle is shut down for 6 or more months due to a condition other than pregnancy, breastfeeding or menopause.

Abnormalities of Secretion by the Ovaries

Hypogonadism. Less than normal secretion by the ovaries can result from poorly formed ovaries, lack of ovaries,
or genetically abnormal ovaries that secrete the wrong hormones because of missing enzymes in the secretory
cells. When ovaries are absent from birth or when they become nonfunctional before puberty, female
eunuchism occurs. In this condition, the usual secondary sexual characteristics do not appear, and the sexual
organs remain infantile. Especially characteristic of this condition is prolonged growth of the long bones
because the epiphyses do not unite with the shafts as early as they do in a normal woman. Consequently, the
female eunuch is essentially as tall as or perhaps even slightly taller than her male counterpart of similar
genetic background.
When the ovaries of a fully developed woman are removed, the sexual organs regress to some extent so
that the uterus becomes almost infantile in size, the vagina becomes smaller, and the vaginal epithelium
becomes thin and easily damaged. The breasts atrophy and become pendulous, and the pubic hair becomes
thinner. The same changes occur in women after menopause.

Irregularity of Menses, and Amenorrhea Caused by Hypogonadism.

As pointed out in the preceding discussion of menopause, the quantity of estrogens produced
by the ovaries must rise above a critical value in order to cause rhythmical sexual cycles. Consequently,
in hypogonadism or when the gonads are secreting small quantities of estrogens as a result of other factors,
such as hypothyroidism, the ovarian cycle often does not occur normally. Instead, several months may elapse
between menstrual periods, or menstruation may cease altogether (amenorrhea). Prolonged ovarian cycles are
frequently associated with failure of ovulation, presumably because of insufficient secretion of LH at the time
of the preovulatory surge of LH, which is necessary for ovulation.

Hypersecretion by the Ovaries.

Extreme hypersecretion of ovarian hormones by the ovaries is a rare clinical entity,
because excessive secretion of estrogens automatically decreases the production of gonadotropins by the
pituitary, and this limits the production of ovarian hormones. Consequently, hypersecretion of feminizing
hormones is usually recognized clinically only when a feminizing tumor develops. A rare granulosa cell tumor can develop in an ovary, occurring more often after menopause than before.
These tumors secrete large quantities of estrogens, which exert the usual estrogenic effects, including
hypertrophy of the uterine endometrium and irregular bleeding from this endometrium. In fact, bleeding is
often the first and only indication that such a tumor exists.


If the ovum is not fertilized, about 2 days
before the end of the monthly cycle, the corpus luteum
in the ovary suddenly involutes, and the ovarian
hormones (estrogens and progesterone) decrease to
low levels of secretion,
Menstruation follows.
Menstruation is caused by the reduction of estrogens
and progesterone, especially progesterone, at the
end of the monthly ovarian cycle. The first effect is
decreased stimulation of the endometrial cells by these
two hormones, followed rapidly by involution of the
endometrium itself to about 65 per cent of its previous
thickness. Then, during the 24 hours preceding the
onset of menstruation, the tortuous blood vessels
leading to the mucosal layers of the endometrium
become vasospastic, presumably because of some
effect of involution, such as release of a vasoconstrictor
material—possibly one of the vasoconstrictor types
of prostaglandins that are present in abundance at this
The vasospasm, the decrease in nutrients to the
endometrium, and the loss of hormonal stimulation
initiate necrosis in the endometrium, especially of the
blood vessels. As a result, blood at first seeps into the
vascular layer of the endometrium, and the hemorrhagic
areas grow rapidly over a period of 24 to 36
hours. Gradually, the necrotic outer layers of the
endometrium separate from the uterus at the sites
of the hemorrhages until, about 48 hours after the
onset of menstruation, all the superficial layers of
the endometrium have desquamated. The mass of
desquamated tissue and blood in the uterine cavity,
plus contractile effects of prostaglandins or other
substances in the decaying desquamate, all acting
together, initiate uterine contractions that expel the
uterine contents.
During normal menstruation, approximately 40
milliliters of blood and an additional 35 milliliters of
serous fluid are lost. The menstrual fluid is normally
nonclotting because a fibrinolysin is released along
with the necrotic endometrial material. If excessive
bleeding occurs from the uterine surface, the quantity
of fibrinolysin may not be sufficient to prevent clotting.
The presence of clots during menstruation is often
clinical evidence of uterine pathology.
Within 4 to 7 days after menstruation starts, the loss
of blood ceases because, by this time, the endometrium
has become re-epithelialized.
Leukorrhea During Menstruation. During menstruation,
tremendous numbers of leukocytes are released
along with the necrotic material and blood. It is probable
that some substance liberated by the endometrial
necrosis causes this outflow of leukocytes. As a result
of these leukocytes and possibly other factors, the
uterus is highly resistant to infection during menstruation,
even though the endometrial surfaces are
denuded. This is of extreme protective value.


Headaches are a type of pain referred to the surface of the head from deep head structures. Some headaches result from pain stimuli arising inside the cranium, but others result from pain arising outside the cranium, such
as from the nasal sinuses.
Headache of Intracranial Origin
Pain-Sensitive Areas in Cranial Vault. The brain tissues themselves are almost totally insensitive to pain. Even cutting or electrically stimulating the sensory areas of the cerebral cortex only occasionally causes pain; instead, it causes prickly types of paresthesias on the area of the body represented by the portion of the sensory cortex stimulated. Therefore, it is likely that
much or most of the pain of headache is not caused by damage within the brain itself.
Conversely, tugging on the venous sinuses around the brain, damaging the tentorium, or stretching the dura at the base of the brain can cause intense pain that is recognized
as headache. Also, almost any type of traumatizing, crushing, or stretching stimulus to the blood
vessels of the meninges can cause headache. An especially sensitive structure is the middle meningeal artery, and neurosurgeons are careful to anesthetize this artery specifically when performing brain operations under local anesthesia.
Areas of the Head to Which Intracranial Headache Is Referred. Stimulation of pain receptors in the cerebral vault above the tentorium, including the upper surface of the tentorium itself, initiates pain impulses in the cerebral portion of the fifth nerve and, therefore, causes referred headache to the front half of the head in the surface areas supplied by this somatosensory portion of the fifth cranial nerve.
Conversely, pain impulses from beneath the tentorium enter the central nervous system mainly
through the glossopharyngeal, vagal, and second cervical nerves, which also supply the scalp above, behind, and slightly below the ear. Subtentorial pain stimuli cause “occipital headache” referred to the posterior part of the head.
Types of Intracranial Headache Headache of Meningitis. One of the most severe
headaches of all is that resulting from meningitis, which causes inflammation of all the meninges, including the sensitive areas of the dura and the sensitive areas around the venous sinuses. Such intense damage can cause extreme headache pain referred over the entire
Headache Caused by Low Cerebrospinal Fluid Pressure.
Removing as little as 20 milliliters of fluid from the spinal canal, particularly if the person remains in an upright position, often causes intense intracranial headache. Removing this quantity of fluid removes part of the flotation for the brain that is normally provided by the cerebrospinal fluid. The weight of the brain stretches and otherwise distorts the various dural
surfaces and thereby elicits the pain that causes the headache.
Migraine Headache. Migraine headache is a special type of headache that is thought to result from abnormal vascular phenomena, although the exact mechanism is unknown. Migraine headaches often begin with various prodromal sensations, such as nausea, loss of vision in
part of the field of vision, visual aura, and other types of sensory hallucinations. Ordinarily, the prodromal symptoms begin 30 minutes to 1 hour before the beginning of the headache. Any theory that explains migraine headache must also explain the prodromal
symptoms. One of the theories of the cause of migraine headaches is that prolonged emotion or tension causes reflex vasospasm of some of the arteries of the head, including arteries that supply the brain. The vasospasm theoretically produces ischemia of portions of the brain,
and this is responsible for the prodromal symptoms.
Then, as a result of the intense ischemia, something happens to the vascular walls, perhaps exhaustion of smooth muscle contraction, to allow the blood vessels to become flaccid and incapable of maintaining vascular tone for 24 to 48 hours. The blood pressure in the
vessels causes them to dilate and pulsate intensely, and it is postulated that the excessive stretching of the walls of the arteries—including some extracranial arteries, such as the temporal artery—causes the actual pain of migraine headaches. Other theories of the cause
of migraine headaches include spreading cortical depression, psychological abnormalities, and vasospasm caused by excess local potassium in the cerebral extracellular
fluid. There may be a genetic predisposition to migraine headaches, because a positive family history for migraine has been reported in 65 to 90 per cent of cases. Migraine headaches also occur about twice as frequently
in women as in men.
Alcoholic Headache. As many people have experienced, a headache usually follows an alcoholic binge. It is most likely that alcohol, because it is toxic to tissues, directly irritates the meninges and causes the intracranial pain.


A lesion in the subthalamus often leads to sudden
flailing movements of an entire limb, a condition called

Hemiballismus is usually characterized by involuntary flinging motions of the extremities. The movements are often violent and have wide amplitudes of motion. They are continuous and random and can involve proximal and/or distal muscles on one side of the body. Some cases even include the facial muscles. It is common for arms and legs to move together. The more a patient is active, the more the movements increase. With relaxation comes a decrease in movements. Physicians can measure the severity of the disorder by having the patient perform a series of basic, predetermined tasks and counting the hemiballistic movements during a set time session. The physicians then rate the patient on a severity scale. This scale gives scientists and clinicians a way to compare patients and determine the range of the disorder.


prosophenosia is inability to recognize faces. This occurs in people who have extensive damage on the medial undersides of both occipital lobes and along the medioventral surfaces of the temporal lobes Loss of these face recognition areas, strangely enough, results in little other abnormality of brain function.
One wonders why so much of the cerebral cortex should be reserved for the simple task of face recognition.
Most of our daily tasks involve associations with other people, and one can see the importance of
this intellectual function.
The occipital portion of this facial recognition area is contiguous with the visual cortex, and the temporal portion is closely associated with the limbic system that has to do with emotions, brain activation, and control of one’s behavioral response to the environment.

Vestibular Sensations and Maintenance of Equilibrium

Vestibular Apparatus
The vestibular apparatus, is the sensory organ for detecting sensations of equilibrium.
It is encased in a system of bony tubes and chambers located in the petrous portion of the temporal bone, called the bony labyrinth.Within this system are membranous tubes and chambers called the membranous labyrinth. The membranous labyrinth is the functional part of the vestibular apparatus It is composed mainly of the cochlea (ductus cochlearis); three semicircular canals; and two large chambers, the utricle and saccule. The cochlea is the major sensory organ for hearing and has little to do with equilibrium. However, the semicircular canals, the utricle, and the saccule are all integral parts of the equilibrium mechanism.

Function of the Utricle and Saccule in the Maintenance of Static Equilibrium
It is especially important that the hair cells are all oriented in different directions in the maculae of the utricles and saccules, so that with different positions of the head, different hair cells become stimulated.The “patterns” of stimulation of the different hair cells apprise the brain of the position of the head with respect to the pull of gravity. In turn, the vestibular, cerebellar,
and reticular motor nerve systems of the brain excite appropriate postural muscles to maintain proper equilibrium.This utricle and saccule system functions extremely effectively for maintaining equilibrium when the head is in the near-vertical position. Indeed, a person
can determine as little as half a degree of dysequilibrium when the body leans from the precise upright position.

“Predictive” Function of the Semicircular Duct System in the Maintenance of Equilibrium.
Because the semicircular ducts do not detect that the body is off balance in the forward direction, in the side direction, or in the backward direction, one might ask:What is the semicircular ducts’ function in the maintenance of equilibrium? All they detect is that the person’s head is beginning
or stopping to rotate in one direction or another. Therefore, the function of the semicircular ducts is not to maintain static equilibrium or to maintain equilibrium during steady directional or rotational movements. Yet loss of function of the semicircular ducts does cause a person to have poor equilibrium when attempting to perform rapid, intricate changing body movements.
We can explain the function of the semicircular ducts best by the following illustration: If a person is running forward rapidly and then suddenly begins to turn to one side, he or she will fall off balance a fraction of a second later unless appropriate corrections are made ahead of time. But the maculae of the utricle and saccule cannot detect that he or she is off balance
until after this has occurred. The semicircular ducts,however, will have already detected that the person is turning, and this information can easily apprise the central nervous system of the fact that the person will fall off balance within the next fraction of a second or so unless some anticipatory correction is made.
In other words, the semicircular duct mechanism predicts that dysequilibrium is going to occur and thereby causes the equilibrium centers to make appropriate anticipatory preventive adjustments. In this way, the person need not fall off balance at all before he or she begins to correct the situation.
Removal of the flocculonodular lobes of the cerebellum prevents normal detection of semicircular duct signals but has less effect on detecting macular signals.
It is especially interesting that the cerebellum serves as a “predictive” organ for most rapid movements of the body, as well as for those having to do with equilibrium.

Female reproductive system

The female reproductive system is illustrated to the right. “Eggs” are produced in the ovaries, but remember from our discussion of meiosis, that these are not true eggs, yet, and will never complete meiosis and become such unless/until first fertilized by a sperm. Within the ovary, a follicle consists of one precursor egg cell surrounded by special cells to nourish and protect it. A human female typically has about 400,000 follicles/potential eggs, all formed before birth. Only several hundred of these “eggs” will actually ever be released during her reproductive years. Normally, in humans, after the onset of puberty, due to the stimulation of follicle-stimulating hormone (FSH)one “egg” per cycle matures and is released from its ovary. Ovulation is the release of a mature “egg” due to the stimulation of leutenizing hormone (LH), which then stimulates the remaining follicle cells to turn into a Corpus luteum which then secretesprogesterone to prepare the uterus for possible implantation. If an egg is not fertilized and does not implant, the corpus luteum disintegrates and when it stops producing progesterone, the lining of the uterus breaks down and is shed.
Each “egg” is released into the abdominal cavity near the opening of one of the oviducts or Fallopian tubes. Cilia in the oviduct set up currents that draw the egg in. If sperm are present in the oviduct (if the couple has recently had intercourse), the egg will be fertilized near the far end of the Fallopian tube, will quickly finish meiosis, and the embryo will start to divide and grow as it travels to the uterus. The trip down the Fallopian tube takes about a week as the cilia in the tube propel the unfertilized “egg” or the embryo down to the uterus. At this point, if she had intercourse near the time of ovulation, the woman has no idea whether an unfertilized “egg” or a new baby is travelling down that tube. During this time, progesterone secreted by the corpus luteum has been stimulating the endometrium, the lining of the uterus, to thicken in preparation for possible implantation, and when a growing embryo finally reaches the uterus, it will implant in this nutritious environment and begin to secrete its own hormones to maintain the endometrium. If the “egg” was not fertilized, it dies and disintegrates, and as the corpus luteum also disintegrates, its progesterone production falls, and the unneeded, built-up endometrium is shed.
The uterus has thick, muscular walls and is very small. In a Nulliparous woman, the uterus is only about 7 cm long by 4 to 5 cm wide, but it can expand to hold a 4 kg baby. The lining of the uterus is called the Endometrium and has a rich capillary supply to bring food to any embryo that might implant there.
The bottom end of the uterus is called the Cervix The cervix secretes mucus, the consistency of which varies with the stages in her menstrual cycle. At ovulation, this cervical mucus is clear, runny, and conducive to sperm. Post-ovulation, the mucus gets thick and pasty to block sperm. Enough of this mucus is produced that it is possible for a woman to touch a finger to the opening of her vagina and obtain some of it. If she does this on a daily basis, she can use the information thus gained, along with daily temperature records, to tell where in her cycle she is. If a woman becomes pregnant, the cervical mucus forms a plug to seal off the uterus and protect the developing baby, and any medical procedure which involves removal of that plug carries the risk of introducing pathogens into the nearly-sterile uterine environment.
The vagina is a relatively-thin-walled chamber. It servs as a repository for sperm (it is where the penis is inserted), and also serves as the birth canal. Note that, unlike the male, the female has separate opening for the urinary tract and reproductive system. These openings are covered externally by two sets of skin folds. The thinner, inner folds are the Labia Minora and the thicker, outer ones are the labia majora. The labia minora contain erectile tissue like that in the penis, thus change shape when the woman is sexually aroused. The opening around the genital area is called the vestibule. There is a membrane called the Hymen that partially covers the opening of the vagina. This is torn by the woman’s first sexual intercourse (or sometimes other causes like injury or some kinds of vigorous physical activity). In women, the openings of the vagina and urethra are susceptible to bacterial infections if fecal bacteria are wiped towards them. Thus, while parents who are toilet-training a toddler usually wipe her from back to front, thus “imprinting” that sensation as feeling “right” to her, it is important, rather, that that little girls be taught to wipe themselves from the front to the back to help prevent vaginal and bladder infections. Older girls and women who were taught the wrong way need to make a conscious effort to change their habits.
At the anterior end of the labia, under the pubic bone, is the Clitoris the female equivalent of the penis. This small structure contains erectile tissue and many nerve endings in a sensitive glans within aprepuce which totally encloses the glans. This is the most sensitive point for female sexual stimulation, so senstiive that vigorous, direct stimulation does not feel good. It is better for the man to gently stimulate near the clitoris rather than right on it. Some cultures do a procedure, similar to circumcision, as a puberty rite in teenage girls in which the prepuce is cut, exposing the extremely-sensitive clitoris. There are some interesting speculations on the cultural significance of this because the sensitivity of the exposed clitoris would probably make having sexual intercourse a much less pleasant experience for these women.

Male Reproductive System

The male reproductive system is illustrated to the right. Sperm are produced in the testes located in the scrotum. Normal body temperature is too hot thus is lethal to sperm so the testes are outside of the abdominal cavity where the temperature is about 2° C (3.6° F) lower. Note also that a woman’s body temperature is lowest around the time of ovulation to help insure sperm live longer to reach the egg. If a man takes too many long, very hot baths, this can reduce his sperm count. Undescended testes (testes are supposed to descend before birth) will cause sterility because their environment is too warm for sperm viability unless the problem can be surgically corrected.
From there, sperm are transferred to the Epididymis coiled tubules also found within the scrotum, that store sperm and are the site of their final maturation (Coiled tubules in the scrotum that store sperm) coiled tubules also found within the scrotum, that store sperm and are the site of their final maturation.
In Ejaculation: expulsion of semen vas deferens (plural = vasa deferentia). From the epididymis, the vas deferens goes up, around the front of, over the top of, and behind the bladder. A vasectomy is a fairly simple, outpatient operation that involves making a small slit in each scrotum, cutting the vasa deferentia near where they begin, and tying off the cut ends to prevent sperm from leaving the scrotum. Because this is a relatively non-invasive procedure (as compared to doing the same to a woman’s oviducts), this is a popular method of permanent birth control once a couple has had all the children they desire. Couples should carefully weigh their options, because this (and the corresponding female procedure) is not designed to be a reversible operation.
The ends of the vasa deferentia, behind and slightly under the bladder, are called the ejaculatory ducts. The seminal vesicles are also located behind the bladder. Their secretions are about 60% of the total volume of the semen (= sperm and associated fluid) and contain mucus, amino acids, fructose as the main energy source for the sperm, and prostaglandins to stimulate female uterine contractions to move the semen up into the uterus. The seminal vesicles empty into the ejaculatory ducts. The ejaculatory ducts then empty into the urethra (which, in males, also empties the urinary bladder).
The initial segment of the urethra is surrounded by the Prostate Gland: the largest of the accessory glands which puts its secretions directly into the urethra prostate gland(note spelling!). The prostate is the largest of the accessory glands and puts its secretions directly into the urethra. These secretions are alkaline to buffer any residual urine, which tends to be acidic, and the acidity of the woman’s vagina. The prostate needs a lot of zinc to function properly, and insufficient dietary zinc (as well as other causes) can lead to enlargement which potentially can constrict the urethra to the point of interferring with urination. Mild cases of prostate hypertrophy can often be treated by adding supplemental zinc to the man’s diet, but severe cases require surgical removal of portions of the prostate. This surgery, if not done very carefully can lead to problems with urination or sexual performance.
The bulbourethral glands or Cowper’s glands are the third of the accessory structures. These are a small pair of glands along the urethra below the prostate. Their fluid is secreted just before emission of the semen, thus it is thought that this fluid may serve as a lubricant for inserting the penis into the vagina, but because the volume of these secretions is very small, people are not totally sure of this function.
The urethra goes through the penis. In humans, the penis contains three cylinders of spongy, erectile tissue. During arousal, these become filled with blood from the arteries that supply them and the pressure seals off the veins that drain these areas causing an erection, which is necessary for insertion of the penis into the woman’s vagina. In a number of other animals, the penis also has a bone, the baculum, which helps to stiffen it. The head of the penis, the glans penis, is very sensitive to stimulation. In humans, as in other mammals, the glans is covered by the foreskin or prepuce, which may have been removed bycircumcision. Medically, circumcision is not a necessity, but rather a cultural “tradition”. Males who have not been circumcised need to keep the area between the glans and the prepuce clean so bacteria and/or yeasts don’t start to grow on accumulated secretions, etc. there. There is some evidence that uncircumcised males who do not keep the glans/prepuce area clean are slightly more prone to penile cancer.

Myocardial Infarction

Immediately after an acute coronary occlusion, blood
flow ceases in the coronary vessels beyond the occlusion
except for small amounts of collateral flow from
surrounding vessels.The area of muscle that has either
zero flow or so little flow that it cannot sustain cardiac
muscle function is said to be infarcted. The overall
process is called a myocardial infarction.
Soon after the onset of the infarction, small amounts
of collateral blood begin to seep into the infarcted area,
and this, combined with progressive dilation of local
blood vessels, causes the area to become overfilled with
stagnant blood. Simultaneously the muscle fibers use
the last vestiges of the oxygen in the blood, causing
the hemoglobin to become totally de-oxygenated.
Therefore, the infarcted area takes on a bluish-brown
hue, and the blood vessels of the area appear to be
engorged despite lack of blood flow. In later stages, the
vessel walls become highly permeable and leak fluid;
the local muscle tissue becomes edematous, and the
cardiac muscle cells begin to swell because of diminished
cellular metabolism.Within a few hours of almost
no blood supply, the cardiac muscle cells die.
Cardiac muscle requires about 1.3 milliliters of
oxygen per 100 grams of muscle tissue per minute just
to remain alive.This is in comparison with about 8 milliliters
of oxygen per 100 grams delivered to the
normal resting left ventricle each minute.Therefore, if
there is even 15 to 30 per cent of normal resting
coronary blood flow, the muscle will not die. In the
central portion of a large infarct, however, where
there is almost no collateral blood flow, the muscle
does die.
Subendocardial Infarction. The subendocardial muscle
frequently becomes infarcted even when there is no
evidence of infarction in the outer surface portions of
the heart. The reason for this is that the subendocardial
muscle has extra difficulty obtaining adequate
blood flow because the blood vessels in the subendocardium
are intensely compressed by systolic contraction
of the heart, as explained earlier. Therefore, any
condition that compromises blood flow to any area of
the heart usually causes damage first in the subendocardial
regions, and the damage then spreads outward
toward the epicardium.


When a specific allergen is injected
directly into the circulation, the allergen can react with
basophils of the blood and mast cells in the tissues
located immediately outside the small blood vessels
if the basophils and mast cells have been sensitized
by attachment of IgE reagins.Therefore, a widespread
allergic reaction occurs throughout the vascular
system and closely associated tissues. This is called
anaphylaxis. Histamine is released into the circulation
and causes body-wide vasodilation as well as increased
permeability of the capillaries with resultant marked
loss of plasma from the circulation. An occasional
person who experiences this reaction dies of circulatory
shock within a few minutes unless treated with
epinephrine to oppose the effects of the histamine.
Also released from the activated basophils and mast
cells is a mixture of leukotrienes called slow-reacting
substance of anaphylaxis.These leukotrienes can cause
spasm of the smooth muscle of the bronchioles, eliciting
an asthma-like attack, sometimes causing death by
Urticaria. Urticaria results from antigen entering specific
skin areas and causing localized anaphylactoid
reactions. Histamine released locally causes (1) vasodilation
that induces an immediate red flare and (2)
increased local permeability of the capillaries that
leads to local circumscribed areas of swelling of the
skin within another few minutes. The swellings are
commonly called hives. Administration of antihistamine
drugs to a person before exposure will prevent
the hives.
Hay Fever. In hay fever, the allergen-reagin reaction
occurs in the nose. Histamine released in response to
the reaction causes local intranasal vascular dilation,
with resultant increased capillary pressure as well as
increased capillary permeability. Both these effects
cause rapid fluid leakage into the nasal cavities and
into associated deeper tissues of the nose; and the
nasal linings become swollen and secretory. Here
again, use of antihistamine drugs can prevent this
swelling reaction. But other products of the allergenreagin
reaction can still cause irritation of the nose,
eliciting the typical sneezing syndrome.
Asthma. Asthma often occurs in the “allergic” type of
person. In such a person, the allergen-reagin reaction
occurs in the bronchioles of the lungs. Here, an important
product released from the mast cells is believed
to be the slow-reacting substance of anaphylaxis, which
causes spasm of the bronchiolar smooth muscle. Consequently,
the person has difficulty breathing until the
reactive products of the allergic reaction have been
removed. Administration of antihistaminics has less
effect on the course of asthma because histamine does
not appear to be the major factor eliciting the asthmatic


A clinical condition known as leukopenia occasionally
occurs in which the bone marrow produces very few
white blood cells, leaving the body unprotected against
many bacteria and other agents that might invade the
Normally, the human body lives in symbiosis with
many bacteria, because all the mucous membranes of
the body are constantly exposed to large numbers of
bacteria. The mouth almost always contains various
spirochetal, pneumococcal, and streptococcal bacteria,
and these same bacteria are present to a lesser extent
in the entire respiratory tract. The distal gastrointestinal
tract is especially loaded with colon bacilli. Furthermore,
one can always find bacteria on the surfaces
of the eyes, urethra, and vagina. Any decrease in the
number of white blood cells immediately allows invasion
of adjacent tissues by bacteria that are already
Within 2 days after the bone marrow stops producing
white blood cells, ulcers may appear in the mouth
and colon, or the person might develop some form of
severe respiratory infection. Bacteria from the ulcers
rapidly invade surrounding tissues and the blood.
Without treatment, death often ensues in less than a
week after acute total leukopenia begins.
Irradiation of the body by x-rays or gamma rays, or
exposure to drugs and chemicals that contain benzene
or anthracene nuclei, is likely to cause aplasia of the
bone marrow. Indeed, some common drugs, such as
chloramphenicol (an antibiotic), thiouracil (used to
treat thyrotoxicosis), and even various barbiturate
hypnotics, on very rare occasions cause leukopenia,
thus setting off the entire infectious sequence of this
After moderate irradiation injury to the bone
marrow, some stem cells, myeloblasts, and hemocytoblasts
may remain undestroyed in the marrow and are
capable of regenerating the bone marrow, provided
sufficient time is available.A patient properly treated
with transfusions, plus antibiotics and other drugs to
ward off infection, usually develops enough new bone
marrow within weeks to months for blood cell concentrations
to return to normal.

The Leukemias

Uncontrolled production of white blood cells can be
caused by cancerous mutation of a myelogenous or
lymphogenous cell. This causes leukemia, which is
usually characterized by greatly increased numbers
of abnormal white blood cells in the circulating
Types of Leukemia. Leukemias are divided into two
general types: lymphocytic leukemias and myelogenous
leukemias.The lymphocytic leukemias are caused
by cancerous production of lymphoid cells, usually
beginning in a lymph node or other lymphocytic tissue
and spreading to other areas of the body. The second
type of leukemia, myelogenous leukemia, begins by
cancerous production of young myelogenous cells in
the bone marrow and then spreads throughout the
body so that white blood cells are produced in many
extramedullary tissues—especially in the lymph nodes,
spleen, and liver.
In myelogenous leukemia, the cancerous process
occasionally produces partially differentiated cells,
resulting in what might be called neutrophilic
leukemia, eosinophilic leukemia, basophilic leukemia,
or monocytic leukemia. More frequently, however, the
leukemia cells are bizarre and undifferentiated and
not identical to any of the normal white blood cells.
Usually, the more undifferentiated the cell, the more
acute is the leukemia, often leading to death within a
few months if untreated.With some of the more differentiated
cells, the process can be chronic, sometimes
developing slowly over 10 to 20 years. Leukemic
cells, especially the very undifferentiated cells, are
usually nonfunctional for providing the normal protection
against infection.
Effects of Leukemia on the Body
The first effect of leukemia is metastatic growth of
leukemic cells in abnormal areas of the body.
Leukemic cells from the bone marrow may reproduce
so greatly that they invade the surrounding bone,
causing pain and, eventually, a tendency for bones to
fracture easily.
Almost all leukemias eventually spread to the
spleen, lymph nodes, liver, and other vascular regions,
regardless of whether the origin of the leukemia is in
the bone marrow or the lymph nodes. Common effects
in leukemia are the development of infection, severe
anemia, and a bleeding tendency caused by thrombocytopenia
(lack of platelets). These effects result
mainly from displacement of the normal bone marrow
and lymphoid cells by the nonfunctional leukemic
Finally, perhaps the most important effect of
leukemia on the body is excessive use of metabolic
substrates by the growing cancerous cells. The
leukemic tissues reproduce new cells so rapidly that
tremendous demands are made on the body reserves
for foodstuffs, specific amino acids, and vitamins. Consequently,
the energy of the patient is greatly depleted,
and excessive utilization of amino acids by the
leukemic cells causes especially rapid deterioration of
the normal protein tissues of the body.Thus, while the
leukemic tissues grow, other tissues become debilitated.
After metabolic starvation has continued long
enough, this alone is sufficient to cause death.

Primary Sensations of Taste

The identities of the specific chemicals that excite different taste receptors are
not all known. Even so, psychophysiologic and neurophysiologic studies have
identified at least 13 possible or probable chemical receptors in the taste cells,
as follows: 2 sodium receptors, 2 potassium receptors, 1 chloride receptor,
1 adenosine receptor, 1 inosine receptor, 2 sweet receptors, 2 bitter receptors,
1 glutamate receptor, and 1 hydrogen ion receptor.
For practical analysis of taste, the aforementioned receptor capabilities have
also been grouped into five general categories called the primary sensations of
taste. They are sour, salty, sweet, bitter, and “umami.”

Sour Taste. The sour taste is caused by acids, that is, by the hydrogen ion concentration,
and the intensity of this taste sensation is approximately proportional
to the logarithm of the hydrogen ion concentration.That is, the more acidic
the food, the stronger the sour sensation becomes.
Salty Taste. The salty taste is elicited by ionized salts, mainly by the sodium ion
concentration. The quality of the taste varies somewhat from one salt to
another, because some salts elicit other taste sensations in addition to saltiness.
The cations of the salts, especially sodium cations, are mainly responsible for
the salty taste, but the anions also contribute to a lesser extent.
Sweet Taste. The sweet taste is not caused by any single class of chemicals. Some
of the types of chemicals that cause this taste include sugars, glycols, alcohols,
aldehydes, ketones, amides, esters, some amino acids, some small proteins,
sulfonic acids, halogenated acids, and inorganic salts of lead and beryllium. Note specifically that most of the substances that cause a sweet taste are organic chemicals. It is especially interesting that slight changes in the chemical structure, such as addition of a simple radical, can often change the substance from sweet to bitter.
Bitter Taste. The bitter taste, like the sweet taste, is not caused by any single type of chemical agent. Here again, the substances that give the bitter taste are almost entirely organic substances. Two particular classes of substances are especially likely to cause bitter taste sensations: (1) long-chain organic substances that contain nitrogen, and (2) alkaloids. The alkaloids include many of the drugs used in medicines, such as quinine, caffeine, strychnine, and nicotine. Some substances that at first taste sweet have a bitter aftertaste.This is true of saccharin, which makes this substance objectionable to some people. The bitter taste, when it occurs in high intensity, usually causes the person or animal to reject the food. This is undoubtedly an important function of the bitter taste sensation, because many deadly toxins found in poisonous plants are alkaloids, and virtually all of these cause intensely bitter taste, usually followed by rejection of the food.
Umami Taste. Umami is a Japanese word (meaning “delicious”) designating a pleasant taste sensation that is qualitatively different from sour, salty, sweet, or bitter. Umami is the dominant taste of food containing L-glutamate, such as meat extracts and aging cheese, and some physiologists consider it to be a separate, fifth category of primary taste stimuli. A taste receptor for L-glutamate may be related to one of the glutamate receptors expressed in neuronal synapses of the brain. However, the precise molecular mechanisms responsible for umami taste are still unclear.

Horner’s Syndrome.

(click to view in zoom)
The sympathetic nerves to the eye are
occasionally interrupted. Interruption frequently occurs
in the cervical sympathetic chain. This causes the clinical
condition called Horner’s syndrome, which consists
of the following effects: First, because of interruption of
sympathetic nerve fibers to the pupillary dilator muscle,
the pupil remains persistently constricted to a smaller
diameter than the pupil of the opposite eye. Second, the
superior eyelid droops because it is normally maintained
in an open position during waking hours partly
by contraction of smooth muscle fibers embedded in the
superior eyelid and innervated by the sympathetics.
Therefore, destruction of the sympathetic nerves makes
it impossible to open the superior eyelid as widely as
normally.Third, the blood vessels on the corresponding
side of the face and head become persistently dilated.
Fourth, sweating (which requires sympathetic nerve
signals) cannot occur on the side of the face and head
affected by Horner’s syndrome

Pupillary Reflexes or Reactions in Central Nervous System Disease

A few central nervous system diseases damage
nerve transmission of visual signals from the retinas to
the Edinger-Westphal nucleus, thus sometimes blocking
the pupillary reflexes. Such blocks frequently occur as a
result of central nervous system syphilis, alcoholism,
encephalitis, and so forth.The block usually occurs in the
pretectal region of the brain stem, although it can result
from destruction of some small fibers in the optic
The final nerve fibers in the pathway through the pretectal
area to the Edinger-Westphal nucleus are mostly
of the inhibitory type. When their inhibitory effect is
lost, the nucleus becomes chronically active, causing the
pupils to remain mostly constricted, in addition to their
failure to respond to light.
Yet the pupils can constrict a little more if the
Edinger-Westphal nucleus is stimulated through some
other pathway. For instance, when the eyes fixate on a
near object, the signals that cause accommodation of
the lens and those that cause convergence of the two
eyes cause a mild degree of pupillary constriction at
the same time. This is called the pupillary reaction to

accommodation. A pupil that fails to respond to light

but does respond to accommodation and is also very

small (an Argyll Robertson pupil) is an important diagnostic

sign of central nervous system disease—often



“Glaucoma,” a Principal Cause of Blindness. Glaucoma is one
of the most common causes of blindness. It is a disease
of the eye in which the intraocular pressure becomes
pathologically high, sometimes rising acutely to 60 to
70 mm Hg. Pressures above 25 to 30 mm Hg can cause
loss of vision when maintained for long periods.
Extremely high pressures can cause blindness within
days or even hours. As the pressure rises, the axons of
the optic nerve are compressed where they leave the
eyeball at the optic disc.This compression is believed to
block axonal flow of cytoplasm from the retinal neuronal
cell bodies into the optic nerve fibers leading to
the brain. The result is lack of appropriate nutrition of
the fibers, which eventually causes death of the involved
fibers. It is possible that compression of the retinal
artery, which enters the eyeball at the optic disc, also
adds to the neuronal damage by reducing nutrition to
the retina.
In most cases of glaucoma, the abnormally high pressure
results from increased resistance to fluid outflow
through the trabecular spaces into the canal of Schlemm
at the iridocorneal junction. For instance, in acute
eye inflammation, white blood cells and tissue debris
can block these trabecular spaces and cause an acute
increase in intraocular pressure. In chronic conditions,
especially in older individuals, fibrous occlusion of the
trabecular spaces appears to be the likely culprit.
Glaucoma can sometimes be treated by placing drops
in the eye that contain a drug that diffuses into the
eyeball and reduces the secretion or increases the
absorption of aqueous humor.When drug therapy fails,
operative techniques to open the spaces of the trabeculae
or to make channels to allow fluid to flow directly
from the fluid space of the eyeball into the subconjunctival
space outside the eyeball can often effectively
reduce the pressure.

Glaucoma is a condition of increased fluid pressure inside the eye. The increased pressure causes compression of the retina and the optic nerve which can eventually lead to nerve damage. Glaucoma can cause partial vision loss, with blindness as a possible eventual outcome.