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(OMS1) Neuro exam 3 > Thyroid Gland physiology > Flashcards

Thyroid Gland physiology Flashcards

1
Q

What hormones does the thyroid gland produce?

A

Active T3 (triiodothyronine) and inactive T4 (tetraiodothyronine)

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2
Q

Describe the structure of the thyroid gland:

A

Thyroid follicle are surrounded by epithelial cells. Lumen in the center where thyroid hormones are stored in the colloid.
Also has parafollicular C cells that secrete calcitonin

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3
Q

What is the back bone of the thyroid hormone?

A

Thyroglobulin

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4
Q

What molecule is important for thyroid hormone synthesis?

A

Iodine (I2) from diet converted into I- and brought into thyroid gland via the iodide trap. Attached to the thyroid hormone

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5
Q

Draw out the synthesis equation of T3 and T4. What is the major product of this pathway?

A

Inactive T4. Later converted to T3 when needed via peripheral conversion

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6
Q

Draw the conversion pathway of T4 to T3

A

Ok

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7
Q

Peripheral conversion of T4 to active T3 can be hindered by …

A

Fasting
Physical stress
Catabolic disease

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8
Q

Draw the synthesis pathway of T3 and T4 inside the thyroid follicle

A

Ok

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9
Q

What enzyme recycles Thyroglobulin and Iodine? What happens if this is deficient?

A

Intrathyroidal deiodinase. Deficiency mimics Iodine dietary deficiency.

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10
Q

If there is low Iodine available, what is the favored product of thyroid synthesis?

A

T3 (requires less iodine)

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11
Q

What transports Iodine into the lumen of the thyroid follicle?
What happens if there is a mutation in this transporter?

A

Pendrin (a chloride iodide pump). Mutation = hypothyroidism = goiter and hearing loss since cochlear pendrin is also mutated.

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12
Q

How does hypothyroidism cause goiter?

A

TSH keeps stimulating the thyroid trying to make it make thyroid hormones = hyperplasia

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13
Q

What is perchlorate and thiocyanate?

A

Anions that compete with iodine binding to transporter. Decreases synthesis of thyroid hormones

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14
Q

How does PTU disrupt thyroid hormone synthesis?

What effect does this cause?

A 
Disrupts peroxidase (which combines Iodine with TG)
Causes buildup of Iodine which inhibits further synthesis of hormoness (Wolff-Chalkoff effect)
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15
Q

How does radioactive iodine uptake relate to thyroid gland activity?

A 
Hyperthyroidism = more iodine uptake
Hypothyroidism = less iodine uptake
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16
Q

What are the main binding proteins for thyroid hormones in the bloodstream?

A

Thyroxine binding globulin (TBG, higher affinity for T4)
Transthyretin (in brain tissue)
Albumin (everything else)

All of these are formed in the liver

17
Q 
Predict the T4 and resin uptake in these conditions (remember the pattern)
Hyperthyroidism
Hypothyroidism
High TBG
Low TBG
Hepatic failure
Pregnancy
A

Ok

18
Q

Draw the HPT axis

A

OK

19
Q

What is the pathway of TSH action on the thyroid gland?

A

TSH > GPCR > Adenlyl Cyclase > cAMP > mediate lots of things that help with T3/T4 production as well as thyroid gland growth

20
Q

What is the mechanism of action of thyroid hormones?

A

-Act like steroid hormones (nuclear receptor)

21
Q

Functions of thyroid hormones:

A

Growth
Synapse plasticity
BMR increase
Increase in cardiac output and B-adrenergic receptors

22
Q

How exactly do thyroid hormones increase basal metabolic rate?

A

Thyroid hormone increases activity of Na/K ATPase leading to increase of O2 consumption and heat production]
Effect of T4 (thyroxine) is usually long lasting

23
Q

Effects of thyroid hormone on lipid metabolism:

A
  • Increase fat mobilization and FA oxidation
  • Blood cholesterol level inversely correlated with thyroid hormone levels
  • needed for carotene conversion to Vitamin A (eye problems and jaundice in hypothyroid patients)
24
Q

Describe the effect of thyroid hormones on cardiovascular system:

A

Thyroid > T4 > T3 > Na/K ATPase > increase tissue thermogenesis > decrease systemic vascular resistance > increase speed and force of cardiac contraction > increase cardiac output > increase blood volume

25
Q

Describe how thyroid hormones directly stimulate cardiac muscle:

A

Bind to B1 adrenergic receptors during sympathetic stimulation > increase in cardiac rate

26
Q

What are the other effects of thyroid hormones?

A 
Growth (working with growth hormone) 
CNS maturation (synaptic plasticity
27
Q

What happens to neurons when there is thyroid deficiency?

A

Abnormal development of synapse, decreased dendrites or myelination
If in prenatal period = congenital hypothyroidism

28
Q

What happens to TSH levels in primary hyperthyroidism?

How about ins secondary hyperthyroidism?

A

Lots of Thyroid hormones feedback and stop production of TSH

TSH levels are elevated since the defect is in the AP

29
Q

What causes grave’s disease?

A

Thyroid stimulating immunoglobulins act as agonist for TSH which causes release of thyroid hormones that feedback to TSH

30
Q

Symptoms of Grave’s disease:

A

Exophthalmos (eyeball protrusion) and periorbital edema

Elevated thyroid hormones, goiter. Presence of TSI in the blood (defining feature of Grave’s)

31
Q

What are the primary causes of hypothyroid?

A

Destruction of gland (as in Hashimoto’s thyroiditis)
Thyroid hormone synthesis inhibition
Agenesis of thyroid
Short term reasons (after surgery/postpartum etc.)

32
Q

How do you treat hypothyroidism?

A

Replacement doses of T4 (half life increases with age so younger patients need more doses)
Overprescribing T4 can lead to osteoporosis in menopausal women

33
Q

Hashimoto’s thyroiditis:
Cause
Clinical

A

-Thyroid gland defective even if I2 is sufficient
Caused by thyroglobulin or TPO antibodies which affects synthesis and secretion
-TSH levels are high because TSH keeps poking the thyroid gland to make hormones (trophic effect = goiter)

34
Q

Congenital hypothyroidism:
Cause
Clinical

A
  • Iodide deficiency or taking anti-thyroid meds during pregnancy leading to impaired development of thyroid gland
  • protruding tongue, curse facial features, growth and mental retardation, hypotonia and jaundice
35
Q

Iodide deficiency

A
  • No iodine = can’t make proper hormones

- TSH will be elevated since it keeps poking the thyroid gland to make hormones, can lead to goiter

36
Q

Sheehan syndrome:
Cause
Clinical

A
  • Necrosis of pituitary gland usually postpartum

- difficulties with lactation, no menses ( amenorrhea), hypothyroidism, other endocrine dysfunction also present

37
Q

Generally what are the symptoms of hyper and hypothyroidism?

A

Hyper: weight loss, sweating, rapid HR and high BP because there’s too much thyroid in the body and increases body functions
Hypo: weight gain, cold intolerance, fatigue because there’s too little thyroid in the body and decreases body functions

38
Q

Goiter development in hyperthyroidism:

A

TSH or something else stimulates/attacks the thyroid gland too much that it swells

39
Q

Goiter development in hypothyroidism:

A

I2 deficiency or thyroiditis (TSH pokes the thyroid gland too much in causes it to hypertrophy)

(OMS1) Neuro exam 3 (14 decks)

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