The endocrine system physiology

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Endocrine signaling
Paracrine signaling Synaptic signaling
Autocrine signaling
Neuroendocrine signaling

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6. Three general classes of hormones exist:
1. Proteins and polypeptides, including hormones secreted by the
anterior and posterior pituitary gland, the pancreas (insulin and
glucagon), the parathyroid gland (parathyroid hormone), and … .
2. Steroids secreted by the adrenal cortex (cortisol and
aldosterone), the ovaries (estrogen and progesterone), the testes
(testosterone), and the placenta (estrogen and progesterone).
3. Derivatives of the amino acid tyrosine, secreted by the thyroid
(thyroxine and triiodothyronine) and the adrenal medullae
(epinephrine and norepinephrine).
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8. The locations for the different types of hormone receptors are
generally the followings:
1. In or on the surface of the cell membrane. The membrane
receptors are specific mostly for the protein, peptide, and
catecholamine hormones.
2. In the cell cytoplasm. The primary receptors for the different
steroid hormones are found mainly in the cytoplasm.
3. In the cell nucleus. The receptors for the thyroid hormones are
found in the nucleus and are believed to be located in direct
association with one or more of the chromosomes.
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Growth hormone has several metabolic effects including:
1) Increased rate of protein synthesis in most cells of the body
(enhancement of amino acid transport through the cell
membranes, enhancement of RNA translation to cause protein
synthesis, increased nuclear transcription of DNA to form RNA,
decreased catabolism of protein and amino acids)
2) Increased mobilization of fatty acids from adipose tissue,
increased free fatty acids in the blood, and increased use of fatty
acids for energy causing Ketosis
3) Decreased rate of glucose utilization throughout the body
(including: decreased glucose uptake in tissues, increased glucose
production by the liver, and increased insulin secretion)
Thus, in effect, growth hormone enhances body protein, decreases
fat stores, and conserves carbohydrates.

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Some specific functions of the thyroid hormones are:
 Increased body growth;
 Increased cellular metabolic activity;
 Increased basal metabolic rate;
 Increased requirement for vitamins;
 Increased blood flow and cardiac output;
 Increased heart rate;
 Increased heart strength;
 Normal arterial pressure because of elevated systolic blood
pressure and decreased diastolic blood pressure;
 Increased respiration;
 Increased gastrointestinal motility;
 Excitatory effects on the central nervous system;
 Increased muscle strength;
 Increased difficult to sleep;
 Increased secretion of the other endocrine glands.

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The best known anti-thyroid drugs are:
Thiocyanate, Perchlorate, and Nitrate ions decrease iodide trapping
does not stop the formation of thyroglobulin. therefore, it can lead to the
development of a greatly enlarged thyroid gland, which is called a goiter;
Propylthiouracil, Methimazole and Carbimazole prevents formation of
thyroid hormone from iodides and tyrosine via blocking the peroxidase
enzyme.
Iodides in High Concentrations decrease all thyroid activity and thyroid
gland size.

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TSH (thyrotropin) has the following specific effects on the thyroid gland:
 Increased proteolysis of the thyroglobulin;
 Increased activity of the iodide pump;
Increased iodination of tyrosine to form the thyroid hormones;
Increased size and increased secretory activity of the thyroid cells;
Increased number of thyroid cells.

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(Oligomenorrhea)
(Exophthalmos)
(Myxedema)
(Hashimoto’s disease) (Grave’s disease)

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The cells of zona glomerulosa is
controlled by the extracellular fluid
concentrations of angiotensin II and
potassium.
The zona fasciculata and the zona
reticularis are controlled in by ACTH.
All human steroid hormones
synthesized from cholesterol.
Adrenocortical hormones are highly
bounded to plasma proteins.
The adrenal steroids are degraded
mainly in the liver and are conjugated
especially to glucuronic acid and, to a
lesser extent, to sulfates.

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In the last-half of nephrone tubule, and
also in sweat glands, salivary glands,
intestinal epithelial cells aldosterone
increases renal tubular reabsorption of
sodium and secretion of potassium.
Excess aldosterone increases
extracellular fluid volume and arterial
pressure but has only a small effect on
plasma sodium concentration.
Excess aldosterone causes hypokalemia
and muscle weakness.
Aldosterone deficiency causes
hyperkalemia and cardiac toxicity.
Excess aldosterone increases tubular
hydrogen ion secretion and causes
alkalosis.

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The following factors are known to play essential roles in
regulation of aldosterone:
1. Increased potassium ion concentration in the extracellular fluid
greatly increases aldosterone secretion.
2. Increased angiotensin II concentration in the extracellular fluid
also greatly increases aldosterone secretion.
3. Increased sodium ion concentration in the extracellular fluid
very slightly decreases aldosterone secretion.
4. ACTH from the anterior pituitary gland is necessary for
aldosterone secretion but has little effect in controlling the rate of
secretion in most physiological conditions.

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A- EFFECTS OF CORTISOL ON CARBOHYDRATE METABOLISM:
1- Stimulation of gluconeogenesis via increasing the enzymes
required to convert amino acids into glucose in liver cells,
mobilization of amino acids from the extrahepatic tissues, mainly
from muscle, and antagonizing insulin’s effects to inhibit
gluconeogenesis in the liver.
2- Decreasing of glucose utilization by cells via decreasing of
translocation of the glucose transporters GLUT4 to the cell
membrane, especially in skeletal muscle cells, leading to insulin
resistance or adrenal diabetes.

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B- EFFECTS OF CORTISOL ON PROTEIN METABOLISM:
1- Reduction in protein stores in essentially all cells of the body
except those of the liver. This reduction is caused by both decreased
protein synthesis and increased catabolism of protein.
2- Increasing liver and plasma proteins.
3- Increasing blood amino acids.
4- Diminished transport of amino acids into extrahepatic cells.
5- Enhanced transport into hepatic cells.

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C- EFFECTS OF CORTISOL ON FAT METABOLISM:
1- Mobilization of fatty acids from muscles and adipose tissue that
increases the concentration of free fatty acids in the plasma, which
also increases their utilization for energy.
2- Enhancement of the oxidation of fatty acids in the cells.
Excess cortisol causes a peculiar type of obesity, with excess
deposition of fat in the chest and head, giving a buffalo-like torso
and a rounded “moon face”. This obesity results from excess
stimulation of food intake.

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D- ANTI-INFLAMMATORY EFFECTS OF CORTISOL:
1- Stabilizing lysosomal membranes;
2- Decreasing permeability of the capillaries;
3- Decreasing both migration of white blood cells into the
inflamed area and phagocytosis of the damaged cells, because
cortisol diminishes formation of prostaglandins and leukotrienes;
4- Suppressing the immune system, causing lymphocyte
reproduction to decrease markedly;
5- Attenuating fever mainly because it reduces release of
interleukin-1 from white blood cells.

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A- EFFECT OF INSULIN ON CARBOHYDRATE METABOLISM:
1- Promoting muscle glucose uptake and metabolism and also
storage of glycogen in muscles;
2- Promoting liver uptake, storage, and use of glucose;
a- Insulin inactivates liver phosphorylase, the principal enzyme
that causes liver glycogen to split into glucose.
b- Insulin causes enhanced uptake of glucose from the blood by the
liver cells by increasing the activity of the enzyme glucokinase.
c- Insulin also increases the activities of glycogen synthase.
d- Insulin activates liver glucose phosphatase for using glucose.
3- Promoting conversion of excess glucose into fatty acids
4- Inhibiting gluconeogenesis in the liver.

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B- EFFECT OF INSULIN ON FAT METABOLISM:
1- Insulin increases the transport of glucose into the liver cells that
have a direct effect to activate acetyl-CoA carboxylase, the enzyme
of the first stage of fatty acid synthesis;
2- Insulin activates lipoprotein lipase in the capillary walls of
the adipose tissue, which splits the triglycerides again into fatty
acids;
3- Insulin inhibits hormone-sensitive lipase that causes the
hydrolysis of triglycerides. So, insulin deficiency increases plasma
free fatty acids and cholesterol.

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C- EFFECT OF INSULIN ON PROTEIN METABOLISM:
1- Stimulating transport of many of the amino acids into the cells,
specially valine, leucine, isoleucine, tyrosine, and phenylalanine;
2- Increasing translation of messenger RNA;
3- Increasing the rate of transcription of selected DNA genetic
sequences in the cell nuclei;
4- Inhibiting catabolism of proteins;
5- Depressing the rate of gluconeogenesis in the liver.

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The major metabolic effects of glucagon are:
1- Breakdown of liver glycogen (glycogenolysis);
2-Increased gluconeogenesis in the liver;
3- Activates adipose cell lipase.
Glucagon in high concentrations also (1) enhances the strength of
the heart; (2) increases blood flow in some tissues, especially the
kidneys; (3) enhances bile secretion; and (4) inhibits gastric acid
secretion.

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Calcium plays a key role in many physiological processes,
including contraction of skeletal, cardiac, and smooth
muscles, blood clotting, and transmission of nerve impulses
and ...
Increases in calcium ion concentration above normal
(hypercalcemia) cause progressive depression of the nervous
system and muscle activity.
Decreases in calcium concentration (hypocalcemia) cause
the nervous system to become more excited and tetany.

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Organic Matrix of Bone:
Is 90 to 95 percent collagen fibers, and the remainder is a
homogeneous gelatinous medium (ground substance) which is
composed of extracellular fluid plus proteoglycans, especially
chondroitin sulfate and hyaluronic acid.
Bone Salts:
The crystalline salts deposited in the organic is hydroxyapatite.
Magnesium, sodium, potassium, and carbonate ions are also present
among the bone salts, although

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1- The initial stage in is the secretion of collagen molecules and
ground substance (mainly proteoglycans) by osteoblasts.
2- The collagen monomers polymerize rapidly to form collagen fibers;
the resultant tissue becomes osteoid.
3- Then, some of the osteoblasts become entrapped in the osteoid and
become quiescent that they are called osteocytes.
4- Within a few days after the osteoid is formed, calcium salts begin to
precipitate on the surfaces of the collagen fibers and after weeks
hydroxyapatite crystals are formed.

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Bone is continually being
deposited by osteoblasts, and it
is continually being reabsorbed
where osteoclasts are active.
The villi of osteoclasts secrete
two types of substances:
1- Proteolytic enzymes, released
from the lysosomes;
2- Several acids, including citric
acid and lactic acid, released
from the mitochondria and
secretory vesicles.

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The other actions of vitamin D:
Promoting phosphate
absorption by the intestines;
Decreasing renal calcium
and phosphate excretion;
Promoting bone calcification
in smaller quantities, and
causing reabsorption of bone
in extreme quantities.

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