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thyroid gland Flashcards

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1
Q

 Major hormones produced by thyroid gland are,

A 
 Tri-iodothyronine (T3)-9-10% of thyroid hormone (TH)
 Tetraiodothyronine or thyroxine (T4
)-90% of TH
 Reverse T3- 1% of TH
 Calcitonin
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2
Q

thyroglobulin

A

Follicular cavity is filled with a colloidal
substance
secreted by follicular cells.

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3
Q

calcitonin

A

parafollicular (C

cells) are present. They secrete

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4
Q

SYNTHESIS OF THYROID HORMONES

A
  1. Thyroglobulin synthesis.
  2. Iodide trapping or iodide pump.
  3. Oxidation of iodide.
  4. Iodination of tyrosine.
  5. Coupling reactions.
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5
Q

Daily average requirement of I2 in adult is

A

150 microg

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6
Q

absorbed by

the gastrointestinal tract (GIT)

A

Ingested Iodine (I2) is converted to iodide (I-)

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7
Q

Wolff-Chaikoff

effect.

A

Normal dose of I2 stimulated thyroid hormone (TH), but high

dose inhibit TH synthesis.

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8
Q
  1. Thyroglobulin (Tg) synthesis
A

 The endoplasmic reticulum & Golgi apparatus in follicular
cells are synthesize and secrete the Tg and it stored in
follicle

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9
Q
  1. Iodide trapping or iodide pump.
A

Iodide is carried by secondary active transport from the blood into the colloid by sodium-iodide
(Na+/I−) symporters (NIS) in the
basolateral membrane of the follicular cells. This process is
process called iodide trapping.
 Two Na+
ions are transported inside the follicular cells with
each iodide molecule.
 Na+
is pumped back into the interstitium by Na+/K+ -ATPase

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10
Q
  1. Oxidation of iodide (I-) to Iodine (I2)
A

 The oxidation of iodide into iodine occurs apical portion of
follicular cells in the presence of thyroperoxidase (TPO).
 Absence or inhibition (propylthiouracil-PTU) of this enzyme
stops the synthesis of TH.
 Iodine is transported into the lumen of thyroid follicles by
chloride-iodide (Cl-—I
-
) ion counter-transporter molecule
called pendrin.

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11
Q

Absence or inhibition (propylthiouracil-PTU

A

stops the synthesis of TH.

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12
Q

thyroperoxidase (TPO)

A

oxidation of iodide into iodine

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13
Q

pendrin

A

chloride-iodide (Cl-—I

-) ion counter-transporter

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14
Q
  1. Iodination of tyrosine
A 
 Combination of Iodine with tyrosine is know as iodination. Its
take place in thyroglobulin.
 The binding of iodine with Tg is
called organification of the
thyroglobulin
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15
Q

organification of the

thyroglobulin

A

e binding of iodine with Tg

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16
Q
  1. Coupling reactions
A 
 Thyroid peroxidase-TPO enzyme is
involved in coupling reactions.
 I2 + Tyrosine= Monoiodotyrosine (MIT)
 MIT+MIT= Diiodotyrosine (DIT)
 DIT+MIT= T3
 MIT+DIT= Reverse T3
 DIT+DIT= T4
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17
Q

 Thyroid peroxidase-TPO

A

involved in coupling reactions

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18
Q

STORAGE OF THYROID HORMONES

A

Thyroid hormones remain attached to the thyroglobulin and

are stored in colloid up to 2 to 3 months

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19
Q

RELEASE OF THYROID HORMONES

A

 When thyroid hormones required, thyroglobulin-hormone complex is
taken back into the follicular cells by
endocytosis mediated by megalin
protein.
 These complex bind fuse with lysosomes, it digest Tg and release
hormones.
 T3, T4 and reverse T3 only diffuse into blood.
 MIT & DIT are not released into blood. These are deiodinated
by thyroid deiodinase and iodine is recycled for further
hormone synthesis

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20
Q

BINDING OF THYROID HORMONES

A

 TH are transported in the blood by 3 types of proteins;

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21
Q

 TH are transported in the blood by 3 types of proteins;

A
  1. Thyroxine-binding globulin (TBG)-great affinity
  2. Thyroxine-biding prealbumin (TBPA)
  3. Albumin
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22
Q

Normal total plasma T4

level in adults-

A

8µg/dL

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23
Q

Normal total plasma T3

level in adults

A

0.15µg/dL

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24
Q

hypothyroidism

A

Low secretion of TH than normal levels

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25
hyperthyroidism
Excess secretion of TH than normal levels
26
REGULATION OF THYROID HORMONE SECRETION
The pituitary and hypothalamus both control | the thyroid.
27
TSH Releasing Hormone (TRH), is secreted | by
hypothalamus and stimulates the section of thyroid stimulating hormone (TSH) from anterior pituitary
28
TSH increases synthesis & secretion of | thyroid hormone via
adenylate cyclase-cAMP | mechanism.
29
TH regulate their own secretion through | negative feedback control,
by inhibiting | release of TRH and TSH.
30
FUNCTIONS OF THYROID HORMONES
1. Action on basal metabolic rate (BMR) 2. Effect on metabolism 3. Effect on body temperature 4. Action on growth 5. Action on blood 6. Action on CVS 7. Action on CNS 8. Action on gastrointestinal system 9. Action on skeletal muscle 10. Action on sleep 11. Action on sexual function
31
1. Action on basal metabolic rate (BMR)
high BMR by increasing the oxygen consumption of the tissues | TH increase the activity of Na K ATPase pump.
32
TH BMR in most of the tissues except
adult brain, testes, | uterus, spleen
33
hyperthyroidism
BMR 60-100% was increased increases energy expenditure and causes weight loss
34
hypothyroidism
20-40% was decreased decrease metabolism and causes weight gain
35
2. Effect on metabolism
TH increase absorption of glucose from GI tract. |  TH increase glycogenolysis, gluconeogenesis
36
TH stimulate both
protein synthesis & protein degradation
37
 Low levels of TH
enhance the amino acid uptake into cells.
38
High levels of TH
protein catabolism
39
TH decrease the fat storage
increasing mobilization of lipids from fatty tissue | increase free fatty acids in plasma
40
3. Effect on body temperature
 TH increase heat production  During hyperthyroidism, body temperature increases resulting in excess sweating
41
4. Action on growth
TH is very important for normal growth, maturation, proper bone and teeth development Hypothyroidism arrest the growth, early close of epiphysis
42
5. Action on blood
TH accelerates erythropoiesis. Polycythemia is common in | hyperthyroidism
43
6. Action on CVS
 heart rate.  force of contraction of heart. But hyperthyroidism heart become weak due to excess activity and protein catabolism, leads to cardiac decompensation.  TH vasodilation on blood vessels.
44
hyperthyroidism
increased blood volume & blood flow leads to increase cardiac output, finally its causes increased blood pressure.
45
7. Action on CNS
TH promote growth & development of brain in fetal and | infants
46
Hypersec | retion of TH
causes excess stimulation of CNS, leads to extreme nervousness, anxiety & worries. Also causes irritable, emotional, unstable and restless
47
hypothyroidism
person develops low memory power, | slowness of speech, lethargy and somnolence (excess sleep)
48
8. Action on gastrointestinal system
 TH stimulate GIT motility
49
9. Action on skeletal muscle
 TH essential of normal activity of skeletal muscle.  In hyperthyroidism, TH causes weakness of muscle due to catabolism of proteins, this condition is called thyrotoxic myopathy. Also causes tremor.
50
thyrotoxic | myopathy
weakness of muscle due to | catabolism of proteins
51
10. Action on sleep
Excess TH stimulate CNS and muscles, so person feels tired, | cannot sleep. Hyposecretion causes somnolence.
52
11. Action on sexual function
 Hypothyroidism leads to complete loss of libido and hyperthyroidism leads to impotence In women, hypothyroidism causes menorrhagia and hyperthyroidism leads to amenorrhea
53
DISORDERS OF THYROID GLAND
1. Hyperthyroidism 2. Hypothyroidism 3. goitre
54
1. Hyperthyroidism
 Increased secretion of TH is called hyperthyroidism. | T3 & T4 and TSH
55
1. Hyperthyroidism | caused by :
1. Graves disease (thyrotoxicosis) and 2. Thyroid adenoma
56
Graves disease
autoimmune disease B lymphocytes produce autoimmune antibodies called thyroid-stimulating autoantibodies (TSAbs) These antibodies act like TSH by binding receptors on thyroid follicular cells and prolonged effect up to 12 h, results hypersecretion of TH, tsh is low concentration
57
2: Thyroid adenoma
high T3 & T4 and low TSH
58
clinical features of thyroid adenoma
 Exophthalmos; increasbody e weight loss; increase sweating  Nervousness & fine tremors; muscle weakness; diarrhea  BMR; cardiac output; Tachycardia
59
2. Hypothyroidism
Myxedema | Cretinism
60
Myxedema causes
a. Iodine deficiency | b. Hashimoto’s thyroiditis-Autoimmune disease.
61
myxedema
 Myxedema patients have obesity, puffy face, low BMR, | bradycardia, dry skin, hypoglycemia, intolerance to cold.
62
Cretinism
 Hypothyroidism in children, caused stunted growth.  Cretinism due to congenital absence of thyroid gland, genetic disorder or lack of iodine in the during pregnancy.  Features like sluggish movement, croaking sound while crying, wide place eyes, large protruding tongue & dwarf.
63
Goiter
 Goiter means enlargement of thyroid gland. |  It occurs in both hypothyroidism & hyperthyroidism.
64
type of goiter
A. Goiter in hyperthyroidism-Toxic goiter | B. Goiter in hypothyroidism-Non-toxic goiter
65
A. Goiter in hyperthyroidism-Toxic goiter
Toxic goiter is enlargement of thyroid gland with increased | secretion of thyroid hormones, caused by thyroid tumor
66
B. Goiter in hypothyroidism-Non-toxic goiter
 Non-toxic goiter is the enlargement of thyroid gland without increase in hormone secretion.  It is also called hypothyroid goiter
67
non-toxic hypothyroid goiter is classified into two types
1. Endemic colloid goiter | 2. Idiopathic non-toxic goiter
68
1. Endemic colloid goiter or iodine deficiency goiter
caused by iodine deficiency. intake is less than 50 µg/day Lack of iodine causes decreased production of TH and increased TSH. TSH increases secretion of thyroglobulin, its accumulation causes enlargement of gland
69
2. Idiopathic non-toxic goiter
iodine uptake is normal, but there is deficiency of enzymes such as peroxidase, iodinase and deiodinase involved in the synthesis of T3 & T4 Goitrogens are interfere with iodine uptake, commonly found in cabbage & cauliflower

Integration finals (19 decks)

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