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MEH A > Session 9 > Flashcards

Session 9 Flashcards

1
Q

Where are the adrenal glands?

A

They cap the upper poles of the kidneys and lie against the diagphragm in the retroperitoneal space

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2
Q

What is the structure of the adrenal glands?

A

2 regions - outer cortex and inner medulla

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3
Q

What is the outer cortex made up of?

A

Zone glomerulosa, zone fasiculata and zone reticularis

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4
Q

What is excreted from the zone glomerulosa?

A

Mineralocorticoids eg aldosterone

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5
Q

What is secreted from the zone fasiculata?

A

Glucocorticoids eg cortisol

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6
Q

What is secreted from the zone reticularis?

A

Secreted glucocorticoids and small amounts of androgens (dehydroepiandosterone)

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7
Q

What is the medulla made up of?

A

Chromaffin cells that produce adrenaline (80%) and noradrenaline (20%)

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8
Q

What is the cortex derived from?

A

Mesoderm

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9
Q

What is the medulla derived from?

A

Neural crest cells

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10
Q

What is outside the adrenal cortex?

A

Connective tissue capsule which contains plexus of blood vessels

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11
Q

What is a corticosteroid?

A

Any group of steroid hormone produced in adrenal cortex

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12
Q

What are the key features of steroid hormones?

A

Synthesised from cholesterol, lipid soluble

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13
Q

How do steroid hormones work?

A

They bind to nuclear receptors to modulate gene transcription

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14
Q

Examples of steroid hormones?

A

Glucocorticoids, mineralocorticoid, androgens, oestrogens

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15
Q

What is the most abundant mineralocorticoid?

A

Aldosterone

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16
Q

Where is aldosterone synthesised and released from?

A

Zona glomerulosa of adrenal cortex

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17
Q

What is the carrier proteins for steroid hormones?

A

Albumin

18
Q

How does aldosterone exert its effects?

A

Experts its actions by regulating gene transcription

19
Q

What is the most abundant corticosteroid?

A

Cortisol

20
Q

Where is cortisol synthesised and released from?

A

Zone fasiculata in response to ACTH

21
Q

What is the carrier proteins in plasma?

A

Transcortin

22
Q

How does the cortisol receptor exert its actions?

A

By regulating gene transcription

23
Q

Why do all steroid hormones need to be bound to plasma proteins when travelling in the blood?

A

Because steroid hormones are lipophilic

24
Q

What are the effects of cortisol?

A 
Inc protein breakdown in muscle
Inc gluconeogenesis
Inc lipolysis in fat 
Dec peripheral uptake of glycolysis 
Dec immune response
25
Q

What can chronic high levels of cortisol result in?

A

Redistribution of fat especially in the abdomen, subclavicular fat pads and dorsal-cervical fat pad and on the face

26
Q

How does cortisol affect glucose uptake?

A

Cortisol inhibits GLUT4 translocation in muscles therefore preventing glucose uptake

27
Q

What does the hypothalamic-pituitary-adrenal axis do?

A

Regulates cortisol secretion

28
Q

What does ACTH stand for?

A

Adrenocorticotropic hormone

29
Q

What is ACTH?

A

Single chain polypeptide hormone

30
Q

What is the initial precursor of ACTH?

A

POMC - large protein

31
Q

How is ACTH released?

A

Released in circadian rhythm

32
Q

What are the features of ACTH?

A

Hydrophillic and interacts with high affinity receptors on the surface of cells in the zone fasiculata and reticularis

33
Q

What is the function of ACTH?

A

Causes conversion of cholesterol esters to free cholesterol.

34
Q

What happens if you get too much aldosterone produced?

A

Hyperaldosteronism

35
Q

What are the different types of hyperaldosteronism?

A

Primary and secondary

36
Q

What happens in primary aldosteronism?

A

Defect in the adrenal cortex caused by hyperactivity on or both adrenal glands.

37
Q

What is a diagnostic feature of primary hyperaldosteronism?

A

Low renin levels but no decrease in aldosterone levels. (High aldosterone:renin ratio).

38
Q

What is the cause of secondary hyperaldosteronism?

A

Overactivity of RAAS.

39
Q

What is the diagnostic feature of hyperaldosteronism?

A

High renin levels (low aldosterone:renin ratio)

40
Q

What are the signs of hyperaldosteronism?

A

High blood pressure, left ventricular hypertrophy, stroke, hypernatraemia and hyperkalaemia.

41
Q

What is the treatment for hyperalsoteronism?

A

Depends on type

MEH A (19 decks)

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