Adrenal Glands Part2 Flashcards
What is cortisol response to each of the following & effect? [3]
Starvation [1]
Infection [1]
Hypotension [1
Starvation: High cortisol: will start to breakdown body tissues
Infection: acts as anti-inflammatory
Hypotension: raises BP
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.
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.
How does Cushings syndrome present?
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.
80% of cases of Cushing’s syndrome are []
80% of cases of Cushing’s syndrome are hypertensive
What are causes of Cushings syndrome?
- Pituitary tumour:Corticotropic adenoma
- Ectopic ACTH secretng tumour
- Cortisol secreting adrenal adenoma
- Bilateral adrenal hyperplasia.
How do you diagnose Cushings syndrome?
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
What imaging would use for Cushings syndrome?
What treatment if pituitary tumour? [3] if adrenal tumour? [3]
What is Addisons disease? [1]
What is Addisons disease caused by? [2]
Addisons disease: A failure of cortisol to rise (less than double the baseline)
Caused by:
* Autoimmune attack
* TB
What are symptoms of Addisons disease?
Fatigue, weakness, myalgia, anorexia, weight loss, hyperpigmentation (from increased ACTH on melanocortin 1 receptor)
What is Addisons crisis? What do Ptx present with?
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
Diagnosis of Addisons? [3]
- 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
Management of Addisons disease? [2]
Management of Addisons crisis? [2]
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.
What is the most abundant steroid in the circulation? [1]
Dehydroepiandrosterone (DHEA)
What is 21-hydroxylase enzyme a key pathway in? [1]
To develop cortisol and aldosterone
How does 21-hydroxylase deficiency present [4] and why [1] ?
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
What is the precursor for catecholamines in adrenal medulla? [1]
tyrosine
What is the conversion of noradrenaline to adrenaline catalysed by? [1]
Which molecule upregulates ^? [1]
catalysed by PNMT
Up regulated by cortisol (so when cortsiol passes from cortex to medulla - increased adrenaline production)
Adrenaline reponds to []
Noradrenaline responds to []
Adrenaline reponds to hypoglycaemia
Noradrenaline responds to hypovolemia
KNOW !
Binding of catecholamines to each of the following causes what repsonse?
A1 [2]
A2
B1
B2
B3
D1
D2
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.
What are symptoms of catecholamine XS
Impending doom
Diaphoresis
Dyspnea
Headache
Hypertension
Palpitation
Tremor
Nausea and vomiting
Fatigue
Orthostatic hypotension
Hyperglycemia
Weight loss
Epigastric and chest pain
Congestive heart failure
Chromaffin cell tumours can be categorised as PPGL. What does this mean? [2]
PPGL:
Phaeochromocytoma: Arising from within the adrenal medulla
Paraganglioma: Extra-adrenal tumours
Chromaffin cell tumours can be categorised as PPGL. What does this mean? [2]
PPGL:
Phaeochromocytoma: Arising from within the adrenal medulla
Paraganglioma: Extra-adrenal tumours
How would you detect PPGL? [5]
Hyperadrenergic spells
Resistant hypertension
Familial syndrome
Incidentally discovered adrenal mass
Early onset hypertension
Dilated cardiomyopathy.
How would you diagnose PPGL? [4]
24 hour urine metanephrines
Plasma metanephrines
CT/MRI adrenals and abdomen
123I-MIBG scingraphy - to light up tumours radioacvely.
Treatment for PPGL? [4]
What should not be given?
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.
