LECTURE 11 (Thyroid & Adrenals) Flashcards
Describe Thyroid Histology
- Thyroid gland contains “follicles”
- Follicles filled with COLLOID (protein materials)
- Thyroid hormone synthesised by follicular cells
What are the different types of Thyroid dysfunction?
Hypothyroidism & Hyperthyroidism
What does Iodine deficiency lead to?
Hypothyroidism
Explanation: Thyroid hormones contain Iodine -> normal level of iodine in diet is mandatory -> Iodine mixed in table salt to prevent iodine deficiency
What are the two types of thyroid hormones synthesised in the body?
- T3 - Triiodothyronine
- T4 - Thyroxine
What are Thyroid hormones synthesised from?
Tyrosine & Iodine
What is Thyroglobulin?
- Large protein produced by thyroid follicular cells
- “backbone” containing numerous tyrosine molecules
What must happen to iodide in our diet for thyroid hormone synthesis?
1) Taken up by follicular cells
2) Oxidised to I2 “OXIDATION”
3) Added to organic/carbon structures “ORGANIFICATION”
What are the symptoms of Hypothyroidism?
- Weight gain
- Puffy face
- Decreased sweating
- Constipation
- Slow heart rate
- Irregular and heavy periods
What are the symptoms of Hyperthyroidism?
- Weight loss or gain
- Diarrhoea
- Increased sweating
- Racing heart
- Short and light periods
Which symptoms are found in both Hypothyroidism and Hyperthyroidism?
- Fatigue
- Insomnia
- Hair loss
Describe Thyroid hormon synthesis
1)Iodide enters the Follicular cell via NA-IODINE SYMPORTER with Sodium
2) “OXIDATION” Iodide is oxidised to I2 via THYROID PEROXIDASE
3) “ORGANIFICATION” Tyrosine + Iodine (I2) is converted to either MONOIODOTYROSINE (MIT) [1 iodine] or DIIODOTYROSINE (DIT) [2 iodine] via THYROID PEROXIDASE
4) “COUPLING REACTIONS” MIT + DIT = TRIIODOTHYRONINE (T3) or DIT + DIT = THYROXINE (T4)
What is the function of Thyroid Peroxidase (TPO)?
It catalyses
- Oxidation of iodide
- Organification into MIT/DIT
- Coupling of MIT/DIT into T3/T4
TPO antibodies are common in which disease?
Autoimmune thyroid disease
What is produced more, T3 or T4?
T4 (>90% of thyroid hormone produced in T4)
Explanation: More T4 is produced but more T3 is needed since it is a more POTENT hormone, thus T4 must be converted to T3 via 5’-DEIODINASE
Which enzyme converts T4 to T3?
5’-DEIODINASE
[most conversion occurs in peripheral tissues]
What are some different Hyperthyroid medications?
- Propylthiouracil (PTU)
- Methimazole
- Propranolol
Describe the MOA of Propylthiouracil (PTU)
- Inhibits TPO (Thyroid peroxidase) -> decreases T3/T4 from thyroid gland
- Inhibits 5’-deiodinase -> decreased T4 into T3 conversion in peripheral tissues
Describe the MOA of Methimazole
Inhibits TPO (Thyroid peroxidase) -> decreases T3/T4 from thyroid gland
Describe the MOA of Propranolol
- Beta-blocker
- Weak inhibitor of 5’deiodinase
- Used in thyrotoxicosis (inappropriately high levels of thyroid hormones) -> blocks catecholamines + T4 to T3 conversion
Describe the Adrenal glands
- Located above kidneys
- CORTEX synthesises 3 groups of hormones (Mineralocorticoids, Glucocorticoids & Androgens)
- MEDULLA synthesises Epinephrine & Norepinephrine -> sympathetic nervous system control
Which parts of the cortex synthesises the three different groups of hormones?
- Zona Glomerulosa = Mineralocorticoids (Aldosterone)
[regulated by Angiotensin II] - Zona Fasciculata = Glucocorticoids (Cortisol)
[regulated by ACTH + CRH] - Zona Reticularis = Androgens (DHEA)
[regulated by ACTH + CRH]
What is the HPA axis?
A major neuroendocrine system that controls reactions to stress
Hypothalamus produces CRH (Corticotrophin-releasing hormone) -> Pituitary gland produces ACTH (Adrenocorticotropic hormone) -> Adrenal gland produces Cortisol
What are the Effects of Cortisol?
- Increased serum glucose
[induces glucose production in liver since increased synthesis of glucose-6-phosphatase + PEPCK -> gluconeogenesis & less glucose taken up peripherally + more glycogen storage in liver] - Fat deposition
[activation of lipolysis in adipocytes -> stimulate adipocyte growth] - Long-term steroid use -> diabetes
[enhanced effects of glucagon and epinephrine -> long-term leads to insulin resistance] - Muscle atrophy
- Thin skin, Easy bruising & Striae (stretch marks)
[blunted epidermal cell division in skin] - Osteopenia & Osteoporosis
[Inhibits osteoblasts]
What is Cushing’s syndrome?
A set of symptoms resulting from exposure to increased levels of cortisol - Endogenous or exogenous sources of excess cortisol
CAUSES:
- Long-term use of glucocorticoid medications
- Pituitary tumour (Cushing’s disease)
- Ectopic ACTH-producing tumour
- Adrenal tumour
SYMPTOMS:
- Moon face
- Buffalo hump
- Muscle wasting & thin extremities
- Stretch marks, weight gain, obesity & easy bruising
= Skin & bone thinning
FEMALES:
- Hirsutism (where women have thick, dark hair on their face, neck, chest, tummy, lower back, buttocks or thighs)
- Menstrual changes
- Decreased Libido
