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Endo/Eye/Derm - Women/Men > EXAM 3 Thyroid and Antithyroid drugs Dr. Pond > Flashcards

EXAM 3 Thyroid and Antithyroid drugs Dr. Pond Flashcards

1
Q

What are the cells of thyroid glands called?

A

Follicle cells
-> secrete thyroid hormones

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2
Q

What is the lumen of follicle cells of thyroid glands filled with?

A

Colloid

Thyroglobulin -> precursor for thyroid hormones

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3
Q

What is a function of Colloids?

A

Precursor for thyroid hormones

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4
Q

What are the cells that lie in between follicle cells?

A

Parafollicle cells or extra-follicle cells

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5
Q

What is the function of Parafollicle cells?

A

Calcitonin secretion

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6
Q

What is the function of Calcitonin?

A

it inhibits osteoclastic bone resorption
-> decrease in Ca2+ and phosphate

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7
Q

What are the thyroid hormones?

A

Thyroxine = T4 (4 iodines)

Triiodothyronine = T3 (3 iodines)

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8
Q

Which protein binds to thyroid hormones in the blood?

A

Thyroxine binding globulin (TBG)

Thyroid hormones are lipophilic and dont like to stay in the blood unbound

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9
Q

Thyroid hormones are derived from which amino acid?

A

Tyrosine

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10
Q

How is iodide from the bloodstream taken up by follicular cells?

A

Iodide trap

Na+-iodide co-transporter: Na+ comes in towards its gradient and iodide comes with it against its gradient (so Na+ carries iodide along)

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11
Q

What happens to iodide after uptake into follicular cells?

A

Oxidation
-> it loses an electron: from iodide (-I) to iodine (I)

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12
Q

What happens to iodine in the Colloid?

A

it will bind to tyrosine residues if Thyrosine globulines

IODINATION

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13
Q

How do iodide levels affect thyroid hormone levels?

A

low level of iodide -> decrease in T3 and T4 (since iodide is needed for synthesis)

high level of iodide -> may inhibit the synthesis and release of thyroid hormones (negative feedback)

-> we don’t want too level or too high levels od iodide

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14
Q

Which stages of thyroid hormone synthesis are affected by high concentrations of iodide?

A

Iodination of Thyroid globulins (tyrosine residues)

Proteolysis of thyrosinglobulins in lysosomes

-> inhibition due to negative feedback

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15
Q

What happens after iodine binds to thyroid globulins?

A

tyrosine residues of the thyroids couple in thyrosind globulins and are stored that way -> until the signal (TSH) for the need for thyroid hormones occur

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16
Q

What is the signal that causes Pinocytosis (uptake of thyroid globulin cells into follicular cells)?

A

TSH binding to receptor cells on the thyroid glands
-> the need for thyroid hormone synthesis

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17
Q

What happens when the signal for the need for thyroid hormones occurs?

A

Thyroid globulins are taken up follicular cells and fused with lysosomes (contain proteases) to phagolysosomes

-> proteases cut all the other amino acids within the thyroid globulins -> and the thyroid hormones with the coupled tyrosine bonds stay intact
-> release into the bloodstream

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18
Q

Hypothalamus-Pituitary-Thyroid-Axis

A

Hypothalamus -> releases TRH (thyroid releasing hormone)

TRH binds to the anteroir pituitary gland -> leading to release of TSH (thyroid stimulating hormone)

TSH binds to thyroid glands -> release in thyroid hormones (T4 and T3)

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19
Q

What are factors that increase thyroid hormone release?

A

-acute psychosis
-cold
-circadian and pulsatile rhytms

-high TRH, high TSH

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20
Q

What are factors that decrease thyroid hormone release?

A

-severe stress
-corticoids (like cortisol) or dopamine

-high levels of T3 and T4 (negative feedback)

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21
Q

What is the ultimate function of thyroid hormones?
MOA

A

regulation of gene transcription
-> by binding to nuclear receptors (thyroid receptor) on the DNA

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22
Q

What happens to T4 once it enters the cell?

A

Deiodination of the outer ring (thyroxin T4 to Triiodothyronine T3)

by 5´DI: 5´deiodinase !!!

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23
Q

What is the state of the thyroid receptor before T3 binds?

A

bound to another thyroid hormone receptor (homodimer) and a corepressor
-> INACTIVATED

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24
Q

What is the state of the thyroid receptor after T3 binds?

A

the second thyroid hormone receptor leaves -> the corepressor leaves

the retinoid X receptor binds to the first thyroid hormone receptor (heterodimer) -> Coactivator binds to the first thyroid hormone receptor

-> ACTIVATION

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25
Which region of the DNA are thyroid receptors bound to?
TRE thyroid response elements (regulatory sequences) when T3 binds to the receptor, the receptor changes its conformation -> Co-activator binds
26
What is the recommended daily uptake of iodide?
150 μg 75 μg is used daily for hormone synthesis, the rest is excreted
27
What is considered the reverse T3?
during deiodination, the iodide is removed from the wrong ring (inner ring) -> this compound is inactive
28
Which of the thyroid hormones is produced in higher amounts?
T4 with 75 mcg VS T3 with 25 mcg
29
Which of the thyroids is preferred in therapy?
T4 -> due to its longer half-life (7 days; 1 day for T3) -> it is the natural way of metabolism when using T4 and let the boy convert it to T3
30
Which drugs may affect the metabolism of T4 and T3?
-CYP 3A4 inhibitors like phenobarbital, phenytoin -> increase their metabolism -> decreases level -> not an an issue in euthyroid patients bc healthy thyroid can compensate for the defecit
31
How do thyroid hormones affect anticoagualtion therapy?
in hyperthyroidism -> lower dose of warfarin in hypothyroidism -> higher dose of warfarin
32
What are the 2 forms of T3 receptors?
alpha and beta -depending on the expression pattern and the tissue and can have different responses to thyroid hormones
33
What is the overall effect of thyroid hormones in the body?
many different metabolic effects -> overall an increase in basometabolic rate (BMR) -> stimulates calorigenes, increased breakdown of energy -> stimulates growth hormones -> growth in children (children with hypothyroidism don't grow well) -> regulates the effects of the nervous system and the heart to catecholamines (NE, epinephrine, dopamine) increasing the number of adrenergic receptors on the heart -> development of the nervous system -> hypothyroidism in children may lead to learning defects and mental retardation
34
What is the permissive effect of thyroid hormones?
Hormone A is required for hormone B to have its maximum effect the thyroid hormones will increase the effect of adrenergic receptors in the heart and in the nervous system -> mimicking sympathetic effects of the NS (sympathomimetic)
35
What is the BBW for thyroid hormones?
they should not be used solely or with other agents for weight loss
36
Patient presentation in Hypothyroidism
-Myxedema (puffiness) -cold (due to low heat predection) -dry skin/hair -weight gain (metabolic rate is low) -lethargy -slowed mental processes - in adults -mental retardation - in children -cretinism in children (severe physical and mental retardation) -infertility, impotence -arrhythmias, bradycardia, decreased SV and CO -> due to decreased number of adrenergic receptors in the heart
37
What is the most common cause of Hypothyroidism?
Hashimito's disease -> autoimmune destruction of thyroids 5x more come in women
38
When might Hashimoto's disease present in women?
occasionally occurs during or after pregnancy
39
What is a Goiter and when does it present in patients?
-enlargement of the thyroids -seen early in Hashimoto's disease bc of the inflammation that is going on during the autoimmune destruction -absent later, as the thyroid is destroyed -degree of hypothyroidism might be mild to severe
40
Treatment of Hypothyroidism
supplementation -Levothyroxine (Synthroid): I-isomer of thyroxine T4 -> long half-life (7days), converted to T3 intracellular -Liothyronine (T3): 3-4x more potent, but short hafl-life (24h) -> more expensive -> greater risk fo cardiotoxicity -> more difficult to monitor in lab
41
Which drug contains T4 and T3?
Liotrix (thyroxine T4 and liothyronine T3) -> expensive
42
Which thyroid hormone drug is of animal origin?
Desiccated thyroid ->more unstable -> variable hormone concentration -> may be seen in older patients who had been using it for a long time and didn't switch
43
Not enough VS too much thyroids
Not enough: -constipation -cold intolerance -weight gain -fatigue, lethargy -impaired intellectual performance or other mental status changes (e.g., depression) -bradycardia Too much: diarrhea heat intolerance/sweating weight loss hyperactivity, tremor, insomnia emotional lability, irritability & anxiety tachycardi
44
Patient presentation of Hyperthyroidism
-Exophthalmos: increased pressure behind the eyes, bulding eyes -tachycardia (sympathomimetic effect) -Hot (high metabolism) -lose weight -decreased fertility -menstrual irregularities
45
What is the most common cause of Hyperthyroidism?
Graves disease -autoimmune disorder -more often in women -occasionally during or after pregnancy
46
What are the symptoms of Grave's disease?
-bulding eyes -Goiter (diffuse toxic goiter - historically bc patients had enlarged thyroid and were feverish) -> Grave's disease is also called thyrotoxicosis -10x more in women
47
How is Grave's disease different from Hashimoto's disease?
in Graves's disease the body produces TSI (thyroid stimualting immunoglobulin) -> that binds to TSH receptors but stiumlates the thyroid longer and stronger than TSH -> overproduction of thyroid -> in Hashimoto's disease the thyroid gets destroyed immune cells
48
How would the levels of T4, T3 and TSH look like in Grave's disease?
-high T4 and T3 -> overproduction stimulated by TSI -low TSH -> negative feedback
49
How are the symptoms of Exophthalmos (bulging eyes) explained?
TSI binds to TSH receptors in tissue behind the eyes and causes inflammation and swelling
50
Which drug is used to treat Exophthalmos? (don't need to know)
teprotumumab-trbw (Tepezza) -blocks IGF-1 receptor on the tissue behind the eye
51
Treatment approaches for Hyperthyroidism
-agents that interfere with the production of thyroid hormones -agents that interfere with the release of thyroid hormones -Glandular destruction with radiation or surgery
52
Which drug is used for Hyperthyroidsim?
Thioamides -Propylthiouracil (PPT) -methimazole -most useful in young patients with mild disease -> remission of 12-18 months -> 70-80% incidence of relapse
53
MOA of Propylthiouracil (PPT) and methimazole
-inhibit oxidation (catalyzed by peroxidase) of iodide to iodine -inhibit Iodination of tyrosine residues of thyroid gloublins -slow onset, since the synthesis is targeted -> so it will still release what is there until it works
54
Why is there a slow onset when using thioamides?
because the colloids have thyroid globulins stored -> the actual effect is seen after the the remaining thyroid is depleted -> onset of 3-4 weeks
55
Toxicites of Thioamides
-GI and nausea -Rash (maybe with fever) -Agranulocytosis: rare, but potentially fatal (higher risk with high doses in elderly) for Methimazole: -altered sense of taste/smell -cholestatic jaundice (can be fatal) for propylthiouracil PPT: -Hepatitis
56
Kinectics of Thioamides
-not predictable in regards to half-life since they accumulate in the thyroid -PPT has a half-life of 1.5 hr but is given q6-8h -methimazole has a half-life of 6hr and can be given once daily -it may cross the placenta and concentrate in the fetal thyroid -> CAUTION in pregnant (since they occasionally suffer from hyperthyroidism during or after pregnancy)
57
Which molecule may be used as a drug for hyperthyroidism?
Iodide -it inhibtis iodination of thyroid globulins -it inhibits proteolysis of thyroid globulins -> no release of thyroid hormones
58
What is the time of onset when using Iodides?
2-7 days (faster than with thioamides) -> because the release is inhibited -but it is only a temporary effect
59
What is the role of Iodide in therapy?
-used acutely and temporarily, maybe in the meantime of scheduling surgery -has a disadvantage: it increases iodine storage which delays the therapy with thioamide, also prevents the use of radioactive iodine therapy for several weeks -cross the placenta and cause fetal goiter
60
Iodide ADE
ADEs are uncommon -rash -swollen salivary glands, mucous membrane ulcerations -conjunctivitis -runny nose -bleeding disorder
61
Which isoform of radioactive iodine is used for treatment?
I-131 -other ones are only used for imaging
62
How does radioactive iodine work in hyperthyroidism?
-Emits β rays -range: 400-2000 μm -half-life of 5 days -Destroys thyroid: epithelial swelling and necrosis, follicular disruption, edema, leukocyte infiltration
63
Advantages and disadvantages of I-131
advantage: easy, effective, cheap, relatively pain-free disadavatnage: -the parathyroid may be affected -patients have a fear of radioactive agents -it crosses the placenta and is excreted in breast milk -> affects fetal thyroid
64
What must be done after surgery or radioactive-induced thyroid destruction?
thyroid supplementation -Levothyroxine (Synthroid) - T4 -Liothyronine T3

Endo/Eye/Derm - Women/Men (30 decks)

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