REPRODUCTION REVISION QUESTIONS:
Birth control pills:
- It inhibits female fertility
- Prevents ovulation by suppressing the release of gonadotropins
- Progesterone negative feedback decreases the pulse frequency of
gonadotropin- releasing hormone released by the hypothalamus,
which decreases the release of FSH and greatly decreases the release
of LH by the anterior pituitary
- Decreased levels of FSH inhibit follicular development, preventing an
increase in estradiol levels
- Progesterone negative feedback and the lack of estrogen positive
feedback on LH release prevent a mid-cycle LH surge
- Inhibition of follicular development and helps prevent ovulation
Describe how the secretion of hormones from the testes and the
ovary is controlled:
GnRH reaching the anterior pituitary gland via the hypothalamo-
pituitary portal vessels triggers the release of both LH and FSH from the
same cell type. FSH acts primarily on the sertoli cells to stimulate the
secretion of paracrine agents required for spermatogenesis. While, LH
acts primarily on the leydig cells to stimulate testosterone secretion.
When testosterone levels rise above normal, GnRH and LH secretion
are inhibited. The level of testosterone is under negative feedback
control: a rising level of testosterone suppresses the GnRH from the
Hormones from the pituitary gland, luteinizing hormone, or LH, and
follicle-stimulating hormone, or FSH, regulate the activity of the Leydig
cells and can alter the amount of testosterone that is produced. When
testosterone levels are low, the hypothalamus releases a hormone
known as GnRH, or gonadotropin-releasing hormone. GnRH stimulates
the anterior pituitary to release LH and FSH, which stimulate the Leydig
cells and increase testosterone production. Increasing levels of
testosterone cause the hypothalamus to decrease the production and
release of GnRH. Without this hormone, LH and FSH will no longer be
released. Without these two pituitary hormones, the Leydig cells will not
be stimulated and testosterone production will decrease. This entire
process is known as a negative feedback loop.
Hypothalamus -> GnRH -> Anterior pituitary -> LH -> Testes ->
The synthesis of estrogens is stimulated by FSH, which is, in turn,
controlled by the hypothalamic GnRH. High levels of estrogens
suppress the release of GnRH providing a negative feedback control of
Estrogen, in low plasma concentrations, causes the anterior pituitary
gland to secrete less FSH and LH in response to GnRH and also may
inhibit the hypothalamic neurons that secrete GnRH. Estrogen, when
increasing dramatically, causes anterior pituitary gland to secrete more
LH and FSH in response to GnRH. Estrogen can also stimulate the
hypothalamic neurons that secrete GnRH.
Hypothalamus -> GnRH -> Anterior pituitary -> FSH -> Follicle ->
Whereas, progesterone is secreted by LH, which is also stimulated by
GnRH. Plasma concentrations of progesterone, in the presence of
estrogen, inhibit the hypothalamic neurons that secrete GnRH
Hypothalamus -> GnRH -> Anterior pituitary -> Corpus luteum ->
Discuss the processes involved from ejaculation to implantation. Be
sure to consider embryonic and hormonal events.
During sexual excitement, parasympathetic nerves to penile arteries
release nitric oxide, which relaxes smooth muscles that causes vessels
to dilate, increase the blood flow to the penis, vascular channels
become engorged with blood, which then leads to an erection.
Ejaculation occurs when impulses provoking an erection reach a
critical point. The bladder sphincter muscle constricts to prevent sperm
and urine from expelling at the same time, and the reproductive ducts
and accessory glands contract, where finally, the bulbospongiosum
muscle of the penis contracts to eject semen.
The production of sperm takes place in the testes in the seminiferous
tubules, where in order to get sperm from the testes to outside of the
body, it travels through a series of tubes. Sperm is ejaculated from the
epididymis into the vas deferens. As the tube, ejaculatory duct, is
joined to the vas deferens and joins to the urethra, sperm is travelled
from the vas deferens down to the ejaculatory duct, where it is then
expelled through the urethra causing ejaculation to occur.
In order for fertilization to occur, sexual intercourse must take place a
few days leading up to ovulation, or on the day of ovulation.
Fertilisation occurs when sperm weaves through the granulosa cells of
the corona radiata, where the sperm then binds to the zona pellucida,
which causes calcium levels to increase in sperm. This leads to
acrosomal reaction to occur, which is the breakdown of membranes. Acrosomal enzymes digest holes in the zona pellucida, as an
acrosomal process is formed at the tip of the sperm, which allows it to
bind to the receptors on the egg. Finally, the sperm and oocyte
membranes fuse, releasing sperm DNA into an egg.
As soon as the oocyte is fertilized, it becomes a zygote. The zygote
undergoes division, and as the collection of cells exceeds 16, it is
known as a morula. The cells of the morula continues to divide, until a
fluid filled cavity forms and the zone pellucida starts to break down,
where it becomes a blastocyst. The implantation of the blastocyst
occurs about 6-7 days after fertilization. Trophoblast adheres to site in
the endometrium with mature receptors and chemical signals. Further
digestion occurs until the blastocyst has buried itself in the rich
endometrial environment. Successful implantation takes about 5 days,
where the embryo signals to the corpus luteum to continue to produce
progesterone and estrogen. DIGESTION REVISION QUESTIONS:
Why is the enteric nervous system referred to as the gut brain?
The enteric nervous system is referred to as the gut brain as it controls
gut functions from the outer or inner input from extrinsic/internal nerves.
It is able to control gut functions independently. Gut nerves from
outside the gut, innervating the gut, the gut can still control its own
functions by its own intrinsic within the gut nerves.
Explain the roles of sensory, autonomic, enteric, somatic nerves in
the defecation reflex.
Mass movements move the fecal matter from the sigmoidal colon to
the rectum. This causes the stretch of rectal well, which activates
stretch receptors. By activating the sensory nerves, it gives information
to the spinal cord neurons, which activates autonomic nerves due to
parasympathetic nerves. The parasympathetic nerves cause the rectal
wall to constrict. There are 2 anal sphincters – internal and external. The
internal anal sphincter is made up of smooth muscles, which is
controlled by autonomic nerves. The activation of enteric/myenteric
nerves causes the rectum to contract, while the internal anal sphincter
relaxes. The parasympathetic nerves cause the internal anal sphincter
to relax. Conscious control activates somatic motor nerves, which
innervates skeletal muscles of the external anal sphincter. This leads to
the relaxation of the external and internal anal sphincter, which causes
feces to be excreted.
What triggers the defecation reflex? How do we control the final
part of this reflex?
A normal functioning defecation reflex produces a muscular
contraction that serves as a signal to the body that it is time to move
the bowels and eliminate stools. A wave of intense contractions, mass
movement, spreads rapidly over the transverse segment of the large
intestine towards the rectum. The anus, the exit from the rectum, is
normally closed by the internal anal sphincter, composed of smooth
muscle, and the external anal sphincter, composed of skeletal muscle
under voluntary control. The sudden distension of the walls of the
rectum produced by the mass movement of fecal material into it
initiates the defecation reflex. The conscious urge to defecate,
mediated by the mechanoreceptors, accompanies distension of the
rectum. The defecation reflex response consists of a contraction of the
rectum and relaxation of the internal anal sphincter but contraction of
the external anal sphincter and increases peristaltic activity in the
sigmoid colon. Finally, a pressure is reached in the rectum that triggers
reflex relaxation of the external anal sphincter, allowing feces to be
However, brain centers can override the defecation reflex signals that
cause the sphincter to relax, thus keeping the external anal sphincter
closed and allowing the person to delay defecation. The prolonged distension of the rectum initiates a reverse peristalsis, driving the rectal
contents back into the sigmoid colon. The urge to defecate subsides
until the next mass movement propels more feces into the rectum,
increasing its volume and initiating the defecation reflex.
Hirschsprung’s disease is associated with aganglionic sections of the
large intestine. What is meant by aganglionic and why does these
diseases lead to bowel obstruction and constipation?
Hirschsprung’s disease is a blockage of the large intestine due to
improper muscle movement in the bowel. Muscle contractions,
peristalsis, in the gut help digested material move through the intestine.
Hirschsprung’s disease lacks the nerves from a part of the bowel. As
areas without such nerves cannot push material through, which causes
blockage. Aganglionic means that ganglion cells are absent. The lack
of ganglion cells in the myenteric plexus, which is responsible for
moving food in the large intestine. Blockage causes the intestinal
contents to build up behind the blockage, which causes the bowel
and abdomen to become swollen. As the path for digested material is
blocked, constipation can occur.
Is removal of the gall bladder likely to have any significant effects
on normal digestive function? Explain your answer.
The gall bladder stores secreted bile until the liver needs it for digestion
and concentrates the organic molecules in bile by absorbing salts and
water. Bile contained bile salts, cholesterol, phospholipids, and bile
pigments. Removal of the gall bladder is going to inhibit the digestion
and absorption of fats and other fat soluble substances. As the function
of bile is to emulsify fats in foods as the fats leave the stomach and
enter the small intestine. Without the gall bladder, fats will still be
emulsified, but not to the same extent. So, for meals containing a lot of
fat and lipids, much of the fat will not be emulsified and won’t get
Describe the anatomy of the enteric nervous system
The principle components of the enteric nervous system are two
networks or plexuses of neurons, both of which are embedded in the
wall of the digestive tract and extend from the esophagus to the anus.
- The myenteric plexus is located between the longitudinal and circular
layers of muscle in the tunica muscularis and, approximately, exerts
control primarily over digestive tract motility.
- The submucous plexus is buried in the submucosa. Its principle role is in
sensing the environment within the lumen, regulating gastrointestinal
blood flow and controlling epithelial cell function. In regions where
these functions are minimal, such as the esophagus, the submucosal
plexus is sparse and may actually be missing in sections.
Within the enteric plexuses, there are three types of neurons:
- Sensory neurons receive information from sensory receptors in the mucosa and muscle. They compile a comprehensive battery of
information on gut contents and the state of the gastrointestinal wall.
- Motor neurons within the enteric plexuses control gastrointestinal
motility and secretion, and possibly absorption. They act directly on a
large number of effector cells, including smooth muscle, secretory cells
(chief, parietal, mucous, enterocytes, pancreatic exocrine cells) and
gastrointestinal endocrine cells
- Interneurons are largely responsible for integrating information from
sensory neurons and providing it to enteric motor neurons.
Fatty foods are retained from the stomach for longer periods than
starches. Describe how CCK slows the release of fatty chime from
stomach to the duodenum.
CCK is a peptide hormone of the gastrointestinal system responsible for
stimulating the digestion of fat and protein. It is appropriate that the
stimuli for its release are fatty acids and amino acids in the duodenum.
It is synthesized by the I-cells in the mucosal epithelium of the small
intestine and secreted in the duodenum, the first segment of the small
intestine, and causes the release of digestive enzymes and bile from
the pancreas and gallbladder. Secretion of CCK by the duodenal and
intestinal mucosa is stimulated by fat or protein-rich chyme entering the
duodenum. It then inhibits gastric emptying and gastric acid secretion
and mediates digestion in the duodenum. CCK also causes the
increased production of hepatic bile, and stimulates the contraction of
the gall bladder and the relaxation of the Sphincter of Oddi, resulting in
the delivery of bile into the duodenal part of the small intestine.
Cholecystokinin CCK) inhibits gastric emptying, thus regulating the flow
of chyme from the stomach into the duodenum. As we discussed
earlier, CCK is released as partially digested food enters the
duodenum. In addition to regulating flow, its other primary role is to
trigger the pancreas and gallbladder to respectively release digestive
enzymes and bile, thereby assisting in the digestion down the line of the
proteins and fats entering the duodenum. ENDOCRINOLOGY REVISION QUESTIONS:
Answer the following questions for insulin – dependent diabetes
Explain the cause and the key endocrine events that occur.
Diabetes mellitus is a condition in which the pancreas no longer
produces enough insulin or cells stop responding to the insulin that is
produced, so that glucose in the blood cannot be absorbed into the
cells of the body. The immune system, the body's defense system
against infection, is believed to be triggered by a virus or another
microorganism that destroys cells in the pancreas that produce insulin.
Insulin is the protein that is responsible for transporting glucose
(secreted by pancreatic a cells) from the blood into the cells, where
the glucose is metabolized for energy. When b cells are killed the body
has no way of producing insulin, so glucose levels in the blood are
unable to be controlled, leading to hyperglycemia, or high blood
What are the effects of these endocrine events?
Without insulin, the body’s cells cannot turn glucose (sugar), into
energy. Without insulin the body burns its own fats as a substitute. Unless
treated with daily injections of insulin, people with type 1 diabetes
accumulate dangerous chemical substances in their blood from the
burning of fat. Long term complications of hyperglycemia include
cardiovascular, kidney, and eye diseases, as well as various nervous
What are the major clinical symptoms?
Symptoms include frequent urination, lethargy, excessive thirst, and
How can the disorder be treated?
The treatment includes changes in diet, oral medications, and in some
cases, daily injections of insulin.
Discuss how the synthesis and secretion of the hormones produced
by the hypothalamus and anterior pituitary gland are regulated.
HORMONES PRODUCED IN THE HYPOTHALAMUS:
- Thyrotropin-releasing hormone (TRH)
- Gonadotropin-releasing hormone (GnRH)
- Growth hormone-releasing hormone (GHRH)
- Corticotropin-releasing hormone (CRH)
- Oxytocin (secreted into the bloodstream by the ppg)
- Antidiuretic hormone (ADH)/Vasopressin TRH is produced by the hypothalamus in medial neurons of the
paraventricular nucleus. It travels across the median eminence to the
anterior pituitary gland via the hypophyseal portal system, where it
stimulates the release of thyroid-stimulating hormone (TSH) and excess
levels inhibit dopamine, which will then stimulate the release of
prolactin, which in turn decreases GnRH.
GnRH is a trophic peptide hormone responsible for the release of FSH
and LH from the anterioir pituitary. GnRH is synthesized and released
from neurons within the hypothalamus. It is secreted in the hypophysial
portal bloodstream at the median eminence. The portal blood carries
the GnRH to the pituitary gland.
GHRH is a releasing hormone for growth hormone. It is released from
neurosecretory nerve terminals of arcuate neurons, and is carried by
the hypothalamo-hypophyeal portal system to the anterior pituitary
gland, where it stimulates GH secretion by stimulating the growth
hormone-releasing hormone receptor. The actions of GHRH are
opposed by somatostation (growth hormone-inhibiting hormone).
Somatostatin is released from neurosecretory nerve terminals of
periventricular somatostatin neurons, and is carred by the
hypothalamo-hypophysial portal circulation to the anterior pituitary,
where it inhibits GH secretion.
CRH is a peptide hormone and neurotransmitter involved in the stress
response. Its main function is the stimulation of the pituitary synthesis of
ACTH. It is secreted by the paraventricular nucleus of the
hypothalamus in response to stress. CRH is released at the median
eminence from neurosecretory terminals of these neurons into the
primary capillary plexus of the hypothalamo-hypophyseal portal system.
The portal system carries the CRH to the anterior lobe of the pituitary,
where it stimulates corticotropes to secrete ACTH.
Somatostatin is a peptide hormone produced by neuroendocrine
neurons of the periventricular nucleus of the hypothalamus. These
neurons project to the median eminence, where somatostatin is
released from neurosecretory nerve endings into the hypothalamo-
hypophyseal system through neuron axons. It is released by the
hypothalamus to inhibit the release of growth hormone (GH,
somatotropin) and TSH from the anterior pituitary.
Oxytoxin is produced in the hypothalamus and is secreted into the
bloodstream by the posterior pituitary gland. Secretion depends on
electrical activity of neurons in the hypothalamus – it is released into
the blood when these cells are excited. Oxytocin is controlled by a
positive feedback mechanism. When contraction of the uterus starts,
oxytocin is released which stimulates more contractions and more oxytocin to be released. There is also a positive feedback involved in
melk-ejection reflex. When a baby sucks on the nipple, the stimulation
leads to oxytocin secretion into the blood which then causes milk to be
let down into the breast. Production of oxytocin is stopped after the
baby is delivered or when the baby steps feeding. A number of factors
can inhibit oxytocin release, among them acute stress. For example,
oxytocin neurons are repressed by catecholamines, which are
released from the adrenal gland in response to many types of stress.
The most important variable regulating antidiuretic hormone secretion
is plasma osmolarity, or the concentration of solutes in blood.
Osmolarity is sensed in the hypothalamus by neurons known as an
osmoreceptors, and those neurons, in turn, stimulate secretion from the
neurons that produce antidiuretic hormone. When plasma osmolarity is
below a certain threshold, the osmoreceptors are not activated and
secretion of antidiuretic hormone is suppressed. When osmolarity
increases above the threshold, the ever-alert osmoreceptors recognize
this as their cue to stimulate the neurons that secrete antidiuretic
hormone. As seen the the figure below, antidiuretic hormone
concentrations rise steeply and linearly with increasing plasma
osmolarity. Osmotic control of antidiuretic hormone secretion makes
perfect sense. Imagine walking across a desert: the sun is beating
down and you begin to lose a considerable amount of body water
through sweating. Loss of water results in concentration of blood solutes
- plasma osmolarity increases.
HORMONES PRODUCED IN THE ANTERIOR PITUITARY GLAND:
- Follicle-stimulating hormone (FSH)
- Luteinizing hormone (LH)
- Growth hormone (GH) or somatotropin
- Thyroid-stimulating hormone (TSH)
- Adrenocortiotropic hormone (ACTH) or corticotropin
Production of growth hormone is modulated by many factors,
including stress, exercise, nutrition, sleep and growth hormone itself.
However, its primary controllers are two hypothalamic hormones and
one hormone from the stomach:
Growth hormone-releasing hormone (GHRH) is a
hypothalamic peptide that stimulates both the synthesis and
secretion of growth hormone.
Somatostatin (SS) is a peptide produced by several tissues in the
body, including the hypothalamus. Somatostatin inhibits gro