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Flashcards in thyroid metabolic hormones Deck (63)
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1
Q

all thyroid hormones

A

thyroxine and triidothyronine (T4 AND T3 ) and calcitonin

2
Q

function

A

increase metabolism

3
Q

metabolically active hormone secreted by thyroid is

A

thyroxine which is coverter to triidothyronine later and its the most potent hormone

4
Q

anatomy of thyroid gland

A

has follicles
that has secretory substance called colloid and cuboidal epithelial cells which scerete the hormone into the follicles and also the follicles have glycoprotein which is thyroglobulin which contains the hormone and secretes it back into the follicles and they need to cross the follicular epithelium into the blood to go to the target organ

5
Q

what is required to form thyroxine

A

iodine
50 milligram per year as iodide which is present in table salt
1/mg per week

6
Q

iodine fate when ingested

A

secreted by kidney

1/5th is taken by thyroid cells in the circulatory system for synthesis of thyroid hormone

7
Q

sodium idodide symporter

A

The
basal membrane of the thyroid cell has the specific ability
to pump the iodide actively to the interior of the cell. This
pumping is achieved by the action of a sodium-iodide
symporter, which co-transports one iodide ion along with
two sodium ions across the basolateral (plasma) membrane into the cell.

8
Q

energy for sumporter comes from

A

na-k atpase pump which pumps na ions out making the inside deficient in na and makes a concentration gradient for symporter to function

9
Q

iodide trapping

A

This process of concentrating the iodide in the cell is

called iodide trapping

10
Q

how iodiide is transported from the thyroid cells into the follicles

A

pendrin

chloride iodine co transportation ( combines with amino acid tyrosine inside the follicles)

11
Q

how thyroid hormone is formed

A

Each molecule of thyroglobulin contains about 70 tyrosine amino acids, and they are the major substrates
that combine with iodine to form the thyroid hormones.
Thus, the thyroid hormones form within the thyroglobulin molecule. That is, the thyroxine and triiodothyronine
hormones formed from the tyrosine amino acids remain

12
Q

Oxidation of the Iodide Ion

A

iodide
ions to an oxidized form of iodine, either nascent iodine
(I0
) or I3
which is then capable of combining directly
with the amino acid tyrosine. This oxidation of iodine is
promoted by the enzyme peroxidase and its accompanying hydrogen peroxide, which provide a potent system
capable of oxidizing iodides.

13
Q

The
binding of iodine with the thyroglobulin molecule is
called

A

organification of the thyroglobulin.

14
Q

iodination
of tyrosine and final formation of the two important
thyroid hormones, thyroxine and triiodothyronine

A

Tyrosine is first iodized to monoiodotyrosine and then to diiodotyrosine. Then, during the next few minutes, hours, and
even days, more and more of the iodotyrosine residues
become coupled with one another.
he molecule thyroxine (T4), which is formed when two
molecules of diiodotyrosine are joined together; the thyroxine then remains part of the thyroglobulin molecule.
Or one molecule of monoiodotyrosine couples with
one molecule of diiodotyrosine to form triiodothyronine
(T3), which represents about one fifteenth of the final
hormones. Small amounts of reverse T3 (RT3) are formed
by coupling of diiodotyrosine with monoiodotyrosine,
but RT3 does not appear to be of functional significance
in humans.

15
Q

release of thyroxine and triiodothyronine

A

The apical surface of thyroid cells sends out pseudopod extensions that close around small portions of the colloid to form pinocytic vesicles that enter the apex of the thyroid cell. Then lysosomes in the cell cytoplasm immediately fuse with these vesicles to form digestive vesicles containing digestive enzymes from the lysosomes mixed with the colloid. Multiple proteases among the enzymes digest the thyroglobulin molecules and release thyroxine and triiodothyronine in free form, which then diffuse through the
base of the thyroid cell into the surrounding capillaries.
Thus, the thyroid hormones are released into the blood

16
Q

why iodine deficiency happens

A

About three quarters of the iodinated tyrosine in the thyroglobulin never become thyroid hormones but remain monoiodotyrosine and diiodotyrosine. During the digestion of the thyroglobulin molecule to cause release of thyroxine and triiodothyronine, these iodinated tyrosines also are freed from the thyroglobulin molecules. However, they are not secreted into the blood. Instead, their iodine is cleaved from them by a deiodinase enzyme that makes virtually all this iodine available again for recycling within the gland for forming additional thyroid hormones. In the congenital absence of this deiodinase enzyme, many persons become iodine deficient because of failure of this recycling process.

17
Q

Thyroxine and Triiodothyronine Are Bound to

Plasma Proteins

A

They combine
mainly with thyroxine-binding globulin and much less so
with thyroxine-binding prealbumin and albumin.

18
Q

latency of these hormones are caused by

A

the prolonged period of action
of these hormones are probably caused by their binding
with proteins both in the plasma and in the tissue cells,
followed by their slow release.

19
Q

general affect of thyroid hormone

A

activate nuclear transcription of many genes

20
Q

THYROID HORMONES INCREASE

CELLULAR METABOLIC ACTIVITY

A

then thyroxine or triiodothyronine
is given to an animal, the mitochondria in most cells of the animal’s body increase in size and number. Furthermore, the total membrane surface area of the mitochondria increases almost directly in proportion to the increased metabolic rate of the whole animal.
One of the enzymes that increases its activity in response to thyroid hormone is
Na-K-ATPase. This increased activity in turn increases the rate of transport of both sodium and potassium ions through the cell membranes of some tissues. Because
this process uses energy and increases the amount of heat produced in the body, it has been suggested that this might be one of the mechanisms by which thyroid hormone increases the body’s metabolic rate.

21
Q

an important effect of thyroid hormones on body

A

growth of skeletal features and growth of brain in fetus and post natal life

22
Q

Stimulation of Carbohydrate Metabolism

A

increase carbo metabolism
increase insulin secretions
increase glucose uptake, absorption from git, glycolysis, gluconeogenesis

23
Q

Stimulation of Fat Metabolism

A

increase fat mobilization from adipose tissue and increase fatty acid oxidation for energy

24
Q

Effect on Plasma and Liver Fats

A

increased thyroid
hormone decreases the concentrations of cholesterol,
phospholipids, and triglycerides in the plasma
increases secretions of above mention in feces and bile secretions by liver
and also by activating low density lipo protein receptors on liver which remove low density lipo proteins from the liver

25
Q

Increased Requirement for Vitamins

A

high thyroid secretions decreases the vitamin quantities as it increases the need for vitamins by increasing the quantities of enzymes

26
Q

Decreased Body Weight

A

increase thyroid decreases the weight and vice versa

27
Q

Increased Blood Flow and Cardiac Output

A

increase thyroid hormone increases metabolism which increases 02 utilization
causes vasodilation specially in skin. also increases blood flow everywhere for heat elimination and increases cardiac output

28
Q

Increased Heart Rate

A

Therefore, thyroid hormone seems to have a direct effect
on the excitability of the heart, which in turn increases
the heart rate.
. This effect is especially important because
the heart rate is one of the sensitive physical signs that the
clinician uses in determining whether a patient has excessive or diminished thyroid hormone production

29
Q

Increased Heart Strength

A

increase thryoid glang increase enzymatic activity which in turn increases the heart strrngth
also increase throyd hormone depresses the heart and can causes cardiac decompensation secndarily to myocardial failure and increase work load due to increase cardiac output

30
Q

Normal Arterial Pressure.

A

The mean arterial pressure
usually remains about normal after administration of thyroid hormone. Because of increased blood flow
through the tissues between heartbeats, the pulse pressure is often increased, with the systolic pressure elevated
10 to 15 mm Hg in hyperthyroidism and the diastolic pressure reduced a corresponding amount

31
Q

increased respiration

A

increase o2 utilization and co2 production icnreases the rate of respiration

32
Q

Increased Gastrointestinal Motility

A

increases secretions of gastric juices (enzymes)
hyperthyroidism - diarrehao
hypothyroidism- constipation

33
Q

Excitatory Effects on the Central Nervous System

A

In
general, thyroid hormone increases the rapidity of cerebration, although thought processes may be dissociated;
conversely, lack of thyroid hormone decreases rapidity of
cerebration. A person with hyperthyroidism is likely to be
extremely nervous and have many psychoneurotic tendencies, such as anxiety complexes, extreme worry, and
paranoia

34
Q

Effect on the Function of the Muscles

A

slight increase- muscles become vigor
excessive - become weakened because of excessive protein catabolism
less- become sluggish

35
Q

Muscle Tremor

A

One of the most characteristic signs of
hyperthyroidism is a fine muscle tremor
it is not as it happens in parkinsons but by placing a piece of paper on the finger and seeing the degree of vibration which is causes by increase activity of neuronal synapses in the area of spinal cord which is responsible for muscle tone
The tremor is an
important means for assessing the degree of thyroid
hormone effect on the central nervous system

36
Q

Effect on Sleep

A

hyperthyroidism because of increase activity of muscles and cns person is always tired by increase activity of synapses the person will have difficulty sleeping
people with somnolence can sleeo for 12-14 hours a day

37
Q

Effect on Other Endocrine Glands

A

increasing glucose metabolism increase s insulin production
increasing bone formation increases parathyroid hormone secretions
also increases the rate of inhibition of glucocorticoid hormones by adrenal through liver which increases the secretions of adrenocorticotropic from anterior pituatry which increases the secreyions of glucocorticoid from adrenal glands

38
Q

effect of sexual function

A

In men, lack of thyroid hormone
is likely to cause loss of libido; a great excess of the hormone, however, sometimes causes impotence. In women, lack of thyroid hormone often causes menorrhagia and polymenorrhea—that is, excessive and frequent menstrual bleeding, respectively. Yet, strangely
enough, in other women a lack of thyroid hormone may cause irregular periods and occasionally even amenorrhea (absence of menstrual bleeding). Hypothyroidism in women, as in men, is likely to result
in a greatly decreased libido. To make the picture still more confusing, in women with hyperthyroidism, oligomenorrhea (greatly reduced bleeding) is common, and
occasionally amenorrhea occurs

39
Q

effect of tsh released by anterior pituitary

A
  1. increase iodine trapping by increasing the activity of iodine pump
  2. increase iodinization of tyrosine
  3. increasing the site and number of thyroid cells
  4. increase proteolysis of thyroglobulin
  5. increase secretory activity of thyroid cells
40
Q

secretion of tsh is controlled by

A

Anterior pituitary secretion of TSH is controlled by a
hypothalamic hormone, thyrotropin-releasing hormone
(TRH), which is secreted by nerve endings in the median
eminence of the hypothalamus. From the median eminence, TRH is then transported to the anterior pituitary
by way of the hypothalamic-hypophysial portal blood,

41
Q

Antithyroid Substances Suppress

Thyroid Secretion

A

thiocyanate, propylthiouracil, and high concentrations of inorganic iodides.

42
Q

Thiocyanate Ions Decrease Iodide Trapping

A

The same
active pump that transports iodide ions into the thyroid
cells can also pump thiocyanate ions, perchlorate ions, and
nitrate ions. Therefore, the administration of thiocyanate
(or one of the other ions as well) in a high enough concentration can cause competitive inhibition of iodide transport
into the cell—that is, inhibition of the iodide-trapping
mechanism.
The decreased availability of iodide in the glandular cells
does not stop the formation of thyroglobulin; it merely
prevents the thyroglobulin that is formed from becoming iodinated and therefore from forming thyroid hormones.
This deficiency of thyroid hormones in turn leads to increased secretion of TSH by the anterior pituitary gland, which causes overgrowth of the thyroid gland even though the gland still does not form adequate quantities of thyroid hormones. Therefore, the use of this cyanates and some
other ions to block thyroid secretion can lead to the development of a greatly enlarged thyroid gland, which is called
a goiter.

43
Q

goiter.

Propylthiouracil Decreases Thyroid Hormone Formation

A

it blocks the affect of peroxidase which is important in the iodinization of tyrosine and it stops the coupling of 2 iodized tyrosine to form thyroxine and trridothyronine causes goiter

44
Q

Iodides in High Concentrations Decrease Thyroid

Activity and Thyroid Gland Size.

A

reduce the rate of iodide trapping so
that the rate of iodination of tyrosine to form thyroid hormones is also decreased. Even more important, the normal
endocytosis of colloid from the follicles by the thyroid glandular cells is paralyzed by the high iodide concentrations.
Because this is the first step in release of thyroid hormones
from the storage colloid, there is almost immediate shutdown of thyroid hormone secretion into the blood
decreases thyroid activity, the size of thyroid gland and blood supply
thats why its administered into patients before thyroid removal surgery to decrease the blood flow through the gland

45
Q

grave disease

A

Graves’ disease, the most common form of hyperthyroidism, is an autoimmune disease in which antibodies called thyroid-stimulating immunoglobulins (TSIs) formagainst the TSH receptor in the thyroid gland. These antibodies bind with the same membrane receptors that bind TSH and induce continual activation of the cAMP system of the cells, with resultant development of hyperthyroidism. The TSI antibodies have a prolonged stimulating effect on the thyroid gland, lasting for as
long as 12 hours, in contrast to a little over 1 hour for TSH. The high level of thyroid hormone secretion caused by TSI in turn suppresses anterior pituitary formation of TSH. Therefore, TSH concentrations are less than normal (often essentially zero) rather than enhanced in almost all patients with Graves’ disease. The antibodies that cause hyperthyroidism almost certainly occur as the result of autoimmunity that has developed against thyroid tissue

46
Q

Thyroid Adenoma.

A

Hyperthyroidism occasionally
results from a localized adenoma (a tumor) that develops
in the thyroid tissue and secretes large quantities of thyroid hormone As long
as the adenoma continues to secrete large quantities of
thyroid hormone, secretory function in the remainder of
the thyroid gland is almost totally inhibited because the
thyroid hormone from the adenoma depresses the production of TSH by the pituitary gland

47
Q

synptoms of hyperthyroidism

A

(1) a high state of excitability, (2) intolerance to
heat, (3) increased sweating, (4) mild to extreme weight
loss (sometimes as much as 100 pounds), (5) varying
degrees of diarrhea, (6) muscle weakness, (7) nervousness
or other psychic disorders, (8) extreme fatigue but inability
to sleep, and (9) tremor of the hands.

48
Q

what is exophthalmos

A

Most people with hyperthyroidism
exhibit some degree of protrusion of the eyeballs, as
in Figure 77-8. This condition is called exophthalmos

49
Q

what effects does exophthalmos has on eyes

A

ulcers of cornea, irritation and dryness of cells of eye epithelium
and damage to optic nerve affecting eye vision

50
Q

cause of protruding eyes

A

edematous swelling
of the retro-orbital tissues and degenerative changes in the
extraocular muscles. I

51
Q

Diagnostic Tests for Hyperthyroidism.

A
  1. The basal metabolic rate is usually increased to +30 to +60 in severe hyperthyroidism.
  2. The concentration of TSH in the plasma is measured by radioimmunoassay. In the usual type of thyrotoxicosis, anterior pituitary secretion of TSH is so completely suppressed by the large amounts of circulating thyroxine and triiodothyronine that there is almost no plasma TSH.
  3. The concentration of TSI is measured by radioimmunoassay. This concentration is usually high in thyrotoxicosis but low in thyroid adenoma.
52
Q

Treatment in Hyperthyroidism.

A

removal of thyroid gland by first administrating propylthiouracil and then iodide to decrease the size of thyroid gland and diminish the blood supply

53
Q

Hypothyroidism

A

Hypothyroidism, like hyperthyroidism, is often initiated by autoimmunity
against the thyroid gland (Hashimoto’s disease), but in this case the autoimmunity destroys the gland rather than
stimulates it. The thyroid glands of most of these patients first demonstrate autoimmune “thyroiditis,” which means
thyroid inflammation. Thyroiditis causes progressive deterioration and finally fibrosis of the gland, with resultant
diminished or absent secretion of thyroid hormone.

54
Q

enlarged thyroid gland in hypothyroidism

A

goiter

55
Q

Endemic Colloid Goiter Caused by Dietary Iodide Deficiency

A

Swiss Alps, the Andes, and the Great Lakes region of the United States, insufficient iodine is present in the soil for the foodstuffs to contain even this minute quantity. Therefore, in the days before iodized table salt, many people who lived in these areas developed extremely large
thyroid glands, called endemic goiters.
The following mechanism results in the development of large endemic goiters: Lack of iodine prevents production
of both thyroxine and triiodothyronine. As a result, no hormone is available to inhibit production of TSH by the anterior pituitary, which causes the pituitary to secrete
excessively large quantities of TSH. The TSH then stimulates the thyroid cells to secrete tremendous amounts of thyroglobulin colloid into the follicles, and the gland grows larger and larger. However, because of lack of iodine,
thyroxine and triiodothyronine production does not occur in the thyroglobulin molecule and therefore does not
cause the normal suppression of TSH production by the anterior pituitary. The follicles become tremendous in size,
and the thyroid gland may increase to 10 to 20 times its normal size.

56
Q

Idiopathic Nontoxic Colloid Goiter

A

but most
of these patients show signs of mild thyroiditis; therefore,
it has been suggested that the thyroiditis causes slight
hypothyroidism, which then leads to increased TSH
secretion and progressive growth of the noninflamed portions of the gland.

57
Q

abnormalities in nontoxic idiophatic colloid goiter

A
  1. A deficient iodide-trapping mechanism, in which
    iodine is not pumped adequately into the thyroid
    cells
  2. A deficient peroxidase system, in which the iodides
    are not oxidized to the iodine state
  3. Deficient coupling of iodinated tyrosines in the thyroglobulin molecule so that the final thyroid hormones
    cannot be formed
  4. Deficiency of the deiodinase enzyme, which prevents
    recovery of iodine from the iodinated tyrosines that
    are not coupled to form the thyroid hormones (this
58
Q

Physiological Characteristics of Hypothyroidism

A

They
include fatigue and extreme somnolence, with persons
sleeping up to 12 to 14 hours a day, extreme muscular
sluggishness, a slowed heart rate, decreased cardiac
output, decreased blood volume, sometimes increased
body weight, constipation, mental sluggishness, failure
of many trophic functions in the body as evidenced by
depressed growth of hair and scaliness of the skin, development of a froglike, husky voice, and, in severe cases, development of an edematous appearance throughout the body
called myxedema

59
Q

myxedema

A

shows such a patient, demonstrating bagginess under the
eyes and swelling of the face. In this condition, for reasons that are not explained, greatly increased quantities of hyaluronic acid and chondroitin sulfate bound with protein form excessive tissue gel in the interstitial spaces, which causes the total quantity of interstitial fluid to increase

60
Q

atherosclerosis

A

decrease level of thyroid gland increases blood cholesterol level which increases the chances of atherosclerosis and other vascular diseases specially people who have myxedema and are prone to more peripheral vascular diseases like deafness and coronary artery diseases

61
Q

Diagnostic Tests for Hypothyroidism

A

The basal metabolic rate in myxedema ranges between −30 and −50. In addition, the secretion of TSH by the anterior pituitary when a test dose of TRH is administered is usually greatly increased (except in the rare instances of hypothyroidism caused by depressed response of the pituitary gland to TRH).

62
Q

treatment of hypothyroidism

A

daily ingestion of thyroid hormones

63
Q

what is cretinism

A

This condition is characterized especially by failure of body growth and by mental
retardation. It results from congenital lack of a thyroid
gland (congenital cretinism), from failure of the thyroid
gland to produce thyroid hormone because of a genetic
defect of the gland, or from a lack of iodine in the diet
(endemic cretinism).