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Endocrine Physiology
Trophic hormones Functions Clinical signs of
of hyposecretion,
Adenohypophy is hypersecretion
stimulates secretion of glucocorticoid ACTH deficiency can either be
1 ACTH steroid hormones from adrenal cortex cells congenital or acquired Symptoms include
weight loss, lack of appetite (anorexia),
muscle weakness, nausea and vomiting,
and low blood pressure (hypotension)
regulates the development, growth, pubertal In men with high FSH levels due to a
2 FSH maturation and reproductive processes of gonadotroph adenoma, symptoms result
the human body. from the mass effect (eg, headaches,
visual impairment, hormonal
deficiencies).
In women with high FSH levels from a
gonadotroph adenoma, symptoms are
frequently due to mass effect (eg,
headaches, visual changes,
hypopituitarism).
helps control the menstrual cycle. Hypersecretion of luteinizing hormone
3 LH (LH) is a significant cause of infertility
and miscarriage in women with the
polycystic ovary syndrome.
regulate the production of hormones by the Fatigue, Increased sensitivity to cold,
4 TSH thyroid gland. Constipation, Dry skin, Weight gain,
Puffy fase, Hoarseness,
Muscle weakness.
B) Extisctic:
1. Nutrition (food supply
Light availability
Available nutrients
Water in the soil
Competition with other plants
Physical activities such as running, jogging, and aerobics are a great way
to physically relieve stress and tension.
Relaxing physical activities such as yoga or tai chi can help to work your
body while relaxing your mind. Try these yoga poses to relieve stress.
Mindfulness techniques such as meditation can strengthen your emotional
responses to stress.
Reducing stress in different areas of your life, when possible, can help to
lessen your exposure to chronic stressors.
C) Hormones:
In order to maintain a normal balanced hormone production, growth
hormone-releasing hormone, somatostatin, growth hormone and insulin-like
growth factor 1 levels are regulated by each other. The consequence of
growth hormone-releasing hormone action is an increase in the circulating
levels of growth hormone and insulin-like growth factor 1 which, in turn, act
back on the hypothalamus to prevent growth hormone-releasing hormone
production and to stimulate somatostatin secretion. Somatostatin then
prevents the release of growth hormone from the pituitary gland and growth
hormone-releasing hormone production by the hypothalamus, therefore
acting as a powerful suppressor of growth hormone secretion.
3. Name disorders of growth
1. Hypothyroidism
Hypothyroidism can be the result of a congenital disorder, meaning it is
present from birth. It is known as an endocrine disorder, the result of a
hormone imbalance. It can also occur later in some children as the result
of an autoimmune disorder.
2. Growth hormone deficiency (GHD)
In GHD, the portions of the brain responsible for stimulating and
secreting growth hormone may not be working properly or could be
damaged. In other cases, GHD can be caused by a hormone imbalance.
This means that growth hormone is not released in high enough levels to
stimulate normal growth.
3. Malnutrition and malabsorption.
Malnutrition directly affects the release of growth hormones, lowering
the amount in the body. Unfortunately, children that are malnourished
will have reduced growth. In Crohn’s disease, the level of growth failure
is directly related to the severity of the disease.
4. Chronic kidney disease (CKD)
Poor growth is a common problem for children with CKD. It can occur
when the glomerular filtration rate (GFR), a measurement of kidney
function, becomes too low. Many factors contribute to poor growth in
patients with CKD, for example the child may be getting inadequate
nutrition (calorie intake).
5. Turner syndrome (TS)
The cause of TS is not fully understood; however, we know it is the
result of a genetic issue. Girls with TS lack some sections on the X
chromosome.
6. Silver-Russell syndrome (SRS)
SRS is a genetic growth disorder caused by errors in different parts of
some genes. It was originally documented in the 1950s by ‘Silver’ and
‘Russell’, who reported a number of children with low birth weights and
short stature.
7. Skeletal displasias
Skeletal dysplasias are regulated by several hormonal and genetic
factors, and any fault in these factors can lead to impairment of growth.
Skeletal dysplasias often lead to neurological issues and problems with
the bones and cartilage that may not see in other growth disorders.
8. Prader-Willi syndrome (PWS)
The cause of PWS is genetic and it can also affect a number of hormonal
processes. A few different genes are affected, leading to a number of
health issues. In nearly 80% of PWS cases, the body may not produce
enough growth hormone leading to short stature.
9. Noonan syndrome (NS)
NS is caused by mutations to certain genes critical for the growth and
regulation of cells, which is why NS can lead short stature, along with a
number of health problems.
10. Small for gestational age (SGA)
Impaired growth of the baby while in the womb can be caused by a
number of factors, including genetic, maternal, placental and
demographic. Often the exact cause is not known.
11. Idiopathic short stature (ISS)
ISS can be caused by mutations to genes involved in the function of
growth hormones and growth plate physiology; however, many causes
are still unknown.
12. Familial short stature
Children with familial short stature tend to fall at the lower extreme of
the growth chart (below the 3rd percentile) and their growth is usually
impacted by their parents’ heights. This does not tend to impact their
overall health and their height is generally considered to be appropriate
for their genetic potential based on their parents’ heights.
13. Constitutional delay of growth and puberty
Constitutional growth delay refers to children who are small for their age
but who grow at a normal rate. They often have a delayed bone age,
meaning their skeletal maturation is younger than their age in years.
Although puberty may be delayed, they tend to catch up with their peers
when they reach adult height.
4. Effects (functions) of oxytocin:
Sucking Reflex
When does the sucking reflex develop? Sucking reflex and nursing
The sucking reflex develops when a baby is The sucking reflex happens in two stages. When
still in the womb. The earliest it develops is a nipple either from a breast or bottle is placed in
in week 32 of pregnancy. It is generally the baby’s mouth, they will automatically start
fully developed by week 36 of pregnancy. sucking. With breastfeeding, the baby will place
their lips over the areola and squeeze the nipple
between their tongue and roof of the mouth.
Rooting versus sucking They will use a similar movement when nursing
on a bottle.
reflex
There is another reflex that goes along with
sucking called rooting. Babies will root around or
search for the breast instinctually before latching How to test a baby’s sucking reflex
on to suck. While these two reflexes are related,
they serve different purposes. Rooting helps a You can test a baby’s sucking reflex by placing a
baby find the breast and nipple. Sucking helps a nipple (breast or bottle), clean finger, or pacifier
baby extract breastmilk for nutrition. inside the baby’s mouth. If the reflex has fully
developed, the baby should place their lips around
the item and then rhythmically squeeze it between
their tongue and palate.
Nursing problems and seeking
help
Kangaroo care Rooting reflex
Wake for feedings
Assume the position Rooting and sucking reflexes go together. Your baby
Try other positions will turn their head when their cheek or the corner of
Increase your let-down reflex. their mouth is stroked. It’s as if they’re trying to find
Stay positive the nipple.
To test for the rooting reflex:
1. Muscular work
- This paper reports on an experiment concerning the involvement of
catecholamines in the biosynthesis of nucleic acids and proteins at
muscular levels, using various types of skeletal muscles (psoas,
diaphragm, soleus) and heart muscles from male Wistar rats treated with
adrenalin
2. Hemorrage
- Neurogenic pulmonary edema (NPE) occurs frequently after aneurysmal
subarachnoid hemorrhage (SAH), and excessive release of
catecholamines (epinephrine/norepinephrine) has been suggested as its
principal cause.
3. Hypoglycemia
- Catecholamines are found to contribute to human glucose
counterregulation because an early phase of hypoglycemia throughout;
they exert effects both at the liver and at the muscle level; their
counterregulatory effects are not compensated by other hormones, in
particular glucagon; thus, the failure of catecholamines to exert their
effects in hypoglycemia, such as during α,β pharmacological blockade,
results in severe hypoglycemia, despite increase in other
counterregulatory hormones.
4. Exposure to cold
- These rats were treated with adrenaline, noradrenaline or propranolol
(400 micrograms/kg subcutaneously) or were exposed to a temperature of
15 degrees C for 2 hours before and after propranolol injection (400
micrograms/kg). The metabolic rate (MR), respiratory quotient (RQ) and
the levels of free fatty acids, glucose and urea in the plasma were
determined.
11. Characterize differences between notions “eustress” and “distress”
and their clinical meaning.
Endocrine Physiology
air pollution or whose mothers smoked during pregnancy. The kids with
stressed out parents had a substantially higher risk of developing asthma .
14.A famous author of stress concept Hans Selye has an expression: “Stress
does not ruin us, but only our perception of it” (“Stress without distress”,
1977). Explain physiological mechanisms of anti-stress influence on
human health:
Incorporate some relaxing practice.
Look for activities to renew yourself physically and psychologically: rest,
leisure activities, relaxation techniques, physical activities such as walking or
swimming.
Take care of your diet. Eat a healthy diet and avoid caffeine and alcohol
abuse.
Distinguish between what 'you can do' and what 'you cannot do'; we all have
limits.
Prioritize your activities to be able to manage your time more effectively.
Learn to tell what happens to you.
Give yourself permission to say 'no' and to feel what you feel.
Set realistic and achievable goals.
Strive for a balance between obligations and pleasures.
Strengthen yourself when you achieve a goal.
If you want to make changes, it is better to start with those that are smaller.
Remember that it is easier to add new behaviors than to remove old ones.
Changes in blood glucose concentrations during a typical 24 h period. Note
that glucose concentration increases after each meal, more so after larger
meals, and then returns to the premeal concentration in short while. The
profile shown here is that of a person who is homeostatic for blood glucose,
even though concentrations of this sugar vary considerably throughout the
day.
Endocrine Physiology
15.Define factors that hormonal control calcium metabolism
- In terrestrial vertebrates, including humans, maintenance of adequate
concentrations calcium ion in the extracellular fluid requires the activity
of two hormones, parathyroid hormone (PTH) and a derivative of
vitamin D called calcitriol. In primitive vertebrates living in a marine
environment, guarding against excessively high concentrations of
calcium requires another hormone, calcitonin, which appears to have
only vestigial activity in humans. Calcium enters into a wide range of
cellular and molecular processes. Changes of its concentration within
cells regulate enzymatic activities and fundamental cellular events such
as muscular contraction, secretion, and cell division. Normally, adults
are in calcium balance; that is, on average, daily intake equals daily loss
in urine and feces. The cellular mechanisms by which extracellular
calcium regulates PTH secretion are poorly understood. In addition to
the primary endocrine regulators of calcium balance, it is apparent that
many other endocrine and paracrine factors influence calcium balance.
Many of the systemic hormones directly or indirectly have an impact on
calcium balance. All of the hormones that govern growth—namely,
growth hormone, the insulin-like growth factors, and thyroidal and
gonadal hormones—directly or indirectly influence the activity of bone
cells and calcium balance. Defects in calcium metabolism are also seen
in hyperthyroidism and in conditions of excess or deficiency of adrenal
cortical hormones.