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Integration finals > thyroid gland > Flashcards

thyroid gland Flashcards

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
Q

hyperthyroidism

A

Excess secretion of TH than normal levels

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26
Q

REGULATION OF THYROID HORMONE SECRETION

A

The pituitary and hypothalamus both control

the thyroid.

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27
Q

TSH Releasing Hormone (TRH), is secreted

by

A

hypothalamus and stimulates the section
of thyroid stimulating hormone (TSH) from
anterior pituitary

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28
Q

TSH increases synthesis & secretion of

thyroid hormone via

A

adenylate cyclase-cAMP

mechanism.

29
Q

TH regulate their own secretion through

negative feedback control,

A

by inhibiting

release of TRH and TSH.

30
Q

FUNCTIONS OF THYROID HORMONES

A
  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
Q
  1. Action on basal metabolic rate (BMR)
A

high BMR by increasing the oxygen consumption of the tissues

TH increase the activity of Na K ATPase pump.

32
Q

TH BMR in most of the tissues except

A

adult brain, testes,

uterus, spleen

33
Q

hyperthyroidism

A

BMR 60-100% was increased
increases energy expenditure and causes
weight loss

34
Q

hypothyroidism

A

20-40% was decreased
decrease metabolism and
causes weight gain

35
Q
  1. Effect on metabolism
A

TH increase absorption of glucose from GI tract.

 TH increase glycogenolysis, gluconeogenesis

36
Q

TH stimulate both

A

protein synthesis & protein degradation

37
Q

 Low levels of TH

A

enhance the amino acid uptake into cells.

38
Q

High levels of TH

A

protein catabolism

39
Q

TH decrease the fat storage

A

increasing mobilization of lipids from fatty tissue

increase free fatty acids in plasma

40
Q
  1. Effect on body temperature
A

 TH increase heat production
 During hyperthyroidism, body temperature increases
resulting in excess sweating

41
Q
  1. Action on growth
A

TH is very important for normal growth, maturation, proper bone and teeth development
Hypothyroidism arrest the growth, early close of epiphysis

42
Q
  1. Action on blood
A

TH accelerates erythropoiesis. Polycythemia is common in

hyperthyroidism

43
Q
  1. Action on CVS
A

 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
Q

hyperthyroidism

A

increased blood volume & blood flow leads
to increase cardiac output, finally its causes increased blood
pressure.

45
Q
  1. Action on CNS
A

TH promote growth & development of brain in fetal and

infants

46
Q

Hypersec

retion of TH

A

causes excess stimulation of CNS, leads
to extreme nervousness, anxiety & worries. Also causes
irritable, emotional, unstable and restless

47
Q

hypothyroidism

A

person develops low memory power,

slowness of speech, lethargy and somnolence (excess sleep)

48
Q
  1. Action on gastrointestinal system
A

 TH stimulate GIT motility

49
Q
  1. Action on skeletal muscle
A

 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
Q

thyrotoxic

myopathy

A

weakness of muscle due to

catabolism of proteins

51
Q
  1. Action on sleep
A

Excess TH stimulate CNS and muscles, so person feels tired,

cannot sleep. Hyposecretion causes somnolence.

52
Q
  1. Action on sexual function
A

 Hypothyroidism leads to complete loss of libido and
hyperthyroidism leads to impotence
In women, hypothyroidism causes menorrhagia and
hyperthyroidism leads to amenorrhea

53
Q

DISORDERS OF THYROID GLAND

A
  1. Hyperthyroidism
  2. Hypothyroidism
  3. goitre
54
Q
  1. Hyperthyroidism
A

 Increased secretion of TH is called hyperthyroidism.

T3 & T4 and TSH

55
Q
  1. Hyperthyroidism

caused by :

A
  1. Graves disease (thyrotoxicosis) and 2. Thyroid adenoma
56
Q

Graves disease

A

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
Q

2: Thyroid adenoma

A

high T3 & T4 and low TSH

58
Q

clinical features of thyroid adenoma

A

 Exophthalmos; increasbody e weight loss; increase sweating
 Nervousness & fine tremors; muscle weakness; diarrhea
 BMR; cardiac output; Tachycardia

59
Q
  1. Hypothyroidism
A

Myxedema

Cretinism

60
Q

Myxedema causes

A

a. Iodine deficiency

b. Hashimoto’s thyroiditis-Autoimmune disease.

61
Q

myxedema

A

 Myxedema patients have obesity, puffy face, low BMR,

bradycardia, dry skin, hypoglycemia, intolerance to cold.

62
Q

Cretinism

A

 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
Q

Goiter

A

 Goiter means enlargement of thyroid gland.

 It occurs in both hypothyroidism & hyperthyroidism.

64
Q

type of goiter

A

A. Goiter in hyperthyroidism-Toxic goiter

B. Goiter in hypothyroidism-Non-toxic goiter

65
Q

A. Goiter in hyperthyroidism-Toxic goiter

A

Toxic goiter is enlargement of thyroid gland with increased

secretion of thyroid hormones, caused by thyroid tumor

66
Q

B. Goiter in hypothyroidism-Non-toxic goiter

A

 Non-toxic goiter is the enlargement of thyroid gland without
increase in hormone secretion.
 It is also called hypothyroid goiter

67
Q

non-toxic
hypothyroid goiter is classified into two
types

A
  1. Endemic colloid goiter

2. Idiopathic non-toxic goiter

68
Q
  1. Endemic colloid goiter or iodine deficiency goiter
A

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
Q
  1. Idiopathic non-toxic goiter
A

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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