Thyroid Flashcards

1
Q

What is the histology of the thyroid

A

single layer of cuboidal cells surrounded by basement membrane

composed of thyroid follicles, which are lined by follicular cells that make iodine

Innactive follicular cell- simple flat columnar
active follicular cells- simple tall columnar
paarafollicular cells- synethsise calcitonin

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2
Q

What is the process for TSH production

A

paraventricular nucleus in hypothalamus release TRH onto ant. pitiutary. Thyrocytes in the gland then stimulated to release TSH, which then enters circulation. TSH binds to Gs on thyroid gland to make…. PKA, which causes production of thyroglobulin. Iodide then enters gland which is oxidised via TPO to iodine. TPO then iodinates thyroglobulin by attaching iodine to tyrosine AA. TPO then fuses DIT-DIT (T4) and MIT-DIT (T3), which are then endocytosed out of cell

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3
Q

How does thyroid hormone control basal metabolic rate

A

hormone increase BMR, rate of O2 comsumption. BMR directly proportional to cellular metabolism

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4
Q

How does thyroid hormone effect Na+/K+ pumps

A

thyroid hormone stimulates synthesis of additional Na+/K+ pumps, which require ATP to pump Na+ from cytosol into ECF. Release of ATP is exothermic reaction, therefore more heat given off, body temp rises causing a calorigenic effect

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5
Q

How does thyroid hormone regulate metabolism

A

stimulates protein synthsis and increase glucose and FA use in ATP production
Increase lipolysis and cholesterol excretion, which reduces cblood cholesterol levels

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6
Q

How does thyroid hormone effect catechalamine

A

thyroid hormone upregulates β-receptors thus enhancing actions of nor/epinerphrine to increase BP

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7
Q

How does thyroid hormone effect body growth

A

It can stimulate synthesis of type 1 collagen, ALP and osteoblast activity which can cause accelerated body growth esp nervous and skeletal system

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8
Q

What is hypothyroidism

A

primary hypothroidism- underactive thyroid, where not enough thyroxine is produced for body causing decreased T3 and T4 and high levels of TSH. Hashimoto’s most common disease as immune response to thyroid autoantigens leading to depletion of thyroid epithelial cells (lymphocyte infiltration and fibrosis) mediated by CD8+ cytotoxic killing T cells and cytokine mediated death

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9
Q

How does hypothyroidsm clinically present

A

painless enlargement of thyroid, increased cold sensitivity, poor conc, depression, constipation , muscle cramps, skin cool and pale, non-pitting oedema due to accumulation of matrix substances e.g GAGs, hylaruronic acid

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10
Q

What are other types of hypothyroidism

A

secondary due to problems with pituitary release and tertiary problems with hypothalamic release

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11
Q

What is hyperthryoidism

A

excess free T4/3 due to thyroid gland overactivity resulting in thyrotoxicosis

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12
Q

Primary hyperthryoidism causes

A

Grave’s disease (IgG antibodies similar structure to TSH continues activation)
Toxic multinodular goitre or adenoma will produce excess thyroid hormone

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13
Q

How can thyrotoxicosis occur without hyperthyroidism

A

Excessive T4 administration
Postpartum- after pregancy causes inflammed thyroid due to thyroid antibody production

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14
Q

What are the clinical features of hyperthyroidism

A

weight loss, increased apetite, heat intolerance, fatigue, hyperactivity ,tremor, lid-lag, hyper-feflexia, tachycardia

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15
Q

MOA Carbimazole

→ it inhibits TPO so no thyroxine is made or thyroglobulin therefore no T4, T3

A

it inhibits TPO so no thyroxine is made or thyroglobulin therefore no T4, T3

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16
Q

MOA Levothyroxine

→ synthetic form of T4

A

synthetic form of T4

17
Q

MOA Propanalol

→ β-AR antagonist, thus preventing bondong of catechalamine so blocks β1-R on cardia myocytes, blocking cAMP, blocking PKA, decrease Ca2+ influx, decrease HR and contractility, decreases renin from kidney

A

β-AR antagonist, thus preventing bondong of catechalamine so blocks β1-R on cardia myocytes, blocking cAMP, blocking PKA, decrease Ca2+ influx, decrease HR and contractility, decreases renin from kidney