Adrenal Glands Part2 Flashcards

1
Q

What is cortisol response to each of the following & effect? [3]
Starvation [1]
Infection [1]
Hypotension [1

A

Starvation: High cortisol: will start to breakdown body tissues
Infection: acts as anti-inflammatory
Hypotension: raises BP

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2
Q

Effect of cortisol:

  • [] the availability of blood glucose to the brain.
  • In the liver, high cortisol levels increase [] and [] glycogen synthesis.
  • muscle cells [] glucose uptake and consumption and [] protein degradation
  • In adipose tissues, cortisol [] lipolysis
  • In the pancreas, [] insulin and [] glucagon.
A

Effect of cortisol:

  • increases the availability of blood glucose to the brain.
  • In the liver, high cortisol levels increase gluconeogenesis and decreases glycogen synthesis.
  • muscle cells decrease glucose uptake and consumption and increases protein degradation (for GNG substrates)
  • In adipose tissues, cortisol increases lipolysis
  • In the pancreas, decreases insulin and increases glucagon.
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3
Q

How does Cushings syndrome present?

A

Dorsal fat pad
Thin skin + easy bruising
Enlarged heart + high BP
Purple striae
Central obesity - but skinny arms and legs. Caused by increase in visceral fat deposition.
Muscle weakness + osteoporosis
Ulcers
Diabetes - because of increased gluconeogenesis.
Breaking down tissue for gluconeogenesis - raised glucose levels.

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4
Q

80% of cases of Cushing’s syndrome are []

A

80% of cases of Cushing’s syndrome are hypertensive

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5
Q

What are causes of Cushings syndrome?

A
  • Pituitary tumour:Corticotropic adenoma
  • Ectopic ACTH secretng tumour
  • Cortisol secreting adrenal adenoma
  • Bilateral adrenal hyperplasia.
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6
Q

How do you diagnose Cushings syndrome?

A

Overnight dexamethasone suppression test:

measure cortisol levels after giving dexamethasone: should suppress ACTH levels; given at bed time so by morning shouldn’t create cortisol - if they are it’s pathological

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7
Q

What imaging would use for Cushings syndrome?

What treatment if pituitary tumour? [3] if adrenal tumour? [3]

A
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8
Q

What is Addisons disease? [1]

What is Addisons disease caused by? [2]

A

Addisons disease: A failure of cortisol to rise (less than double the baseline)

Caused by:
* Autoimmune attack
* TB

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9
Q

What are symptoms of Addisons disease?

A

Fatigue, weakness, myalgia, anorexia, weight loss, hyperpigmentation (from increased ACTH on melanocortin 1 receptor)

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10
Q

What is Addisons crisis? What do Ptx present with?

A

Addisonian crisis is the term used to describe an acute presentation of severe Addisons, where the absence of steroid hormones leads to a life threatening presentation. They present with:

Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia, hyperkaemia
Patients can be very unwell

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11
Q

Diagnosis of Addisons? [3]

A
  • Low morning cortisol (should be high)
  • High ACTH
  • Short synacthen test (injection of synthetic ACTH) - would expect a rise in cortisol -> in addison’s, no rise = addison’s
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12
Q

Management of Addisons disease? [2]

Management of Addisons crisis? [2]

A

Management of Addisons disease? [2]
Replace steroids:
* Hydrocortisone (glucocorticoid - synthetic cortisol
* Fludrocortisone (mineralocorticoid synthetic aldosterone)

Management of Addisons crisis? [2]
IC fluids - resus.
IM hydrocortisone.

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13
Q

What is the most abundant steroid in the circulation? [1]

A

Dehydroepiandrosterone (DHEA)

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14
Q

What is 21-hydroxylase enzyme a key pathway in? [1]

A

To develop cortisol and aldosterone

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15
Q

How does 21-hydroxylase deficiency present [4] and why [1] ?

A

Causes no cortisol or aldosterone to be produced: no -ve feedback on ACTH: increase in testosterone (substances that are usually used to form cortisol and aldosterone instead build up in the adrenal glands and are converted to androgens)

Presentation:
* Salt-losing
* Adrenal Insufficiency
* Virilisation
* Adrenal hyperplasia

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16
Q

What is the precursor for catecholamines in adrenal medulla? [1]

A

tyrosine

17
Q

What is the conversion of noradrenaline to adrenaline catalysed by? [1]

Which molecule upregulates ^? [1]

A

catalysed by PNMT

Up regulated by cortisol (so when cortsiol passes from cortex to medulla - increased adrenaline production)

18
Q

Adrenaline reponds to []
Noradrenaline responds to []

A

Adrenaline reponds to hypoglycaemia

Noradrenaline responds to hypovolemia

19
Q

KNOW !

Binding of catecholamines to each of the following causes what repsonse?

A1 [2]
A2

B1
B2
B3

D1
D2

A

A1 - vascular/SM contraction + gluconeogenesis in liver
A2 - inhibitory to noradrenaline release -> supresses BP. In pancreas - inhibit insulin release.
B1 - positvely ionotropic in heart. Increase glycolysis and glycogenolysis.
B2 - smooth muscle relaxation. And glycogenolysis
B3 - burning fat
D1 - small vessel dilatation in kidney + brain + heart
D2 - presynaptic inhibitory release of prolactin.

20
Q

What are symptoms of catecholamine XS

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

21
Q

Chromaffin cell tumours can be categorised as PPGL. What does this mean? [2]

A

PPGL:

Phaeochromocytoma: Arising from within the adrenal medulla
Paraganglioma: Extra-adrenal tumours

22
Q

Chromaffin cell tumours can be categorised as PPGL. What does this mean? [2]

A

PPGL:

Phaeochromocytoma: Arising from within the adrenal medulla
Paraganglioma: Extra-adrenal tumours

23
Q

How would you detect PPGL? [5]

A

Hyperadrenergic spells
Resistant hypertension
Familial syndrome
Incidentally discovered adrenal mass
Early onset hypertension
Dilated cardiomyopathy.

24
Q

How would you diagnose PPGL? [4]

A

24 hour urine metanephrines
Plasma metanephrines
CT/MRI adrenals and abdomen
123I-MIBG scingraphy - to light up tumours radioacvely.

25
Q

Treatment for PPGL? [4]
What should not be given?

A

Surgical resection

Pre-operative A + B adrenoreceptor blockade - very dangerous if not given:
* Phenoxybenzamine A blocker
* Propranolol: B blocker

Acute crisis:
* IV phentolamine
* .nicardipine.

Malignant disease:
131I- MIBG therapy

DON’T USE opiates - can stimulate catecholamine release.