GHM L8 Flashcards
sDescribe the anatomy of thyroid gland
Butterfly-shaped, bilateral
2 lobes joined by isthmus
Front of neck, around cartilages of larynx
DIAGRAM
Functional units of thyroid gland - Follicles
Follicles contain follicular cells - produce colloid
Colloid (gelatinous proteins) - made of thyroglobulin (Tg), precursor to thyroid hormones (T3 and T4)
Tg facilitates assembly of thyroid hormones
T4 - Thyroxine
T3 - Triiodothyronine
This happens in thyroid follicular lumen
In thyroglobulin, its the tyrosine molecule that becomes modified, tyrosine is modified into T3 and T4
State the function of C cells in the thyroid gland follicles
C cells secrete CALCITONIN
State the function of follicular cells
Secrete
Tg into colloid with IODINE
Describe the process of TSH stimulation
TSH secreted from anterioir pituitary
Stimulates thyroid gland to secrete T3 and T4 - bloodstream
(Follicular cells reabsorb iodinated Tg, degreade it, releasing T3 and T4)
State the functions of T3 and T4
- Homeostasis
-Cell differentation
-Growth
-Metabolism
Describe the process of iodine trapping
- Iodine from diet (e.g. spinach), travels through bloodstream in form an iodide ion (I-)
- I- accumulate in thyroid via active transport
- Na+ cotransported with iodide from basolateral membrane
- Concentrated in thyroid follicles
What stimulates iodine trapping ?
TSH
What region of the thyroid contains the most iodide ions?
FOLLICLE
State examples of iodine sources
- Cow’s milk
- DIARY PRODUCTS yoghurt etc
- Meat
Describe the function of TPO
TPO: thyroperoxidase
- TPO found outer-membrane of follicular cells
- Catalyses oxidation of I- by H2O2 (adds H2O2) to a reactive iodine intermediate
- This intermediate iodises tyrosine - (iodine added to tyrosine to form T3 and T4, t3 - 3 iodines, t4 - 4 iodines)
This whole process is controlled by TSH (upregulates TPO expression)
Where is thyroglobulin synthesised and secreted?
ER
Secreted in colloid by exocytosis
Describe the proteolysis of Tg with release of T3 and T4
T4 and T4 synthesised + stored within thyroglobulin
Protelysis of modifed thyroglubulin occurs
Modified thyroglublin (Tg) taken back into the folicular cell via endocytosis (phagacytosis), then undergoes proteolytic cleavage (proteolysis) to release + produce the mature T3 and T4 hormones which are then secreted into circulation
State the name of the transporter on the apical side of follilcular cell membrane
PENDRIN (I-/Cl-)
State the name of the transporter on the apical side of follilcular cell membrane
Na+/I- symporter
What stimulates endocytosis of iodinated Tg back into the cell?
Megalin binding to iodinated thyrogloblin
TSH
Which thyroid hormone is more abundant in the body?
T4
Where in the body is T4 produced?
ONLY THYROID Gland
State the 2 processes producing T3 in the body
80% produced from DE-IODINATION of T4 (peripheral tissues)
20% direct thyroid secretion (thyroid gland)
State 3 enzymes and locations which de-iodinate T4 into T3
Type I Enzyme: Thyroid, pituitary, liver, kidney - 80% MOST
Type II: CNS, pituitary, brown adipose tissue, heart
Type III: Placenta, CNS This deiodinase converts T4 into rT3 which is inactive
State the differences between hypothyrodism and hyperthyroidism
HYPOthyrodism
-Forgetfullness
-Moodiness
-Irratibility
-THINNING HAIR/HAIR LOSS
-WEIGHT GAIN
-DRY PATCHY SKIN
-HYPERLIPIDEMIA
-PUFFY EYES
-GOITER
-DEEPENING VOICE
-PERSISTANT DRY SORE THROAT
-BRADYCARDIA
-DIFFICULTY SWALLOWING
-INFERTILITY
-HEAVY PERIOID
HYPERthyroidism
-SUDDEN PARALYSIS
-sleepless
-BULGING EYES
-GOITER
-WARM MOST PALMS
-SWEATING
-MUSCLE FATIGUE
-TACHYCARDIA
-WEIGHT LOSS
-FREQUENT BOWEL MOVEMENT
-LIGHT PERIOD
-INFERTILITY
Describe 3 types of hypothyroidism
Primary: Thyroid destruction MOST COMMON
Secondary: Lesion to anterioir pituitary gland (tumour-CRANIOPHARYNGIOMA) therefore, deficient TSH secretionn + Congenital (less common)
TERTIARY (CENTRAL): Lesion (growth/tumour) of pituitary stalk + hypothalamus (which are above the level of pituitary), therefore, defisient TSH stimulation
(less common than secondary)
Primaty hypothyroidism
- Autoimmune disorder
-Autoimmune antibodies against thyroperoxidase (TPO)
-Less TPO
-More TSH to compensate, as TSH upregulates TPO, therefore, TSH high
Secondary hypothyroidism
Lesions compressing pituitary (adenoma, enuryssm carotid artery) leading to LOW TSH
Another cause: autoimmune
thalassemia = iron overlead
TB, SYPHILIS
TREATMENT:
-SURGERY
-RADIATION at Pituitary
Central / Tertiary Hypothyoidism
- Lesion to levels above anterioir pituitary including infundipular stalk + HYPOTHALAMUS
- Insuficient TSH
CAUSES:
- CONGENITAL
- IODINE DEFICIENCY IN PERGNANCY
TREATMENT:
DAILY DOSE OF THYROXINE
Describe the causes of hyperthyroidism
- Grave’s Disease - aka toxic diffuse goiter
-Autoimmune
-Antibodies bind to + activate TSH receptor
-more TSH, more TPO upregulated, more T3 and T4
Describe characteristics of hyperthyroidism Grave’s disease
EXOPTHALMOS - popping / bulging eyes
WHY?
Autoimmune inflammation of periorbital connective tissue + extraocular muscles
TREATMENT:
Radioidine, surgery, antithyroid drugs
State examples of drugs that increase TBG
Oral contraceptives (sources of oestrogen)
METHADONE (ANALGESIC)
Clofibrate (reduces cholestrol)
5-flurobacil (cancer)
HEROIN
Tamoxifen (BREAST CANCER)
Give examples of conditions which increase TBG
- Pregnancy
- Infectious / chronic active hepatitis
- HIV infection
- Billary cirrhosis
- Acute intermittent porphyria
- Genetic factors
State the effect of drugs and conditions decreasing and increasing TBG
Increase in TBG: Increase T4 and T3 Levels
Decrease in TBG: Decrease T4 and T3 levels
State examples of drugs that decrease TBG
- Glucocorticoids
- Androgens
- L-asparaginase
- Salicylates
- Mefenamic acid (anti-inflammatory)
- Antiseizure medications
- Furosemide
State examples of conditions that decrease TBG
- Genetic factors
-Acute + chronic ilness
Give an adaptation of the thyroid gland to its function of hormone production
RICH BLOOD SUPPLY
Why is T3 more active than T4?
T4 pro-hormone for T3
(precursor)
T4 less active than T3
Has reduced of the affinity for nuclear receptor than T3
State the enzyme used to convert T4 into T3
Monodeiodinase (5’ deiodination)
Describe how T4 and T3 play a major role in growth and development
Increase protein sytnthesis
Increases ATP synthesis
Increases O2 utilisation
Increases heat production
Increases fat metabolism (therefore, decreases fat store)
-Essental for NORMAL BRAIN DEVELOPMENT
Describe how T4 and T3 play a major role in growth and development
Increase protein sytnthesis
Increases ATP synthesis
Increases O2 utilisation
Increases heat production
Increases fat metabolism (therefore, decreases fat store)
-Essental for NORMAL BRAIN DEVELOPMENT
Describe how thyroid hormone is essential for childhood growth
-Increases protein synthesis, ATP synthesis, O2 utilsation, fat metabolism, normal brain development
Describe the severity of untreated congenital hypothyroidism
aka chronic hypothyrodism
- incomplete development
-mental retardation
Describe how thyroid hormone stimulates protein synthesis
Thyroid hormone binds to nuclear receptors
This modulates gene transcription
Stimulates protein formation
Give common symptoms between hypothyrodism and hyperthyroidism
- Infertility
- Goiter
Describe the metabolic effects of T3
Stimulates lipolysis - release of free fatty acids, glyceol
Stimulates metabolism of cholestrol to bile acids and rapid removal of cholestrol from plasma
Stimulates protein degradation
Converts Carotene to Vit A
Describe the location of the parathyroid glands
- 4 small glands
-Posterior surface of thyroid, also can be in chest
-Upper pair - superioir parathyroid gland
-Lower pair - inferioir parathyroid gland
State two tyes of cells present in parathyroid gland
- Chief cells -
- Oxyphil cells - larger, stain differently, derivede from chiefc cells, INCREASE IN NUMBER WITH AGE, embedded in MATRIX or STOMA
- Adipose cells (if adipose cells present, person older as adipose cells appear with age)
- Lots of blood capillaries
State where parathyroid hormone is produced
Chief cells in parathyroid gland
PTH
