Endocrine Adrenal Disorders Flashcards
Name the 6 Adrenal disorders
(IX& RX)
- Cushings-Excess cortisol/ ATCH Rx surgery
- Primary Hyperaldosteronism – (high)Aldosterone : (low) renin ratio Rx spironolactone & amiloride
- Congenital Adrenal Hyperplasia (21 hydroxylase, 11 hydroxylase )= decrease cort. Increase androgenic steroids
- Hypoadrenalism Addison’s – Short synactin test Rx steroids
- Pheochromocytoma Medulla – Fractionated metanophrines 2ndln catacolamines
- PCOS – testosterone
Where corticotropin-releasing hormone, known as CRH
1. made,
2.What stimulates release 3. where dose it act
- Made in the hypothalamus
- Low cortisol
- Acts on the pit gland
Where is cortisol produce
What stimulates it
What dose it stimulate
- Zona faciularis
- inhibitory effect on Hypothalamus CRH
- inhibitory effect pit. ATCH
What does Cortisol do? (6)
- Stimulates glycogenesis
- Break down proteins
- Break down Lipid
- Reduce inflammation
- Increased sensitivity to catecholamines
- Inhibits proliferation of T lymphocytes
What does High levels of Cortisol do
reduce CRH in hypothalamus
Reduce pituitary production of ATCH
Main cause of excess endogenous cortisol
Pituitary adenoma= increase ATCHproduction = Cushing disease
What is produced in excess in Cushing’s
ATCH
Other causes of endogenous Cushing d’s (4)
- Pituatory adenoma
- Ectopic tumour in small cell Lung Ca
- Adrenal adenomas
4.Adrenal Carcinomas (Malignant)
3 Main lab test for Cushings
- 24-hour urine cortisol sample
- overnight (low does) dexamethasone suppression (Should have low serum cort levels mean neg feedback from pit intact; cortisol levels remain unchanged pituitary isn’t working
3.High does dex test:
Will suppress pituitary adenoma =Low ATCH low cort levels
overnight (low does) dexamethasone suppression (1mg)
Low Cortisol
Pituitary -ve feedback working
extra source no present
overnight (low does) dexamethasone (1mg) suppression
high Cortisol
pituitary response isnt working or
another sours of cortisol
Do high does Dex test
High dexamethasone suppression (8 mg)
Low ATCH and low Cortisol
pit adenoma effected
High dexamethasone suppression (8 mg)
High Cortisol and low ATCH
Another source outside the pituitary gland
High dexamethasone suppression (8 mg)
High ATCH and High Cort
paraneoplastic syndrome
What is released in the zona glomerulosa
aldosterone
-Adrenal cortex (mnemonic GFR - ACD
What is released in the * zona fasciculata
Cortisol
-Adrenal cortex (mnemonic GFR - ACD
What is released in the zona reticularis
dehydroepiandrosterone (DHEA)
-Adrenal cortex (mnemonic GFR - ACD
What is the function of Aldosterone? (5)
- HIGH androgens - FM Masculinization
- LOW aldosterone Salt wasting (HypoNA HyperK, Hypotension)
- LOW Corisol - Hypoglycemia
21 hydroxylase
Deficiency
Screen for at birth
Congenital Adrenal Hyperplasia
-
HIGH androgens-Masculinization FM
2.LOW aldosterone But HTN - Low cortisol
11 Beta hydroxylase
deficiency
But buildup of 11deoxcorticosterone weaker, earlier version of aldosterone = HTN
-
Low androgens - Poorly develop secondary sex characteristics Males
2.Low aldosterone But HTN & hyperNa, HyOPK, - *Low Cort**
17 Alpha hydroxylase
But buildup of 11deoxcorticosterone & corticosterone
High= hyperNa, HYPOK, HTN
Rx CAH (3)
Aldosterone, steroids, sex hormones’
- What stimulates Aldosterone?
- FX of aldosterone (2)
Stim by renin
1. Increases absorption of NA on the na/k pump in the DCT =Higher BP
2. Stimulates H+/APTase pumps in alpha intercalated cells = more protons out of the cells & HCO3 into cells = increase in pH
Cause of Acute primary adrenal insufficiency ,
Waterhouse-Friderichsen syndrome
=sudden increase in BP –> blood vessels in the adrenal cortex to rupture,–> filling up the adrenal glands with blood = causing tissue ischemia and adrenal gland failure.
What is Waterhouse-Friderichsen syndrome
=sudden increase in BP –> blood vessels in the adrenal cortex to rupture,–> filling up the adrenal glands with blood = causing tissue ischemia and adrenal gland failure.
Cause of Chronic Adrenal insufficiency?
Addison’s disease
Hormones released by they hypothalamus?
Hormones released by ant. Pit
What is the Synacthen test?
Ideally in AM Measure cortisol then give synactin (synthetic ATCH )and measure cort. 30 mins & 60 min. Normally cortisol would double ;
No raise in cort = Primary adrenal insufficiency
Result of Synacthen test indicating Primary Adrenal Insufficiency
No raise in cort = Primary adrenal insufficiency
Hypertension, HyPER Na, HyPOkalaemia, Hypo MG, metabolic ALKalosis may indicate
Primary hyperaldosteronism
Primary hyperaldosteronism causes (4)
- Bilateral idiopathic adrenal hyperplasia -is the cause in up to 70% of cases.
- Adrenal adenoma/ Conn’s syndrome )- previously thought to be most commonly cause
- Family Hyperaldosteron
- Adrenal carcinoma -v rare
Secondary hyperaldosteronism causes (3)
Renal artery stenosis
Heart failure
Liver cirrhosis and ascites
Perceive low BP= High levels of Renin Causing High levels of aldosteronism
Secondary hyperaldosteronism
High aldosterone & LOW renin
hyperaldosteronism
Drugs that should be stopped for 4-6 wk to test for hyperaldosteronism (5)
- Beta blker (Suppress Renin )
- Reduce aldosterone:
Spiro, CCB,ACEi & angiotensin antagonist =Increase renin ; stop for
Imaging
Rx for
Hormones released by post pit
How to EXPLAIN hypoglycemia
Exogenous drugs (alcohol, pentamidine, quinine quinolones )
Pituitary insufficiency (No GH or cort)
Adrenal failure (no cort )
Insulinoma / Immune hypoglycaemia
Non-pancreatic neoplasm (retroperitoneal sarcoma)
Stim of renin
(3)
Secretion is Low BP
Stim sympathetic nervous system
Low Na
What is the action renin?
via angiotensin and aldosterone increase BP
Fx Angiotensin
narrows your blood vessels and aldosterone causes your kidneys to retain water and salt.
Where a chromaffin cells (4) & what do they produce (2)?
Adrenal Medulla, carotid, bladder, Adom. aorta
Produce Catecholamines (nor epinephrine & Epinephrine)
Fx of Epinephrine(5)
Hrt
Eyes
Mscl
Glucose
- Increase CO
- BP
- Dilates pupils
- Increase blood flow to mscls
- Increase Glucose
Pheochromocytoma causes (3)
- MEN2a & MEN2b ( due to mutation in RET gene)
- VLH (mutation in VLH gene))
- Neurofibromatosis 1 = mutation in NF1 gene)
Ix for Pheochromocytoma
- 24 hr urinary or plasma collection of metanephrines (sensitivity 97%*)
- this has replaced a 24 hr urinary collection of catecholamines (sensitivity 86%)
Rx Pheochromocytoma
Surgery is the definitive management.
Pt first however be stabilized with:
Phenoxybenzamine very potent alpha blker (More than doxazosin. ).Then add beta blker . Labatalol is recommended
3ps of Men 1
4 pancreatic ca of MEN 1
2 ps of men 2a
1 P of Men 2b
Men 2b body habitus and skin
