Lecture 6: Thyroid (Exam I) Flashcards
Where does thyroid hormone secretion start?
What is released?
- Hypothalamus
- The hypothalamus releases TRH (thyrotropin-releasing hormone).
What can trigger the hypothalamus to secrete TRH?
- ↑ stress
- ↓ temp
Describe the circulatory path from hypothalamus to thyroid (include pertinent released hormones).
Hypothalamus - TRH → portal system → anterior pituitary - TSH → general circulation → thyroid.
What occurs whenever TSH reaches the thyroid?
T₃ and T₄ production is stimulated.
What two things are necessary for thyroid hormone and precursor production?
- Iodine
- Tyrosine
What is the result of a single iodine molecule combined with a tyrosine base?
- Monoiodotyrosine (T₁)
What is the result of two iodine molecules combined with a tyrosine base?
- Di-iodotyrosine (T₂)
How is T₃ created? What is its proper name?
- Triiodothyronine (T₁ + T₂ = T₃)
How is T₄ created? What is its proper name?
- Thyroxine (T₂ + T₂ = T₄)
What structural difference separates a molecule with a -tyrosine suffix vs a -thyronine suffix?
- One benzene ring = -tyrosine
- Two benzene rings = -thyronine
What hormones are secreted from the adenohypophysis?
- TSH (thyroid-stimulating hormone)
- GH (growth hormone)
- LH (luteinizing hormone)
- FSH (follicle-stimulating hormone)
- Prolactin
- Corticotropin
What organ does FSH interact with?
- Ovaries
What organ does LH interact with?
- Ovaries
What organ does prolactin interact with?
- Mammary glands
What is the pathway for Corticotropin causing increased serum insulin levels?
Adenohypophysis - corticotropin → Adrenal cortex - ACH → increased glucose → pancreas increases insulin release.
Which thyroid hormone is more active intracellulary?
T₃
What percentage of T₃ vs T₄ is delivered to the tissue?
- T₃ = 15% of hormone delivered.
- T₄ = 85% of hormone delivered.
How do thyroid hormones affect mitochondria?
- T₃-T₄ increase the size and number of mitochondria.
How do thyroid hormones affect the Na⁺K⁺ATPase pump?
- ↑Thyroid hormones cause ↑ ICF Na⁺ = increased Na⁺K⁺ATPase activity.
Do thyroid hormone increase gluconeogenesis or glycolysis?
- Trick question. Thyroid hormones increase both gluconeogenesis and glycolysis.
_________ will convert T₄ to T₃ for intracellular use.
- Iodinase
How do thyroid hormones get into cells?
What happens when they are in the cell?
- Lipid diffusion
- Gene transcription causing upregulating of essentially all cellular activity.
What innervates the voicebox?
What are these branches of?
Why are they named the way they are?
- Right & Left Recurrent Pharyngeal Nerves
- Branches of the vagus nerve
- “Recurrent” due to looping characterstic. The right loops under the subclavian artery and the left loops under the aortic arch.
Where would an emergent cricothyrotomy be performed? Describe its location.
- A. Ligament immediately inferior to the thyroid cartilage.
What considerations should be given to the thyroid when performing an emergency airway?
- The thyroid might be in the way and is highly vascularized with arteries.
What is an increase in thyroid size called? What can occur from this?
- Goiter
- Increased pressure on the voicebox = hoarseness. Possible compression of tracheal rings in worst case scenarios.
What is the main source of dietary iodine intake?
How much iodine is needed per year?
- Iodized salt
- 50mg of Iodine needed per year. No single dose, need a steady consumption.
What is the rate-limiting step for thyroid precursor formation?
- H₂O₂ (Peroxidase)
I₂ → H₂O₂ → I + tyrosine = precursors.
What type of molecule are T₃ and T₄ ?
Why is this pertinent?
- Steroids
- Need transport proteins for circulatory movement and lipid solubility makes membrane diffusion easy.
What transport proteins carry thyroid hormones?
(list in order of importance)
- TRG (Thyroxine-binding globulin)
- Thyroxine-binding pre-albumin
- Albumin
Where are thyroid transport proteins created?
Why is this clinically relevant?
- Thyroid transport proteins are made in the liver and are subject to deficiencies from various liver pathologies (ex. cirrhosis)
Describe the process for thyroid hormone creation inside the thyroid itself as well as secretion.
- Thyroglobulin combines iodine + tyrosine to produce 60-70 T₃ & T₄ per thyroglobulin.
- Thyroglobulin is dissolved to secrete hormones.
When does T₄ effect peak when injected intravenously? Why?
- Lag time of ~ 10 days due to gene transcription MOA of T₃ & T₄
What two causes of hyperthyroidism were discussed in lecture?
- Primary Tumor
- Autoimmune (Graves disease)
What is the pathology of Graves disease?
- TSH receptors are stimulated via auto-antibodies thus eventually increasing T₃ and T₄.
What are the four generalized treatment options for hyperthyroidism?
- Surgery
- Radioactive Iodine
- Drugs
- Iodine Overdosing
What are the possible consequences of surgery for hyperthyroidism?
- Possible loss of ability to speak
- Possible bleeding
Why is radioactive iodine a good option for hyperthyroidism treatment?
- Selectively shrinks thyroid gland with no other tissues uptaking iodine.
What drugs are used to treat hyperthyroidism?
What should be known the MOA of each?
What is the general drawback of both?
- Thiocyanate - competitor for Iodine transporter
- Propothiouracil - Inhibits peroxidase
Both take 60 - 90 days to work.
What drugs are used to treat hyperthyroidism?
What should be known about the MOA of each?
What is the general drawback of both?
- Thiocyanate - competitor for Iodine transporter
- Propothiouracil - Inhibits peroxidase
Both take 60 - 90 days to work.
How would Iodine overdosing actually treat hyperthyroidism?
- Overwhelms Iodine oxidizing process (thus inhibiting formation of MIT, DIT, T₃, & T₄)
What what drug has a large amount of Iodine in it? How much?
Does this drug cause hypothyroidism or hyperthyroidism?
- Amiodarone (35% Iodine by mass)
- Both ↓THY & ↑THY are possible from excess Iodine.
What are four possible causes of hypothyroidism?
- Iodine deficiency
- Autoimmune disease (Hashimoto’s)
- Genetic mutations
- Idiopathic (5% of population)
What is Hashimoto’s disease?
What is the treatment?
- Autoimmune disease where antibodies attack thyroid tissue.
- Steroids & plasmapheresis
What is the clinical significance of hypothyroidism?
↓ NMJ excitability
- ↓ awareness
- longer wake times
- susceptibility to NMBs
What is the consequence of hypothyroidism for younger patients?
What is the treatment?
- Cretinism (stunted growth)
- Levothyroxine (difficult to dose & adhere to).
What are the general cardiac responses to increased thyroid hormone?
- ↑ HR
- ↑ SV
- No change in MAP
- ↑ PP
- ↓ cholesterol
- ↓ triglycerides
Why is there an increased pulse pressure when the body is exposed to increased thyroid hormones?
- ↑sBP & ↓dBP
- Occurs from peripheral vasodilation so nutrients can flow in and byproducts can flow out.
Why is cholesterol decreased in hyperthyroidism?
- Cholesterol gets used for energy and has increased GI excretion as well.
What are the general neuromuscular effects of hyperthyroidism?
- ↑ awareness & harder to put to sleep
- ↑ NMJ excitability = tremor
What symptoms would you expect to see from thyroid storm?
What does acute care involve?
- ↑HR, ↑Temp, ↑RR, etc.
- Supportive care (ex. cooling)
What disorder might be expected from these lab values:
- ↓ TSH
- ↓ TRH
- ↑ T₄
- Primary T₄ secreting tumor
What disorder might be expected from these lab values:
- ↑ TSH
- ↓ TRH
- ↑ T₄
- Primary TSH secreting tumor
What disorder might be expected from these lab values:
- ↓ TSH
- ↑ T₃
- ↑ T₄
- Grave’s Disease
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What disorder might be expected from these lab values:
- ↓ T₄
- ↑ TRH
- ↑ TSH
- Iodine deficiency
