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CJ: UoL Medicine Semester Two (ESA2) > MEH - Adrenal Glands > Flashcards

MEH - Adrenal Glands Flashcards

1
Q

What are the three general areas of the kidney called?

A

Capsule, cortex, medulla (innermost)

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2
Q

What are the three parts of the cortex called?

A

Zona glomerulosa, zona fasiculata, zona reticularis

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3
Q

What is found in the medulla of the kidney?

A

Chromaffin cells, which secrete adrenaline and noradrenaline

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4
Q

What does the zona glomerulosa secrete?

A

Mineralocorticoids, eg aldosterone

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5
Q

What does the zona fasiculata secrete?

A

Glucocorticoids such as cortisol

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6
Q

What does the zona reticularis secrete?

A

Androgens

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7
Q

What are steroid hormones synthesised from?

A

Cholesterol, in the adrenal glands and gonads

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8
Q

Steroid hormones are lipid soluble, true or false?

A

True

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9
Q

How do steroids interact with cells?

A

They bind to nuclear receptors to modulate gene transcription

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10
Q

How do corticosteroids exert their actions?

A
  • diffuse across plasma membrane
  • bind to glucocorticoid receptors which causes dissociation of chaperone proteins
  • receptor ligand complex translocates to nucleus and dimerises with other receptors
  • receptors bind to GREs or other transcription factors
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11
Q

What class of steroid is aldosterone?

A

It is the most abundant mineralocorticoid

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12
Q

Where is aldosterone made?

A

Synthesised and released by the zona glomerulosa of the adrenal cortex

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13
Q

Which proteins are used to transport aldosterone?

A

Serum albumin and transcortin

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14
Q

What is aldosterone’s main action?

A

Promotes expression of the Na+/K+ pump in the nephron, which influences water retention and blood volume and therefore blood pressure

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15
Q

What triggers aldosterone release from the kidneys?

A

Angiotensin II

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16
Q

What is hyperaldosteronism?

A

Too much aldosterone produced by the body

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17
Q

What are the two categories of hyperaldosteronism?

A

Primary - defect in adrenal cortex

Secondary - overactivity of the RAAS

18
Q

What are the signs of hyperaldosteronism?

A
  • high blood pressure
  • left ventricular hypertrophy
  • stroke
  • hypernatraemia
  • hypokalaemia
19
Q

How is hyperaldosteronism treated?

A

Aldosterone-producing adenomas can be removed by surgery, or spironolactone can be given

20
Q

How does spironolactone work?

A

It is a mineralocorticoid receptor antagonist

21
Q

What class of steroid is cortisol?

A

Most abundant corticosteroid

22
Q

Where is cortisol synthesised?

A

In the zona fasiculata, in response to ACTH

23
Q

What is cortisol’s carrier protein in plasma?

A

Transcortin

24
Q

What are the actions of cortisol?

A
  • increases protein breakdown in muscle, gluconeogenesis in the liver and lipolysis in fat
  • in charge of resistance to stress
  • anti-inflammatory effects (inhibits macrophages and mast cell degranulation)
  • depression of immune response
25
Q

Describe the sequence of events from the hypothalamus to release of cortisol from the kidneys

A
  • hypothalamus produces corticotropin releasing hormone (CRH)
  • anterior pituitary releases adrenocorticotropic hormone in response to this (ACTH)
  • adrenal cortex releases cortisol
26
Q

What are the net effects of glucocorticoids on metabolism?

A
  • increased glucose production
  • breakdown of protein
  • redistribution of fat
27
Q

What is Cushing’s Syndrome?

A

Chronic excessive exposure to cortisol

28
Q

What are the signs and symptoms of Cushing’s syndrome?

A
  • moon shaped face
  • buffalo hump fat pad
  • abdominal obesity
  • purple striae
  • acute weight gain
  • hyperglycaemia
  • hypertension
29
Q

What are the external causes of Cushing’s syndrome?

A

Prescribed glucocorticoids (most common cause)

30
Q

What is the difference between Cushing’s disease and Cushing’s syndrome?

A

Cushing’s disease is due to a benign pituitary adenoma secreting ACTH, while Cushing’s syndrome is an umbrella term for excessive cortisol exposure

31
Q

What are steroid drugs used for?

A

Used to treat inflammatory disorders such as asthma, IBD, RA, etc.

32
Q

What is Addison’s disease?

A

Chronic adrenal insufficiency, usually caused by autoimmune response

33
Q

What are the signs/symptoms of Addison’s disease?

A
  • postural hypotension
  • lethargy
  • weight loss
  • anorexia
  • increased skin pigmentation
  • hypoglycaemia
34
Q

Why does hyperpigmentation occur in Addison’s?

A
  • decreased cortisol means that negative feedback on the anterior pituitary is reduced
  • this means that more POMC (building block) is required to form ACTH
  • POMC makes both ACTH and MSH (which forms melanin), so to maintain ACTH levels, more MSH is made as a byproduct
35
Q

What is an Addisonian crisis?

A

Life threatening emergency due to adrenal insufficiency caused by severe stress, infection, trauma, cold, abrupt withdrawal of steroids, salt deprivation etc

36
Q

What are the symptoms of an Addisonian crisis?

A

Nausea, vomiting, pyrexia, hypotension, vascular collapse

37
Q

What is the treatment for an Addisonian crisis?

A

Fluid replacement and cortisol

38
Q

What are the androgens that are released from the zona reticularis?

A

DHEA and androstenedione

39
Q

What do 20% of chromaffin cells in the adrenal medulla lack?

A

N-methyl transferase, meaning they secrete noradrenaline instead of adrenaline

40
Q

Which GCPRs can adrenaline act on?

A

B1 and B2, a1 and a2

41
Q

What are the effects of adrenaline on the heart, lungs and blood vessels?

A

Heart - increase heart rate and contractility (B1)
Lungs - bronchodilation (B2)
Blood vessels - vasoconstriction in skin and gut (a1) or vasodilation (B2) in skeletal muscle

42
Q

What is a pheochromocytoma?

A

Chromaffin cell tumour which secretes noradrenaline. It may cause life-threatening hypertension. Symptoms of anxiety, weight loss, headaches etc

CJ: UoL Medicine Semester Two (ESA2) (87 decks)

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