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Biochemistry And Endocrinology > Adrenal Medulla And Hypertension > Flashcards

Adrenal Medulla And Hypertension Flashcards

1
Q

Where are catecholamine made?

A

Sympathetic nervous system and the medulla

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2
Q

What are catecholamines involved in?

A

Fight and flight

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3
Q

What are 2 branches of the autonomic nervous system?

A

Parasympathetic and sympathetic

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4
Q

What influence does the sympathetic nervous system have?

A

Dilates pupils, decreases saliva, dilates lung airways, increases heart rate, decrease gut movement, increases secretion of Noradrenaline and adrenaline, decreases bladder, increasing sweating and vessel contraction, increases BP

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5
Q

What does the parasympathetic nervous system do?

A

Decreases Dilation of pupils, increases saliva, decrease dilation of lung airways, decreases heart rate, increase gut movement, increases bladder, decreases vessel contraction, decreases BP

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6
Q

Biochemical markers of deficiency in catecholamines?

A

Low BP
Bowel habit disruption, diarrhoea.
Impaired urinary continuance and sexual arousal
Less sweating
Low glucose and low hypoglycaemic awareness
Eventually cardiovascular instability

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7
Q

You can also get selective adrenal catecholamine loss - what is this? is it serious?

A

When adrenal is damaged but isn’t too serious as there is normally other places catecholamines (particularly noradrenaline) can be released

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8
Q

Does adrenaline have a role in maintaining glucose?

A

Yes

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9
Q

Does adrenaline maintain glucose on its own and if not what does it do it with?

A

No - cortisol, growth hormone and glucagon

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10
Q

What does a profound loss of cortisol do to adrenaline?

A

Decreases adrenaline

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11
Q

Catecholamines -what are these products and do they have alpha or beta characteristics?

A

Adrenaline - alpha
Noradrenaline - beta

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12
Q

What does adrenaline have a role in?

A

Excess is, raising glucose and delivering it to tissue

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13
Q

Where do catecholamines act on?

A

9 receptors - alpha and beta adrenergic receptors

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14
Q

What drugs can block alpha affects

A

Doxazosin
Phenyoxybenzamine

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15
Q

What drugs block beta affects?

A

Propranolol

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16
Q

What happens if you get catecholamine excess? More alpha

A

Vasoconstriction - high BP, pale skin
Reduced gut activity and blood flow - nausea, butterfly’s
Headaches

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17
Q

What happens if you get catecholamine excess? More beta?

A

Heart racing - palpatations
Tendency to crease glucose
Phychological arousal - on edge, anxious, fearful
Overbreathe (airways dilation)

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18
Q

If you have intermittent excess catecholamines what symptoms do you get?

A

blood pressure variable
postural drops in blood pressure on standing
get attacks of panic+palpitations

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19
Q

What causes increase catecholamines?

A

Phaeochromocytoma (paraganglioma = outside adrenal, only some make cathechoamines)

Drugs – eg antidepressants (tricyclic, MAOIs), some cold cures (ephidrine, pseudoephedrine)

Physiological – severe stress/illnes

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20
Q

What are concerning signs of a phaeochromocytoma?

A

Headache, sweating, palpitations, high blood pressure, panic attacks and fear

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21
Q

What do you tests to see if someone has phaeochromocytoma

A

Metanephrons

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22
Q

What are the inactive forms of adrenaline and noradrenaline?

A

Normetadrenaline and metadrenaline

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23
Q

What is the pathway of release of catecholamine and metanephrines?

A

Dopamine goes into vesicles which gather at the membrane and are released by nerve signal.

In the alternative pathway the vesicles break spilling adrenaline and noradrenaline back into the cytoplasm and COMT turns them into metanephrones - this is bad

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24
Q

How would you diagnose a phaeochromocytoma?

A

24 urine to screen for metanephrines,

To localise it use MRI/CT or abdomen and pelvis.
MIGB scans
Venous sampling

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25
How do you manage a phaeochromocytoma?
- Initiate alpha blockade with phenyoxybenzamine - Then beta blockade with propranolol - surgery
26
After you remove consider if the phaeochromocytoma was part of a syndrome - what are these syndromes?
Von Hippel Lindau cerebellar - retinal, ± renal/pancreatic tumours/cysts MENII - medullary carcinoma thyroid, hyperparathyroidism, mucosal neuromas etc Paragangliomas - SDHB, SDHC, SDHD. Paragangliomas in neck imprinting ect. Neurofibromatosis - skin neurofibromas, multiple pigmented patches
27
Hypertension - what is too high?
Over 140/90
28
Is BP constant?
No
29
When will BP alter?
Normally lower at night can be affected with how its measured,
30
What tests are done to diagnose hypertension?
Should allow several readings over 5 minutes while person relaxingif seems raised should ideally average assessments over few weeks
31
Is hypertension important?
Yes as it is a risk factor for CVD
32
What are the 3 main CVD’s
Coronary heart disease - includes MI Cerebrovascular disease - dementia, stroke Arterial disease - peripheral vascular disease, renal impairment, renal artery stenosis, abdominal aortic aneurysms.
33
What are risk factors for CVD?
Hypertension, hyperglycaemia smoking, family history, poor history, obesity, insulin resistance, kidney disease, dyslipidaemia
34
What is hypercholesterolanemia?
High cholesterol
35
What two diagnostic tests are needed to make a hypertension diagnosis?
Clinical BP and ABPM/Home BP
36
How many grades of hypertension is there and a d what are these called?
Normal BP, High normal BP, Hypertension, Grade 1, grade 2 and grade 3
37
What is white coat hypertension?
Only hypertension due to the white coat affect
38
What are some key signs of hypertension that isn’t blood pressure?
Target organ damage (heart, eyes, kidneys) Life threatening symptoms (confusion, chest pain, heart failure an AKI) Accelerated hypertension
39
What grades of hypertension would get treatment?
Grade 1 (some people Grade 2 - 3 all people
40
What guidance would you give people with hypertension and an increased risk of CVS? What advice gets given to everyone?
➔advice about lifestyle changes to moderate BP (aim for weightin ideal range, limit salt intake, regular exercise etc) ➔BP kept under review (may be just x1-2/year if mild)and ➔may warrant drug treatment eventually if remain hypertension
41
What guidance would you give someone high risk of hypertension?
Anti-hypertensive drug treatment
42
What other situations would you start someone on anti-hypertensives?
ii) Established Cardiovascular disease– e.g. past heart attack (MI), stroke (CVA), definite angina etc iii)Target organ damage– e.g. heart ➔enlarged, kidney➔protein in urine, retinal damage (back of eye) iv)Especially vulnerable to raised blood pressure- e.g. diabetes, chronic kidney disease (especially proteinuria:albumin/creatinine>70) v)If at high Cardiovascular Disease (CVD) risk-usually 10-year CVD Risk, less if other increased CVD risk factors- e.g. Family history- relatives (especially close/many/young) with CVD eve
43
What are some BP target exceptions?
In cases of chronic kidney disease, diabetes or people who are frail and it could be risky lowering BP
44
What is resistant hypertension?
If blood pressure is high and the 3x drugs (ACE inhibitor or angiotensin, calcium blockers or thiazide-like diuretic) doesn’t help it
45
What would you do if someone had resistant HT?
Specialist, spironolactone drug and look for secondary causes
46
What causes hypertension?
Genetics Fetal programming - if you are born underweight Environment - diet, salt, stress
47
What is seen in all hypertension?
Impairment in the kidney regulation of body salt balance
48
What is secondary hypertension?
Hypertension with a clear cause that can be fixed by fixing the cause
49
What is primary hypertension associated with?
Metabolic syndrome
50
What is primary hypertension rick factors?
Western diet, high salt, low K, high Caroline, low fibre, physical inactivity, alcohol, stress
51
What is secondary hypertension associated with?
Endocrine Renovascular Renal Drugs Coarctation Others-e.g. Sleep Apnoea
52
Endocrine Secondary hypertension - what specific things can cause this?
Mineralocorticoid-salt retention Phaeochromocytoma etc Others: Thyroid dysfunction Cushing’s syndrome(incl GC drugs) Hyperparathyroidism Acromegaly Endocrine drugs such as oral contraceptives
53
What would you ask when investigating secondary hypertension?
History and examination - does this suggest a specific secondary HT e.g. hypokalaemia, alkalosis Drugs - oestrogen containing pill, liquorice, glucocorticoids Cushings, acromegalic appearance - is there young/severe/resistant HT for example is it caused by target organ damage
54
What are the biochemical tests you would ask about when investigating secondary hypertension?
Recent glucose, HbA1c, potassium, HC, calcium, thyroid function test, 1) aldosterone and renin 2) 24hr urine metadrenaline 3) renal ultrasound (only if you suspect a renal disease)
55
adrenal related endocrine hypertension - what causes mineralocorticoid excess?
Bilateral hyperplasia Unilateral (Conn’s) tumour Rarities eg GRA (FH1), FH2+3, low 17alpha OHase and 11βOHase
56
What is the rare mineralocorticod excess conditions?
Resemblance to Aldo excess but Aldo suppressedeg SAME, Liddle’s syndrome, activating MR mutations
57
What is primary aldosteronism?
Aldosterone excess,-driven by a primary adrenal abnormality (raised renin-angiotensin or body K+) -above physiological requirements (BP high) It isn’t suppressed by sodium loading
58
How do you diagnose aldosteronism?
Screening hypertensives ➔measure aldo/renin ratio (ideally off all interfering medication)
59
When should you diagnose someone with primary aldosteronism?
If they have all: ➔ ARR >40 [pmol/miU/L] if renin assay = direct renin concentration (DRC) ➔Aldosterone >300-400pmol/L (sitting) (ie >upper part normal range or supranormal ➔Aldosterone that is abnormally resistant to suppression – often by assessing ARR when on high salt intake- but may require salt-loading/saline infusion tests
60
What are the two common causes of primary aldosteronism?
BAH Conns tumour
61
What is conns tumour?
Unilateral aldosterone producing adenoma– potentially benefitting from surgery
62
What is BAH?
bilateral adrenal hyperplasia,– often shows adrenal hyperplastic nodules not tumours), increases with age– not helped by surgery
63
What is rare causes of primary aldosteronism?
FH, GRA
64
how do you treat primary aldosteronism?
Drugs (spironolactone, Eplerenone) If conns tumour once sure of location do a adrenalectomy (surgery)
65
How would you distinguish conns tumour and BAH?
Adrenal venous sampling = best but invasive and difficult Imaging - adrenal CT/MRI - look for non functional nodules (useful in people under 40 but people over that age tend to have these naturally)
66
What are the controversial tests to distinguish a conns tumour and BAH?
Potassium level, BP, 18OH cortisol, novel imaging and C-metomidate PET-CT scan.
67
What is venous sampling/ how is it done?
Catheter put in and thread into adrenal to collect fluid
68
What are the trends of age with Conn’s tumour, BAH and GRA?
Conns tumour - Rare in childhood but has a slow increase BaH - over age 40 GRA - born with it
69
What causes glucorticoid remediable aldosteronism (GRA)?
The 11-OHase accidentally combines with a aldosterone which means when you are given glucocorticoids it releases aldosterone
70
What can you suppress GHA with?
Dexamethasone
71
Is GHA autosomal recessive?
No dominant
72
What is GRA also called?
Fh1
73
What is the biochemistry of GRA?
Potassium normal 18OH cortisol high
74
How is GRA tested for?
Genetic test showing the abnormal chimeric gene present
75
How is GRA managed?
Combination of dexamethasone and eplerenone/amiloride
76
What are some other mineralocorticoid disorders affecting BP?
11 beta HSD2 deficiency Mutations promoting ENaC half life Inactive MR mutations Inactivating ENaC mutations Hypertension form activating MR mutations Aldosterone excess and deficiency

Biochemistry And Endocrinology (16 decks)

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