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Adrenal Flashcards

Adrenal gland, function, control axis affects and pathology

1
Q

Location of Adrenal gland

A 
The adrenal (or suprarenal) gland sits on top of the
kidney (ad – near, supra – above, renal –kidney).
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2
Q

Divisions of Adrenal Gland

A 
Zona glomerulosa(cortex)
 Zona fasciculata(cortex)
Zona reticularis(cortex)
Adrenal Medulla
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3
Q

What does zona fasiciculata produce and what enzyme does it lack

A

glucocorticoid cortisol

lacks aldosterone synthase

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4
Q

What does zona reticularis produce and what enzyme does it lack

A

lacks aldosterone synthase
adrenal androgens
androstenedione
dehydroepiandrosterone acetate (DHEA)

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5
Q

What is Acth derived from

A

ACTH derived from pro-opiomelanocortin

POMC

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6
Q

What other products do you get from POMC breakdown

A

g-lipotrophin (g-LPH),b-MSH ACTH main ones

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7
Q

REGULATION OF SYNTHESIS of cortisol brief outline involving axis

A

hypothalamus releases CRH, causes anterior pituitary corticotrophs to release acth, causes cortex to synthesis and release cortisol. negatuve feedback from cortisol to hypothalamus and pituitary

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8
Q

What molecule are all steroid hormones derived from

A

Chlesterol

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9
Q

What receptor does ACTH act on

A

ACTH acts on a G-protein coupled receptor
(melanocortin 2 receptor, MC2R) to activate adenyl
cyclase which leads to an increase in cAMp level and activation of PKA

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10
Q

What enzymes are involved in synthesis of cortisol in zona fascicuclata

A

cholesteryl ester hydrolase (CEH)

cholesterol 20,22-hydroxylase also referred to as
desmolase

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11
Q

What enzyme is the rate limiting step in cortisol synthesis

A

desmolase

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12
Q

Describe action of the enzymes in synthesis of cortisol

A

All steroid hormones are derived from cholesterol.
ACTH acts on a G-protein coupled receptor
(melanocortin 2 receptor, MC2R) to activate adenyl
cyclase which leads to an increase in cAMP levels.
This in turn activates protein kinase A which activates
cholesteryl ester hydrolase (CEH) which liberates
cholesterol from lipid droplets. There is also stimulation
of cholesterol 20,22-hydroxylase also referred to as
desmolase which is the first enzyme in the pathway and
is the rate limiting step. This leads to increased synthesis
of cortisol.

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13
Q

Name the five steroid hormones produced by adrenal gland

A

cortisol, corticosterone, aldosterone, DOC(Deoxycorticosterone), DHEA(Dehydroepiandrosterone)

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14
Q

How is cortisol transported in the blood plasma

A

CBG corticosteroid binding globulin 75% , albumin 15% , free 10%

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15
Q

How is aldosterone transported in the blood plasma

A

free 40%, albumin bound 40% and CBG 20%

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16
Q

When steroid hormone binds to cytoplasmic receptor what protein dissociates from receptor

A

Steroid hormone enters cells by diffusion and binds to
cytoplasmic receptor. This leads to dissociation of Heat
Shock Protein (hsp90) from the receptor.

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17
Q

Once steroid hormone has bound to cytoplasmic receptor outline what occurs

A

The hormone-receptor complex dimerises and is
translocated to nucleus. The complex binds to hormone
responsive element (HRE) on DNA which leads to an
increase in mRNA production and subsequently to
increased protein synthesis.

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18
Q

Why is steroid action have a slower effect on the body

A

The complex binds to hormone
responsive element (HRE) on DNA which leads to an
increase in mRNA production and subsequently to
increased protein synthesis.
Protein sythesis is slow

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19
Q

EFFECTS OF GLUCOCORTICOIDS (cortisol) on glucose

A

decrease glucose uptake
decrease glucose use
increase gluconeogenesis
“hyperglycaemia”

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20
Q

EFFECTS OF GLUCOCORTICOIDS (cortisol) on proteins

A

decrease protein synthesis
increase protein breakdown
“muscle wasting”

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21
Q

EFFECTS OF GLUCOCORTICOIDS (cortisol) on calcium

A 
decrease Ca2+ absorption in gut
increase Ca2+ excretion in kidney
decrease activity of osteoblasts
increase activity of osteoclats 
"osteoporosis"
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22
Q

EFFECTS OF GLUCOCORTICOIDS (cortisol) on inflammatory early phase

A

anti-inflammatory effects
early phase
reduce redness, heat, pain, swelling

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23
Q

EFFECTS OF GLUCOCORTICOIDS (cortisol) on inflammatory late phase

A

late phase

reduce wound healing, repair, proliferation

24
Q

EFFECTS OF GLUCOCORTICOIDS (cortisol) on immune response

A 
decreases expression of COX2 (cyclo-oxygenase 2)
cytokine production
complement in plasma
nitric oxide (NO) production
histamine release
IgG production
25
Q

How is cortisol action on mineralcorticoid recptors prevented

A 
cortisol has higher affinity for mineralocorticoid
receptor than glucocorticoid receptor
11bHSD
cortisol ------→cortisone
active inactive
11bHSD 11bhydroxysteroid dehydrogenase
11bHSD2 isoform expressed in aldosterone
sensitive tissues
converts cortisol ---→ cortisone
11bHSD1 isoform expressed in liver,adipose,
muscle
converts cortisone ---→ cortisol
26
Q

What causes Cushing syndrome

A 
Cushing syndrome due to
prolonged exposure to
elevated levels of cortisol
or exogenous
glucocorticoid drugs
27
Q

What symptoms associated with cushing syndrome

A 
Osteoporosis
Negative nitrogen
balance
Increased appetite
Obesity
Increased susceptibility to
infection
28
Q

What drugs can be used to treat cushing syndrome and how do they work

A 
Metyrapone
11b hydroxylase inhibitor
• Ketoconazone (withdrawn in Europe)
inhibits steroid biosynthesis
• Pasireotide (somatostatin analogue)
SSTR5 agonist
● Cabergoline (dopamine D2 agonist)
● Mifeprestone
glucocorticoid receptor antagonist
progestogen receptor antagonist
29
Q

What causes Addison disease

A

Low cortisol- Chronic adrenal insufficiency

30
Q

Symptoms associated with Addisons

A

Hypotension, weight loss, hyperpigmentation,gastro disturbances

31
Q

What androgen do adrenal glands secrete and which zone does this occur in

A

zona reticularis DHEA
and its sulphate, and
androstenedione

32
Q

What happens to androgens secreted by adrenal gland in periphery

A

n the pre-menopausal woman 50% of androstenedione
is derived from the adrenal and is converted in peripheral
tissue to oestrogen and testosterone. Excess secretion
of these androgens in women can lead to hirsutism and
virilisation.
In the post-menopausal woman, with the regression of
the ovary, the main oestrogen in oestrone. As peripheral
conversion takes place in adipose tissue the production
of oestrone is higher in the obese postmenopausal
woman than in the thin woman.

33
Q

What is function of aldosterone (mineralococortoid)

A 
Aldosterone
Effects in distal tubule & collecting duct in kidney
Increased number of sodium channels in apical
membrane (ENaC epithelial Na channel)
Increase in Na +
/K +ATPase in basolateral
membrane
Increased Na/K exchange
34
Q

What drug can be used to reduce aldosterone action

A

Spironolactone
Aldosterone antagonist
Used as K+ sparing diuretic

35
Q

Adrenaline and Nora adrenaline are examples of

A

Catecholamines

36
Q

Hypofunction of the adrenal gland causes which pathology

A

Addisons

37
Q

Hyperfunction of adrenal gland causes which pathologyies

A

– Cushing’s (high cortisol)
– Pheochromocytoma
– Conn’s / hyperaldosteronism (high aldosterone)

38
Q

Primary Hypoadrenalism (issue at adrenal level) caused by

A 
Autoimmune, Abrupt discontinuation of exogenous steroids, body system out of sync, tubercolosis, surgery, 
Haemorrhage/ infarction
– Meningococcal septicaemia (Waterhouse
Friderichsen Syndrome)
• Infiltration – Malignancy, amyloid
39
Q

symptoms of primary hypoadrenalism

A

weight loss, diahorrea, nausea/vomiting, hypotension, myalgia

40
Q

signs of hypoadrenalism

A 
Pigmentation – new scars
buccal
palmar creases
• Postural hypotension
• Wasting
• Dehydration
• Loss of body hair
41
Q

how do you investigate suspected hypoadrenalism

A 
Random cortisol
• Short synacthen test
• Plasma ACTH
• Urea and electrolytes
• Adrenal antibodies
42
Q

How do you treat adrenal failiure

A 
Emergency, life-threatening adrenal crisis
– ICU care
– Fluids, sodium
– IV hydrocortisone @ high dose
• Maintenance treatment
– Glucocorticoid (hydrocortisone, prednisolone)
– Mineralcorticoid (fludrocortisone)
– ?DHEA
43
Q

If high cortisol is ACTH dependent at what level is the issue with axis likely to be at

A

pituitary, Cushing’s disease

44
Q

If high cortisol is ACTH independent at what level is issue with axis likely to be at

A

Adrenal level, potential adrenal adenoma or carcinoma

45
Q

Taking too many steroids can cause what pathology

A

hyperadrenalism

46
Q

What are the signs of Cushings

A 
Hypertension
 Osteoporosis
 Pathological #
 Kyphosis
 Buffalo hump
 Striae
 Oedema
 Proximal myopathy
 Diabetes mellitus
47
Q

How can you diagnose cushings or high cortisol

A

Dynamic Investigations
TO CONFIRM DIAGNOSIS
• Low dose dexamethasone suppression test
• 24 hour urinary cortisol
• Loss of diurnal rhythm (mid-night cortisol).
test conc of acth,

48
Q

how do you treat hyperadrenalism

A

Laparoscopic adrenalectomy
• Replacement GC (after removing part of adrenal gland you can become hypo)
– Hydrocortisone
– Periodic withdrawal
• Many of the features improve
– BP, diabetes, psychological disturbance may
continue

49
Q

What is Phaeochromoctoma

A

Tumour of the adrenal medulla. Increase of NA and Adr can be bilateral or malignant

50
Q

How does Phaeochromoctoma present

A 
Headaches
• Palpitations
• Sense of Doom
• Chest pain
• Sweating
• Weight loss
SNS Over stimulation
51
Q

How does Phaeochromoctoma get diagnosed

A 
Diagnosis with
• 24 HOUR – urine catecholamines
• OR
• Metanephrines either 24 HOUR urine
• OR plasma
52
Q

How does Phaeochromoctoma get treated

A

Surgical removal after
– Pretreatment with alpha and B blockade
• Phenoxybenzamine
• Doxazosin

53
Q

what does aldosterone do to BP and serum potassium

A

• Raised BP and low serum potassium

54
Q

Conn’s syndrome= primary

hyperaldosteronism chracterised by

A

Hypertension, hypokalaemia, alkalosis

55
Q

Treatment of Conn’s syndrome?

A 
Remove the adenoma
– Laparoscopic
• Drug treatment
– Spironolactone
– Eplerenone

HD (18 decks)

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