endocrinology 4 - adrenal cortex Flashcards

1
Q

Name the 3 zones of the cortex?

A
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2
Q

What does the zona reticularis produce?

A

sex hormones

(low affinity androgens)

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3
Q

What does zona fascicularis produce?

A

glucocorticoids (cortisol)

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4
Q

What does the zona glomerulosa produce?

A

aldosterone

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5
Q

name 3 types of cholesterol (steroid hormones)

A

aldosterone

cortisol

sex hormones

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6
Q

What type of secretion regulates glucocorticoid release?

A

diurnal rhythm (it has a circadian rhythm but can be induced)

–> inducible in response to stress

i.e a rhythmic inducible release

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7
Q

Name the primary glucocorticoid

A

cortisol

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8
Q

What hormone is released from the hypothalamus to stimulate ACTH?

A

CRH

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9
Q
A

ACTH promote cholesterol to make cortisol

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10
Q

What tissue doe cortisol have an effect on?

A

IMMUNE system

liver

muscle

adipose tissue

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11
Q

What does ACTH bind in the adrenal cortex?

A

membrane-bound receptors on cells of zona fasciculata

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12
Q

What is the long-term mediator of stress response?

A

cortisol

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13
Q

Does cortisol help with hypoglycaemia?

A

yes

opposes insulin

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14
Q

How does cortisol prevent hypoglycaemia?

A

stimulates gluconeogenesis

breaks down fat and uses A as energy source

breaks down protein into AA for use as energy source

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15
Q

What is gluconeogenesis?

A

glucose form non-carbohydrate source

(not glycogen)

can use glycogen if it really needs to

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16
Q

How does cortisol have an effect on immune function?

A

supress inflammatory immune response

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17
Q

Does cortisol help with proper development?

A

yes

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18
Q

What effect does cortisol have on brain function?

A

mood

learning and memory

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19
Q

What are the non-essential functions of cortisol?

A

growth

reproduction

20
Q

What hormones does cortisol have an effect on?

A

required for full glucagon and catecholamine activity

stimulates expression of their receptors

enhance cardiovascular drive and respiratory

21
Q

androgens male or female?

A

male/female

22
Q

What do low affinity androgens make?

A

testosterone (male)

estrogen (female)

these are made in non-adrenal tissues

23
Q

Where are low affinity androgen secreted from?

A

cortex

24
Q

What does aldosterone regulate?

A

minerals e.g. na and k

25
Q

What does the liver constitutively release?

A

angiotensinogen

(does not have an effect)

26
Q

What does the kidney release if blood volume decreases?

A

release renin

27
Q

What does angiotensinogen and renin make?

A

angiotensin I

ACE converts this to

agII

28
Q

What is the effect of agII on the kidney?

A

stimulates aldosterone

29
Q

What is the effect of aldosterone on the kidney?

A

increase na permeability/reabsorption

increase water conservation

hold onto water and maintain electrolyte balance

30
Q

What is the aldosterone receptor?

A

mineralocorticoid receptors (intracellular)

31
Q

What is a drop in blood volume?

A

haemorrhage or dehydration

(*increase na levels)

32
Q

Where in the kidney does ag II bind?

A

binds receptors on the surface of zona glomerulosa cells

this activates biosynthesis of aldosterone

33
Q

What is the syndrome associated with hypercortisolism?

A

cushings syndrome

34
Q

What is a predictable sign of hypercortisolism?

A

diabetagenic (hyperglycaemia) –> excessive gluconeogenesis

tissue wasting –> muscle, fat and bone breakdown

‘plumping’ of trunk and ‘moon face’ –> redistribution of fat

mood disorder/immunosuppression

hypertension (enhanced adrenaline and/or aldosterone-like effects incraesed blood pressure)

35
Q

What area have tissue wasting in hypercortisolism?

A

muscle

fat

bone breakdown

(skinny legs)

moon face

36
Q

What is the primary cause of hypercorticolsim?

A

adrenal tumour that autonomously produces cortisol (not controlled by ACTH)

37
Q

What is the secondary cause of hypercorticolism?

A

pituitary tumour autonomously secretes ACTH (not controlled by CRH or -ve feedback)

cushings disease

38
Q

What is an iatrogenic cause of hypercorticolism?

A

occurs following glucocorticoid therapy for another condition

  • commonly used as topical or systemic anti-inflammatory drugs
39
Q

treatment for hypercorticolism?

A

removal of tumour

stop glucocorticoid therapy - has to be gradual

40
Q

What syndrome is associated with hypocorticolism?

A

addisons disease

41
Q

What is addisons disease associated with?

A

hypoglycaemia

hypotension

hyponatremia/hyperkalemia- loss of salt balance
–> dehydration and cardiovascular risk

mood disorders/ weakness/lethargy

skin pigmentation

42
Q

What is the primary cause of adrenal insufficiency?

A

loss of adrenal cortical function (90%)

tuberculosis, invasive tumours, autoimmune attack, genetic

following minor stress/illness

43
Q

What percentage loos of adrenal function occurs before symptoms of adrenal insufficiency is apparent?

A

90%

44
Q

What are the causes of secondary adrenal insufficiency?

A

pituitary disease –> ACTH deficiency

symptoms less dramatic - aldosterone not affected (ACTH independent)

45
Q

What is the treatment for adrenal insufficiency?

A

daily oral administration of glucocorticoids and mineralocorticoids

careful dietary/fluid management

treatment of causative disorder

46
Q

How is cushings syndrome relevant to dentistry?

A

suppressed immune/inflammatory systems
–> risk of infection/ poor wound healing

diabetic consideration

emotionally liable (jumpy, hyperactive)

hypertension (LA effected)

47
Q

What are the implications for addison’s disease for the dentist?

A

pigmentation

hypotension

they are on steroid management