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Systems Physiology > Thyroid Physiology > Flashcards

Thyroid Physiology Flashcards

1
Q

Which hormones are classified as glycoproteins?

A

Glycoproteins:

FSH, Human chorinoic gonadotropin, LH, TSH (thyroid stimulating hormone)

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2
Q

Which hormones are classified as steroids?

A 
Steroids: 
Aldosterone
Cortisol
Estradiol
Progesterone
testosterone
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3
Q

which hormones are classified as Amines?

A

Amines:

Epinephrine, Norepinephrine, melatonin ,dopamine, Thyroxine (T4) and Triiodothyronine (T3)

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4
Q

Which hormones are considered peptides, polypeptides and proteins?

A

Peptides, polypeptides, and proteins:
ACTH (adrenocorticotropic hormone), angiotensin, calcitonin, cholecystokinin, erythropoietin, gastrin, glucagon, growth hormone, insulin, somatomedins, nerve growth factor, oxytocin, parahormone, prolactin, relaxin, secretin, somatostatin, vasopressin

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5
Q

Explain why the thyroid hormones (T3, T4) do not behave like other amines?

A

T3, T4 do NOT behave like other amines because:

  1. They do NOT have Rapid (enzymatic) synthesis
  2. They are NOT stored in secretory granules (thyroid hormones stored outside cells)
  3. They are NOT water soluble (thyroid hormones need binding proteins)
  4. They do NOT have a short half- life (thyroid hormones have long half-lives, day, or 7 days (t4)
  5. They do NOT have a membrane receptor (t3, t4 have receptors in nucleus)
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6
Q

Describe the characteristics of thyroid gland? What happens if you repeatedly stimulate thyroid. What conditions could occur?

A

Thyroid gland: Bow tie shape composes of 2 lobes
Size of thyroid INCREASES when you repeatedly stimulate it.
You can get a goiter due to iodine insufficiency. When you repeatedly stimulate thyroid, you will get hyperplasia (increase number of cells)

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7
Q

Where are thyroid hormones stored?

A

Thyroid hormones are stored in COLLOID

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8
Q

Describe the change in structure of colloid in resting state vs stimulated form? What surrounds the colloid?

A

The follicular cells surround the colloid in a spherical shape. In resting state, colloid is hollow and follicular cells are sphere shaped.
In stimulated form, follicular cells become columnar shaped, due to hyperplasia (increase in cells)

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9
Q

What are the three major steps for thyroid hormone synthesis?

A

Three major steps for thyroid hormone synthesis:

  1. Uptake and concentration of Iodide (I-) in the gland
  2. Oxidation and incorporation of Iodine to Tyrosine’s phenol ring
  3. Coupling of two iodinated tyrosines to form t4 or T3.
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10
Q

Elaborate on iodide uptake. Why is Iodine important and how do we obtain it? What is the minimum daily requirement for Iodine? How does this compare to avg U.S. consumption?

A

Step 1 of thyroid hormone synthesis:
1. Iodide uptake
Iodine is a critical micronutrient (obtained from our DIET)
-Few food sources are rich in iodine: like Seaweed (Kombu kelp, wakame, nori, IODIZED Table salt.
-Minimum daily requirement: 80 ug
-80 ug is taken up daily by thyroid gland
Us avg daily intake is 300-400 ug
So you have stored Iodine within thyroid gland that is 100x greater than daily need (protected for 2 months from iodine deficiency)

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11
Q

What happens when you have low levels vs high levels of Iodine intake?

A

Low levels of Iodine intake DECREASES rate of thyroid synthesis
HIGH levels of iodine intake (greater than 2mg/day), SUPPRESSES rate of thyroid synthesis due to Wolf-chaikoff effect.

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12
Q

What is the Wolf-Chaikoff effect?

A

Wolf-Chaikoff effect: autoregulatory phenomenon that occurs when you ingest too much Iodine, it will INHIBIT or shut down thyroid hormone synthesis for 10 days (won’t make any iodine).

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13
Q

Further elaborate on what occurs in Iodide uptake? how is Iodine able to be transported into thyroid gland? What kind of transport is needed? What molecules block active transport of I- ?

A

Iodide uptake:
-I is actively transported into thyroid gland vs an electrochemical gradient by 2 Na+ 1 I- SYMPORTER
The Na+ K+ ATPASE allows Na+ to go DOWN its concentration gradient and Iodine go up its concentration gradient. (hence Na+ move across thyroid cell and I move across thyroid cell in same direction).
CLO4-, SCN- BLOCK the active transport of I-

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14
Q

Explain what happens in step 2 of thyroid hormone synthesis? What products are formed?

A

Step 2: Tyrosine iodination
- The glycoprotein THYROGLOBULIN is a scaffold structure that contains lots of tyrosine.
I- is oxidized and incorporated into tyrosine by enzyme THYROID PEROXIDASE (TPO)
This is where oxidation and organification and oxidation of iodine by TPO occurs.
The products of MIT (moniodotyrosine) and DIT (diodotyrosine) are formed after oxidation/incorporation of I- into tyrosine.

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15
Q

Explain what occurs in step 3 of Thyroid hormone synthesis. What process occurs and what products are formed?

A

Step 3: Coupling of Iodinated molecules with Thyroglobulin (by TPO).
TPO will help couple MIT and DIT with thyroglobulin to form T3 (triodothyronine)
TPO also couples 2 DIT molecules with thyroglobulin to form T4 (thyroxine)

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16
Q

What is the ratio of T4 to T3 synthesized?

A

Ratio of T4 to T3 synthesized: 10-20:1 (unless I- is limited) Usually higher amount of T4 than T3.

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17
Q

Explain how thyroid hormone is eventually secreted. What processes occur?

A

Secretion of thyroid hormone:
occur when thyroglobulin is ENDOCYTOSED and HYDROLYZED
1. Thyroglobulin enters the thyroid follicular cell via endocytosis
2. Lysosomal proteases Hydrolyze the thyroglobulin
3. This causes T3 an T4 to be released
4. MITs and DITs are also DEIODINATED and I- is recycled

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18
Q

How much of T3, T4 and reverse T3 is secreted from thyroid? How do you get T3 and T4?

A 
Secretion from thyroid: 
- 90% T4
9& of T3
-1% rT3 (reverse T3)
-Peripheral conversion of T4 to T3
T4 is the prohormone (or precursor) that will converted into T3.
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19
Q

which hormone is active vs inactive out of T3 and T4? How does the conversion of one into other occur?

A

T4 is NOT active
T3 is the ACTIVE hormone
T4 can convert into T3 by priming the outer ring structure of T4
T4 can also encounter 5MD and convert into reverse T3.
Also with COLD TEMPS, T4 converts into T3.

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20
Q

What thyroid hormone is produce more when body is cold, during illness, aging,

A

When the body is cold, more T3 is made

During starving, illness, aging, you make more of Reverse T3.

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21
Q

Which thyroid hormone would be made during fasting, malnutrition, Drugs (PTU, DEX, propranolol , amiodarone)?

A

During fasting, malnutrition, physical trauma or drugs, there would be a decrease in T4 and a conversion into T3.

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22
Q

If one were starving and cold, which factors wins out? What hormone is produced?

A

If one were starving and cold, which factor wins out?

- Being cold would kill the person, so cold wins and T3 would be made.

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23
Q

Describe what occurs with thyroid hormones T4 and T3 in blood. How much of the thyroid hormone is bound vs free?

A

Thyroid hormones circulate BOUND to plasma proteins or FREE
-70% thyroid hormones bound to THYROIXINE-BINDING GLOBULIN (TBG)
TBG made from liver
-29.5% Bound to Prealbumin and Albumin
-FREE HORMONE: Low levels but critical
-0.03% of T4
-0.3% of T3

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24
Q

What is the role of free thyroid hormone and binding proteins?

A

Free thyroid hormones: low levels, but critical: achieve thyroid hormone’s effects and responsible for feedback
Binding proteins create a reservoir of hormone
-protects against acute changes in thyroid gland function
Binding proteins also makes proteins more soluble.

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25
Q

Describe the equilibrium that exists between bound and free T4.

A

An equilibrium exists between bound and free T4
-A decrease in plasma free T4 causes by decrease in thyroid gland secretion; which Can be REVERESED via dissociation of Bound T4.

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26
Q

What occurs if there is a change in [TBG] ?

A

A change in [TBG], (binding protein )disturbs the Ratio of Free to bound
-Thyroid gland must compensate (increase or decrease) until free T4 levels are normal
alterations in TBG do NOT DISTURB Biological function (if thyroid gland is normal).
Temporary state: will INCREASE TSH (?) come back to this

27
Q

What is the major stimulator of thyroid hormone secretion?

A

Major stimulator of thyroid hormone secretion: THYROID-STIMULATING HORMONE (TSH)
it stimulates almost every step in the pathway of TH synthesis
-uptake and oxidation of iodide
-Thyroglobulin synthesis
-Iodination and coupling
-Endocytosis of thyroglobulin and colloid
-Thyroglobulin proteolysis
TSH also stimulates GROWTH and VASCULARITY of thyroid gland.

28
Q

Explain the inhibitory and stimulatory affects for hormones involved in thyroid hormones synthesis.

A

Inhibitory/stimulatory effects of thyroid hormone:
TRH (thyroid releasing hormone) STIMULATES thyroid stimulating hormone
TSH stimulates Thyroid gland and almost every step of thyroid synthesis.
Both T3 and T4 can feedback and INHIBIT hypothalamus and anterior pituitary.
High levels of T3 and T4 inhibit TRH (thyroid releasing hormone). They can also inhibit TSH.
Hypothalamus stimulates the release of TRH (thyroid releasing hormone) and anterior pituitary stimulates release of TSH
Dopamine and somatostatin also INHIBIT Thyroid stimulating hormone.

29
Q

What is minor vs major form of T3.

A

Minor form of T3- when thyroid gland stimulates T3 directly

Major form of T3- when T4 is deiodinated and moves through PERIPHERAL TISSUE to convert into T3.

30
Q

Explain how thyroid hormone is under Sensitive Feedback control.

A

Changes in thyroid hormone levels of only 10-30% are enough to change TSH in the opposite direction
If Thyroid hormone levels increase by 10-30%, it will negative feedback and decrease TSH levels.
if thyroid hormone DROPS by 10-30%, increase TSH levels.
Feedback on T3 on Anterior pituitary: (if T3 levels high)
-Represses Transcription of TSH gene
-Suppresses TSH release
-Down-Regulates TRH receptors.

31
Q

What is half life for T4 and T3? Which hormone is biologically active hormone and why?

A

T4 (thyroxine) has a half life of 6 days, due to T4 having a HIGHER AFFINITY for Binding protein. Hence it cannot get metabolized and will stay in blood longer (longer half-life).
T3 has a short half life since it has HIGH Affinity for Receptor which makes it Biologically ACTIVE.

32
Q

Compare and contrast the characteristics for Levothyroxine (T4) and Liothyronine (T3)

A 
T4 vs T3: 
Levothyroxine (T4): 
-Mimics true physiology
-LOW cost
-Stability (2 years in dark bottle)
-Lack of allergens
-EASY Lab Measurement
-LONG Half life (1 dose a day)
-2 hormones in 1; because T4 converts to T3 (2 in 1)

Liothyronine (T3):

  • SHORTER half-life (multiple doses/day)
  • More EXPENSIVE
  • Harder to monitor
  • Higher activity (Dangerous to heart; may cause palpitations)
33
Q

What is the synthetic form of T3 and T4, that can also be used as drugs for patients?

A

Synthetic form T3: Liothyronine (TRIO= LIO)

Synthetic form T4 Levothyroxine

34
Q

When treating hypothyroidism, why do we give synthetic T4 (levothyroxine) instead of Synthetic T3 (liothyronine)

A

Synthetic T4 (Levothyroxine) is given to treat hypothyroidism instead of synthetic T3 because The body actively makes T3 already and T4 will eventually convert into T3?

35
Q

What are the main functions of T3 (thyroid hormone)?

A 
T3's functions (4B's): 
Brain maturation
Bone growth
Beta-adrenergic effects 
-BMR increases
36
Q

Describe the physiological effects of thyroid hormones.

A

Action of thyroid hormones:

  1. T4 gets iodinated to convert into T3
  2. T3 then binds to Nuclear receptor and influences transcription of DNA which leads to translation of mRNA and synthesis of new proteins.
  3. Synthesis of new proteins leads to stimulation of many factors:
    - Growth- growth formation and bone maturation
    - CNS- maturation of CNS
    - BMR- Increase in Na+K+ ATPase, increase in O2 consumption, increase in Heat production, and increase in BMR.
    - Metabolism: Increase in glucose absorption, increase in Glycogenolysis, increase in gluconeogenesis, increase in lipolysis and increase in protein synthesis and degradation (net catabolic).
    - Cardiovascular- increase in Cardiac output.
37
Q

What are the main functions of T3 (thyroid hormone)?

A 
T3's functions (4B's): 
Brain maturation
Bone growth
Beta-adrenergic effects (increase in catecholamine (NE/E affects)
-BMR increases
38
Q

Explain how Thyroid hormones are transported and how long it takes for T3 effects to be seen.

A

Thyroid hormones require TRANSPORTER PROTEINS for transport across cell membranes
-Transporters associated with clinical disorders: Monocarboxylate Transporter (MCT) 8, and Organic anion Transporting polypeptide (OATP) 1C1.
Because T3 acts through gene transcription, 12-48 hour delay before effects seen. Thus, several weeks until consequences of T3 deficiency are corrected.

39
Q

Further elaborate on how T3 regulates basal metabolic rate (BMR). What other factors are affected?

A

T3 Regulates Basal Metabolic Rate (BMR):
-increases Number and size of mitochondria
-increase O2 consumption
-Increases substrate use (Synthesis and oxidation of fatty acids and Glucose
-increases Na, K ATPase.
also increases heat production by FUTILE CYCLING
(Na K+ ATPASE and substrate use all use ATP)

40
Q

How does hypothyroidism or hyperthyroidism affect oubain? What is the role of Oubain?

A

Hyperthyroidism- INCREASES Oubain
Hyothyroidism decreases Oubain
Oubain- plant derived toxic substance that binds to and inhibits Na+ K+ ATPase.
also used as cardiac glycoside; treat heart failure in Africa.

41
Q

How does thyroid hormone affect futile cycling?

A

Thyroid hormone influences futile cycling which increases heat production and ATP is used in this process
Futile cycling (make something or break down something) which uses a lot of ATP, generating heat
Heat production increases during synthesis of fatty acid oxidation and synthesis of glucose.

42
Q

Differentiate between the factors affected in hypothyroidism vs hyperthyroidism

A

Hyperthyroidism: O2 consumption goes up in most tissues, Increases Na+ K+ ATPASE
Hypothyroidism: low thyroid hormone, low O2 consumption.

43
Q

How does Thyroid hormone T3, affect Cardiovascular System? How does this hormone affect SERCA2, B-1 adrenergic, Na/Ca, and phospholamban?

A

Cardiovascular: T3 Increases Cardiac Output which ensures that tissues get adequate nutrients and O2.
- increase Heart Rate, Stroke volume and contractility. Increase SBP (systolic Blood pressure) and decrease DBP (diastolic Blood pressure), decrease vasodilation and decrease SVR (systemic vascular resistance)
Thyroid hormone POSITIVELY regulates SERCA2, Beta 1 adrenergic, NA/K
Thyroid hormone NEGATIVELY regulates Na/Ca, Phospholamaban

44
Q

Why is Thyroid hormone(T3) described as Sympathomiemtic?

A

Thyroid hormone (T3) is seen as sympathomimetic:
because many actions of High thyroid hormone levels resemble increase Endogenous SNS (sympathetic nervous system) activity.
-It reinforces Cardiovascular responses to Epinephrine an NE.
-Increases number of Beta and alpha1- adrenergic receptors
-Thyroid hormone has Permissive effect for Epi and NE on lipolysis, glycogenolysis, and Gluconeogenesis (thyroid increases activity of these processes).

45
Q

What effect does thyroid hormone alone, vs epinephrine and a combination of thyroid hormone and epinephrine have on fatty acids?

A

Thyroid hormone alone has LITTLE or NO Fatty acids released
Epinephrine has SMALL amount of fatty acids released
Epinephrine AND thyroid hormone has LARGE amount of Fatty acids released.

46
Q

Explain how thyroid hormone affects Growth?

A

Growth:
Thyroid hormone STIMULATES linear growth, development and Maturation of Bone
-T3 (via IGF): stimulates activity of chondrocytes in the growth palate
-T3 also stimulates SECRETION Of GH
-also affects TOOTH Development and Eruption
-T3 stimulates RENEWAL of Epidermis and hair follicles
-Th ACCELERATES shedding of skin and hair.

47
Q

How does Thyroid hormone affect CNS Development? How does thyroid hormone affect CNS in children and adults?

A

CNS (Central Nervous System Development):
Thyroid hormone T3 is expressed in brain throughout Fetal life.
-Activity of 5’ Deiodinase is AUGMENTED (catalyze inactivation of T4 into T3 (active)
-Degradation of T3 is DIMINISHED.
In children and adults: Thyroid hormone ENHANCES the speed and amplitude of reflexes, wakefulness, alertness, responsiveness to various stimuli, awareness of hunger, memory and learning capacity.
-Thyroid Hormone also Stimulates normal emotional tone.

48
Q

What happens to CNS (Central Nervous system ) development if deficient in thyroid hormone in Utero?

A

CNS Development:
if deficient in Thyroid hormone in UTERO:
-IMPAIRED growth of cerebral and cerebellar cortex
-IMPAIRED Proliferation of axons and branching dendrites
-Impaired MYELINIZATION
-Irreversible Brain damage if thyroid deficiency is NOT treated immediately after birth
-biochemically: Decrease in RNA and protein content, protein synthesis, enzymes for DNA synthesis, and NT receptors, NT (neurotransmitter) synthesis

49
Q

Differentiate between what is seen in X-ray of hand of 13 year old with normal thyroid vs one with hypothyroid child.

A

In normal 13 year old with Normal Thyroid: you see X-ray of hand (with bones in place) and normal bone growth
In HYPOTHYROID child: you see spaces between bones in hand, due to bone growth impairment and lack of development or maturation of bone due to low levels of thyroid hormone.

50
Q

Describe what occurs in a 28 year old with Congenital Hypothyroidism.

A 
Congenital Hypothyroidism (in 28 year old):
The woman has SHORT stature, Malformed legs, dull expression, Intellectual disabilities, delayed puberty and muscle weakness. 
This thyroid hormone deficiency occurs in a baby after birth, and it occurs when thyroid fails to develop properly or fails to function properly.
51
Q

Describe what occurs in hypothyroidism and the symptoms associated with it.

A

Hypothyroidism: A DEFICIENCY of Thyroid hormones
Symptoms:
-Fatigue, lethargy
-Weight gain
-Cold intolerance (Decrease BMR) GET COLD
-Muscle aches, stiffness
-Somnolence (or drowsiness)
-Thinning hair
-Dry skin
-Prolonged Reflex times
-Depression
-Mental Slowness
-Constipation
-Amenorrhea (HEAVIER than normal or irregular periods)
-Puffy face (myxedema)- due to fibroblast stimulation
-can have GOITER (can cause trouble breathing or swallowing)

52
Q

Further elaborate on why people with Hypothyroidism have myxedema (puffy face)

A

People with hypothyroidism have a puffy face (myxedema) due to FIBROBLAST STIMULATION: Increase in deposition of mucopolysaccharides into skin, which draws H2O into the interstitial space and leads to swelling.

53
Q

Why does hypothyroidism lead to goiter?

A

People with hypothyroidism can have goiter because goiter is caused by Iodine DEFICIENCY. The anterior pituitary can detect the low iodine levels and stimulate the thyroid to create more thyroid hormone. This will cause Thyroid to ENLARGE to capture more iodine to make more of thyroid hormone. The enlargement of thyroid will then cause goiter.
If you have low thyroid hormone, you have low iodine as well?

54
Q

What are the main causes of hypothyroidism?

A

Causes of Hypothyroidism:
1. Primary (thyroid failure)
-Hashimoto’s Thyroiditis- the MOST COMMON cause of hypothyroidism
-Autoimmune, thyroid ANTIBODIES Damage Thyroid (produce no T3, T4)
-you will have LOW LEVELS of T3, T4 and high TSH.
2. Secondary (pituitary or hypothalamic failure)
-you will have LOW levels of TSH (since problem in pituitary) and hence Low T3, T4
3. IODINE DEFICIENCY
If you have low iodine levels, you will have low thyroid hormone, hence LOW T3 and T4 levels. But TSH will be very high. You may also have thyroid failure.
You will have the LARGEST GOITER.

55
Q

Explain why you can have goiter with Hashimoto vs not with secondary hypothyroidism cause ( pituitary failure)

A

with Hashimoto you can have goiter, you have high TSH, and Low T3, T4 (due to thyroid failure)

56
Q

What is Hashimoto’s disease?

A

Hashimoto’s disease- when immune system attacks your thyroid gland (butterfly shaped organ)
eventually inflammation due to autoimmune reaction (formation of antibodies) prevents thyroid from not being able to make thyroid hormone (leading to hypothyroidism)

57
Q

Describe what occurs in hyperthyroidism and symptoms that occur.

A

HYPERTHYROIDISM- EXCESS of thyroid hormone
symptoms:
-Heat tolerant (Increase in BMR), get very hot
-Weight LOSS
-Palpitations (heart)
-Nervousness, anxiety, irritability,
-Tremor
-Moist, Warm skin (due to heat release)
-Increase DEFECATION frequency (discharge of feces)
-GOITER (due to overstimulation of thyroid, enlargement)
-Bruit over thyroid (audible vascular sound (turbulent blood flow)
-Pretibial myxedema (condition where lesions occur in skin due to deposition of hyaluronic acid; Grave’s disease)
-Fatigue
-Exophthalmos (Bulging of eyes), lid retraction (grave’s disease)
Exophthalmos (forward displacement of eyeballs)

58
Q

What are the main causes of Hyperthyroidism?

A

Causes of Hyperthyroidism:
1.Primary: GRAVES’ Disease - autoimmune disease in which antibodies target thyroid RECEPTOR, which activates thyroid hormone synthesis
-Thyroid stimulating Immunoglobulins (TSI) (antibodies tell thyroid gland to be more active, producing high amount of thyroid hormone)
Hence, high T3 and T4 levels, but LOW TSH levels.
2. Secondary: Excess TSH or TRH,
when you have too much TSH, or TRH, you get high levels of T3, and T4, and also causes Goiter (since thyroid is overstimulated, causes enlargement)
3. Hypersecreting Thyroid Tumor which is also known as toxic adenoma
A toxic thyroid nodule (tumor) is causing e)
-single nodule (lump) grows on top of thyroid gland, causing thyroid enlarged and produce too much thyroid hormone (hypothyroidism). Tumor causes autonomic secretion of TSH (tropic hormone)
T3, T4 levels are HIGH and LOW TSH.
You have low levels of TSH because of negative feedback. The pituitary gland is trying to compensate for excess T3 and T4, and stopping the production of TSH and hence stopping thyroid hormone.

59
Q

What is Grave’s Disease?

A

Grave’s disease- immune system disorder that results in overproduction of thyroid hormones (hyperthyroidism)
leads to HIGH T3, T4 levels and Low TSH levels.

60
Q

What do High TSH levels, and High T3, and T4 levels indicate?

A

PRIMARY failure of target endocrine organ (thyroid)

-Primary hypothyroidism.

61
Q

What do high T3, T4 levels and low TSH level indicate?

A

SECONDARY Hypothyroidism (tropic hormone deficiency). This means malfunction with pituitary gland or hypothalamus.

62
Q

What do High T3, T4 and High TSH levels indicate?

A

AUTONOMOUS secretion of TSH ( Tropic hormone) due to TSH-secreting tumor. Tumor causing increase in TSH, and hence stimulating thyroid to produce high levels of thyroid hormone.

63
Q

What do High T3 and T4 level and Low TSH levels indicate?

A

AUTONOMOUS secretion of target endocrine organ (thyroid) (Graves disease), overstimulation of thyroid leading to high levels of T3, T4. This causes negative feedback of inhibiting TSH to lower T3, T4.

Systems Physiology (19 decks)

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