Thyroid Flashcards
What is the chemical name for active form of thyroid hormone?
What is the chemical name for inactive form of thyroid hormone?
Liothyronine (T3)
Thyroxine (T4)
Why does the thyroid have such a substantial blood supply? [1]
Very substantial blood supply to trap as much Iodine as possible
Which side would you detect enlarged thyroid / graves disease in first? Why? [1]
Right side is larger
Branchial pouch embryology:
Pouch = endodermal outpouching of pharynx
Which pouch made the inferior parathryoid and thymus? [1]
Which pouch made the superior parathryoid and ultimobranchial body? [1]
Pouch 3 - inferior parathyroid and thymus
Pouch 4 - superior parathyroid and ultimobranchial body
Ultimobranchial body - C-cells
Where does the thryoid originate? [1]
What duct does it move down to get to perm position? [1]
Thyroid originates from foramen cecum
Travels along thyroglossal duct. to cricoid cartilage
Normally thyroglossal duct disappears but in some it can remain: contains thyroid tissue
= Colloid
Thyroid follicle cell:
What receptors does it contain and what do they transport?
MoA of how is T4 / T3 made/
NIS - Na/I symporter - transports 1 iodine with 2 Na+ into the cell.
PDS - transports iodine out of the cell into the colloid.
DUOX2 creates iodine oxidising agent: H2O2 outside of cell
TPO oxidises the iodine with H2O2. Allows it bind it to Tyroglobulin (is produced in the golgi apparatus of the cell and is iodonated)
Tyroglobulin is taken back into the follicular cell. Decomposed to produce T3 and T4 (~80%), which is released into the blood stream/colloid.
IYD - A means of recycling iodide – iodotyrosine dehalogenase 1
TSHR – receptor for thyroid stimulating hormone
What turns on the process of T3 / T4 being made? [1]
Explain the effects xx
TSH binding to TSHR
Causes cAMP
- to make NaI symporter: transports to cell membrane
- to make TPO and will transport to membrane
- increase thyroglobulin production from GA
- Activates PDS
- Activates DUOX2 for H202 production
- Iodinate thyroglobulin
- Iodinated thyroglobulin taken into cell –> T4 / T3
Explain feedback loop of thyroid hormone production
Control of thyroid function
- Classical feedback loop with hypothalamus and pituitary, modulated by additional neuropeptide
- Inverse relationship between the iodine level in the thyroid and the rate of hormone formation - large intraglandular stores of hormone buffers the effect of acute increases or decreases in hormone synthesis.
describe the -ve feedback loop of thyroid hormone production
-ve feedback loop:
- Hypothalamus releases TRH
- TRH stimulates release of TSH in AP
- TSH stimulates release of T4 / T3 from thyroid
- As T4 rises it suppresses TRH and TSH production
Where is T4 –> T3? [2]
Liver
Tissues themselves
How is T3 transported around the body? [3]
Predominately via Thyroid Binding Globulin
Also by albumin and transthyretin
Why are pregnant people in a hypothryoid state?
In pregnancy: the level of oestrogen increases:** increases sialylation of TBG** (increases the half life) so it is cleared slowly from plasma: less free thyroid hormone
T4 -> T3 (activation) of free TH:
What are the effect of Deiodinase enzymes:
D1 & D2? [1]
D3 [1]
Why is this important?
D1 & 2: convert T4 -> T3 - activation
D3: D3 -> inactivates T4 to rT3
Important because another level of control - expression of deiodonase enzymes:
these enzymes will be up/down regulated at certain times to increase/decrease metabolism.
- Learn *
What is main control of thyroid hormone? [1]
What are 3 ways body can locally control thyroid hormone? [3]
Main control:
* Main neg. feedback control. HPT axis.
Local control:
* Transporter expression MCT, OATP
* Deiodinase enzymes up/down reg
* Thyroid hormone receptor expression.
What happens to D2 in hypoT? [1]
D2 is upregulated:
T3 –> T4
What effects does hyperthyroidism have on cardiovascular system? [5]
Hyper metabolic state: need to dissipate the excess heat
TH increases α- to β- myosin ratio so positive inotropic effect
Increased NO: decreased peripheral resistance
Widened pulse pressure!
Palpitations are subjective increase in force or increased pulse
20% toxic patients have AF
Hyperthyroidism:
[] insulin turnover
[] gluconeogenesis
[] insulin secretion
Increased insulin turnover
Increased gluconeogenesis
Reduced insulin secretion
Hyperthyrodism:
Weight [] and []
Protein and lipid []
Heat []
Hyperthyrodism:
Weight loss and myopathy
Protein and lipid degradation
Heat intolerance
Hyperthyroidism:
Effect on Nervous System? [3]
Effect on skin [3]
Effect on eyes? [1]
Hyperthyroidism:
Effect on Nervous System? [3]
* Increased risk of seizures
* Nervousness/tremor.
* Hyperphagia - increased hunger
Effect on skin [3]
* Warm and moist - due to vasodilation + heat loss.
* ‘Plumber’s’ nails. Or soft and crumbling nails.
* Pretibial myxoedema inflammation over the tibia.
Effect on eyes? [1]
* Eyelid retraction and eyelid drag.
Hyperthyroidism
Effect on GI tract? [4]
Effect on bones? [3]
Haematological effect [2]
Effect on reproductive system [3]
Hyperthyroidism
Effect on GI tract? [4]
* Increased appetite
* Weight loss
* Increased gut motility
* Increased liver enzymes - transaminitis.
Effect on bones? [3]
* * Accelerated osteoclast activity - to provide substrates for metabolism.
* Hypercalcemia
* Osteoporosis - in the long term.
Haematological effect [2]
* Pernicious anaemia - coincidental, autoimmune.
* B12 deficiency.
Effect on reproductive system [2]
* Periods stop (oligomenorrhoea)
* Gynecomastia (man boobs)
* Erectile dysfunction.
What is Hashimoto’s disease caused by? [1]
What is the characteristics of it? [1]
TPO antibodys present
Autoimmune destruction of thyroid gland:
- transient hyperthyroidism as stores of TH are released.
- Then hypothyroidism follows.
What is pathophysiology of graves disease? [2]
Antibodies bind to and stimulate TSHR.
Causes hyperthyroidism.
Why does graves disease cause this symptom? [2]
- Fibrocytes behind the eye expresses TSH receptors
- TSHR stimulated, causing inflammation behind the eye -> pushes eyeball forward -> proptosis + lid retraction.
