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PA10315 2nd semester > Adrenal gland > Flashcards

Adrenal gland Flashcards

1
Q

What acts on the adrenal gland

A

Renin-angiotensin system and autonomic nervous system

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2
Q

Medulla function

A

secretes catecholamines eg adrenaline (noradrenaline)

Acts on alpha and beta adrenergic receptors to incr HR and RR
Acute stress response

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3
Q

Cortex function

A

Releases aldosterone (mineralcorticoid): Na+ reabsorption (NA+ leads, H2O follows), incr BV as a result

Releases Glucocorticoids eg cortisol: via glucocorticoid receptors- regulate gene transcription, mobilize glucose into the blood

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4
Q

adrenal glands overall function

A

mediating response to acute and chronic stress

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5
Q

What is acting on glucocorticoids

A

Hypo (CRH) –> Pituitary (ACTH)

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6
Q

Medulla structure

A

modified sympathetic ganglion

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7
Q

Outer cortex 3 zones

A

ZG- mineralocorticoid- aldosterone

ZF- glucorticoid or corticosteroid- cortisol

ZR- androgen precursors

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8
Q

Mineralcorticoids effects

A

blood volume/sodium effects

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9
Q

Glucocorticoids effects

A

metabolic effects

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10
Q

Catecholamines effects

A

bodily symptoms

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11
Q

Regulation of secretion in the adrenal medulla

A

adrenal medulla is part of the sympathetic division of the autonomic nervous system
Considered as specialised group of postganglionic neurones
Secretion of hormones controlled by sympathetic preganglionic nerve fibres

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12
Q

Effects of medullary catecholamines

A

same as direct activation of symp nerves but:

  • lasts longer
  • effects generalised to all cells with alpha and/or beta receptors (GPCRs)

Major effect is on CO and cellular metabolism due to greater effect of adrenaline than NA at beta receptors

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13
Q

action of adrenaline vs noradrenaline

A

Noradrenaline has a more specific action working mainly on alpha receptors to increase and maintain blood pressure whereas epinephrine has more wide-ranging effects. Norepinephrine is continuously released into circulation at low levels while epinephrine is only released during times of stress.

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14
Q

Specific effects of catecholamines

A
  • incr release of glucose from liver
  • incr release of fatty acids from fat stores
  • incr HR
  • incr constriction of visceral BVs
  • incr BP
  • Incr metabolic rate in skeletal muscles
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15
Q

Precursor of aldosterone

A

Cholesterol

Corticosterone

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16
Q

Actions of aldosterone

A

Stimulates reabsorption of Na+/excretion of K+ in cortical collecting ducts
Decr ratio of Na+ to K+ in sweat and saliva
Increases reabsorption of Na+ in the colon and excretion of K+ in the faeces

Overall retain Na+ and lose K+
Net effect incr in plasma vol and hence cardiovascular pressure

17
Q

How does incr aldosterones increase NA+ reabsoprtion in the cortical collecting ducts

A

Increased synthesis of Na+ channels which move Na+ from tubular lumen into ccd cells (ATPase pump moves Na+ into ISF)

18
Q

Renin-Angiotensin system

—-vanders

A

see kidney/CV lectures

BP drop- renin produced from kidney, travels in blood to the liver.

Angiotensinogen is produced by the liver, and is then broken up by renin, an enzyme produced in the kidney, to form angiotensin I.
This travels to the lungs, where the angiotensin converting enzyme converts Angiotensin I to to II

Angiotensin II acts on the adrenal cortex to produce aldosterone, leading to more Na+ reabsorption , incr BV etc which incr BP

Incr BP feeds back -vely to reduce renin secretion

19
Q

Aldosterone anatgonist

A

Spironolactone: potassium-sparing diuretic hyperaldosteronism (Conn’s disease)

20
Q

ACE inhibitors

A

Captopril, enalapril
Anti-hypertensive
Cardiac failure

21
Q

ATII antagonist

A

Losartan

Similar to ACE inhibitors, used in hypertension

22
Q

Common structure in all steroids

A

tetraplanar ring

23
Q

Glucorticoids precursor

A

cholesterol

24
Q

How are most glucorticoids transported

A

Bound to binding proteins

25
Q

Regulation of glucorticoid secretion

A

Hypo, in response to stress releases CRH which acts on pituitary gland to produce ACTH, which acts on adrenal glands to produce cortisol, circulates and acts on tissues

Negative feedback - cortisol switches off pituitary production of ACTH and hypo production of CRH

26
Q

CRH

A

corticotrophin releasing hormone

27
Q

ACTH

A

adreno cortico Trophic hormone

28
Q

Fluctuations in cortisol are caused by

A

fluctuations in ACTH secretion from the pituitary gland

Leads to circadian rhythm

29
Q

Metabolic actions of glucorticoids

A

Stimulate gluconeogenesis in the liver- incr plasma glucose
Incr proteolysis in the muscle- creates AA’s which act as substrates for generation of glucose in the liver
Lipolysis of fat- incr glycerol production - alternative substrate for glucose so incr plasma glucose. Incr FFA production acts as fuel source for muscle and liver

30
Q

Addison’s disease- cortisol deficiency

A

cellular metabolism: hypoglycaemaia, weight loss
CV: vasodilation, hypotension, reduced BV, anaemia and lymphocytosis
CNS: fatigue and anorexia
Salt balance: reduced Na, incr K (mineralcortocoid loss)
Inflammatory and immune system: tendency towards autoimmune disease

31
Q

Corticosteroids

A

Cause rise in plasma glucose levels (release from liver and incr gluconeogenesis)

Causes incr in proteolysis, which can bring about muscle wasting skin thinning
Cause fat redistribution eg moon face (Cushings)
Cause incr breakdown of triglycerides, leading to rise in plasma Fatty acid levels

SUppress inflammation and immune responses

32
Q

Cushing’s disease- cortisol excess

A

cellular metabolism: hyperglycaemia, fat redistribution, truncal obesity. Weak muscles, skin and bone and poor wound healing
CV: hypertension, incr BV, leukocytosis, erthyrocytosis
CNS: depression,euphoria
Salt balance: incr NA, decr K (more mineralocorticoid)
Inflammatory and immune response: decr inflam response, incr infection and decr fibrous tissue formation

PA10315 2nd semester (27 decks)

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