The Thyroid Gland Flashcards
Structure of Thyroid Gland + Its Cells
CONTAINS 2 CELL TYPES:
1. CLEAR CELLS = secrete calcitonin 2. FOLLICULAR CELLS = support TH synthesis & surround hollow follicles
THYROID FOLLICLES:
* SPHERICAL STRUCTURES * WALLS MADE OF FOLLICULAR CELLS * FILLED W/ COLLOID = STICKY GLYCOPROTEIN MATRIX • CONTAIN 2-3 MONTHS SUPPLY OF TH
Production of Thyroid Hormones (how is iodine taken up & how is thyroglobulin transported to colloid + what happens in the colloid + how are thyroid hormones then secreted)
Iodine taken up:
1. IODIDE ENTERS FOLLICULAR CELLS via NA+/I- TRANSPORTER (symport) (Na+ coupling allows iodide to enter against conc. gradient) 2. FOLLICULAR CELLS ACTIVELY CONCENTRATE IODIDE 3. IODIDE then TRANSPORTED INTO COLLOID via PENDRIN TRANSPORTER
Thyroglobulin transported to colloid:
1. FOLLICULAR CELLS MANUFACTURE: ENZYMES PRODUCING TH + THYROGLOBULIN (large protein rich in tyrosine residues) 2. ENZYMES & THYROGLOBULIN PACKAGED INTO VESICLES + EXPORTED FROM FOLLICULAR CELLS = INTO COLLOID
In the colloid:
• IODIDE COMBINES W/ THYROGLOBULIN TYROSINE RESIDUES = FORMS TH
○ TYROSINE & IODINE DERIVED FROM DIET
Thyroid hormone secretion:
1. TSH causes FOLLICULAR CELLS to TAKE UP PORTIONS of COLLOID via ENDOCYTOSIS a. W/O TSH = TH REMAINS IN COLLOID 2. FORM VESICLES INSIDE CELLS - CONTAINING PROTEOLYTIC ENZYMES 3. ENZYMES CUT THYROGLOBULIN TO RELEASE TH
TH transport in plasma + which has higher levels of circulation + which is more physiologically active)
T3 & T4 = LIPID SOLUBLE:
* PASS THROUGH FOLLICULAR LIPID MEMBRANE * Need to BIND TO PLASMA PROTEINS = THYROXINE BINDING GLOBULIN * Then CIRCULATE IN PLASMA
T4 = PRESENT IN HIGHER LVLS AS THYROXIN BINDING GLOBULIN HAS A GREATER AFFINITY FOR IT
= GREATER 1/2-LIFE
T3 = MORE PHYSIOLOGICALLY ACTIVE AS TH RECEPTORS HAVE A HIGHER AFFINITY FOR IT
T4 CAN BE DEIODINATED TO T3 BY DEIODINASE ENZYMES (half deiodinated in plasma - remaining in target cells - this can be adjusted depending on cell’s demand)
Regulation of TH Release (increasing & decreasing circulation)
STIMULI INCREASING TH SECRETION:
* COLD * EXERCISE * PREGNANCY
STIMULI INHIBITING TH SECRETION:
* GLUCOCORTICOIDS = inhibits TSH & conversion of T4 to T3 * SOMATOSTATIN = inhibits TSH * T4 & T3 = -ve feedback control
Thyroid Hormone Functions
TH BINDS TO NUCLEAR RECEPTORS IN TARGET CELLS
• CHANGE TRANSCRIPTION & TRANSLATION = ALTERS PROTEIN SYNTHESIS 1. RAISES METABOLIC RATE + PROMOTES THERMOGENESIS a. By promoting FUTILE CYCLES of simultaneous catabolism & anabolism 2. INCREASES HEPATIC GLUCONEOGENESIS (no net effect on BG as pancreas releases adequate insulin) 3. NET INCREASE in PROTEOLYSIS (+ increase in protein synthesis - more in children) 4. NET INCREASE in LIPOLYSIS 5. CRITICAL FOR GROWTH (stimulates GH receptor expression) 6. ESSENTIAL FOR BRAIN DEVLEOPMENT IN UTERO a. Maternal iodine deficiency = congenital hypothyroidism/cretinism 7. PERMISSIVE ACTION ON EPINEPHRINE
Hyperthyroidism: Causes + Presentation
Causes:
• GRAVES DISEASE = COMMON
○ ANTIBODIES PRODUCED - THESE MIMIC TSH + CONTINUALLY ACTIVATE THYROID GLAND ○ INCREASED RELEASE of TH SWITCH OFF TSH FROM ANTERIOR PITUITARY (TSH lvls in plasma v. low) ○ THYROID GLAND MAY BE 2-3x LARGER due to HYPERPLASIA + HYPERACTIVE CELLS ALSO APPARENT
• THYROID ADENOMA = RARE
○ HORMONE-SECRETING THYROID HORMONE
Presentation:
1. INCREASED METABOLIC RATE & HEAT PRODUCTION a. WGT. LOSS/HEAT INTOLERANCE 2. INCREASED PROTEIN CATABOLISM a. MUSCLE WEAKNESS/WGT. LOSS 3. ALTERED NERVOUS SYSTEM FUNCTION a. HYPEREXCITABLE REFLEXES & PSYCHOLOGICAL DISTURBANCES 4. ELEVATED CV FUNCTION - TH PERMISSIVE TO EPINEPHRINE & BETA RECEPTORS a. INCREASED HR/CONTRACTILE FORCE, INCREASED CO, CARDIAC FAILURE
Goitre
- SIGNIFICANT ENLARGEMENT OF THYROID GLAND
- OCCURS IN BOTH HYPOTHYROIDISM & HYPERTHYROIDISM
MECHANISMS:
* HYPOTHYROIDISM = ENLARGEMENT due to INCREASED TROPIC ACTION of TSH ON THYROID FOLLICULAR CELLS = HYPERTROPHY * HYPERTHYROIDISM (GRAVES DISEASE) = OVERACTIVITY due to AUTOIMMUNE DISEASE = HYPERTROPHY
