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Metabolism 2 > Adrenals > Flashcards

Adrenals Flashcards

1
Q

what foetal tissue does the adrenals come from

A

mesoderm

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2
Q

describe how the adrenals develop

A

 SF1 expression is crucial in adrenal gland development.
 Cells secreting high SF1 levels from the adrenal primordium.
 Migrating neural crest cells enter the AP, forming the adrenal medulla.
 Surrounding mesenchymal cells form a capsule.

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3
Q

what also develops at the urogenital ridge

A

the kidney

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4
Q

what are the two parts of the adrenal gland

A

cortex

medulla

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5
Q

what are the three layers of the adrenal cortex

A

zona glomerulusa
zona fasciularis
zona reticularis

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6
Q

describe the adrenal blood supply

A
  • The blood flow in the adrenal gland starts on the outside and delivers blood to the plexus of blood vessels just under the capsule
  • The blood flow goes through the adrenal cortex in to the medulla
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7
Q

Give an example of how the cortex and medulla are linked

A
  • hormones in the cortex such as cortisol can have an effect on the adrenal medulla hormones
  • for example cortisol produced in the cortex goes via the blood to the adrenal medulla
  • this is where it upregualtes an enzyme that allows the adrenal medulla to produce adrenaline this helps the body to deal with stress
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8
Q

what is the medulla composed of

A
  • groups and columns of chromaffin cells

- smaller islands of these are scattered through the cortex

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9
Q

what does a chromaffin cell look like

A

The cells are large, with large nuclei, and contain fine cytoplasmic granules which stain brown with chromium salts (and are therefore named phaeochromocytes).

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10
Q

what cells secrete what in the medulla

A

.- 80% of the medulla cells secrete adrenaline

  • 20% noradrenaline,
  • a few dopaminergic cells
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11
Q

what causes the adrenal cortex to grow

A

ACTH

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12
Q

Name some types of stress

A
  • Starvation
  • Infection
  • Severe volume loss
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13
Q

why do the areas of the cortex look different

A
  • they look different as they contain different amounts of fat
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14
Q

name some function of the adrenal cortex and medulla

A
  • have mechanism to put the blood pressure up if they do it too much you get hypertension
  • Response to infection leads to hypoerpfustion and hypotension – steroids dampen down response to inflammation
  • Adrenal gland avoids starving to death – helps you breakdown fat, bone and protein in order to provide substrate for gluconeogenssi
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15
Q

what happens if you have too much cortisol versos what happens if you have too little cortisol

A

Too much cortisol
- immunosuppressed, hypertension, diabetes, breakdown muscle,
hypertrophy

Too little cortisol
– hypotensive, hypoglycaemia and wont respond to stresses

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16
Q

How do you provide multiple different hormones from the same organ

A
  • uses cholesterol and depending on what cell type it allows cholesterol to cause factors that allow you to turn it into different hormones
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17
Q

describe the cortex layers and what allows them to produce what they produce

A

In the zona glomerulus – characterised by CYP11B2 means you can produced aldosterone

In the zona fasciculus characterised by CYP11B1 allows you to produce cortisol

In the zona reticularus you produce CYP17A1 to produce testosterone

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18
Q

Why are mineralocorticoids called mineralocorticoids

A
  • named because on the effect that they have on minerals
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19
Q

What is an example of mineralocorticoids

A

aldosterone

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20
Q

Where are mineralocorticoids produced

A
  • zona glomuerlusa
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21
Q

what stimulates release of aldosterone

A
  • rise in potassium

- low blood pressure - therefore an increase in angiotensin II from RAAS and ACTH

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22
Q

What does aldosterone do

A
  • increases sodium reabsorption
  • therefore causes then increase in the reabsorption of water
  • therefore increases the overall circulating volume
  • causes potassium excretion

can lead to a metabolic alkalosis

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23
Q

How does aldosterone do what it does

A
  • aldosterone binds to the mineralocorticoid receptor
  • this increases sodium reabsorption - this happens as the mineralocorticoid inserts more sodium ENac channels in the collecting duct for absorption
  • intercalated cells upregualte the sodium potassium ATPase
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24
Q

How does the renal system acts on aldosterone

A
  • via the principal cell

- via the intercalated cell

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25
Q

what can aldosterone lead to

A
  • metabolic alkalosis
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26
Q

What is the condition called for primary hyperaldosteronism

A

Conns syndrome

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27
Q

how much does primary hyperaldosteronisim cause hypertension

A
  • Conn’s syndrome – 29% cause of hypertension
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28
Q

how is conns syndrome caused

A
  • develop hypertension

- this is because there is suppressed plasma renin activity and increased aldosterone secretion

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29
Q

what is conns syndrome caused by

A
  • Aldosterone producing adenoma

- Bilateral adrenal hyperplasia

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30
Q

How do you diagnose conns syndrome

A

Aldosterone:Renin Ratio
- measure the aldostoenre and renin ratio, if renin levels are 0 and aldosterone is high then conns syndrome

Saline suppression test
- the low fluid volume increases aldosterone production therefore if you give them a bag of saline which raises the fluid level and there aldosterone levels are still high then this is pathological

CT Adrenal

Adrenal venous sampling
- this is when you insert a catheter into the groin and measure the aldosterone level form each adrenal gland

Metomidate PET

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31
Q

How do you treat Conns syndrome

A

Spironolactone = Mineralocorticoid receptor antagonist.

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32
Q

Describe how you can get an mineralocorticoid excess

A
  • lycosrol has an active ingredient which inhibits 11BetaHSD2
  • this increases the level of cortisol that comes into contact with the mineralocorticoid
  • this causes more mineralcoritcoids to develop

-excess mineralocorticoid excess can also be genetic

33
Q

What does 11betaHSD2 usually do

A
  • ## it usually binds to the kidney and inactivates cortisol prevention mineral corticoid receptor binding
34
Q

How do you diagnose a mineralcorticoid excess

A
  • Diagnosis is made on the basis of elevated urinary cortisol to cortisone ratio on a 24 hr urine collection.
35
Q

What is a syndrome in which there is low to normal aldosterone release

A

Liddles syndrome

36
Q

What causes low aldosterone release in Liddles syndrome

A

 Low plasma renin activity, reduced aldosterone output therefore.

37
Q

What does Liddles syndrome lead to

A
  • Hypertension
  • Hypokalemia
  • Metabolic alkalosis
38
Q

What is liddles syndrome

A

Liddle syndrome is a rare hereditary disorder involving increased activity of the epithelial sodium channel (ENaC), which causes the kidneys to excrete potassium but retain too much sodium and water, leading to hypertension
- even though there is low renin and low aldosterone , sodium channels are spontaneously placed on the collecting duct

39
Q

describe the HPA axis for cortisol secretion

A
  • CRH stimulates ACTH which stimulates cortisol then there is a negative feedback in which cortisol inhibits CRH and ACTH
40
Q

what does CRH stand for

A

corticotropin releasing hormone

41
Q

what is ACTH also know as

A
  • ACTH is also called corticotropin
42
Q

describe how POMC is produced in the anterior pituitary and how this leads to ACTH being produced

A
  • Produces POMC this is cleaved by the same enzymes that cleave insulin and PTH
  • Cleavage of POMC produces ACTH
43
Q

what receptors does ACTH bind to

A
  • ACTH this binds to the melanocortin-2 receptor (MC2R)

- this is in the Zona fasciularus and causes the cells to produce cortisol

44
Q

Too little ACTH and hereofre cortisol can cause

A

Addisons disease

45
Q

How can ACTH cause aldosterone production

A
  • CYP11B2 AND CYP11B1 – similar structurally and genetically as they are on the same gene
  • When ACTH binds to the ZF it up-regulates CYP11B2, if you have a mistake being made in division of these cells you can end up where the promoter region for 11b-hydroxylase is attached to the coding region of aldosterone synthase therefore ACTH leads to increase aldosterone secretion instead of cortisol
46
Q

when ACTH causes aldosterone production how do you treat it

A
  • Can treat this condition by lowering the levels of ACTH –
  • Quickest way to do that is steroids
  • This is glucocorticoid remediable aldosteronism
47
Q

describe the circadian rhythm in regards to cortisol

A

Cortisol follows a circadian rhythm, increasing around 3 am and peaking at 7 am; it
decreases after this.

48
Q

what can inhibit the production of cortisol

A
  • opiates
  • oxytoxcin
  • ANP
49
Q

what also inhibits ACTH

A
  • CRIF
50
Q

what can increase ACTH

A
  • Angiotensin II, IL1, IL6, IL2, LIF increases ACTH
51
Q

if you suspect Addisons when do you measure cortisol

A
  • need to measure it in the morning to see if it is lower than normal
52
Q

if you suspect bushings when do you measure cortisol

A
  • need to measure it at bed time to see if it is higher than normal
53
Q

what are the symptoms of Cushing syndrome

A
  • Skinny arms and legs as they are breaking down fat and subcutaneous fat and muscles
  • Weight gain - increase in the amount of visceral fat
  • Dermatological changes.
  • Muscle weakness.
  • Hypertension.
  • Loss of libido.
  • Depression.
  • Kidney stones.
  • breakdown of bones - osteoporosis
54
Q

how does Cushing syndrome act on the visceral fat versus the subcutaneous fat

A

Cushings increases the amount of visceral fat and lowers the amount of subcutaneous fat

55
Q

What are the causes of Cushings syndrome

A
  • Iatrogenic
  • Corticotroph adenoma of the pituitary- most common cause
  • Ectopic ACTH secreting neuroendocrine tumour
  • Cortisol secreting adrenal adenoma
  • Bilateral adrenal hyperplasia
56
Q

How do you diagnose Cushing syndrome

A

Overnight dexamethasone suppression test
– give tablet of dexamethasone at bedtime and measure the next morning they should be 0 or less than 20 nano meteres, if there not then there is a cortisol problem

24 hour urine free cortisol

LDDST: 0.5mg dexamethasone every 6 hours for 48 hours

Cortisol day curve plus midnight sleeping cortisol – measures cortisol throughout the day, if you have cushings disease the levels of cortisol will stay up all long

Blood test – midnight should be low

57
Q

How do you manage cushings treatment

A

treat the underline cause

58
Q

what imaging do you use for Cushings disease

A
  • MRI Pituitary
  • CT Adrenals
  • Inferior petrosal sinus sampling
  • NM: Octreotide uptake scan
59
Q

What is the treatment of Cushings disease

A

Pituitary

  • Transsphenoidal surgery
  • External beam radiotherapy
  • Stereotactic radiosurgery (gamma knife)

Adrenal

  • Adrenalectomy
  • Metyrapone/Ketoconazole/Etomidate
60
Q

What can differitate between a pituitary adenoma and a ectopic ACTH secreting tumour as the cause of Cushings syndrome

A
  • Inferior petrosal sinus sampling distinguishes between a pituitary adenoma and an ectopic ACTH secreting tumour as the cause of Cushing’s syndrome
  • Blood is drawn directly from the venous sinuses around the pituitary.
    High ACTH in the petrosal veins in a patient with confirmed Cushing’s compared to the periphery =
    Pituitary Source of ACTH

ACTH in the petrosal veins equal to the periphery with confirmed Cushing’s = Peripheral source of ACTH

61
Q

what can be used to locate the ectopic neuroendocrine tumour

A
  • octreotide scan
62
Q

what is Addisons disease due to

A

• Primary adrenal failure
– Autoimmune
– Tuberculosis

63
Q

what are the symptoms of Addisons disease

A

• Vague symptoms initially
– Fatigue, weakness, myalgia
– Anorexia, weight loss
– Hyperpigmentation

64
Q

describe Addison crisis symptoms

A 
-	Failure to response to stress
Low Blood pressure 
Low glucose 
Low sodium 
High potassium
65
Q

How do you diagnose Addison disease

A

Low 9am cortisol
High ACTH
Short Synacthen Test – synthetic ACTH – if adrenal glands are working expect to increase the amount of cortisol that is being produced

66
Q

what is congenital adrenal hyperplasia

A
  • 2 1 -hydroxylase – if this doesn’t work
  • Cortisol falls
  • ACTH rises
  • And if you have high levels of ACTH
  • It stimulates cholesterol process and they end up producing more androgens
  • This is called Congenital Adrenal Hyperplasia
67
Q

What is an congenital adrenal hyperplasia due to

A
  • due to 21-hydroxylase deficiency
68
Q

What are the symptoms of a congenital adrenal hyperplasia

A

Salt-losing
Adrenal Insufficiency
Virilisation
Adrenal hyperplasia

69
Q

what does the adrenal medulla do

A

catecholamine biosynthesis

70
Q

Where are chomaffin cells

A 
Adrenal medulla
Para-aortic sympathetic chain
Organ of Zuckerkandl
Wall of urinary bladder
Neck and mediastinal sympathetic chain
71
Q

what are the two types of tumours from chromaffin cells

A

phaeochromocytoma
paraganglioma

  • These together are called PPGL
72
Q

where do the two types of tumours from chromaffin cells originate from

A

• Phaeochromocytoma
– Arising from within the adrenal medulla
• Paraganglioma
– Extra-adrenal tumours

73
Q

name the adrenoreceptors and what they do

  • alpha 1
  • alpha 2
  • b1
  • b2
  • b3
  • d1
  • d2
A
  • α1 vascular and smooth muscle contraction
  • α2 presynaptic, inhibitory to noradrenaline release - suppresses BP
  • β1 positive inotropic and chronotropic in the heart; increased renin; lipolysis
  • β2 bronchial, vascular, uterine smooth muscle relaxation; glycogenolysis
  • β3 Lipolysis, energy expenditure, eg at brown fat tissue
  • D1 cerebral, renal, mesenteric, coronary vasculature dilatation
  • D2 presynaptic inhibition of noradrenaline and prolactin release
74
Q

what are the symptoms of catecholamine excess

A
  • Impending doom
  • Diaphoresis
  • Dyspnea
  • Headache
  • Hypertension
  • Palpitation
  • Tremor
  • Nausea and vomiting
  • Fatigue
  • Orthostatic hypotension
  • Hyperglycemia
  • Weight loss
  • Epigastric and chest pain
  • Congestive heart failure
75
Q

What are the main producers of catecholamine

A

chromaffin cells

76
Q

How do you detect PPGL

A
  • Hyperadrenergic spells
  • Resistant hypertension and desceibed panic attacks should be thinking about PPGL
  • Familial syndrome
  • Incidentally discovered adrenal mass
  • Pressor response during general anaesthesia
  • Early onset hypertension
  • Dilated cardiomyopathy
77
Q

how do you make a diagnosis of PPGL

A 
•	24 hour urine metanephrines
•	Plasma metanephrines
•	CT/MRI adrenals and abdomen
•	123I-MIBG scintigraphy
- MIBG – tracer taken up ny neuroendocrine cells and localise din the granules where they caetcholamines are made
78
Q

What is the treatments of PPGL

A

• Surgical resection
• Pre-operative alpha and beta-blockade – because the symptoms of these tumours are due to too much alpha and beta cell stimulus, can lead to anaesthetic bad reaction without these
– Phenoxybenzamine 10mg bd and titrate
– Propranolol 10mg qds and titrate
• Acute crisis: IV phentolamine or nicardipine
• Avoid opiates – adrenal cells have opiate receptors on them
• 131I-MIBG therapy for malignant disease

79
Q

What would happen if you treatment a patient with a phaemochromocytoma with beta blockers alone

A
  • the tumour balances the catecholamine with stimulus of A1 and b2 adrenoreceptor
  • A1 causes vasoconstriction and b2 causes vasodilation
  • if you were to use a beta blocker you would block B2 and therefore block vasodilation
  • therefore vasoconstriction would happen and this would cause the blood pressure to increase

Metabolism 2 (40 decks)

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