The document discusses the thyroid gland, including its histology, hormones, synthesis and storage of hormones, functions, and disorders. Key points include:
- The thyroid gland secretes T4, T3, and calcitonin hormones. T4 is the main hormone secreted.
- Hormones are synthesized from tyrosine and iodine within the thyroid follicles and stored in thyroglobulin.
- The thyroid regulates metabolism, growth, and many other bodily functions.
- Disorders include hyperthyroidism (overactive thyroid) and hypothyroidism (underactive thyroid). Goiter is an enlargement of the thyroid gland.
Hyperthyroidism is a very common name, when it comes to lifestyle diseases. Often a deeper and holistic approach towards your health will help you find long term solution, and hence you will be able to recognize your symptoms of Hyperthyroidism. Your thyroid gland, when starts secreting more amount of hormone, the condition is referred as hyperthyroidism. Thereby speeding up the bodily functions, including metabolism.
As a part of my M.Sc. Nursing course, I have prepared PPT on Bengin Prostate Hyperplasia, which is an important topic from clinical as well as exam point of view. I hope this material will be helpful to the prospect nursing student. However, refer books for the better understanding of the topic.
Hyperthyroidism is a very common name, when it comes to lifestyle diseases. Often a deeper and holistic approach towards your health will help you find long term solution, and hence you will be able to recognize your symptoms of Hyperthyroidism. Your thyroid gland, when starts secreting more amount of hormone, the condition is referred as hyperthyroidism. Thereby speeding up the bodily functions, including metabolism.
As a part of my M.Sc. Nursing course, I have prepared PPT on Bengin Prostate Hyperplasia, which is an important topic from clinical as well as exam point of view. I hope this material will be helpful to the prospect nursing student. However, refer books for the better understanding of the topic.
Thyroid storm is basically a life threatening acute exacerbation of the clinical features of thyrotoxicosis.
Thyroid storm also known as thyroid crisis is an acute, life threatening hypermetabolic state induced by excessive activity of thyroid hormones in individuals with thyrotoxicosis.
Exact pathogenesis not understood.
No clear cut clinical feature separation from thyrotoxicosis.
precipitants of thyroid storm include the following
Infection, especially pneumonia
Cerebrovascular accident
Acute coronary syndrome, Congestive heart failure
Pulmonary embolus
Diabetic ketoacidosis
Parturition / toxemia
Major trauma
Surgery
Iodine 131 Rx or iodine contrast agents
Rapid withdrawl of antithyroid medications
Although the exact pathogenesis of thyroid storm is not fully understood, the following theories have been proposed:
Patients with thyroid storm reportedly have relatively higher levels of free THs than patients with uncomplicated thyrotoxicosis, although total TH levels may not be increased.
Adrenergic receptor activation is another hypothesis. Sympathetic nerves innervate the thyroid gland, and catecholamines stimulate TH synthesis. In turn, increased THs increase the density of beta-adrenergic receptors, thereby enhancing the effect of catecholamines.
The dramatic response of thyroid storm to beta-blockers and the precipitation of thyroid storm after accidental ingestion of adrenergic drugs such as pseudoephedrine support this theory. This theory also explains normal or low plasma levels and urinary excretion rates of catecholamines.
However, it does not explain why beta-blockers fail to decrease TH levels in thyrotoxicosis.
Another theory suggests a rapid rise of hormone levels as the pathogenic source. A drop in binding protein levels, which may occur postoperatively, might cause a sudden rise in free hormone levels. In addition, hormone levels may rise rapidly when the gland is manipulated during surgery, during vigorous palpation during examination, or from damaged follicles following RAI therapy.
Other proposed theories include alterations in tissue tolerance to THs, the presence of a unique catecholaminelike substance in thyrotoxicosis, and a direct sympathomimetic effect of TH as a result of its structural similarity to catecholamines.
General symptoms
Fever
Profuse sweating
Poor feeding and weight loss
Respiratory distress
Fatigue (more common in older adolescents)
GI symptoms
Nausea and vomiting
Diarrhea
Abdominal pain
Jaundice
Neurologic symptoms
Anxiety (more common in older adolescents)
Altered behavior
Seizures, coma
Thyroid disease in_pregnancy
Presented by: Dr. Ahmad mukhtar
M.B.B.Ch., M.Sc Obstetrics and GynecologyAssistante lecturer of Obstetrics and Gynecology
Faculty of Medicine, Zagazig University
Hirsutism _ excesive terminal hair growth in the women on a male pattern distribution-face, body(sexual hear,androgendependent)-common in PCOS
Hypertricosis_ can involve of vellus, lanugo, nonpigmanted hair and terminal hear occupying the entire body surface including the face ( androgen independent disorder)- congenital, caused by drugs, hypothyroidism, anorexia nervosa
Virilization _ production of androgens in women is extremely high (presence of clitoromegaly,alopecia- balding, deepening of the voice- bariphonia, male body habitus)-usually caused by androgen producing tumors, CAH
Acne _ du to hyperceratosis and occlusion of duct of sebaceum gland plus inflammation( multifactoral, androgendependent)
Acanthosis nigricans _ skin grey- brown ,velvety appearance mainly in the neck, axillae,vulva and groin (local hyperpigmentation of skin on specific area-marker of hyperinsulinemia/insulinresistance)
Congenital Adr Hyperplasia (CAH) can appear at any age from birth to puberty where it can lead to ambiguous genitalia. It is due to absolute or relative deficiency of 17 Hydroxylase or 21 Hydroxylase enzyme.
Thyroid storm is basically a life threatening acute exacerbation of the clinical features of thyrotoxicosis.
Thyroid storm also known as thyroid crisis is an acute, life threatening hypermetabolic state induced by excessive activity of thyroid hormones in individuals with thyrotoxicosis.
Exact pathogenesis not understood.
No clear cut clinical feature separation from thyrotoxicosis.
precipitants of thyroid storm include the following
Infection, especially pneumonia
Cerebrovascular accident
Acute coronary syndrome, Congestive heart failure
Pulmonary embolus
Diabetic ketoacidosis
Parturition / toxemia
Major trauma
Surgery
Iodine 131 Rx or iodine contrast agents
Rapid withdrawl of antithyroid medications
Although the exact pathogenesis of thyroid storm is not fully understood, the following theories have been proposed:
Patients with thyroid storm reportedly have relatively higher levels of free THs than patients with uncomplicated thyrotoxicosis, although total TH levels may not be increased.
Adrenergic receptor activation is another hypothesis. Sympathetic nerves innervate the thyroid gland, and catecholamines stimulate TH synthesis. In turn, increased THs increase the density of beta-adrenergic receptors, thereby enhancing the effect of catecholamines.
The dramatic response of thyroid storm to beta-blockers and the precipitation of thyroid storm after accidental ingestion of adrenergic drugs such as pseudoephedrine support this theory. This theory also explains normal or low plasma levels and urinary excretion rates of catecholamines.
However, it does not explain why beta-blockers fail to decrease TH levels in thyrotoxicosis.
Another theory suggests a rapid rise of hormone levels as the pathogenic source. A drop in binding protein levels, which may occur postoperatively, might cause a sudden rise in free hormone levels. In addition, hormone levels may rise rapidly when the gland is manipulated during surgery, during vigorous palpation during examination, or from damaged follicles following RAI therapy.
Other proposed theories include alterations in tissue tolerance to THs, the presence of a unique catecholaminelike substance in thyrotoxicosis, and a direct sympathomimetic effect of TH as a result of its structural similarity to catecholamines.
General symptoms
Fever
Profuse sweating
Poor feeding and weight loss
Respiratory distress
Fatigue (more common in older adolescents)
GI symptoms
Nausea and vomiting
Diarrhea
Abdominal pain
Jaundice
Neurologic symptoms
Anxiety (more common in older adolescents)
Altered behavior
Seizures, coma
Thyroid disease in_pregnancy
Presented by: Dr. Ahmad mukhtar
M.B.B.Ch., M.Sc Obstetrics and GynecologyAssistante lecturer of Obstetrics and Gynecology
Faculty of Medicine, Zagazig University
Hirsutism _ excesive terminal hair growth in the women on a male pattern distribution-face, body(sexual hear,androgendependent)-common in PCOS
Hypertricosis_ can involve of vellus, lanugo, nonpigmanted hair and terminal hear occupying the entire body surface including the face ( androgen independent disorder)- congenital, caused by drugs, hypothyroidism, anorexia nervosa
Virilization _ production of androgens in women is extremely high (presence of clitoromegaly,alopecia- balding, deepening of the voice- bariphonia, male body habitus)-usually caused by androgen producing tumors, CAH
Acne _ du to hyperceratosis and occlusion of duct of sebaceum gland plus inflammation( multifactoral, androgendependent)
Acanthosis nigricans _ skin grey- brown ,velvety appearance mainly in the neck, axillae,vulva and groin (local hyperpigmentation of skin on specific area-marker of hyperinsulinemia/insulinresistance)
Congenital Adr Hyperplasia (CAH) can appear at any age from birth to puberty where it can lead to ambiguous genitalia. It is due to absolute or relative deficiency of 17 Hydroxylase or 21 Hydroxylase enzyme.
Thyroid function tests help to determine if your thyroid is not working correctly. If blood levels of thyroid hormone are high, the brain senses this and sends a message to stop producing TSH.
This is a content made by the students of Pharmacy dept of Comilla University about the Endocrine system, In this you can easily find the glands in out body and their functions. and specific organs which secrete specific hormones for our body. figures are added to make it more convenient. thank you all.
Thyroid hormone (The Guyton and Hall physiology)Maryam Fida
THYROID HORMONE
Location:
The thyroid gland located below the larynx on each side of and anterior to the trachea.
Largest Endocrine Hormone
Secretion:
secretes:
1. thyroxine (T4)
2. triiodothyronine (T3)
3. Also secretes calcitonin (an important hormone for calcium metabolism)
Cell: Thyrotopes
secretion is controlled by thyroid-stimulating hormone (TSH) from the anterior pituitary gland.
93% T4 & 7% T3
T4→T3 in tissues
Qualitatively same
Differ in Rapidity & Intensity of action.
T3 is 4 times more potent than T4, but decrease conc. In blood & decrease half life.
T3 and T4 combine mainly with thyroxine-binding globulin.
More than 90% of Thyroid hormone that binds with cellular receptors is T3.
T4
No effect for 2-3 days after injection
Long Latent Period.
Activity peaks in 10-12 days & ↓↓ with a half life of 15 days.
In some cases it takes 6 weeks-2 months.
T3
4 times rapid
Latent Period 6-12 hours
Peak in 2-3 days
Composed of large numbers of closed follicles filled with colloid and lined with cuboidal epithelial cells that secrete into the interior of the follicles
The major component of colloid is the large glycoprotein Thyroglobulin contains the thyroid hormones within its molecule.
50mg/year, 1mg/week
Ingested iodine in the form of iodides
Iodides ingested orally are absorbed from GIT
⅕ removed from the blood by thyroid cells for synthesis of hormones; rest excreted through kidneys.
Basal membrane of thyroid cells has an active pump to push iodides to interior (Iodine Pump).
Normally 30% more conc. Inside
Max. active 250% more conc. Inside
The rate of Iodine trapping is influenced by conc. of TSH
TSH stimulates and hypophysectomy greatly diminishes the activity of the iodide pump in thyroid cells.
The content of presentation is as follows
- introduction to thyroid
- thyroid hormone synthesis
- type of thyroidism
- difference between hyperthyroidism and hypothyroidism
-treatment of hypothyroidism
- anti thyroid drug classification
- mechanism of anti thyroid drugs
-
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
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4. INTRODUCTION
• An endocrine gland , at the root of neck on either side of trachea.
• Two lobes connected by isthmus
HISTOLOGY
• Composed of large number of closed follicles , lined with follicular cells , in
between are present parafollicular cells.
• Follicular cells secrete thyroglobulin( colloidal
substance)which fills follicular cavity and also
secretes T4 and T3 .
• Both T4 and T3 are derivatives of amino acid
tyrosine.
5. HORMONES
• Secretes 3 hormones :-
I. Tetraiodothyronine or ( thyroxine ) T4 ------90% of secretion
II. Tri-iodothyronine or T3 -------9% to 10% of secretion
III. Calcitonin
• Strength of T3 is four times more than T4 but duration of T4 action is four
time more than T3 action .WHY??? Reason is less affinity of T3 for plasma
protein , combines loosely with them so released quickly while T4 binds
strongly and is released slowly.
• Degradation of thyroid hormones occur in kidney , liver and muscles.
• Synthesis takes place in thyroglobulin , tyrosine and iodine are essential .
6. STAGES OF SYNTHESIS OF THYROID
HORMONES
Synthesis occurs in 6 stages
1) Thyroglobulin synthesis:- ER and Golgi apparatus in follicular cells synthesize
and secrete thyroglobulin .After synthesis, it stores in follicles .
2) Iodide trapping:- Iodide is actively transported from blood to follicular cells ,
against EC gradient ,along with Na+ through Na-iodide symport pump.
3) Oxidation of iodide:- Iodide oxidizes to iodine inside follicular cells in
presence of thyroid peroxidase because only iodine combines with tyrosine
to form hormone.
7. 4 ) Transport of iodine to follicular cavity:- Transported from follicular cells to
follicular cavity through iodide –chloride pump called pendrin.
5 ) Iodination of tyrosine :- Iodine binds with thyroglobulin, process called
organification . Iodine combines with tyrosine in thyroglobulin , process called
iodination .Iodination of tyrosine occurs in different stages: tyrosine first
transform to mono-iodothyronine (MIT) and later into tri-iodothyronine (DIT).
6 ) Coupling reaction :- the coupling reaction in different configuration, gives
rise to different thyroid hormones.
8.
9. STORAGE OF HORMONES
• Can be stored up to 4 months, remains in form of vesicles in thyroglobulin.
• Only endocrine gland which stores its hormones for long periods, so sign and
symptoms of deficiency don’t appear before 4 months.
RELEASE FROM THYROID GLAND
• Not released in blood directly, hormones are first cleaved from thyroglobulin and then
released.
• Only T3 and T4 are released into blood stream. MIT and DIT are not released in blood
stream, they are deiodinated by enzyme . During congenital absence of enzyme, MIT
and DIT are secreted in urine and iodine deficiency develops.
10. FUNCTIONS OF THYROID GLAND
• Increases basal metabolic rate(BMR) by increasing O2 consumption except in
brain , retina, spleen, testes and lungs.
• Increase synthesis of protein in cells ,and cardiovascular activity and
carbohydrates metabolism.
• Decrease fat storage by mobilizing from adipose tissue and fat depots , increase
the fatty acid level in blood.
• Decreases cholesterol , phospholipids and triglycerides level in plasma. In
hyposecretion of T4, cholesterol level increase ,results in atherosclerosis.
11. • Increase heat production in body, called thyroid hormone-induced
thermogenesis
• Increase growth in children, promote brain development in fetal life, deficiency
leads to mental retardation .
• Decrease body weight, accelerate erythropoietic activity .polycythemia is
common in hyperthyroidism.
• Increase GIT activity ,hypersecretion cause diarrhea, hypo-- cause constipation.
• Maintain normal sleep, hyposecretion cause somnolence .
• Affect muscular activity, hypersecretion cause thyrotoxic myopathy and tremors.
12. • Increase formation of many enzymes, vitamins are
essential. vitamin deficiency is possible during
hyposecretion of T4.
• Essential for normal sexual function. In males ,
hyposecretion cause loss of libido and
hypersecretion cause impotence .In women,
hypersecretion cause oligomenorrhea and
amenorrhea, hyposecretion cause
polymenorrhea and menorrhagia.
13. DISORDERS OF THYROID GLAND
HYPERTHYROIDISM
Increased secretion of thyroid gland .Caused by Graves disease and thyroid adenom
GRAVES’ DISEASE :- Autoimmune disease ,most common cause of hyperthyroidism
B-Lymphocytes produce thyroid stimulating autoantibodies (TBAbe).these antibiotics
act as TSH by binding with membrane receptors and activating cAMP systems of
thyroid follicular cells , results in hyperthyroidism.
THYROID ADENOMA :- sometimes, localized tumor develops in thyroid tissues and
secretes large quantity of thyroid hormones. Not associated with autoimmunity, the
hormone secreted from adenoma depresses the TSH production.
14. Exophthalmos :-
• Most but not all hyperthyroid patient develops Exophthalmos (bulging of eyes)
• Caused due to swelling of retro-orbital tissues and degenerative changes in
extraocular muscles.
• Leads to blindness due to stretch and damage to optic nerve and due to
constant exposure to atmosphere cause dryness ,infection and irritation.
15. HYPOTHYROIDISM
Decreased secretion of thyroid hormone ,leads to myxedema in adults and
cretinism in children.
MYXEDEMA :- edematous appearance. Caused due to thyroid gland , genetic
disorder or iodine deficiency .Common cause is autoimmune disease called
hashimoto’s thyroiditis,common in middle aged
Women.
Sign and symptoms includes features like:-
Swelling of face, bagginess under eyes ,Non-
Pitting type of edema , atherosclerosis.
16. CRETINISM :- Occurs due to congenital absence of thyroid gland, genetical
disorder , or lack of iodine
Features of cretinism include babies with sluggish
movements, croaking sound, mental retardness.
skeleton growth is more affected than soft tissue.
big tongue with dripping saliva.
18. GOITER
Means enlargement of thyroid gland ,Occurs both in hypothyroidism and
hyperthyroidism.
Goiter in hyperthyroidism ---- Toxic goiter :-
Enlarged thyroid gland with increased hormone secretion,
caused by thyroid tumor.
Goiter in hypothyroidism ---- nontoxic goiter :-
Enlarged thyroid gland without increased thyroid
hormone secretion.
19. Based on cause ,nontoxic goiter classified into two types :-
Endemic colloid goiter :- due to iodine deficiency(less than 50ug/day),no
formation of hormones, thyroglobulin accumulates in follicles, increase size of gland
Idiopathic non-toxic goiter :- due to unknown cause, gland enlarges
without iodine deficiency, suggested due to thyroiditis and deficiency of enzymes
(peroxidases, deiodinase…etc.)required for hormone synthesis. some foodstuffs
(turnips,cabbage..etc.) contain goitrogenic substances which suppress hormone
synthesis.
20. TREATMENT OF THYROID DISORDERS
TREATMENT FOR HYPERTHYROIDISM :-
I. BY USING ANTITHYROID SUBSTANCES : Drugs which suppresses hormone
secretion e.g. Thiocyanate ,thiourylenes ,high cons of inorganic iodides.
II. BY SURGRICAL REMOVAL : when antithyroid substances are not possible ,this
process is called thyroidectomy.
TREATMENT FOR HYPOTHYROIDISM :-
Only treatment is administration of thyroid extract or ingestion of pure thyroxine
in form of tablets ,orally.
21. THYROID DIAGNOSTIC TESTS
Functional status of thyroid gland can be assessed by following tests :-
i. Measurement of plasma level of T3 and T4 : measure concentration of
“free” thyroid hormone in plasma.
ii. Measurement of TRH and TSH : these hormones will be total absent in
hyperthyroidism dur to –ive feedback by increased level of thyroid hormone
iii. Measurement of basal metabolic rate : In hyperthyroidism rate increased
by 30% to 60%. In hypothyroidism rate decrease by 20% to 40% .