Pharmacology - Beresford Flashcards

1
Q

What is Prolactomina?

And what often causes it?

A

When there is an overproduction of prolactin

A decrease in dopamine often causes it –> this can be fixed by using a dopamine agonist

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2
Q

What is Panhypopituitarism?

A

A deficinecy in all anterior pituitary hormones

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3
Q

What’s the difference between primary and secondary diseases?

A

Primary –> Defect with the target organ

Secondary –> Problems with the release of the hormones (eg, in the pituatary)

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4
Q

What are the differences between T4 and T3?

A

T4 is a pro-hormone of T3 –> converted by deiodinases

T3 has a shorter half life than T4

T3 has a lower binding affinity for binding proteins, but a higher affinity for receptors

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5
Q

Where are thyroid hormones synthesised?

A

Follicle cells

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6
Q

What is the most common form of hypothyroidism?

A

Atrophic (autoimmune) hypothyroidism

This uses antithyroid antibodies

More common in women –> with the incidence increasing with age

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7
Q

How can we differentiate between primary and secondary hypothyroidism?

A

TSH Levels

High = Primary

Low = Secondary

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8
Q

What’s the common form of hyperthyroidism?

A

Graves Disease

An autoimmune disease that causes the stimulation of TSH receptors

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9
Q

What are the 3 treatment options for hyperthyroidism?

A

Antithyroid Drugs –> Carbimazole/Thiamazole

Radioiodine –> If rendered euthyroid before (normal thyroid gland)

Surgery –> Only if rendered euthyroid before

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10
Q

Where abouts are aldosterone and cortisol specifically made in the adrenal glands?

A

Aldosterone –> Zona Glomerulosa (ZG)

Cortisol –> Zonas fasciculate (ZF) and Zonas reticularis (ZR)

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11
Q

What is aldosterone?

A

A mineralcorticoid

Its secretion is stimulated by elevation in angiotensin II

Binds to the MCR nuclear receptor

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12
Q

What are the 3 triggers for the release of renin?

A

Decrease in BP in the afferent arteriole

Increase in sympathetic nervous activity

Decrease in [NaCl] in the DCT

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13
Q

What are the 3 main effects of primary hyperaldosteronism?

A

Increase plasma Aldosterone:Renin Ratio (ARR)

Increased aldosterone plasma levels –> that cannot be controlled with NaCl infusion

Increased urinary K+ (and so decreased plasma levels)

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14
Q

What is cortisol?

A

A glucocorticoid

In circulation most of it is bound to plasma proteins

Binds to the GCR nuclear receptor

Secretion is stimulated by ACTH from the pituitary

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15
Q

What’s Addison’s Disease?

A

Primary adrenal insufficiency

An autoimmune disease that destroys the adrenal cortex –> so less adrenal steroid production

Characterised by an increase in CRH/ACTH production

Also due to low cortisol levels (due to destruction above) there is a negative feedback loop which creates more CRH/ACTH

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16
Q

What is main reason for people getting secondary adrenal insufficency?

And what does it cause?

A

Long term corticosteorid therapy

Suppress the hypothalamus-pituitary axis

17
Q

How do you manage hypoadrenalism long term?

A

Replacement therapy with gluco/mineralocorticoids

Have a steroid card for emergency services

Keep an ampoule of hydrocortisone at home for injection by carers/family

18
Q

What are the 2 types of hypercortisolism (cushings syndrome)?

And how do you test for them?

A

Primary –> Non ACTH dependent, normally caused by a cortisol-secreting adrenal tumour

Secondary –> ACTH dependent, usually caused by an ACTH-secreting pituitary adenoma (‘cushings disease’)

The high-dose dexamathasone test is the main one

19
Q

How do you pharmacologically inhibit cortisol synthesis in cushings syndrome?

A

Metyrapone and Ketoconazole

These block the adrenal 11(B)-hydroxylase