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Transcript
CHAPTER XII
PDL 101 HUMAN ANATOMY & PHYSIOLOGY
Ms. K. GOWRI. M.Pharm.,
Lecturer.
ENDOCRINE SYSTEM
Introduction :
Endocrine glands consist of groups of secretory cells surrounded by an extensive network of
capillaries which facilitates diffusion of hormones.
The endocrine glands are :
1.
1 pituitary gland
2.
1 thyroid gland
3.
4 parathyroid glands
4.
2 adrenal glands
5.
The pancreatic islets
6.
1 pineal gland or body
7.
1 thymus gland
8.
2 ovaries in the female
9.
2 testes in the male
.
PITUITARY GLAND AND HYPOTHALAMUS
:• Regulate activity of most of endocrine glands.
Pituitary gland lies in the hypophyseal fossa of the sphenoid bone.
•
Anterior pituitary & posterior pituitary
•
Thin strip of tissue called intermediate lobe.
•
Blood supply - arterial blood internal carotid artery
•
Venous blood - venous sinuses between duralayer
The influence of the hypothalamus on the pituitary gland :
•
anterior pituitary - network of blood vessels forms part of the pituitary portal
system.
•
Posterior pituitary – nerve cells called pituicytes hypothalamohypophyseal
tract)
´ Anterior pituitary :
Growth hormone (GH It release is stimulated by growth hormone releasing hormone
(GHRH) & supressed by growth hormone release inhibiting hormone
(GHRIH).
•
Sleep , exercise, hypoglycaemia, stimulates release.
•
Thyroid stimulating hormone (TSH) :
•Hormone thyroxine (T4) & triiolothyronine (t3).
•Release decreases in evening & highest -> night.
•Regulated by negative feed back mechanism.
Adrenocorticotrophic hormone (corticotropin ACTH)
•From hypothalamus -> synthesis of ACTH
•Increases of conc of cholesterol & steroids within the adrenal cortex & the output.
•Associated with sleep pattern -> shift work changes.
•Secretion by negative feed back mechanism.
Prolactin :
•Stimulates lactation & has a direct effects on breasts immediately after parturition
(child birth)
•Lowered by prolactin inhibiting hormone.
•Prolactin together & oestrogens, corticosteroids, insulin & thyroxine is involved.
Gonadotrophins :
•Sex hormones secreted by anterior pituitary in response to luteinising hormone
releasing hormone (LHRH) also known as gonadotrophin releasing hormone (GnRH)
•In females – LH & FSH ->oestrogen, progesteron
•In males -> LH,ICSH - >testosterone.
Posterior pitutary :
• oxytoxin & antidiuretic hormone are synthesized in the hypothalamus.
• they act on non-endocrine tissue and their release by exocytosis is stimulated by nerve
impulses.
Oxytocin
•Stimulates two target tissues
•Increased oxytocin during parturition
•Positive feedback mechanism
•Suckling inhibits the release of prolacting inhibiting hormone
Antodiuretic hormone (ADH) or vaso pressin :
•Reduce urine output
•Reabsorption of water from glomerular filtrate is increased
Glucagon :
•Conversion of glycogen to glucose
• glucogenesis
Somastatin :
• by hypothalamus
• increase in insulin & glucagon.
Pineal gland or body :
•Metatonin
• optic pathways light
• coordination of circadian n diurnal rythms of tissues.
• inhibition of growth.
• synthesis of release of gonadotropins prevented
.
Thymus gland :
• thymosin- by thymus gland
• histamine , serotonin, prostaglandins
• inflammatory response
• potentiating pain, fever
• regulating blood pressure
• blood clotting
• uterine contractions during labour
• erythropoietin
• gastrointestinal hormone
Disorders of anterior pitutary :
• commonly caused by tumours or autoimmune diseases .
• hypersecretion of hormones.
• hyposecretion of hormones.
Hyper :
• hyposecretion of hormone releasing factors by the hypothalamus.
• damage to the optic nerves causing visual disturbances.
• gigantism – excess GH
• acromegaly – large extremities
• hyperprolactinanemia
Hyposecretion :
• tumours of hypothalamus or pitutary .
• trauma , usually caused by fractured base.
•ischaemic neuroses
• pitutary dwarfism ,genetic abnormality.
• frohilch’s syndrome
Disorders of posterior pitutary :
• diabetes insipidus – hyposecretion of ADH
THYROID GLAND
THYROID DISORDER
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THYROID HORMONES
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DISEASE OF THE THYROID GLAND :
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ANATOMY AND PHYSIOLOGY OF
ADRENAL GLANDS
♥10 grams in weight
♥4cm long and 3cm thick
ADRENAL CORTEX
♥Produces three groups of
hormones
♥Glucocorticoids
♥Mineralocorticoides
♥Androgens(sex
hormones)
ADRENAL GLANDS
GLUCOCORTICOIDS
‰
‰
‰
‰
‰
‰
‰
‰
‰
‰
‰
‰
PRODUCED BY ZONE OF FASICULATA
21 carbon steroids.
Stimulated by ACTH by anterior pituitary and stress.
High levels ofharmones occur between 4am to 8am and lowest
between midnight and 3am.
BIOCHEMICAL FUNCTION
Effect of Carbohydrate Metabolism.
Effert on Lipid Metabolism.
Effect on Water and Electrolye Metabolism.
Effect on Protien and Nucleic acid Metabolism.
MECHANISM OF ACTION
Binds to specific receptor on target cell and bring about the action.
Act at transcription level and control the protine synhtesis.
MINERALOCORTICOIDS
Most active and potent mineralocorticoids is aldosterone.
It promote sodium reabsorption at distal convulated tubules of kidney.
Sodium retention is accompanied by excretion of potassium,hydrogen
and ammonium ions.
REGULATION OF ALDOSTERONE SYNTHESIS
™
™
™
™
Renin angiotension.
Potassium.
Sodium.
ACTH.
MECHANISUM OF ACTION
™
™
It binds to specific receptors on the target tissues and
promotes transcription and translation.
Stimulates the active transport and absorption of sodium
ions.
ADDISON’S DISEASE
•
Addison’s disease is a disorder that results in insufficient
amounts of certain important like glucocorticoids and
mineralocorticoids
CLINICAL FEATURES
Weight and decreasd appetite
Glucocorticoids Insufficiency
Malaise,Anorexia,Nausea,vomiting
Gastrointestinal diarrhea Constipation
HYPOGLYCEMIA
Increased ACTH secrtion
Pigmentation – Sun exposed area,HYPOTENTION
Decreased body hair espically in female
Mineralocorticoids insufficiency
Postural hypotension
Loss of Adrenal Androgen
CAUSES
COMMON
AUTOIMMUNE
Spordiac
™
Polyglandular deficiency type 1
™
Polyglandular deficiency type 2
™
Tuberculosis
™
Bilateral adrenalectomy
RARE
™
Metastatic tumour
™
Lymphoma
™
Amyloid
™
Bleeding into the adrenal glands
™
Other infections on adrenal glands
™
spread of cancer to the adrenal glands
™
INVESTIGATION
ACTH stimulation test
o
Measurment of plasma ACTH
Blood glucose
o
Plasma rennin activity and aldosterone
o
Plasma electrolytes
Insulin induced hypoglycemia test
o
Imaging tests
TREATMENTS
”
”
”
”
”
”
”
”
”
Required treatment with glucocorticles and
mineralocorticoides
Hydrocortisone 20 mg in morning and 10mg in
evening
Glucocorticles of choice cordisone 12.5mg -37.5mg
orally daily
Fludro Cortisone -50mg -30mg orally/daily.
Accute adrenocortical insufficincy.
Addisional crisis
Treatment with salt, water, glucose should be replaced
with I.V.dextrose.(5%) plus isotonic saline solution.
Hydrocortisone 100mg I.V.should be given
immediately.same oral hydrocortisone and cortisone is
started with high doses 50mg every six hours of
hydrocortisone and maintaince dose according to the
requirement.
ADRENAL CORTICAL HYPERACTIVITY
CUSHING’S SYNDROME
™
Cushing’s syndrome, also known as
hypercortisolism,occurs when a person’s
tissuesare exposed to an excess of the
hormone cortisol.
APPROPRIATE AMOUNT OF CORTISOL
™
™
™
™
Regulate blood pressure
Energy production
Ability to fight disease
CLINICAL FEATURES
Extremed weight gain
Growth retardation
Missed periods in teenage girls
Excess hair growth
Acne
Reddish-blue streaks on the skin
High blood pressure
Tiredness and weakness
Either very early or late puberty
Muscle and bone weakness
Moodiness, irritability,or depression
Sleep disturbance
High bloodpressure
Menstual disorders in women and decreased fertility in man.
CAUSES
´
´
´
´
´
´
Persons take certain hormones for a long time as a
treatment for another disorders or disease,taking steroidal
anti-inflammatory for arthrities.
The body produces too cortisol, when the pituitary and
adrenal glands are not working properly.
Certain type of cancerous tumors in other part of the body
Growth on the adrenal glands,that may or may not be
cancerous, can cause the adrenal glands to relase extra
cortisol
A noncancerous tumor of the pituitary gland that produces
incresed amount of the ACTH produces adrenal glands to
produces too munch cortisol .
This form of cushing’s syndromes is known “Cushing’s
disease”
INVESTIGATION
´
´
´
´
´
´
´
´
´
Seeing if there is too much cortisol in the body.
Discovering the cause of extra cortisol.
A urine test to measure cortisol is being produced.
Dexamethasone suppresion test.
CRH stimulation tests.
Scans –This may inculde CT and MRI scans of
pituitary, adrenal gland,chest and abdomen.
Ultrasound imaging of the adrenal gland.
Chests X-rays.
Iodo cholestrol scan.
Petrosal sinus sampling.
TREATMENT
´
´
´
´
´
Treament upon the specific reasons for cortisol excess and
include
Oral medication.
Radiation
Surgery to remove a tumour
A combination of tumour that pepends upon the causes