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MEH * > 9.1 - The Adrenal Glands > Flashcards

9.1 - The Adrenal Glands Flashcards

1
Q

What are the components of each of the layers of the adrenal glands?

A

Capsule

Cortex

  • zona glomerulosa
  • zona fasicularis
  • zona reticularis

Medulla
- chromatin cells

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2
Q

What does the zona glomerulosa produce?

A

Mineralcorticoids e.g aldosterone

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3
Q

What does the zona fasiculata produce?

A

Glucocorticoids e.g cortisol

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4
Q

What does the zona reticularis produce?

A

Androgens e.g testosterone and oestrogen

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5
Q

What are steroid hormones?

A

Lipid soluble hormones synthesised from cholesterol in the adrenal glands and gonads

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6
Q

How do corticosteroids exert their actions?

A

Gene transcription

  • readily diffuse across the plasma membrane
  • bind to glucocorticoid receptors
  • binding causes dissociation of chaperone proteins e.g heart shock protein 90
  • receptor ligand complex trans locates to nucleus.
  • dimerisation with outer receptors can occur
  • receptor binds to glucocorticoid response elements (GREs) or other transcription factors.
  • receptor ligand complex translocates to nucleus
  • dimerisation with outer receptors can occur
  • receptors bind to glucocorticoid response elements or other transcription factors
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7
Q

What the main role of aldosterone?

A

Main actions in distal tubules and collecting ducts of nephron where it promotes expression of Na/K pump, promoting reabsorption of Na and exertion of K thereby influencing water retention, blood retention and thereby blood pressure

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8
Q

What is primary hyperaldosteronism and what are the causes?

A

Primary = too much aldosterone produced due to defects in adrenal cortex

Causes

  • bilateral idiopathic adrenal hyperplasia
  • aldosterone secreting adrenal adenoma (Conns syndrome)
  • low renin levels (high aldosterone to renin ratio)
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9
Q

What is secondary hyperaldosteronism and what is it caused by?

A

Secondary = to much aldosterone produced due to an overactive renin angiotensin aldosterone (RAAS) system

Causes

  • renin producing tumour e.g juxtaglomerular tumour
  • renal artery stenosis
  • high renin levels (low aldosterone/renin ratio)
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10
Q

How would you differentiate primary from secondary hyperaldosteronism?

A 
Blood test
High renin (low aldosterone /renin ratio) = secondary
Low renin (high aldosterone/renin ratio)= primary
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11
Q

What are the signs of hyperaldosteronism?

A 
High BP
Left ventricular hypertrophy 
Stroke
Hypernatraemia
Hypokalaemia
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12
Q

What’s the treatment for hyperaldosteronism?

A
  • depends on type
  • aldosterone producing adenomas removed by surgery
  • spironolactone (mineralcorticoid receptor antagonist)
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13
Q

What are the actions of cortisol?

A
  • increased protein breakdown in muscle and increased lipolysis in fat
  • increased gluconeogenesis in liver
  • resistance to stress
  • anti inflammatory effects
  • depression of immune response
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14
Q

How does cortisol negative feedback system work?

A
  • stress = stimulus
  • detected by hypothalamus which produced Corticotropin releasing hormone (CRH)
  • goes to anterior pituitary which released Adrenocorticotropic hormone (ACTH)
  • ACTH goes to the adrenal cortex which produces cortisol
  • increase in cortisol levels reduced CRH and ACTH production
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15
Q

What are the actions of glucocorticoids e.g cortisol?

A

Increased glucose production
- therefore increased glycogen storage in liver

Breakdown of protein
- cortisol inhibits GLUT4 translocation in muscle = low muscle uptake so there is a glucose sparing effect

Redistribution of fat
- due to high levels of cortisol

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16
Q

What’s is Cushing’s syndrome and what are the causes?

A

Cushing’s syndrome = chronic excessive exposure to cortisol

External causes
- perceived glucocorticoids

Endogenous

  • benign pituitary adenoma secreting ACTH
  • excess cortisol produced by adrenal tumour (adrenal cushings)
  • non pituitary adrenal tumours producing ACTH e.g small cell lung cancer
17
Q

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

A
  • moon shaped face
  • buffalo hump at the base of the neck
  • abdominal obesity
  • purple striae
  • acute weight gain
  • hyperglycaemia
  • hypertension
18
Q

What are steroid drugs used for?

A
  • asthma
  • inflammatory bowel disease
  • rheumatoid arthritis
  • other autoimmune conditions
  • used to suppress immune reactions to organ transplant
19
Q

What is Addison’s disease?

A

Chronic adrenal insufficiency
Caused by an autoimmune response, fungal infection, adrenal cancer and adrenal haemorrhage
More women effected than men.

20
Q

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

A
  • postural hypotension
  • lethargy
  • weight loss
  • anorexia
  • increased skin pigmentation
  • hypoglycaemia
21
Q

Why does hyperpigmentation occur in Addison’s?

A

Decreased cortisol =
Decreased negative feedback on ant pit
= more POMC required to synthesise Adrenocorticotropic hormone and as a byproduct of this synthesis you get melanocytes stimulating hormone

22
Q

What are the androgens and what do they do?

A

Dehydroepiandrosterone (DHEA) and androstenedione

In males DHEA is converted to testosterone
In females androgens promote libido and are the only source of oestrogen after menopause

Promote axillary and pubic hair growth in both sexes

23
Q

What do chromatin cells act as?

A

In adrenal medulla, they lack axons but act themselves as postganglionic nerve fibres that release hormones into the blood e.g adrenaline and noradrenaline (20% of c ells lack N methy transferase so secrete NA)

24
Q

What receptor increases HR and contractility?

A

B1

25
Q

What receptor causes bronchodilator?

A

B2

26
Q

What receptors cause vasoconstriction and vasodilation?

A 
Constriction = a1
Dilation = b2
27
Q

How does adrenaline increase HR?

A

B1 adrenoreceptors = stimulators
CAMP activates HCN channels responsible for pacemaker current

PKA phosphorylates HCN channels = modulates function

PKA phosphorylates L type Ca channels = potentiates opening, increasing the slope of the upstroke of the action potential

28
Q

What’s a phaeochromocytoma?

A 
Chromatin cell tumour 
Causes
- severe hypertension
- headaches
-palpitations 
- diaphoresis (sweating) 
- anxiety
- weight loss
- elevated blood glucose

MEH * (21 decks)

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