THE ADRENAL GLAND Moderator : Dr Lalitha firstname.lastname@example.org
ANATOMY • Situated on Posterior Abdominal Wall - over upper pole of kidneys • Hence k/a SUPRARENAL GLANDS - 50 mm in height , 30 mm in breadth , 10 mm thickness • weighs 5 gms, medulla forming one tenth • Right – pyramidal Left - semilunar
Suprarenal Glands Divided into two parts; each with separate functions Suprarenal Cortex (mesodermal origin) Suprarenal Medulla (neural crest origin)
Arterial supply The arterial blood supply to each adrenal gland is via three adrenal arteries: • The superior suprarenal artery, a branch of the inferior phrenic artery • The middle suprarenal artery, a branch of the aorta • The inferior suprarenal artery, a branch of the renal artery.
The venous drainage of the adrenal glands is via the suprarenal veins which drain into different main veins on each side: • the right into the inferior vena cava • the left into either the left renal or left inferior phrenic vein.
Nerve supply - rich nerve supply through myelinated pre ganglionic sympathetic fibres Branches from the coeliac plexus and the thoracic splanchnic nerves supply the chromaffin cells of the medulla
FUNCTIONAL ANATOMY Figure 25.9a
The Adrenal Glands • Adrenal medulla • Adrenal cortex • Three specific zones and each produces a specific class of steroid hormone • Zona glomerulosa – mineralocorticoids (Aldosterone) • Zona fasciculata – glucocorticoids ( Cortisol ) • Zona reticularis - androgens
Medullary hormones • Amines : adrenaline (epinephrine), noradrenaline (norepinephrine), dopamine • Others: acetylcholine, metenkephalin, chromogranin A
1 IN RECUMBENT HUMANS, THE NORMAL PLASMA LEVEL OF FREE NOREPINEPHRINE IS ABOUT 300pg/ml [1.8 n mol/L] . 2 THE FREE EPINEPHRINE LEVEL IS NORMALY ABOUT 30pg/ml [0.16n mol/L]. 3 THE PLASMA FREE DOPAMINE LEVEL IS ABOUT 35pg/ml [0.23n mol/L] .
a catecholamine-secreting tumour of chromaffin cells of the adrenal medulla • paraganglioma – a catecholamine secreting tumour of the sympathetic paraganglia adrenal pheochromocytoma (90%) extra-adrenal pheochromocytoma
Mineralocorticoidsfrom zonaglomerulosa • ALDOSTERONE – 95% • DESOXYCORTICOSTRONE • CORTISOL
Aldosterone • Steroid hormone • Essential for life • responsible for regulating Na+ reabsorption in the distal tubule and the cortical collecting ducts • Leads to secretion of K • target cells are called “principal (P) cell” • stimulates synthesis of more Na/K ATPase pumps
Effects of Aldosterone • Renal and circulatory effects … - Excess aldosterone Na retention ECF volume increase increased CO & BP - Excess aldosterone K decreased skeletal muscle weakness & paralysis
Promotes reabsorption of sodium from ducts of sweat and salivary glands during excessive sweat/saliva loss. - Enhances absorption of sodium from intestine esp. colon. – absence leads to diarrhoea.
Regulation of Aldosterone Release • direct stimulators of release - increased extracellular K+ - decreased osmolarity • indirect stimulators of release (RAAS) - decreased blood pressure - decreased macula densa blood flow
Half life of aldosterone : 20 mins 90% of it is cleared by the liver in a single passage Hyperaldosteronism is k/a Conn’s Disease
Glucocorticoids • Cortisol • Corticosterone • cortisone
Cortisol • Enhances gluconeogenesis & inhibits periph glucose utilization inc blood glucose - protein catabolism - fatty acid metabolism - anti-inflammatory - crucial for norepi epi conversion (critical for expression of enz phenylethanolamine N methyl transferase) - Breakdown of bone matrix (high doses)
Effect on Blood Cells and Immunity • Decrease production of eosinophils and lymphocytes • Suppresses lymphoid tissue systemically therefore decrease in T cell and antibody production thereby decreasing immunity • Decrease immunity could be fatal in diseases such as tuberculosis • Decrease immunity effect of cortisol is useful during transplant operations in reducing organ rejection.
Stressor Brain Stem (e.g. LC) Stressor
REGULATION OF CORTISOL SECRETION DIURNAL RHYTHM HYPOTHALAMUS STRESS + - + CRH ANTERIOR PITUITARY INCREASED BLOOD GLUCOSE BLOOD AA BLOOD FATTY ACIDS - ACTH ADRENAL CORTEX CORTISOL TARGET ORGANS
Regulation of Cortisol Release cont Enhanced release can be caused by: • physical trauma • infection • extreme heat and cold • exercise to the point of exhaustion • extreme mental anxiety
“Diurnal ryhthm” Peak plasma cortisol level : 8- 25 ug/dl shortly after awakening ACTH Cortisol
In systemic circulation : 80 – 90% bound to specific globulin TRANSCORTIN • Unbound cortisol is biologically active • Elimination half time : 70 mins • Degradation : Liver 17 hydroxycorticosteroid excreted in urine
Classification of adrenal disorders • Insufficiency • Primary adrenal insufficiency (Addison’s) • due to adrenal insufficiency (marked skin pigmentation due to high ACTH levels) • Secondary adrenal insufficiency • Pituitary or hypothalamic Insufficiency (no skin pigmentation) • Excess • Cushing's disease/syndrome • Primary hyperaldosteronism (Conn’s) • Resistance • adrenal virilism and congenital adrenal hyperplasia (21-hydroxylase deficiency)
Cushing Syndrome Endogenous • Pituitary hypersecretion of ACTH • Adrenal hypersecretion of cortisol (adenoma, carcinoma, nodular hyperplasia) • Ectopic ACTH (small cell lung cancer) Exogenous 4. Adm. of exogenous glucocorticoids
Cushing Syndrome – Clinical Features • Hypertension • Weight gain: • Truncal obesity • “moon” face • “buffalo hump” • Decreased muscle mass • Hyperglycemia • Catabolic effect on proteins with loss of collagen: cutaneous striae, easy brusing, osteoporosis • Hirsutism, amenorrhea • Increased risk of infections (because of decreased immune response)
Cushing’s : Diagnosis • Distinguish between: • Cushings Disease -Pituitary Causes • Cushing’s Syndrome -Adrenal causes of cortisol excess; -Ectopic sources of ACTH or Ectopic CRH (Corticotropin Releasing Hormone)
Diagnosis : Anatomical Details • Pituitary: Skull X ray C T M R I • Adrenals: U S C T M R I Scintigraphy - cholesterol scan - N P 59 scan • Search for ectopic ACTH source C T chest Angiography
Laboratory • Serum Cortisol is elevated (normal:13 – 20 mg/d) • Abnormal tests can be seen in up to 30% of hospitalized and/or depressed patients • 24 hour free urinary cortisol can be a useful adjunct • Overnight Dexamethasone suppression test……
Overnight Dexamethasone Suppression Test: 1 gram at 11pm, measure plasma cortisol at 8 am the next morning • The normal response is suppression to less than 3mcg/dl • If no suppression, they have ectopic or adrenal production • If supression, they may have pituitary cause
CUSHING’S/hypercortisolism • RX • 80-90% due to ant pituitary tumor • Transphenoidal exc pituitary gland tumor • Adrenalectomy for adrenal cortex tumor • Pituitary irradiation with bilateral Adrenalectomy with adrenal adenoma/carcinoma
Anaesthetic considerations • Plasma cortisol level rise 2 – 10 folds induction, during sx, post op • Return to normal 24 – 72 hrs post op
Anaesthetic Considerations • Preop • Eval BP • Eval electrolytes • Evaluate blood glucose • Does the pt have osteoporosis?
difficult intubation, airway.. Because of moon facies • Delicate oral mucosa • Attempts to dec adrenal cortex activity with opioids, barbiturates, or volatile agents is futile…. any drug induced inhibition is over ridden by surgical stimulus Choice of sedatives, induction agents not influenced by elevated cortisol
Etomidate dec of synthesis & release cortisol is transient • Careful use of relaxants in face of skeletal muscle weakness/hypokalemia MONITOR
Regional OK-remember possibility of osteoporosis and effects on vertebral bodies • But.. Mechanical ventilation is recommended dec strength in muscles of breathing
Osteoporosis tendency = positioning considerations • Skin issues (prone to bruising, easy damage)=need for special handling • Fluid mx :Will be prone to water overload and hyponatremia
Plasma cortisol levels decrease promptly after gland excision need replacement • Consider steroid infusion : hydrocotisone 100mg/d iv
Na retention and K excretion HTN, hypokalemia • Primary (Conn syndrome) • Adrenal cortical adenoma • Suppression of RAA: plasma renin = low • Secondary • Due to decreased renal perfusion (renal artery stenosis, arteriolar nephrosclerosis, CHF) • Activation of RAA: plasma renin = high