L8 - Adrenal causes of hypertension COPY Flashcards
ADRENAL HYPERTENSION
i) name the three main causes of hypertension
ii) what is the main cause of adrenal hypertension? what happens? what layer of the adrenal cortex is implicated?
iii) name three causes of this
iv) name a rare tumour of the adrenal medulla that may cause this
v) name one other cause of adrenal hypertension
i) essential, renal and endocrine
ii) main cause is primary hyperaldosteronism
- increased aldosterone production from the zona glomerulosa
iii) primary HAS can be caused by an adenoma, hyperplasia of the adrenals or a rare genetic cause
iv) phaeochromcytoma
v) congenital adrenal hyperplasia (enzyme defect in the adrenals)
PATHWAY FOR ALDOSTERONE SECRETION
i) which enzyme travels to the adrenal cortex and allows the zona glomerulosa to produce aldo?
ii) what does aldosterone cause in the nephron? what happens as a consequence of this?
iii) what ion is brought into the blood and what ion is excreted into the urine under aldosterone control?
iv) name two things that can cause inappropriate aldo release
v) name four classes of drugs which can be used to decrease aldosterone production
i) angiotensin II
ii) causes salt and water to be reabsorbede
- results in expansion of plasma volume (kidney recognises low BP and releases renin)
iii) Na+ moves into the blood and K+ moves into the urine
iv) adenomas and hyperplasia of the adrenals can cause inapprop aldo release
v) renin inhibitors, ACE inhibitors, aldosterone antagonists, AGII receeptor blockers (ARBs)
SCREENING FOR PRIMARY HYPERALDOSTERONISM
i) which two types of pathology do individuals with PA have more of compared to people with essential HT?
ii) name three sequalae of this
iii) give three indications for screening
iv) high aldosterone exists across a spectrum of hypertension
true or false?
i) renal and vascular
ii) can cause stroke, cardiac and renal problems
iii) hypokalemia, resistant HT (inadequate control on 3 drugs), younger people with HT
iv) true
DOES THIS PATIENT HAVE PRIMARY HYPERALDOSTERONISM?
i) which two things may be seen on initial screening in relation to renin and aldosterone? which parameter should be looked at first?
ii) what confirmatory test is commonly used? what are the expected findings if patient has PA or not?
i) supressed renin (this is the first thing to look at as aldo negatively feeds back to renin)
- aldosterone may be normal or high
ii) use oral or IV Na+ supression test to confirm (dynamic test)
- if healthy should see decrease in aldo as plasma vol increases
- if PA then you may not see a decrease in aldo
ONCE PA DX CONFIRMED - WHERE IS THE LESION?
i) name three tests that can be carried out
ii) name two things you may find in these tests
iii) which test may allow you to see which adrenal the excess aldosterone is coming from?
iv) what is administered before doing a metomidate PET CT? why?
i) 1) adrenal CT scan to look fr nodules
2) adrenal venous sampling
3) metomidate PET CT
ii) a secreting adenoma or bilateral hyperplasia
iii) do adrenal venous sampling to see which adrenal the excess aldo is coming from
iv) give dexamethasone to supress cortisol function (so you can see the aldo secretion) then give isotope - light intensity indicates aldo production as cortisol has been turned off
TREATMENT FOR HA
i) what is the main treatment for a unilateral adenoma? what may also be given?
ii) what is the main type of treatment for bilateral hyperplasia? name the drug class
iii) which specific drugs may be given for bilateral hyperplasia?(2) give a disadvantage of each
i) laproscopic adrenalectomy
- may also be given medical treatment
ii) bilat hyperplasia - get medical treatement (aldosterone antagonists)
iii) give spironolactone - cheap but also activates the oestrogen receptor so can cause gynaecomastia in men
- eplereinone - not as effective as spironolac
THE ADRENAL MEDULLA
i) where does the adrenal medulla recieve innervation from? what NT is used? are these pre or post ganglionic?
ii) what are the two main products of the adrenal medulla?
iii) which has the largest biological effect?
iv) which precursor is stimulated by the medulla to make L-DOPA?
i) from pre ganglionic sympathetic neurons in the spinal cord
- uses Ach
ii) adrenaline and noradrenaline
iii) NA has biggest effect
iv) tyrosine
CATECHOLAMINES
i) what allows the conversion of noradrenaline to adrenaline? where does this come from?
ii) what is produced by phaeochromocytomas?
iii) what do paragangliomas produce? why?
iv) name another catecholamine produced by the adrenal medulla
i) need high levels of cortisol to convert NA to adren
- cortisol comes from the adrenal cortex
ii) Phaeochromocytomas produce adrenaline
iii) paragangliomas produce more noradrenaline than adrenaline as they dont sit close to cortisol producing areas
iv) dopamine
BIOLOGICAL EFFECTS OF CATECHOLAMINES
i) which two receptors does NA stimulate? (2) what effect does it have on blood vessels? what two things does this cause?
ii) what effect does NA have on glucose?
iii) which two receptors does adrenaline stimulate? (3) what four things does this cause?
i) NA = alpha 1 and 2
- causes vasoconstriction
- causes increased BP and pallor of skin
ii) NA causes glycogenolysis (increases blood glucose)
iii) adrenaline stimulates alpha 1 and beta 1 & 2
- causes bv to vasoconstrict
- vasodilation in muscles
- tachycardia
- sweating
PHAEOCHROMOCYTOMA
i) which hormones do these tumours make? (2)
ii) what % are diagnosed post mortem?
iii) name five symptoms that present in ‘spells’
iv) name one other principal presenting symptom that can be permanent or intermittent
v) what other part of the history may be specifically relevant when making a diagnosis?
i) adrenal medulla hormones - adrenaline and NA
ii) 20%
iii) headaches, palpitations, pallor, sweating and anxiety
iv) hypertension - can cause strokes and cardiac failure
v) family history of auto dominant conditions
GENETIC CONDITIONS ASSOCIATED WITH PHAEOS
i) name three genetic conditions associated with phaeochromocytoma
ii) which one has medullary carcinoma of the thyroid as the usual presenting symptom?
iii) which conditions has lots of skin nodules?
iv) which two conditions often present with bilateral phaeos?
i) neurofibromatosis 1
MEN 2
Von hippau lindau
ii) thyroid carcinoma = MEN (multiple endocrine neoplasia)
iii) NF1 has lots of skin nodules
iv) MEN and VHL often have bilateral tumours
BIOCHEMICAL DIAGNOSIS OF PHAECHROMOCYTOMA
i) name two possible presenting features (symptoms)
ii) which two parameters are looked at for biochem diagnosis?
iii) name three chemicals/hormones checked in each test
iv) which will always be high in phaeos?
i) tachycardia and anxiety
ii) 24 urine and plasma
iii) 24 hr urine - metanephrines, normetanephrins and 3 methoxytyromine (to see if making lots of DA)
plasma - NA and adrenaline and metanephrins
iv) metanephrins will always be high in phaeos
OTHER CAUSES OF ELEVEATED CATECHOLAMINES
i) name four other causes of high measured catecholamines
ii) which hypotensive drug with beta blocking activity should not be used for treating phaeos? why?
iii) where does urine dopamine come from? (2) should this be measured? if not, what should be measured instead/
i) obstructive sleep apnoea, labetalol, amphetamine drug use, L-DOPA
ii) labetalol - can increase catecholamine levels
iii) urine dopamine comes from the kidney and nervous system (not the adrenal medulla) - measure urine methoxytyramine
DX IMAGING FOR PHAEOCHROMOCYTOMAS
i) name two diagnostic imaging tests
ii) what is each test used for?
i) MIBG scan for phaeos (produce catecholamines - take up MIBG)
ii) PET CT for paragangliomas (extra renal phaeos) and for mets
MANAGEMENT OF PHAEOS
i) what is the main class of drug used? give two examples
ii) what action does this drug have?
iii) what other class of drug may also be used? give an example
iii) if patient is going to receive surgery - what must happen first? why?
i) alpha blockers
- pheoxybenzamine and doxazocin
ii) alpha blockers lower BP (good to do before surgery)
iii) can also use beta blockers eg propanolol to stop tachycardia
iii) before surgery patient should have medical treatment to block NA/adrenaline activity to stop the tumour leaking
