Thyroid Flashcards

(40 cards)

1
Q

Which statement aligns best with how many people are unaware of their thyroid issues?

A

About 60% are unaware.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which stats most accurately reflect the prevalence worldwide of thyroid disorders?

A

Approximately 10% of the global population.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Graves’ disease comprises 60–80% of hyperthyroidism, yet about half relapse within 1 year after anti-thyroid meds. This suggests what major failing?

A

Treating symptoms not root cause—autoimmunity isn’t addressed; over-reliance on medication alone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

True or False: Women have about three times higher incidence of thyroid cancer than men, with a 283% rise from 1990 to 2013.

A

ture!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

A male 65-year-old has a ~1 cm nodule. What percentage of the population has a thyroid nodule by age 60?

A

About 50%.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why is TSH alone insufficient?

A

It misses FT4/FT3 status; doesn’t detect autoimmunity; pituitary D2 can mask tissue hypothyroid; wide ranges delay care; misses conversion/clearance issues.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which statement about iodine and hypothyroidism is correct?

A

In Hashimoto’s (≈90% of hypothyroid), iodine can worsen disease;

goitrogens may help by lowering iodine uptake.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

A coach prescribes bioidentical T3 without checking deiodinase or hormone fluctuations. Which error is this?

A

Premature T3 replacement without assessing conversion/regulation; ignoring potential fluctuating hypo/hyper.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Thyroid hormones elicit which metabolic activities?

A

Increase BMR/thermogenesis;

regulate lipid and glucose metabolism;

increase cardiac output/HR; support GI motility;

influence mood/cognition;

support growth/bone maturation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

True or False: T4 is a pro-hormone with ~1-week half-life; T3 is more active with a shorter half-life. A:

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

An elevation in parathyroid hormone might be suspected if?

A

Low vitamin D;
low calcium or malabsorption; CKD/secondary hyperparathyroidism;
bone loss.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

TRH has which effects beyond initiating TSH release? A:

A

Stimulates prolactin; CNS effects including arousal/thermoregulation; impacts autonomic tone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

A 28-year-old TSH 1.9 mIU/L at 4pm, no T4/T3. Why might this be inaccurate for subclinical hypothyroidism? A:

A

Afternoon draw and fed state can lower TSH; missing FT4/FT3 prevents identification.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

A 35-year-old male has minimal TSH, normal FT4/FT3, no antibodies, no meds. Best explanation?

A

A: Physiologic low pituitary set point/central adaptation with euthyroid hormones.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

True or False: TSH 1.72 vs 1.01 is associated with higher miscarriage risk. A:

A

True.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

In terms of thyroid hormone output, what percentage is typically T4?

A

A: About 80–90% (roughly 90% T4, 10% T3).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

A 61-year-old with “subclinical low T3,” normal TSH/T4, chronic inflammation. Where to suspect issues?

A

A: Peripheral conversion—deiodinase dysfunction (reduced D1, increased rT3 pathway).

18
Q

How much more metabolically potent is T3 compared to T4?

A

A: Approximately 3–4 times.

19
Q

giver overview of thyroglobulin

A

Follicular storage protein for thyroid hormones; source of T3/T4 when proteolyzed;

TgAb indicates autoimmunity and can interfere with Tg assays;

Tg can rise with tissue destruction or cancer (context-dependent

20
Q

Which two major anti-thyroid antibodies are clinically tested most often

A

A: Anti–thyroid peroxidase (TPO) and anti–thyroglobulin (TgAb).

21
Q

A 46-year-old female has elevated TPO but no hypothyroid signs. Why?

A

A: Euthyroid autoimmunity phase; antibodies can precede dysfunction for years; influenced by iodine/postpartum/immune shifts.

22
Q

Why might a female on the oral contraceptive pill have lowered thyroid function?

A

A: Estrogen increases TBG lowering free T4/T3;
altered hepatic binding/clearance;
potential micronutrient effects on conversion.

23
Q

Which deiodinase is critical for T4→T3 in liver/kidneys and can contribute to rT3 dynamics under stress?

A

A: Type 1 deiodinase (D1): main T4→T3 in liver/kidney; under stress D1 drops while D3 inactivates T4→rT3.

24
Q

Type 3 deiodinase does what?

A

A: Inactivates thyroid hormones: T4→rT3 and T3→T2.

25
how many years can TPO and thyroglobulin antibodies appear before clinical thyroid dysfunction?
up to 7 years
26
- A large glycoprotein made by thyroid follicular cells. - Acts as the scaffold and storage matrix for thyroid hormone production inside the follicle colloid. functions: iodination platform, coupling site (to form T4), storage resoevoir (iodinated TGP stored in cooled until TSH signals release of T4/T3)
27
give overview of try
- Triggers pituitary TSH; also stimulates prolactin; CNS effects on arousal/mood. - in hypothalamus - Stress, pregnancy, and low thyroid hormones modulate TRH.
28
overview of TSH (Thyroid-Stimulating Hormone)
- Source: Anterior pituitary. Role: Master switch—upregulates iodine uptake, thyroglobulin, TPO, and release of T4/T3. Clinical note: Pituitary D2 can normalize TSH even when peripheral tissues are low in T3.
29
overview of T4 (Thyroxine)
Source: Thyroid follicular cells; ~80–90% of output. Role: Pro-hormone reservoir; long half-life (~6–7 days); converted to T3 in tissues. Clinical note: Free T4 (FT4) is the actionable marker; low-normal FT4 links to anemia, metabolic syndrome, depression risk.
30
overview of T3 (Triiodothyronine)
Source: 10–20% from thyroid; majority from peripheral conversion of T4. Role: Active hormone (3–4× potency of T4); regulates BMR, thermogenesis, cardiac output, mood, cognition, bone, GI motility. Clinical note: FT3 reflects tissue availability; drops with inflammation, calorie deficit, selenium/iron/zinc deficits.
31
overview of rT3
Source: Inactive product from T4 via D3 (and reduced clearance when D1 is low). Role: Inactive brake; rises with stress, illness, inflammation, calorie restriction. Clinical note: High rT3 pattern suggests conversion bottleneck and stress physiology.
32
overview of D1
Liver/kidney; converts T4→T3; clears rT3. Suppressed by inflammation/illness.
33
overview of D2
Brain, pituitary, brown fat, muscle; local T4→T3 to maintain central sensitivity (can mask low peripheral T3).
34
overview of d3
D3: Placenta, brain, inflamed tissues; inactivates T4→rT3 and T3→T2.
35
overview of TPO (Thyroid Peroxidase)
Role: Iodide oxidation, iodination of thyroglobulin (MIT/DIT), coupling to form T3/T4. Clinical note: Major autoantigen in Hashimoto’s; TPO Ab often precedes dysfunction.
36
overview of Thyroxine-Binding Globulin (TBG)
Role: Transport proteins; ~99.5% of thyroid hormone is bound. Clinical note: Estrogens (e.g., OCP) raise TBG → lower free fractions; androgens/glucocorticoids lower TBG.
37
overview of Calcitonin
(from C cells) Role: Lowers blood calcium (inhibits osteoclasts; increases renal excretion). Clinical note: Marker for medullary thyroid carcinoma (context-dependent).
38
overview of Parathyroid Hormone (PTH)
[adjacent system] Role: Raises blood calcium; increases renal Ca reabsorption; activates vitamin D; stimulates bone resorption. Clinical note: Elevated in vitamin D deficiency, CKD, calcium malabsorption.
39
overview of Iodine
Role: Essential substrate (T4 has 4 iodine atoms, T3 has 3). Clinical note: Excess iodine can worsen Hashimoto’s; deficiency causes hypothyroid/goiter; balance with selenium.
40
overview of cofactors required for thyroid hormones
Selenium, Iron, Zinc (key cofactors) Selenium: Required for deiodinases (T4→T3). Iron: Needed for TPO activity. Zinc: Supports conversion and receptor function.