Transcript Endocrinology - You Can Do It! | Physical Therapy Students

Endocrinology 2
Lecture Notes
Adrenal Glands
• We have 2 adrenal glands located above the
kidneys.
• The adrenal gland is divided into 3 portions,
the adrenal cortex + the adrenal medulla.
• The adrenal cortex is further divided into 3
layers:
Zona glomerulosa  releases aldosteron
Zona fasciculata  releases cortisol
Zona reticularis  releases sex steroids
Adrenal Medulla
• Adrenal medulla cells secrete catecholamines
(epinephrine & norepinephrine, 4 : 1 ratio ,
more epinephrine secretion)
• It is innervated by sympathetic nerve fibers,
activated by stress, meaning that it will
support the sympathetic nervous system
• Secretion is initiated by stimulation of
preganglionic sympathetic neurons
Adrenal Medulla
• Effects: are very similar to those
caused by stimulation of sympathetic
nervous system, they last 10 times
longer.
• Activation of adrenal medulla along with
the sympathetic nervous system
prepares the body for greater physical
performance (fight-or-flight)
Effects of Fight-or-Flight
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Increase heart rate
Vasoconstricts arterioles to most tissues
Vasodilates arterioles to muscles, lungs and heart
Dilate pupils so more light reaches retina
Stimulates ventilation
Increases glycogenolysis in the liver to provide
energy
Stimulate glucagon  increases blood glucose level
Inhibits insulin  prevent the uptake of glucose from
blood
Increases lipolysis in adipose tissue to provide energy
Increases efficiency of muscle contraction
Increases sweating  heat loss
Adrenal Cortex
• Secrets steroid hormones called
corticosteroids including:
Mineralocorticoids (aldosterone)
Glucocortecoids (cortisol)
Sex steroids (estrogens, androgens)
Adrenal Cortex
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Mineralocorticoids (aldosterone)
 Zona glomerulosa  aldosterone  kidneys  regulates Na+ and K+
balance in body fluids
•
Glucocortecoids (cortisol catabolic hormone):
 ACTH stimulates the zona fasciculata  cortisol is released  acts on
liver, muscle & adipose tissue to regulate carbohydrate, prootein and
fat metabolism leading to:
1. Increase in serum glucose
2. Increase in serum fatty acid
3. Increase in serum amino acid
•
Sex steroids (estrogens, androgens):
 Weak andorgens secreted by different zones of adrenal cortex (Zona
reticularis)
 Not the main sex steroids, the main sex steroids are provided by the
gonads, these are supplement of sex steroids secreted by gonads.
Adrenal Cortex Secretion
Abnormalities
Cushing’s Disease:
• Cause: hypersecretion of
corticosteroids (cortisol) as a result of:
Tumor of adrenal cortex (Cushing's
syndrome)
Oversecretion of ACTH from anterior
pituitary ( Cushing's disease)
Important!
Cushing’s Disease is Different From
Cushing’s Syndrome
Cushing’s Syndrom:
• One cause for Cushing’s syndrome is exogenous
glucocorticoids. Meaning that a person take corisol
exogenously by injections or tablets to treat various
diseases.
• Another cause for Cushing’s syndrome is a tumor of
the adrenal gland, the patient will have high
production of cortisol  it will inhibit ACTH through
negative feedback mechanism.
In these two cases the person is said to have Cushing’s
syndrome
Important!
Cushing’s Disease is Different From
Cushing’s Syndrome
Cushing’s Disease:
• A patient has high secretion of ACTH
from the anterior pituitary  high
ACTH will stimulate the adrenal gland to
produce cortisol
Important!
Cushing’s Disease is Different From
Cushing’s Syndrome
If you take a serum sample from a Cushing’s
Disease patient he will have :
High levels of ACTH + High level of cortisol
If you take a serum sample from a Cushing’s
Syndrom patient he will have :
Low levels of ACTH + High level of cortisol
Important!
Cushing’s Disease is Different From
Cushing’s Syndrome
Changes in the body are the same in the two
cases EXCEPT:
The hyperpigmentation in Cushing’s Disease
patients because of excess ACTH
ACTH is a melanocyte stimulating hormone, it
stimulates the melanocyte , so the patient will
have a darker skin
Cushing’s Disease and
Cushing’s Syndrome
• Characterized by :
Hyperglycemia: because cortisol is a catabolic
hormoneit will cause the breakdown of
carbohydrates  increase level if glucose in the
circulation
Hypertension: because cortisol can stimulate Na
and water retention
Muscular weakness: due to the breakdown of
protiens
Thin arms and legs
Cushing’s Disease and
Cushing’s Syndrome
• Those patients will also have red cheeks because
cortisol stimulates erythropoietin which is the
hormone that causes the production of red blood cells
from the bone marrow.
• The patients also have purple abdominal striae, the
look like stretch marks but they are wider and purple
in color
• Hirsutism: a side effect of the stimulation of ACTH
is the stimulation of the androgens production, and
that’s why growth of excessive hair happens
Addison’s Disease
Cause:
• Inadequate secretion of cortisol and aldosterone
• Characterized by:
 Hypoglycemia: because of low cortisol.
 Na+ loss and K+ retention: because of low aldosterone.
 Dehydration: because of Na+ and water loss.
 Hypotension: because of Na+ and water loss.
 Rapid wieght loss: because cortisol is one of the hormones
that stimulates the appetite.
 Generalized weakness.
 High ACTH causes hyperpigmentation.
 May lead to death if not treated with corticosteroids.
Adrenogenital Syndrome
Cause:
• Hypersecretion of adrenal sex hormones,
particularly androgens
In young children  premature puberty and
enlarged genitals
In mature women  growth of beard (Hirsutism) +
boldness (similar to male boldness)
Thyroid Gland
• Thyroid gland does not have a certain tissue
to act on it acts all over the body
• It secretes:
Thyroxine (T4)
Triiodothyronine (T3)
Calcitonin  responsible for phosphate and Ca
metabolism.
Hypothyroidism
1- Iodine-deficiency (endemic goitre,
meaning it happens in a certain geographic
area):
A form of hypothyroidism, caused by the
lack of adequate iodine in the died
Hypothyroidism
2- Cretinism:
New born infants born in areas of low iodine
intake and endemic goitre.
Symptoms include: mental retardation,
short stature, puffy face and hands, deaf
mutism, etc….
Hypothyroidism
2- Cretinism:
 Happens becase the mother doesn’t provide enough thyroid
hormone to the fetus during the first 3 months.
 Thyroid hormone is important for the development of CNS
 During the first 3 months the fetus can not produce thyroid
hormone but depends on the mother
 After the first 3 month the baby is able to produce thyroid
hormone on its own
 But, if the baby was deprived from thyroid hormone during the
first 3 months, he will still develop cretinism because the damage is
done
Hypothyroidism
3- Infantile hypothyroidism:
Occurs during childhood
Symptoms include:
Retarded growth because thyroid hormone is
needed for the action of growth hormone.
Abnormal bone development.
General lethargy.
Low body temperature because of low BMR .
Hypothyroidism
4- Hashimoto thyroditis:
• Form of hypothyroidism .
• Characterized by a goitre, high concentration
of antibodies, which are directed against
thyroglobulin and thyroid peroxidase.
• The progressive destruction of thyroid
follicular tissue results in hypothyroidism.
Hypothyroidism
5- Myxoedema:
• Hypothyroidism in adulthood
Symptoms include:
Edema
Low basal metabolic rate
Cold intolerance
Lethargy
Weight gain tendency
What’s Happening in The Case of
Iodine-deficiency Hypothyroidism?
1. We have TRH stimulating the pituitary.
2. TSH is secreted stimulating the thyroid gland.
3. The thyroid glad is trying to produce T3 & T4 but it
can’t because of inadequate iodine (We need iodine for
the formation of T3 & T4).
4. We will have low levels of T3 & T4.
5. Low negative feedback will lead to high TSH.
6. TSH will act on the thyroid gland causing it
hypertrophy (become bigger in size) producing a goitre.
Goitres can occur in both
hypothyroidism and
hyperthyroidism
Hyperthyroidism
Grave’s Disease (Toxic Goitre)
• It is an autoimmune disease caused by
antibodies that are similar in structure to
TSH, so they act like causing the growth of the
thyroid associated with hypersecretion of
thyroxine.
• The antibodies will bind to the TSH receptors
on the thyroid gland
• Then they will stimulate thyroid hormone
production + the growth of the gland.
Hyperthyroidism
Grave’s Disease (Toxic Goitre)
• Clinical symptoms include:
 High metabolic rate
 High heart rate
 Wight loss
 Excessive sweating
 Heat intolerance
 Exopthalamus (bulging of the eyes: because
of edema in tissues of eye sochet)
Regulation of Calcium & Phosphate
• Ca+ & phosphate concentration in plasma
is affected by:
 Bone resorption: taking Ca+ and phosphate
out of the bone into the circulation.
 Bone absorption: taking Ca+ and phosphate
into the bone.
 intestinal absorption
 Urinary excretion
Regulation of Calcium & Phosphate
• Regulation of plasma calcium and
phosphate by:
 Parathyroid hormone
 Calcitriol (Dihydroxyvitamin D3)
 Calcitonin
Parathyroid Hormone (PTH)
• Usually 4 parathyroid glands
• PTH is secreted by the parathyroid gland
whenever the plasma concentration of Ca+
begins to fall
• PTH promotes a rise in blood calcium levels by
acting on:
 The bones ( causing bone resorption)
 kidneys ( causing reabsorption)
 Intestines (indirectly)
Parathyroid Hormone (PTH)
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The stimulus of PTH secretion is low Ca+.
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PTH will be released.
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It will act on the bone causing an increase in bone
resorption.
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Ca+ will go from the bone to blood circulation.
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It will also cause an increase in Ca+ reabsorption from the
kidney.
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It will promote formation of 1,25 dihydroxyvitamin D3 by
acting on the kidney.
Calcitriol (1,25 Dihydroxyvitamin D3)
Production starts in the skin where Vitamin D3 (prehormone)
is produced from precursor molecule 7-dehydrocholestrol
under influence of sunlight.
Actions:
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Activity stimulated by PTH
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Helps to raise plasma concentration of Ca+ and phosphate
by stimulating :
 Intestinal absorption of Ca+ and phosphate (main function)
 Resorption of bones
 Renal reabsorption of calcium and phosphate
Calcitonin
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Calcium lowering hormone
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Secreted by the parafollicular cell in the thyroid gland
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It antagonizes the hypercalcemic effect of calcitriol and
PTH
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Is stimulated by high plasma Ca+ and phosphate levels and
acts to lower Ca+ levels by:
 Inhibitong bone resorption ( cause bone absorption)
 Stimulating the urinary excretion of Ca+ and phosphate by
inhibiting their reabsorption by the kidneys
Rickets
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A disease in which the Bones become weaker
Action of Insulin
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After approximately ½ an hour of having a meal we have
the peak of glucose level.
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This will stimulate the secretion of insulin.
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Insulin will cause the glucose to be converted into
glycogen (glycogenesis) in the muscles.
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Insulin will stimulate the uptake of glucose in the liver
to convert it into glycogen and also into triglycerides
(lipogesesis).
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Glucose is also taken into the adipose tissue and
converted into triglycerides.
Action of Glucagon
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When we have low levels of glucose in the circulation
glucagon is secreted.
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It will act in the muscle causing the breakdown of protein
into amino acids.
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It will act on adipose tissue to cause the breakdown of
triglycerides into fatty acids.
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Amino acids + fatty acids will be converted in the liver into
glucose.
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Glucagon will also aid in the breakdown of glycogen into
glucose.
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In the end you’ll have higher glucose level in the circulation
Abnormalities
• Diabetes Mellitus is characterized by:
 Fasting hyperglycemia
 Glucose in the urine
Types of Diabetes Mellitus
• Type 1 diabetes:
 10% of cases
 Also known as insulin dependent diabetes mellitus
 Caused by lack of insulin secretion as a result of
destruction of the beta cells
 Also known as juvenile-onset diabetes
Abnormalities
Types of Diabetes Mellitus
• Type 2 diabetes:
90% of cases
Patients are usually over weight
Also known as insulin independent diabetes mellitus
Large amount of insulin secretion however,
decreased tissue sensitivity to insulin secreted
 Also known as maturity-onset diabetes
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Long Term Complications of Diabetes
Mellitus
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Strokes
Retinopathy
Blindness
Hypertension
Renal failure
Impotence (in males)
Skin infections that might lead to
Gangrene
• Vascular diseases
End of The
Second Lecture