LECTURE 11 (Thyroid & Adrenals) Flashcards

1
Q

Describe Thyroid Histology

A
  • Thyroid gland contains “follicles”
  • Follicles filled with COLLOID (protein materials)
  • Thyroid hormone synthesised by follicular cells
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2
Q

What are the different types of Thyroid dysfunction?

A

Hypothyroidism & Hyperthyroidism

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3
Q

What does Iodine deficiency lead to?

A

Hypothyroidism

Explanation: Thyroid hormones contain Iodine -> normal level of iodine in diet is mandatory -> Iodine mixed in table salt to prevent iodine deficiency

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4
Q

What are the two types of thyroid hormones synthesised in the body?

A
  • T3 - Triiodothyronine
  • T4 - Thyroxine
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5
Q

What are Thyroid hormones synthesised from?

A

Tyrosine & Iodine

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6
Q

What is Thyroglobulin?

A
  • Large protein produced by thyroid follicular cells
  • “backbone” containing numerous tyrosine molecules
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7
Q

What must happen to iodide in our diet for thyroid hormone synthesis?

A

1) Taken up by follicular cells
2) Oxidised to I2 “OXIDATION”
3) Added to organic/carbon structures “ORGANIFICATION”

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8
Q

What are the symptoms of Hypothyroidism?

A
  • Weight gain
  • Puffy face
  • Decreased sweating
  • Constipation
  • Slow heart rate
  • Irregular and heavy periods
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9
Q

What are the symptoms of Hyperthyroidism?

A
  • Weight loss or gain
  • Diarrhoea
  • Increased sweating
  • Racing heart
  • Short and light periods
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10
Q

Which symptoms are found in both Hypothyroidism and Hyperthyroidism?

A
  • Fatigue
  • Insomnia
  • Hair loss
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11
Q

Describe Thyroid hormon synthesis

A

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)

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12
Q

What is the function of Thyroid Peroxidase (TPO)?

A

It catalyses
- Oxidation of iodide
- Organification into MIT/DIT
- Coupling of MIT/DIT into T3/T4

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13
Q

TPO antibodies are common in which disease?

A

Autoimmune thyroid disease

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14
Q

What is produced more, T3 or T4?

A

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

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15
Q

Which enzyme converts T4 to T3?

A

5’-DEIODINASE

[most conversion occurs in peripheral tissues]

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16
Q

What are some different Hyperthyroid medications?

A
  • Propylthiouracil (PTU)
  • Methimazole
  • Propranolol
17
Q

Describe the MOA of Propylthiouracil (PTU)

A
  • Inhibits TPO (Thyroid peroxidase) -> decreases T3/T4 from thyroid gland
  • Inhibits 5’-deiodinase -> decreased T4 into T3 conversion in peripheral tissues
18
Q

Describe the MOA of Methimazole

A

Inhibits TPO (Thyroid peroxidase) -> decreases T3/T4 from thyroid gland

19
Q

Describe the MOA of Propranolol

A
  • Beta-blocker
  • Weak inhibitor of 5’deiodinase
  • Used in thyrotoxicosis (inappropriately high levels of thyroid hormones) -> blocks catecholamines + T4 to T3 conversion
20
Q

Describe the Adrenal glands

A
  • Located above kidneys
  • CORTEX synthesises 3 groups of hormones (Mineralocorticoids, Glucocorticoids & Androgens)
  • MEDULLA synthesises Epinephrine & Norepinephrine -> sympathetic nervous system control
21
Q

Which parts of the cortex synthesises the three different groups of hormones?

A
  • Zona Glomerulosa = Mineralocorticoids (Aldosterone)
    [regulated by Angiotensin II]
  • Zona Fasciculata = Glucocorticoids (Cortisol)
    [regulated by ACTH + CRH]
  • Zona Reticularis = Androgens (DHEA)
    [regulated by ACTH + CRH]
22
Q

What is the HPA axis?

A

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

23
Q

What are the Effects of Cortisol?

A
  • 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]
24
Q

What is Cushing’s syndrome?

A

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