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ENDOCRINE > A. THYROID GLAND AND HORMONES > Flashcards

A. THYROID GLAND AND HORMONES Flashcards

1
Q

where is the thyroid gland

A

under Adam’s apple around trachea

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2
Q

what are the 3 thyroid hormones

A
  1. thyroxine (T4)
  2. tri-iodothyronine (T3)
  3. calcitonin
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3
Q

where is calcitonin produced and what is its role

A

(‘calcium reducing’)
- by parafollicular ‘C’ cells
- to reduce plasma calcium levels

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4
Q

what is parathyroid hormone

A
  • secreted by parathyroid glands which are 4 small glands located on posterior surface of thyroid gland
  • increase plasma calcium levels
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5
Q

what is T4 and T3 made of

A
  • tyrosine and iodine
  • T4 = 2x di-iodotyrosine
  • T3 = 1x mono-iodotyrosine and 1x di-iodotyrosine
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6
Q

what is the role of thyroid peroxidase

A
  • catalyses iodination and coupling of MIT and DIT
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7
Q

what is reverse tri-iodothyronine (rT3)

A
  • biologically inactive
  • antagonist at T3 receptors
  • made of MIT and DIT but different 3D structure to T3
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8
Q

proportions of T4, T3, rT3 in body

A
  • 90-95% T4
  • 5-10% T3
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9
Q

activity of TRH

A
  • tropic: regulates TH production/release
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10
Q

activity of TSH

A
  • tropic: regulates TH production/release
  • trophic: maintains integrity of thyroid gland
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11
Q

how do thyroid hormones act in the circulation

A
  • they are highly lipophilic
  • highly bound to plasma proteins hence biologically inert
  • <0.1% T4 & <1.0% T3 is in unbound (free) form
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12
Q

why measure free T4/T3 for thyroid function

A
  • as 99.9% not readily availible
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13
Q

how is T4 converted to T3

A
  • deiodinase enzymes in periphery which remove iodine
  • T3 is 4-5x more potent than T4
  • T4 functions largely as a pro-hormone
  • T3 is principal active hormone
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14
Q

actions of thyroid hormones

A
  1. increase metabolism in body in nearly all tissues as most have thyroid receptors
    - increased metabolism of CHOs, proteins, fats
    - so increased oxygen consumption and heat production
    i.e. increase basal metabolic rate = basic rate at which cells function at rest
  2. stimulate growth and development
    - good for young children
  3. up regulate expression of B-ARs so promote CV effects
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15
Q

what is a goitre

A
  • enlargement of thyroid gland
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16
Q

what is a diffuse goitre

A
  • whole of thyroid gland
  • occurs when there is overstimulation of thyroid gland by TSH or TSI
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17
Q

what is a nodular goitre

A
  • discrete area clearly different from surrounding thyroid gland eg- a thyroid tumour
  • effects on surrounding cells
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18
Q

hypothyroidism caused by primary failure of thyroid gland

A
  • 90% primary cases caused by this
  • Hashimoto’s thyroiditis
  • autoimmune disease caused by an overactive immune response against substances/tissues normally present in body
  • decreased T3 and T4
  • increased TSH (ie trophic activity)
  • goitre present
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19
Q

hypothyroidism secondary to hypothalamic or anterior pituitary failure

A
  • decreased T3 and T4
  • decreased TSH (ie less trophic activity)
  • no goitre
  • shrinkage of thyroid gland seen
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20
Q

hypothyroidism due to lack of dietary iodine

A
  • decreased T3 and T4
  • increased TSH
  • goitre present: simple, non-toxic
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21
Q

what else can cause hypothyroidism

A
  • drug induced (e.g. anti-thyroid drugs, lithium, amiodarone)
  • radioactive iodine therapy, surgery
  • thyroid hormone resistance
22
Q

how does hypothyroidism affect metabolism

A

REDUCTION in metabolic activity

  • decreased BP
  • decreased body core temperature
  • decreased sweating
  • cold intolerance
  • decreased appetite
  • weight gain due to low metabolism
  • constipation
23
Q

how does hypothyroidism affect CNS

A

SLOWING DOWN

  • depression
  • confusion
  • poor memory
  • difficulty concentrating
  • cretinism (perinatal): dwarfism and mental retardation
24
Q

how does hypothyroidism affect CVS (resting)

A
  • decreased HEART RATE
  • decreased arterial blood pressure
25
Q

what other effects does hypothyroidism have

A
  • growth deficiency (childhood)
  • dry skin
  • hoarse voice
  • menstrual problems

*every newborn tested for TSH and T4 within 5 days of birth

26
Q

diagnosis of hypothyroidism

A

Thyroid function test

  • primary: decreased T3 and T4, increased TSH
  • secondary (usually pituitary disease): decreased T3 and T4, decreased TSH
  • if suspect Hashimoto’s, test for thyroid antibodies
  • anti-microsomal (TPO), anti-thyroglobulin antibodies
27
Q

what is the goal when treating hypothyroidism

A
  • euthyroid state
28
Q

1st drug treatment for hypothyroidism

A

Levothyroxine (T4)
- drug of choice
- orally active
- once a day (long half-life)

29
Q

what cautions need to be taken with levothyroxine

A
  • can switch up metabolism in body and increase expression of B-ARs
  • may worsen or uncover angina
  • angina: give beta-blocker to decrease B-AR enhanced activity
  • baseline ECG with initial dosage
30
Q

2nd drug treatment for hypothyroidism

A

Liothyronine (T3)
- max effect 24h, disappear 24 - 48h
- not used routinely, rapid onset can induce heart
failure due to higher potency
- used in severe hypothyroid states when rapid response is desired (IV)

31
Q

what is thyrotoxicosis

A
  • toxic levels of T3 and T4
32
Q

hyperthyroidism caused by abnormal levels of thyroid-stimulating immunoglobulins

A
  • Graves’ disease
  • increased T3 and T4
  • decreased TSH
  • goitre present due to TSIs
33
Q

hyperthyroidism secondary to excess hypothalamic or anterior pituitary secretion

A
  • increased T3 and T4
  • increased TSH due to increased TRH or tumour
  • goitre present due to increase in trophic activity
34
Q

hyperthyroidism caused by a hyper-secreting thyroid tumour

A
  • increased T3 and T4
  • decreased TSH
  • goitre present: toxic, multinodular, toxic adenoma
35
Q

other causes of hyperthyroidism

A
  • latrogenic (eg - amiodarone, lithium)
36
Q

what is the most common cause of hyperthyroidism

A
  • 90% of cases
  • f:m 10:1
  • autoimmune: TSIs bind to TSH receptors on thyroid gland and activate the thyroid gland to produce and release thyroid hormones
37
Q

symptoms of Graves’ disease

A
  • nervousness
  • palpitations
  • weight loss
  • tremor
  • sweating
  • heat intolerance
  • goitre
  • exophthalmos: distinct for only Graves’
    protrusion of both eyes (30% have)
38
Q

how does hyperthyroidism affect metabolism

A

INCREASE in metabolic activity

  • increased BP
  • increase BMR
  • increased body core temperature
  • increased sweating
  • heat intolerance
  • increased appetite
  • weight loss due to high metabolism (body burning CHOs, fat and proteins to heat)
  • diarrhoea
39
Q

how does hyperthyroidism affect CNS

A

INCREASE in neuronal function
- anxiety
- emotional
- irritable
- restless
- tremor

40
Q

how does hyperthyroidism affect CVS

A

enhancement of B-AR responses so sympathetic nervous system activity enhanced

  • increased heart rate
  • increased arterial BP
  • palpitations
41
Q

what other effects does hyperthyroidism have

A
  • growth acceleration (childhood)
42
Q

diagnosis of hyperthyroidism

A

Thyroid function test

  • increased T3 and T4
  • decreased TSH (Graves’ disease/ tumour)
  • radioactive isotope scan to show regions of thyroid gland
  • presence of thyroid autoantibodies - autoimmune condition
43
Q

what is the goal of hyperthyroidism treatment

A
  • euthyroid state
  • symptomatic relief from increased sympathetic activity
44
Q

what are anti-thyroid drugs are used for hyperthyroidism

A

Thionamides
- Carbimazole and propylthiouracil
- if sensitivity to carbimazole, use propylthiouracil

45
Q

how do carbimazole and propylthiouracil work

A
  • decrease production of thyroid hormones, by inhibiting iodination and coupling processes (via TPO)
  • PTU also blocks T4 to T3 deiodination
  • several weeks for clinical response to occur (due to colloid stores)
  • usually for 12-18 months, but ~50% relapse rate
  • will become hypothyroidic
46
Q

when to use propylthiouracil

A

carbimazole:
- rashes & pruritus are common (2-25%)
- RARE complication (0.1-1.2%) – neutropenia and agranulocytosis (bone marrow suppression)
- reversible

47
Q

what should you use whilst waiting for anti-thryoid drugs to bring about a clinical response

A
  • non-selective beta-blockers
  • reduce actions of catecholamines
  • rapid symptomatic relief of tremor, palpitations, anxiety (within 4 days)
48
Q

dose titration approach with anti-thyroid drugs

A
  • where only anti-thyroid drugs are used
  • doses are adjusted to achieve normalisation of thyroid hormone production
  • 12-18 months
  • lower rate of side effects but both are equally effective
49
Q

block and replace approach with anti-thyroid drugs

A
  • where anti-thyroid drugs are given with thyroxine
    replacement
  • 6-12 months
50
Q

hyperthyroidism treatment with radioactive iodine (131I)

A
  • taken up into thyroid gland and destroys cells with high energy beta-emission
  • first-line for older patients with nodular goitres
    and hyperthyroidism
  • used when thyrotoxicosis recurs after anti-thyroid drug therapy
  • given as single drink or capsule
  • max effect 2-4 months after due to slow destruction of thyroid follicular cells
  • hypothyroidism may result if too many cells destroyed
51
Q

hyperthyroidism treatment with a thyroidectomy (partial)

A
  • not frequently used
  • used when severe thyrotoxicosis associated
    with a large goitre or concern about tumour
    development
  • used when there are obstructive symptoms (breathing and swallowing)
  • hypothyroidism may result

ENDOCRINE (17 decks)

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