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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
Q

How do you manage a phaeochromocytoma?

A
  • Initiate alpha blockade with phenyoxybenzamine
  • Then beta blockade with propranolol
  • surgery
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26
Q

After you remove consider if the phaeochromocytoma was part of a syndrome - what are these syndromes?

A

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

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27
Q

Hypertension - what is too high?

A

Over 140/90

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28
Q

Is BP constant?

A

No

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29
Q

When will BP alter?

A

Normally lower at night
can be affected with how its measured,

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30
Q

What tests are done to diagnose hypertension?

A

Should allow several readings over 5 minutes while person relaxingif seems raised should ideally average

assessments over few weeks

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31
Q

Is hypertension important?

A

Yes as it is a risk factor for CVD

32
Q

What are the 3 main CVD’s

A

Coronary heart disease - includes MI

Cerebrovascular disease - dementia, stroke

Arterial disease - peripheral vascular disease, renal impairment, renal artery stenosis, abdominal aortic aneurysms.

33
Q

What are risk factors for CVD?

A

Hypertension, hyperglycaemia smoking, family history, poor history, obesity, insulin resistance, kidney disease, dyslipidaemia

34
Q

What is hypercholesterolanemia?

A

High cholesterol

35
Q

What two diagnostic tests are needed to make a hypertension diagnosis?

A

Clinical BP and ABPM/Home BP

36
Q

How many grades of hypertension is there and a d what are these called?

A

Normal BP, High normal BP, Hypertension, Grade 1, grade 2 and grade 3

37
Q

What is white coat hypertension?

A

Only hypertension due to the white coat affect

38
Q

What are some key signs of hypertension that isn’t blood pressure?

A

Target organ damage (heart, eyes, kidneys)
Life threatening symptoms (confusion, chest pain, heart failure an AKI)
Accelerated hypertension

39
Q

What grades of hypertension would get treatment?

A

Grade 1 (some people
Grade 2 - 3 all people

40
Q

What guidance would you give people with hypertension and an increased risk of CVS? What advice gets given to everyone?

A

➔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
Q

What guidance would you give someone high risk of hypertension?

A

Anti-hypertensive drug treatment

42
Q

What other situations would you start someone on anti-hypertensives?

A

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
Q

What are some BP target exceptions?

A

In cases of chronic kidney disease, diabetes or people who are frail and it could be risky lowering BP

44
Q

What is resistant hypertension?

A

If blood pressure is high and the 3x drugs (ACE inhibitor or angiotensin, calcium blockers or thiazide-like diuretic) doesn’t help it

45
Q

What would you do if someone had resistant HT?

A

Specialist, spironolactone drug and look for secondary causes

46
Q

What causes hypertension?

A

Genetics

Fetal programming - if you are born underweight

Environment - diet, salt, stress

47
Q

What is seen in all hypertension?

A

Impairment in the kidney regulation of body salt balance

48
Q

What is secondary hypertension?

A

Hypertension with a clear cause that can be fixed by fixing the cause

49
Q

What is primary hypertension associated with?

A

Metabolic syndrome

50
Q

What is primary hypertension rick factors?

A

Western diet, high salt, low K, high Caroline, low fibre, physical inactivity, alcohol, stress

51
Q

What is secondary hypertension associated with?

A

Endocrine
Renovascular
Renal
Drugs
Coarctation
Others-e.g. Sleep Apnoea

52
Q

Endocrine Secondary hypertension - what specific things can cause this?

A

Mineralocorticoid-salt retention
Phaeochromocytoma etc

Others:
Thyroid dysfunction
Cushing’s syndrome(incl GC drugs)
Hyperparathyroidism
Acromegaly
Endocrine drugs such as oral contraceptives

53
Q

What would you ask when investigating secondary hypertension?

A

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
Q

What are the biochemical tests you would ask about when investigating secondary hypertension?

A

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
Q

adrenal related endocrine hypertension - what causes mineralocorticoid excess?

A

Bilateral hyperplasia
Unilateral (Conn’s) tumour
Rarities eg GRA (FH1), FH2+3, low 17alpha OHase and 11βOHase

56
Q

What is the rare mineralocorticod excess conditions?

A

Resemblance to Aldo excess but Aldo suppressedeg SAME, Liddle’s syndrome, activating MR mutations

57
Q

What is primary aldosteronism?

A

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
Q

How do you diagnose aldosteronism?

A

Screening hypertensives ➔measure aldo/renin ratio (ideally off all interfering medication)

59
Q

When should you diagnose someone with primary aldosteronism?

A

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
Q

What are the two common causes of primary aldosteronism?

A

BAH
Conns tumour

61
Q

What is conns tumour?

A

Unilateral aldosterone producing adenoma– potentially benefitting from surgery

62
Q

What is BAH?

A

bilateral adrenal hyperplasia,– often shows adrenal hyperplastic nodules not tumours), increases with age– not helped by surgery

63
Q

What is rare causes of primary aldosteronism?

A

FH, GRA

64
Q

how do you treat primary aldosteronism?

A

Drugs (spironolactone, Eplerenone)
If conns tumour once sure of location do a adrenalectomy (surgery)

65
Q

How would you distinguish conns tumour and BAH?

A

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
Q

What are the controversial tests to distinguish a conns tumour and BAH?

A

Potassium level, BP, 18OH cortisol, novel imaging and C-metomidate PET-CT scan.

67
Q

What is venous sampling/ how is it done?

A

Catheter put in and thread into adrenal to collect fluid

68
Q

What are the trends of age with Conn’s tumour, BAH and GRA?

A

Conns tumour - Rare in childhood but has a slow increase
BaH - over age 40
GRA - born with it

69
Q

What causes glucorticoid remediable aldosteronism (GRA)?

A

The 11-OHase accidentally combines with a aldosterone which means when you are given glucocorticoids it releases aldosterone

70
Q

What can you suppress GHA with?

A

Dexamethasone

71
Q

Is GHA autosomal recessive?

A

No dominant

72
Q

What is GRA also called?

A

Fh1

73
Q

What is the biochemistry of GRA?

A

Potassium normal
18OH cortisol high

74
Q

How is GRA tested for?

A

Genetic test showing the abnormal chimeric gene present

75
Q

How is GRA managed?

A

Combination of dexamethasone and eplerenone/amiloride

76
Q

What are some other mineralocorticoid disorders affecting BP?

A

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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