Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MNE > Adrenal steroid synthesis > Flashcards

Adrenal steroid synthesis Flashcards

1
Q

Choleterol —> pregnenolone

(2 enzymes)

A
  1. choelsterol-ester —-> cholesterol

via esterase (+cAMP)

*****StAR (steroid acute regulatory protein) brings cholesterol into MITOCHONDRIA******

  1. cholesterol —> pregnenolone & isocaproaldehyde

via P450 SCC

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

P450 SCC

A

Side chain cleavage enzyme

Stimulated by: ACTH, LH, angiotensin II, cAMP

Inhibited by: aminoglutethimide

cholesterol —> pregnenolone & isocaproaldehyde

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

Zona specificity

A

Each zona makes specific adrenal hormones because of their enzymatic content

  1. Glomerulosa: Aldosterone/ mineralocorticoid

only one to have 18 hydroxylase & 18 hyrdoxyDH

  1. Fasciculata: Cortisol / glucocorticoid

17 α hydroxylase

  1. Reticulosa: DHEA / androgen

17 α hydroxylase & C17-20 lyase

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

Aldosterone synthesis (mineralocorticoid)

(5 enzymes)

A

Located in Zona glumerulosa

*1. P450 SCC

  1. 3ß hydroxysteroid DH; 5,4 isomerase
  2. 21 hydroxylase
  1. 11ß hydroxylase
  2. 18 hydroxylase

18 hydroxy DH

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

Renin-Angiotensin system

A
  1. Renin production from juxtaglomerular cells of renal afferent arteriole (decreased BP, Na)
  2. Liver –> angiotensinogen –> angiotensin I
  3. angiotensin I –> angiontensin II

via ACE (from lungs)

  1. Angiotensin II negative feedback on juxtaglomerular cells —x renin
  2. angiotensin II activates aldosterone synthesis

Also vasoconstrictive to increase BP

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

Cortisol synthesis (glucocorticoid)

(4 enzymes)

A
  1. P450: 17α hydroxylase (17-20 lyase inactivated)
  2. 3ß hydroxysteroid DH; 5-4 isomerase
  3. 21 hydroxylase
  4. 11 hdyroxylase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Glucocorticoid stimulation and action process

A
  1. stimulated by ACTH
  2. Cortisol is ONLY steroid to feedback inhibit ACTH release
  3. CRH (hypothalamus) —>

POMC —> ACTH (anterior pituitary)

ACTH —> adrenal cortex

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

DHEA synthesis (Androgens)

(3 enzymes)

A

Low levels of 3ß hydroxysteroid DH; 5-4 isomerase in adrenal cortex

  1. P450 SCC
  2. 17α hydroxylase
  3. C17-20 lyase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

C17-20 lyase

Exists on P450 bi-functional enyzme

w/ 17 hydroxylase

A
  1. Found in adrenals and gonads
  2. DHEA —> DHEA-3 sulfate
  3. Travels to gonads by tightly binding to

sex hormone bonding globulin

  1. DHEA –> androstenedione –> testosterone —> Estradiol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Degradation (4)

A
  1. Liver modifications —> more hydrophilic
  2. A ring: reduce double bond —> DIHYDRO
  3. C3 ketone: reduced —> HYDROXY
  4. Add clucuronide or sulphate to hydroxy groups

*Bind less well to carrier proteins & excreted rapidly

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

Transport binding

  1. Aldosterone
  2. Cortisol
  3. Deoxycorticosterone (DHEA)
A
  1. WEAK: albumin & CBG
    - short half-life, 36% free
  2. CBG (weak albumin)
    - long half-life, 8% free
  3. Albumin, CBG
    - 4% free

*CBG= transcortin

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

Addison’s Disease

  1. Deficiency
  2. Cause
  3. Characterization (4)
A
  1. Insufficient GLUCOCORTICOIDS, overproduction of CRH, ACTH and POMC peptides (αMSH)
  2. Caused by destruction of adrenals (usually autoimmune)
  3. intolerance to stress, extreme sensitivity to insulin, pigmentation
    - hypoglycemia, hypovolemic, low Na levels, hypotensive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Secondary Adrenal insufficiency

  1. Deficiency
  2. Cause
  3. Characterization (2)
A
  1. Lack of ACTH
  2. No ACTH production
  3. intolerance to stress & extreme sensitivity to insulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cushing’s syndrome

  1. Mutation
  2. Cause
  3. Characterization (5)
A
  1. Excess GLUCOCORTICOIDS
  2. tumor (Cushing’s disease=+ACTH), pharmacological use
    • moon face =edemous swelling

Redistribution of fat: Truncal obesity, dosro-cervical (neck)

  • hyperglycemia: excess cortisol raises blood sugar
  • Accelerated gluconeogensis (striae due to breakdown of connective tissue)
  • decreased resistance to infection/ decreased inflammatory response/compromised immune system
  • hyperpigmentation in cushing’s DISEASE

*mineralocorticoid activity of cortisol= hypertension, edema, alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Conn’s Syndrome

  1. Mutation
  2. Cause
  3. Characterization (4)
A
  1. MINERALOCORTICOID excess
  2. adenoma (benign tumor) of glomerulosa
  3. Hypertension, edema, alkalosis

renin & angiotensin II levels decrease

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

Secondary Aldosteronism

  1. Mutation
  2. Causes
  3. Characterization (4)
A
  1. Hyperplasia and hyperfunction of juxtaglomerular cells
  2. Renal artery stenosis
  3. Hypertension, edema, alkalosis,

Elevated levels of angiotensin due to cells sensing low BP

17
Q

Andrenogenital snyndrome (Congentinal Adrenal Hyperplasia)

  1. Deficiency
  2. Cause
  3. Characterization
A
  1. ACTH overproduction –> shunt to overproduction of androgens
  2. Deficiency in 21 hydroxylase or 11ß hydroxylase
  3. increased body growth, virilization(clitoromegaly), ambiguous external genitalia

*no cortisol, so no negative feedback

  1. Treatment: cortisol (necessary for life, est. neg feedback to normalize androgen levels)

MNE (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions