Thyroid Physiology and Anatomy Flashcards
Thyroid Gland
Largest endocrine gland
Only endocrine gland which is superficial and allows palpation
Requires substances from the environment to synthesise hormone
Thyroid gland embryology
4th week of human embryogenesis
- Midline thickening at back of the tongue and stretches downwards
- Migrates in front of larynx and comes into close proximity with parathyroid glands
- Comes into contact with cells from lower part of the pharynx (become C-cells - produce calcitonin)
End of 2nd month
- 2 lobes joint at isthmus in front of trachea
- Thyroglossal duct loses contact (does not occur in 15% of population0
Week 12
- Primitive follicles become visible as simple epithelium surrounding central lumen
Thyroid Gland point of origin remnant
Point of origin in tongue persists as foramen caecum
Failure of development
Congenital hypothyroidism
Under or over migration
Lingual or retrosternal thyroid
Failure of thyroglossal duct to recess
thyroglossal cyst
Thyroid gland vertebral levels
C5, C6, C7 and T1
Secretions of. thyroid gland tissues
Thyroxine (T4)
Tri- iodothyronine (T3)
Calcitonin
parathyroid gland secretions
4 parathyroid glands
Secrete parathyroid hormone (PTH)
Thyroid gland shape
‘butterfly shape’
Thyroid gland innervation
Autonomic nerve supply
Parasympathetic
- vagus nerves
Sympathetic
- superior, middle and inferior ganglia of sympathetic trunk
Thyroid gland blood supply
Superior and inferior thyroid arteries
- branch of external carotid
Thyroid gland venous drainage
Superior/ middle thyroid vein
- drains to internal jugular
inferior thyroid vein
- drains to brachiocephalic vein
Thyroid gland support
Supported by ligaments and strap muscles
Posteromedial aspect of the gland is attached by posterior suspensory ligament (Berry ligament)
basic function unit of thyroid gland
Follicle
- colloid surrounded by follicular cells
- parafollicular cells
Richly vascularised and innervated
Control of thyroid gland
Controlled by negative feedback loop
Thyroid is controlled by TSH from the pituitary gland. (in turn regulated by TRH from hypothalamus)
T3 predominantly completes the. negative feedback loop by suppressing the production of TSH and TRH
Underactive thyroid
High TSH as compensatory
Thyroid Hormone Synthesis (6)
- Thyroglobulin synthesis (thyroxine rich protein- exclusively made by follicular cells)
- Uptake and concentration of iodide
- Oxidation of iodide to iodine.
- Iodination of thyroglobulin
- Formation of MIT and DIT
- Secretion
Synthesis and storage of T3 and T4 (4)
- Iodine taken up by follicle cells
- Iodine attached to tyrosine residues on thyroglobulin to form MIT and DIT
- Coupling of
MIT + DIT =T3
DIT + DIT = T4 - Stored in colloid thyroglobulin till required
Effect on carbimazole and Propylthiouracil on synthesis and storage of T3 and T4
Step 3 can be inhibited:
Iodine unable to attach to tyrosine residues on thyroglobulin - No formation of MIT and DIT
Used to treat hyperthyroidism
Thyroid Hormone- T4
Thyroxine
90% of thyroid hormones secreted
Converted to T3 by liver and kidney
Not biologically active
Thyroid Hormone - T3
Tri-iodothyronine
10% of thyroid hormones secreted
Major biologically active thyroid hormone
Thyroid hormone transport
Bound to serum proteins
- thyroxine binding globulin (TBG)
- Thyroxine binding pre-albumin (TBPA)
- Albumin
Only unbound hormones can enter cells
Thyroid binding globulin (TBG)
T4 and T3 are almost entirely bound by plasma proteins
T3 has a more rapid onset and offset of actions as its less avidly bound
Only free/unbound hormone is available to tissues
Metabolic state correlates more freely with the total concentration in the plasma
Concentration of total hormone does not necessarily vary directly with that of free hormones .
Increased TBG
aetiology
Increases total T4 (but not free T4)
Pregnancy Newborn state OCP and other sources. of oestrogen Hepatitis A Chronic active hepatitis Biliary cirrhosis Acute intermittent porphyria Genetics Clofibrate Heroin
Decreased TBG
aetiology
Decreases total T4 (but not free T4)
Androgens Karge doses of glucocorticoids Cushing Syndrome Active acromegaly Severe systemic illness Chronic liver disease nephrotic syndrome Genetics Pheytoin Carbamzepine
Effects of Thyroid Hormone (all cells, especially neurons)
Increased metabolic rate
Increased glucose uptake
Effect of thyroid hormone on liver tissue
Increased glycogenolysis and gluconeogenesis
Decreased glycogenesis
Effect of thyroid hormone on adipose connective tissue.
Increased lipolysis
Decreased lipogenesis
Effect of thyroid hormone on lungs
Increased breathing rate
- Helps meet increased O2 demand for aerobic cellular respiration
Effect of thyroid hormone on heart
Increased heart rate
Increased force of contraction
Helps meet increased O2 demand for aerobic cellular respiration
thyroid hormone physiological effect
target virtually every tissue
Occurs throughout life to alter. gene transcription and protein synthesis
Profound effects on
- metabolism
- growth
- developement
- reproduction
- behaviours
Thyroid Hormone Effect: Metabolic rate
Increases metabolic rate
increase number and size of mitochondria
Increases oxygen use and rates of ATP hydrolysis
Increase synthesis of respiratory chain enzymes
Thyroid Hormone: Thermogenesis
Increases thermogenesis
~ 30 % of temperature regulation due to thyroid hormone thermogenesis
Thyroid Hormone: Carbohydrate metabolism
Increases blood glucose
- stimulation of glycogenolysis and gluconeogenesis
Increased insulin dependent glucose uptake into cells
Thyroid Hormone: Lipid metabolism
Mobilise fats from adipose tissue
Increases fatty acid oxidation in tissues
Thyroid Hormone; Protein Metabolism
Increases protein synthesis
Thyroid Hormone: Growth and Development
Growth Hormone releasing hormone (GHRH) production and secretion requires thyroid hormones
Glucocorticoid-induced GHRH release also dependent on thyroid hormones
GH / Somatomedins require presence of thyroid hormone for activity
Thyroid hormone: development of foetal and neonatal brain
Myelinogenesisi and axonal growth require thyroid hormone
Thyroid Hormone: CNS activity
Hypothyroidism: Slow intellectual functions
Hyperthyroidism: nervousness, hyperkinesis and emotional liability
Thyroid Hormones Permissive Sympathomimetic Action
Thyroid hormones increase responsiveness to adrenaline and sympathetic NS neurotransmitter, noradrenaline, by increasing number of receptors
CV responsiveness also increased due to this affect
- increase force and rate of contraction
use of beta-blocker in hyperthyroidism
Need to use beta-blocker (egg, propranolol) to treat symptoms in initial stages if therapy for hyperthyroidism,
De-iodinase Type 1
D1
Found in liver and kidney
De-iodinase type 2
D2
Found in heart, skeletal muscle, CNS, fat, thyroid and pituitary
De-iodinase type 3
D3
Found in foetal tissue, placenta and brain (except pituitary)
Degradation of thyroid hormones
Thyroid produces T4 and T3 which enter circulation and peripheral tissues
T4
- 15% go to minor degradative pathways
- 45% converted by D3 into inactive reverse T3 and then rapidly excreted
- 40% converted by D1 into T3
T3
- can become biologically active
- converted to Inactive T2 by D3
In the brain and pituitary thyrotroph
- T4 converted to T3 by D2. T3 then contributes to negative feedback on TRH and TSH
Hypothyroidism
Deficiency of thyroid hormones
Hypothyroidism aetiology
Primary (gland) failure
- may be associated with goitre
Secondary to TRH or TSH
- no goitre
lack of iodine in diet
Hypothyroidism symptoms
Reduced BMR Slow pulse rate Fatigue, lethargy. slow response times and mental sluggishness Cold-intolerance Tendency to put on weight easily
In adults
-myxoedema
babies
- Cretinism (dwarfism and limited mental functioning)
Hyperthyroidism Aetiology
Graves Disease
Toxic adenoma
Toxic nodule in MNG
Graves disease
Autoimmune
- TSH receptor antibodies act like TSH but are unchecked by T3 and T4
Exopthalmos (bulging eyes)
Goitre
Hyperthyroidism symptoms
Increased BMR Very fast pulse rate Increased nervousness and excessively emotional Insomnia Sweating and heat intolerance Tendency to lose weight easily
