Disturbances of Adrenal hormones secretion Flashcards
Hypersecretion of Aldosterone is divided into:
- Primary hyperaldosteronism (conn’s Syndrome): tumor in zona glomerulosa secreting excess mineralocorticoids
- Secondary Hyperaldosteronism: in heart failure, Liver cirrhosis or nephrosis –> elevated RAAS
- Glucocorticoid-remediable Aldosteronism (GRA): genetic error causing Zona glomerulosa to be hypersensitive to ACTH (increased All steroid hormones on adrenal gland including Aldosterone)
Explain why liver cirrhosis causes secondary hyperaldosteronism
Decreased Aldosterone reduction and conjugation —> Accumulates (excess)
Explain why Nephrosis causes secondary hyperaldosteronism
- Decreased Albumin in blood (albuminuria)
- leading to decreased osmotic pressure
- edema —> Aldosterone secretion
Features of Hyperaldosteronism
Hypokalemia, leading to:
* Hypokalemic nephropathy –> polyuria
* Hyperpolarisation –> Muscle weakness
* Metabolic Alkalosis (due to H+ excretion) —> decrease plasma Ca2+ —> Tetany
* inhibition of insulin secretion —> decrease glucose utilisation (worsens DM)
Hypertension, cause d by Na+ & water retention –> Expansion of ECFvolume
Explain why in Primary Hyperaldosteronism (conn’s Syndrome) , there is no edema == there is Escape phenomenon
Due to Atrial Naturitic Peptide (ANP):
1. Due to expansion of ECF, central venous pressure increases
2. this stimulates secretion of ANP
3. ANP balances out Na+ & Water retaining effect of Aldosterone by:
* Decrease responsivness to Zona glomerulosa
* Inhibit renin secretion
* Increases GFR & Inhibits Na+ reabsorption
Explain why secondary effects of Glucocorticoid-remedied Aldosteronism (GRA) are minimal
GRA causes secretion of All adrenal steroid hormones —> glucocorticoid corrects effect of Aldosterone
Name disease of glucocorticoid Hypersecretion
Cushing’s Syndrome
Causes of Cushing’s Syndrome
- ACTH independent: Adrenocortical tumors
- ACTH dependent: Bilateral hyperplasia of Adrenal cortex secondary to Hypersecretion of ACTH
- Adminstration of excess cortisone
Levels of ACTH in ACTH independent cushing’s syndrome
Low, due to negative feedback mechanism
Levels of ACTH in ACTH dependent cushing’s syndrome
High
effect of Cushing syndrome on metabolism
Protein metabolism–> Catabolic:
* Thin skin, fragile capillaries, easy bruising
* thin hair
* poor wound healing
* Osteoprosis
* Muscle atrophy
* Suppressed immunity
Fat Metabolism:
* Trunkal obesity —> Moon face & Buffalo hump
* Purple striae in abdomen: Stretch of thin skin by fat, showing underlying vessels
* Hyperlipidemia & ketosis
Carbohydrate Metabolism:
* Increase Gluconeogenesis & decreases peripheral glucose utilisation —> Hyperglycemia (& DM)
effect of Cushing’s syndrome not related to metabolism
CNS:
* Increases apetite
* insomnia
* euphoria
Mineralocorticod effect (when excess) —> Hypertension
Excess Androgen –> Acne & facial hair
Excess ACTH (in ACTH dependent Cushing’s) –> pigmentation (has melanocyte stimulating activity)
Hypersecretion of Adrenal Androgens in Adult females is called:
Adreno-genital syndrome
Hypersecretion of Adrenal Androgens in intrauterine females is called:
Female pseudohermaphrodite
Charactaristics of Adreno-genital syndrome
- facial hair growth
- deep voice
- acne
- balding
- Masculine distribution of body hair
- Atrophy of breast
- Loss of menses
- Enlargement of clitoris
- Masculine muscle development
