Adrenal glands Flashcards
Cushing most frequent type
Iatrogen by steroid medication
2 main types of Cushing
ACTH dependant :
- ACTH producing hypophysis adenoma (m. Cushing, 70%)
- Ectopic ACTH production
ACTH independant
- adrenocortical adenoma
- adrenocortical carcinoma
Cushing Work Up
Dexamethasone stress test (1mg Dexamethasone midnight, Cortisol serum at 8am)
if < 140nm/l = no cushing
If above Head MRI
Cushing treatment
Neurosurgical
Adrenalectomy only als ultima ratio and for adrenal origin
Cushing post op
The healthy side is in hypo.
Substitute with cortisol post operatively.
Conn syndrome
Primary hyperaldosteronism
Conn Syndrome (clinic)
High blood pressure because of hypervolemia
Hypokaliemia and Metabolic alcalosis
Conn Syndrome mechanism
Aldosterone acts mainly on kidney Stimulation of ENaC and ROMK channels increases sodium resorption increases potassium excretion chloride follows sodium Also acts on apical Proton ATPase and causes secretion that acidifies urine and alkalises extracellular fluid
Why renin decrease ?
Elevated blood pressure
- > increased glomerular filtration rate
- > drop in renin (granular cells of the juxtaglomerular apparatus)
Conn main types
idiopathic bilateral 72%
unilateral adenome 28%
adrenal carcinoma seldom
Diagnosis
serum aldosteron concentration (high)
plasma renin activity (low)
Captopril test
Sodium loading test
Fludrocortisone suppression test
CT
Noriodocholesterol scintigraphy
Sampling of venous adrenal veins (gold standard)
Captopril suppression test
Captpril (ACE inhibitor) supresses renin angiotension aldosterone system
Normally, aldosterone should drop and therefore ARR should be lower. In Conn, stays high.
Differential of Conn
Liddle Syndrome (ENAC Mutation) Licorice, pastis (glycyrrhizin)
What to do by IHA
Medication, no surgery
Localised Conn Adenoma
generally less than 2cm
lap adrenalectomy
can go out of BP meds in 60% of cases
Pheochromocytoma (4x10)
10% familial
10% extra-adrenal (paragangliome)
10% malignity (actually higher)
10% bilateral
Pheochromocytoma trias
Headache
Sweating
Palpitations
Pheochromocytoma Diagnosis and Work Up
Plasmatic metanephrine
CT or MRI
if multilocalisation suspected :
MIBG (metaiodobenzylguanidine) Scintigraphy.
Pheochromocytoma peri-operative
10-14 days alpha blockade (Phenoxybenzamin)
To prevent tacharrythmia and hypertensive crisis
Pheochromocytoma operation
if no malignity suspected:
- LAP Adrenalectomy
Pheochromocytoma post operative
24h ICU
- BP surveillance
- Blood sugar surveillance
Screening every year for 10 years.
Adenocortical carcinoma epidemiology
1/3 are endocrine active
virilising / cushing
therefore earlier diagnosis for women
Adenocortical carcinoma work up
Testosterone Dihydroepiandosterone Dexamethasone suppresion test Conn work up if high blood pressure No FNB !!! spread !!
Adrenocortical Carcinoma Staging
I < 5cm N0 M0
II > 5cm N0 M0
III N+
IV M+
Adrenocortical Carcinoma Operation
only for Stage I and II
en bloc extended resection
for III and IV depends on patient and extension
Adrenocortical Carcinoma Survival
Stage I and II 35 months
Stage III and IV 8-10 months
Adrenal metastasis indication
not for SCLC for - NSCLC - Kidney - Colon increases survival
Incidentaloma
Present in 0.6 - 5% of cases
Indication only for hormone active (10%)
Anamnesis
Standard hormone work up
< 10 HU = benign
Washout after 10 mintues 40-50% = benign
MRI chemical shift phenomenon
incidentaloma indication
Hormone activity
Radiologic malignity
> 6cm
if < 4cm observe
4-6 cm depends on age, patient, etc