Transcript Endocrine system: physiological peculiarities, symptoms and

Prevention of diseases of the
endocrine system. Diabetes
mellitus. Endemic goiter.
Thyrotoxicosis.
Sakharova Inna Ye., MD, PhD
Hypothalamus
• consists of very small clusters of cells that
are located just above the pituitary gland
• It controls the function of the pituitary gland,
by producing hormones that induce the
pituitary gland, which in turn affects
hormone secretion of the other glands
• Hormones secreted by hypothalamus include
growth hormone-releasing hormone (GHRH),
somatostatin and dopamine.
Epiphysis (Pineal body)
• Produce melatonin
• Hypofunction: insomnia, increased
anxiety, immune suppression, decreased
basal body temperature and an elevated
level of estrogen/progesterone ratio.
• Hyperfunction: hypotension, inadequate
function of the adrenal and thyroid
glands, decreased estrogen/progesterone
ratio, Seasonal Affective Disorder (SAD).
Hypophysis (Pituitary gland)
• “Master gland” of the organism
• Produce endorphins
ENDOCRINE
GLAND
HORMONES
PITUITARY TSH
•ANTERIOR
ACTH
LOBE
FUNCTIONS
•Thyroid to release
hormones
•Adrenal cortex to
release hormones
FSH,LH
•Growth, maturation &
GH/
SOMATOTROPIN
•Growth of body tissues
PROLACTIN/
LTH
•Development of
function of sex organs
& bones
mammary glands &
lactation
ENDOCRINE
GLAND
HORMONE
ADH
PITUITARY
•POSTERIOR
LOBE
• INTERMEDIATE
LOBE
FUNCTION
•Regulates water
metabolism
OXYTOCIN
•Stimulate uterine
MSH
•Affects skin pigmentation
contractions
•release of milk
Hypofunction (Hypopituitarism):
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Head injuries
Brain tumor
Brain surgery
Radiation treatment
Autoimmune inflammation (hypophysitis)
Stroke
Infections of the brain, such as meningitis
Tuberculosis
Infiltrative diseases, such as sarcoidosi, histiocytosis Xand
hemochromatosis
Severe loss of blood during childbirth, which may cause
damage to the front part of the pituitary gland (Sheehan
syndrome, or postpartum hypopituitarism)
Genetic mutations resulting in impaired pituitary hormone
production
Symptoms of hypopituitarism:
• Growth hormone deficiency:
- Congenital – dwarfism, nanism
short stature (height more than 2 standard
deviations below the mean for age and gender),
muscle hypotonia, delayed motor development,
“childs’ face”, high voice, hypogonadism, normal
mental development
- Aquired – growth retardation, memory problems,
hypogonadism, decresed of muscles strength
• FSH and LH deficiency:
Deficiency of luteinizing hormone (LH) and folliclestimulating hormone (FSH), together referred to as
the gonadotropins, leads to different symptoms in
men and women. Women experience oligo- or
amenorrhea (infrequent/light or absent menstrual
periods respectively) and infertility. Men lose facial,
scrotal and trunk hair, as well as suffering decreased
muscle mass and anemia. Both sexes may
experience a decrease in libido and loss of sexual
function, and have an increased risk of osteoporosis
(bone fragility). Lack of LH/FSH in children is
associated with delayed puberty.
- TSH deficiency:
- Congenital hypothyroidism, cretinism
increased birth weight, edemas, prolonged
jaundice, low voice, enlarged tongue
- ADH (vasopressin) deficiency:
- Diabetes insipidus
excessive thirst, polyuria, hypostenuria,
normal level of glucose in blood, high
sodium level
Hyperfunction (Hypopituitarism):
• Excessive production of growth
hormone:
Childhood: gigantism
Adults: acromegaly
Diagnostics:
• Level of hormones in blood
• X-ray of sella turcica
• X-ray of hands (bone age)
• MRI
• CT scan
ENDOCRINE
GLAND
HORMONE
FUNCTION
THYROID
T3 & T4’
•Regulate metabolic rate
•P,C,F metabolism
•Regulate physical & mental
growth & development
THYROCALCITONIN
PTH
PARATHYROID
•Decrease serum Ca by
increasing bone deposition
•Increase serum calcium by
promoting bone decalcification
• Hypofunction:
• Endemic goiter, Aquired
hypothyroidism, autoimmune
thyroiditis
• Hyperfunction:
• Graves’ disease
Classification of Goiter by Grades
Classification
Description
Grade 0
No palpable or visible goiter.
Grade 1
Mass in the neck that is consistent with
an enlarged thyroid that is palpable but
not visible when the neck is in the
normal position. Moves upward in the
neck as the patient swallows. Nodular
alterations can occur even when the
thyroid is not enlarged.
Grade 2
Swelling in the neck that is visible when
the neck is in a normal position and is
consistent with an enlarged thyroid
when the neck is palpated.
From WHO/UNICEF
Grave’s ophthalmopathy
• Grefe symptom (uncovering sclera during
patient is looking down)
• Koher symptom (uncovering sclera during
patient is looking up)
• Rosenbah symptom (lids tremor)
Diffuse toxic goiter (Graves disease)
Lab. findings :
–  levels of T3 and T4
– Serum TSH, measured by the sensitive
methods, is undetectable or subnormal
• Simple goiter (the convertible terms are 
colloid goiter, adolescent goiter, juvenile
goiter, nontoxic goiter) is an acquired
enlargement of the thyroid gland with normal
function that is not caused by an
inflammatory process or a tumor.
Lab. findings:
– N levels of T3, T4
– N level of thyroid-stimulating hormone
(TSH)
– negative thyroid antibodies
Endemic goiter occurs
iodine-deficient areas.
predominantly
in
Test for diagnosing iodine deficiency:
Extreme deficiency occurs when daily urine
contains less then 25 g of iodine; moderate
deficiency occurs when it is 25-50 g and an
adequate intake is reflected by an excretion
of 100-200 g/day.
Lab. findings in early stages and small iodine
deficiency:
– N or slightly  levels of T3, T4
– N or slightly  level of thyroid-stimulating
hormone (TSH), but these patients are
clinically euthyroid.
Recommended daily Intake of iodine
Adults
150 micrograms/day
Children
90-120 micrograms/day
Pregnant Women
200 micrograms/day
Diagnostics:
• Labs
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– Serum TSH
(0.4 – 6.15 μU/mL)
– Serum Free T4
(0.9 – 1.7 ng/dL)
– Serum T3
(T3 70 – 220 ng/dL)
– Serum T4
(4.5 – 11.5 μg/dL)
– T3 Resin uptake test
(25%-35%)
– Thyroid antibodies
– Serum thyroglobin
Radioactive iodine uptake test
Thyroid scan, radioscan, or scintiscan
USD of thyroid gland
ENDOCRINE
GLAND
HORMONES
FUNCTION
ADRENAL
CORTEX
ALDOSTERONE
•Fluid & electrolyte balance;
•Na reabsorption;
•K excretion
•Glycogenolysis;
•Gluconeogenesis
•Na & water reabsorption
•Antiinflammatory
•Stress hormone
CORTISOL
SEX
HORMONES
•Slightly significant
ENDOCRINE
GLAND
HORMONE
FUNCTION
ADRENAL
MEDULLA
EPINEPHRINE
NOREPINEPHRINE
•Increase heart rate & BP
•Bronchodilation,
•Glycogenolysis
•Stress hormone
Adrenal glands hyperfunction:
Cushing's syndrome
(hypercorticism)
Conn's syndrome
(hyperaldosteronism)
Congenital adrenal
hyperplasia (CAH)
Pheochromocytoma
• Cushing's syndrome is a multisystem
disorder resulting from chronic
exposure to inappropriately elevated
concentrations of free circulating
glucocorticoids.
Etiology of Cushing's syndrome
Endogenous (ACTH dependent 85%)
• Cushing's disease (pituitary)
• Ectopic ACTH syndrome (small cell lung
carcinoma)
• Ectopic CRH syndrome (bronchial carcinoid
tumours)
ACTH independent 15%
• Common: Adrenal adenoma, adrenal carcinoma
• Less common: Micronodular hyperplasia,
macronodular hyperplasia
• Rare: McCune-Albright syndrome, gastric
inhibitory polypeptide
Exogenous
• ACTH treatment
• Glucocorticoid treatment
Pseudo-Cushing's syndrome
• Major depressive disorder
• Alcoholism
• Obesity
Clinical features of Cushing's syndrome
• 90% - Central (truncal) obesity. Fat
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deposits may appear in the cheeks (moon
facies), in the dorsocervical area (buffalo
hump), and the supraclavicular area
85% - Hypertension
65% - Presence of multiple purple striae
with a diameter >1 cm on the abdomen or
proximal extremities
60% - Muscle wasting and weakness
affect the proximal muscles of leg and
shoulder girdle
40% - Easy bruising of the skin
40% - Osteoporosis
• Hyperpigmentation (palmar creases and
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pressure points) in a patient with Cushing's
syndrome strongly suggests an ACTH cause
(Cushing's disease)
Patients may have mild hirsutism and acne,
but severe hirsutism and especially
virilisation strongly suggest an adrenal
carcinoma.
Depression, lethargy, and insomnia often
occur at the same time as other symptoms.
In children the dominant clinical features are
cessation of linear growth and weight gain;
the clinical course is more aggressive than in
adults.
• Conn's syndrome is a disease of the
adrenal glands involving excess
production of a hormone, called
aldosterone.
Another name for the condition is primary
hyperaldosteronism.
Primary Hyperaldosteronism
(Conn's syndrome)
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Solitary adrenal adenomas (80-90%)
Bilateral adrenal hyperplasia (10-20%)
Adrenal Carcinoma (rare)
Unilateral Adrenal Hyperplasia (very
rare)
Clinical features of Conn's
syndrome
• Often asymptomatic
• Frontal headache
• Muscle weakness to flaccid paralysis
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decreased muscle strength (because of
low potassium level)
Polyuria and Polydipsia (carbohydrate
intolerance)
Hypertension
Hypofunction of adrenal glands
Addison's disease
(primery adrenal insufficiency)
The causes of Addison's disease
include:
• Actual destruction of the adrenal glands
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through cancer, infection, or other diseases.
Use of corticosteroids as a treatment causes
a slow down in production of natural
corticosteroids by the adrenal glands.
Certain drugs used to treat fungal infections
may block production of corticosteroids in
the adrenal glands.
Usually, the cause is unknown.
Symptoms:
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Weakness, Fatigue, Dizziness
Arterial hypotension
Dark skin
Black freckles
Bluish-black discoloration
around the nipples, mouth,
rectum, scrotum, or vagina
Lack of appetite
Weight loss
Muscle aches
Nausea, Vomiting, Diarrhoea
Intolerance to cold
Dehydration
Diagnostics of adrenal glands
disorders:
• Hormons level in blood and urine
• Products of hormons’ metabolism in blood
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(hydroxyprogesteron)
Products of hormons’ metabolism in urine
(17-ketosteroids)
Hormons supression tests
Biochemical blood testing (pH,
electrolytes)
Molecular genetics
MRI, CT scan, USD of adrenal glands
QUESTIONS
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