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RED > Adrenal Gland > Flashcards

Adrenal Gland Flashcards

1
Q

In the adrenals what hormones are made and where

A

Capsule
Zona glomerulosa: mineralcorticoids -> aldosterone

Zona fasiculata: glucocortiscoids -> cortisol

Zona reticularis: androgens -> DHEA

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2
Q

If you have adrenal insuffienctly what conditons can you have

A
  • glucocorticoid
  • mineralocorticoid
  • adrenal androgen insufficiency
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3
Q

If you excess GC, MC, and andorgens what conditions do you have

A

Too much

  • glucocorticoid excess → Cushing syndrome
  • mineralocorticoid excess → Conn’s syndrome
  • androgen excess → congenital adrenal hyperplasia, PCOS
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4
Q

What is CAH

A
  • rare disorder
    • affects 1 in 10000
  • genetic disorder
  • there is a lack of enzymes needed to make GC, MC, A
  • (there’s a mutation in the enzyme)
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5
Q

What is the most common form of CAH

A

most common form is 21 hydroxylase deficiency

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6
Q

What enzyme is implicated in 21 hydorxlyase defiency and what does it do

A
  • CYP21A2
  • is needed to to make aldosterone and cortisol
  • stops making GCs, and MCs
    • they have adrenal insufficiency
    • but also excess androgens
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7
Q

Explain how cortisol does negative feedback

A
  • cortisol exerts a negative feedback
    • it stops the pituarity releasing ACTH
    • and stops hypothalamus from producing CRH
  • if there is not enough hormones, then it can amplify the signal even further
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8
Q

What happens to the pituriatry adrenal axis in CAH

A
  • Since we lack cortisol we lack the negative feedback systems, overproduction of CRH, ACTH
    • excess ACTH causes hyperplasia of the adrenal gland
  • excess of adrenal androgens
    • affect the genitalia
  • adrenal insufficiency (lack of cortisol)
  • wasted salt (lack of aldosterone)
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9
Q

In summary what happens to hormones if you have CAH

A
  • lose GC, MCs
  • lots of androgens
  • lots of ACTH, CRH
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10
Q

How do we diagnose CAH

A

look at enzyme before 21 hydorxylase

  • typically we look at 17 OH progesterone as a key marker
    • would be high
    • use as a baseline or measure it after giving ACTH as a stimulation
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11
Q

How do we measure if we are giving someone too much treatment

A
  • We also use androstenedione
    • measures if we are giving too much
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12
Q

What are the two types of CAH

A

classic
androgen excess + cortsiol and aldoestrone defiency

non classic (most common) -> androgen excess (but no cortsiol and aldoestrone defeincy)

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13
Q

Symptoms and signs

What are the symptoms that you can get with CAH

A

Androgen excess
-common ground for classical and non classical
-ambigous genitalia (female babies)
-excess body hair, early sexual development
-irregular periods

Cortisol defiency
-fatigue
-weight loss
-muscle weakness
-emergency -> adrenal crisis

Aldoestrone defienecy
-low bp
-salt cravings
-salt wasting at birth -> emergency

this all depends on the mutation, there can be minor or total impairment

if you have less sevre mutation you have non classic

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14
Q

Signs

What happens to gentalia in CAH

A

46, XX DSD
- external genitalia go through development in the womb
- female fetus with congenital adrenal hyperplasia
- appearance dictated by how much androgen exposure
- if less androgens more “female-looking genitalia”
- more androgens more “male-looking genitalia”

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15
Q

Treatment

How is CAH treated

A

1) Replacement of deficient corticosteroids

  • Glucocorticoid replacement
    • Hydrocortisone,
    • Prednisolone,
    • Dexamethasone
  • Mineralocorticoid replacement (not always)
    • Fludrocortisone

2) Suppression of ACTH-driven androgen excess

  • Higher glucocorticoid doses
    • cortisol exerts a negative feedback
    • androgen excess is driven by excess ACTH
    • so you can dampen the effect of ACTH,
    • so you give higher than normal doses. of GCs
  • Modified-release hydrocortisone
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16
Q

Why is treating CAH described as a balancing act

A
  • need to balance, treatment without causing places
  • if you give to little you don’t dampen ACTH, rise in adrenal androgen
  • can cause things like hiritusim, acne, menstrual irregularietes, reduced fertlity
  • if you give too much, you cause metabolic consequences (cortsiol over replacement)
  • can cause weight gain, central obesity, metabolic syndrome, osteprosis)
17
Q

fertility in CAH

what happens hormonally

A

Too much glucocorticoid

  • Suppression of LH and FSH
  • Oligo-/Amenorrhea

Not enough glucocorticoids

  • Androgen and progesterone excess
  • Anovulation, oligomenorrhoea, failure to implant
18
Q

What is TART

how is it implicated in CAH

A

Testicular adrenal rest tissue (TART)

  • Arises from urogenital ridge,
    • both adrenal and gonadal features come from the urogential ridge go to the gonads and ten start to growth with their adrenal ability when there is increase ACTH
    • TART cells are dormant under ACTH they grow and compress testes inhibiting spermatogensis
    • if you have CAH, growth can occur and effect the other tissues this can impair fertility
19
Q

What are the causes of androgen excess in women

A
  • non classic CAH
  • PCOS
20
Q

PCOS

What are the signs and symptoms of PCOS

A
  • Chronic (or intermittent) Anovulation
    • defined as frequent bleeding at intervals <21 d or infrequent bleeding at intervals >35 d.
  • Mid-luteal D21 progesterone in women with 21-35 day intervals.
  • Polycystic ovarian (PCO) appearance of the ovaries (ultrasound)
    • defined by the presence of 12 or more follicles 2–9 mm in diameter and/or an increased ovarian volume >10 mL(without a cyst or dominant follicle) in either ovary
  • Androgen excess
    • Clinical signs of AE: hirsutism, acne, androgenic alopecia
    • Biochemical evidence of AE: increased serum testosterone
21
Q

Why is PCOS described as metabolic disorder

and why is this a problem long term

A
  • androgen excess
  • can cause irrefular periods, inferiltiy or miscarriages
  • insulin resistance
  • can cause future hypertension, type 2 diabetes, lover disease, cardiovasuclar disease

Lifelong problems
- with no specific treatment and no means of metabolic risk
- PCOS affects multiple body disorders

22
Q

What do they want to rename PCOS

A

FAME
Female AndroMEtabolsic syndrome

23
Q

What needs to excluded before a diagnosis of PCOS

A
  • congenital adrenal hyperplasia
  • adrenal cancer
  • adrenal adenoma
  • Cushings disease
  • ovarian hyperthecosis
  • ovarian tumours
24
Q

IF you see an adrenal incidentalomas you need to two key questions
what are they?

A
  • need to know if its malignant
    • risk is about 5-8%
  • and is this adrenal mass producing hormones in excess
25
Q

Incidentalmoas

Why do we need to know if its malignant

A
  • adrenal cancer very rare and aggressive
  • less than 50% will survive pass 5 years
  • do not want to miss this diagnosis
  • most adrenal tumors will be bengin tumors
26
Q

Incidentalmoas

What is the best way to answer these questions diagnostalicly

like what tool would you use

A
  • imaging
    • good at ruling out malignancy
    • BUT… hard to differentiate from benign from malignant
27
Q

If we have an adrenal tumor what else do we need to look for

apart from maligancny

A
  • tumor size
    • If it is less than 4cm → risk of malignancy is 6-9%
    • If it is more than 4cm → risk of malignancy is 31-34%
    We also look at lipid content
    • we use CT scans without contrast (unenchanced)
    • we look at hounsfield units
    • <10 conclusively exclude malignancy

<10 for phaeochromocytoma also

28
Q

adrenal tumors

How do we exculse hormone excess

what tests would you do

A

Exclude cortisol excess

  • Serum cortisol at 8-9 a.m. after 1mg dexamethasone at 11 pm =
  • 1mg-overnight dexamethasone suppression test (1mg-DST)
  • normal cortisol would be below 50

Exclude aldosterone excess (primary aldosteronism)

  • BP increase or K decreased: Paired Plasma Renin and Plasma Aldosterone

Exclude adrenal androgen excess

  • Serum DHEAS, androstenedione, 17OHP (in tumours >4cm)

Exclude Phaeochromocytoma

  • Plasma metanephrines
29
Q

What is MACS

A

abnormal cortsol secretion typically from an adrenal tumor

30
Q

how do we differneiate whether someone has MACS or cushings

A

based on clinical symptoms

31
Q

Phaeochromocytoma

How do people with Phaeochromocytoma present

A

hypertension + hyperadrenergic spells (headaches, palpitations, profuse sweating)

but 2/3 Phaeochromocytomas present as incidentalomas

32
Q

Phaeochromocytoma

How do we test for Phaeochromocytoma

A

Sensitive test

  • Plasma metanephrines

Slightly less sensitive test, but slightly more specific:

  • 24-h urinary metanephrines
33
Q

Phaeochromocytoma

If in surgery you were to remove a Phaeochromocytoma what would happen

A
  • blood pressure may spike
  • when adrenal mass was removed blood pressure went pack to normal
34
Q

How do we treat Phaeochromocytoma

A

Treatment

α-blockade

  • stops too many catcehlomises being made
  • blocks alpha 1 receptors
    • phenoxybenzamine,
    • doxazosin
35
Q

What do we need to do during surgery of Phaeochromocytoma

A
  • Surgery needs special anaesthesia requirements
    • remember your removing a source of catecholamines which were keeping blood pressures regulated
  • Ensure fluid resuscitation before, during and after surgery
36
Q

Basically theres bits about genes

A

RET protooncogene

Multiple Endocrine Neoplasia (MEN) type 2

1) Phaeochromocytoma

2) Medullary thyroid carcinoma

3) parathyroid hyperplasia/tumour (MEN2A) or mucocutaneous neuroma (MEN2B)

Phaeochromocytoma are ssociated with germline conditions

37
Q

more genes

A

check hamzas notes on what they all mean

38
Q

What is the difference between an adrenal adednomw and cortcial carcinoma

A

Carcinoma
Large and has haemorrhage

Adenoma
Has darker

39
Q

What do we need to rule out before

A

Primary aldosterone plasma renin
Adrenal and DHEA, 17 oh progesterone

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