Adrenal Gland Flashcards

1
Q

What does the adrenal cortex release?

A

Mineralocorticoid-aldosterone (Zona glomerulosa)
Glucocorticoids- cortisol (Zona fasciculata)
Androgens- DHEA and androstenedione (Zona reticularis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does the adrenal medulla release?

A

Epi
NE
Dopa
Dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the rate limiting step for steroid hormone synthesis?

A

Cholesterol to pregnenolone which is catalyzed by 20, 22 desmolase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does the glomerulosa layer of the adrenal cortex lack so it only synthesizes aldosterone?

A

17 alpha-hydroxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the major action of aldosterone?

A

to stimulate the kidney to reabsorb Na and H2O and enhance K secretion @ the distal nephron segments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What do the Fasciculata and reticularis of the adrenal cortex layers lack and what can it synthesize?

A

lack aldosterone synthase but have 17-alpha-hydroxylase so cortisol and androgen synthesis(DHEA/androstenedione) occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does the cortisol feedback loop work?

A

High cortisol levels inhibit expression of CRH receptor and ACTH in the coricotrophs of the anterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the metabolic effects that cortisol has?

A

Stimulates gluconeogenesis in liver
Enhances protein breakdown in muscle
Stimulates lipolysis
Decreases osteoblastic activity and interferes with Ca absorption in the gut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What anti-inflammatory effects does cortisol have?

A

inhibits cytokine production
inhibits production of chemo-attractant molecules
Stabilize lysosomal enzymes
Contributes to vasoconstriction and decreased capillary permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What immunosuppressive effects does cortisol have?

A

Decreases lymphocyte proliferation

inhibits hypersenstivity reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What receptors are on the adrenal cortex cells for ATCH?

A

Melanocortin-2 receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the precursor protein for ACTH and where is it located?

A

Pro-opiomelanocortin POMC–located in the coricotrophs in the anterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When is the highest level of ACTH secretion?

A

morning hours and diminishes late in the afternoon—corresponds to low glucose level in the morning and want to increase blood glucose levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What occurs with 21-a-hydroxylase deficiency?

A

decreased production of cortisol–hypoglycemia/hyperplasia of adrenal gland and aldosterone–loss of salt/hypotension/dehydration

  • -Increased ACTH production–no neg feedback–Adrenal hyperplasia
  • -increased androgen production–ambiguous genitalia in females
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is 21-a-hydroxylase deficiency diagnosed?

A

Elevation of 17-hydroxprogesterone before and after ACTH stimulation test

also molecular genetic analysis of CYP21 gene–encodes 21-a-hydroxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is 21-a-hydroxylase deficiency treated?

A

Glucocorticoids–reduces ACTH levels–decrease hyperplasia and over production of androgens

Mineralocorticoids– used to prevent salt wasting and decreased elevated renin levels

17
Q

What occurs with 17-a-hydroxylase deficiency?

A

Reduced cortisol–hyperplasia of adrenal gland and androgen synthesis

Increased cotisterone and aldosterone–HTN and hypokalemia

Reduced estrogen synthesis–sexual infantilism in females
Pseudohermaphroditism and sexual infantilism in males

18
Q

How is 17-a-hydroxylase deficiency treated?

A

Glucocorticoid—treat HTN and mineralocorticoid excess
Females–estrogen treatment
Males-surgery/testosterone treatment

19
Q

What is Cushings syndrome?

A

Occurs when body’s tissues are exposed to excessive cortisol for long periods of time–excess cortisol of any etiology

20
Q

What is Cushings dz?

A

hypercortisolism secondary to excess production of ACTH from a pituitary gland adenoma

21
Q

What are symptoms seen in Cushings?

A
Moon face
red face
upper body obesity
increased fat around neck
thinning arms and legs
osteopenia
muscle wasting and weakness
increased infections
glucose intolerance 
hypokalemia and HTN
22
Q

What is a dexamethasone suppression test?

A

Dexamethasone acts as cortisol and provides negative feedback to the pituitary to suppress the secretion of ACTH

23
Q

If a pt has an adrenal tumor what will be seen on the Dexamethasone suppression test?

A

Cortisol-high

ACTH-low

24
Q

If a pt has an ACTH production tumor what will be seen on the Dexamethasone suppression test?

A

Cortisol- high

ACTH- high

25
What is seen in a normal pt who undergoes dexamethasone suppression test?
Cortisol and ACTH both low--the dex is suppressing the ACTH secretion by negative feedback--No ACTH-->no cortisol
26
What is Addison's dz?
Hypoadrenal function--failure of the adrenal glands to produce enough cortisol and aldosterone is also deficient in primary adrenal insufficiency Usually due to autoantibodies against adrenal cells containing 21-a-hydroxylase
27
What are the symptoms of Addison's Dz?
Lack of aldosterone--hypotension and hyperkalemia
28
How is Addison's Dz diagnosed?
ACTH stimulation-- Normal response would be rise in blood and urine cortisol levels Adrenal insufficiency results in poor response or none at all CRH stimulation test-- Measure cortisol and ACTH in the blood before/after administration - -Primary adrenal insufficiency- high ACTHs but no cortisol production - -secondary adrenal insufficiency-- deficient cortisol responses and absent/delayed ACTH responses