GINME > Week 8: Adrenal Hyperfunction > Flashcards

Week 8: Adrenal Hyperfunction Flashcards

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1
Q

Identify

A
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2
Q

Identify

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3
Q

Describe adrenal steroidogenesis

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4
Q

Cortex layers and secretions

A

Zona glomerulosa (aldosterone)

Zone Fasiculata (cortisol)

Cona reticularis (andreogens)

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5
Q

Medulla secretions

A

epinephrine and norepinephrine

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6
Q

Zona glomerulosa secretion

A

(aldosterone)

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7
Q

Zona Fasicularis secretions

A

Cortisol

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8
Q

Zona reticularis secretions

A

Androgens

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9
Q

Adrenal steroidogenesis things to know

A

ACTH is the stimulus for adrenal steroidogenesis and cholesterol is needed (from de novo from acetate or taken from LDL or HDL from the circulation)

Cholesterol -STAR protein-> brings cholesterol into the mitochondria to start steroidogenesis)

*1st step is the rate-limiting step* (shown below)

Cholesterol -cholesterol desmolase or CYP11A1-> Progenolone

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10
Q

Describe the Hypothalamic-pituitary-adrenal axis and regulatory mechanisms

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11
Q

What are the acute effects of ACTH?

A

increased conversion of cholesterol to Pregnenolone via activation of CYP11A1

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12
Q

What are the chronic effects of ACTH?

A
  • Increased synthesis of the enzymes involved in steroidogenesis
  • Increased RNA and DNA synthesis
  • Increased Cell growth
  • Increased synthesis of LDL and HDL receptors
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13
Q

Systems affected by cortisol

11 listed

A
  • Increased production of glucose (gluconeogenesis)
  • Carbohydrate metabolism
  • Protein metabolism
  • Lipid Metabolism
  • Immune System
  • Body Water
  • Mineralocorticoid activity
  • Arterioles
  • Osteoblasts
  • Hepatocytes
  • Cardiomyocytes
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14
Q

Cortisol effects on metabolism

9 listed

A
  • Antagonizes secretion and action of insulin
  • Decreased peripheral uptake of glucose
  • insulin resistance
  • Increased gluconeogenesis
  • Increased protein breakdown
  • Increased nitrogen excretion
  • Decreased protein synthesis
  • Free fatty acid mobilization
  • Activation of cellular lipase
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15
Q

Cortisol effects on the immune system

6 listed

A
  • Maintains vascular responsiveness to circulating vasoconstrictors
  • Opposes increase in capillary permeability during acute inflammation
  • Leukocytosis (release from bone marrow and inhibition of movement through the capillary wall)
  • Impairs cell-mediated immunity
  • Inhibits production and action of mediators of inflammation (Leukotrienes, Prostaglandins, IL-2)
  • Blocks histamine release from mast cells
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16
Q

Cortisol effects on body water

4 listed

A
  • Promotes renal water excretion
  • inhibition of vasopressin excretion
  • Increase glomerular filtration rate
  • Direct action of the renal tubule
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17
Q

Cortisol mineralocorticoid effects

A

Weak mineralocorticoid effects

  • Promotes renal tubular Na+ reabsorption
  • Increase urine potassium excretion
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18
Q

Cortisol effects on the vascular system

A
  • Upregulates α1-receptors on arterioles → increased sensitivity to norepinephrine and epinephrine
  • Opposes capillary permeability during acute inflammation
  • Maintains vascular responsiveness to circulating vasoconstrictors
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19
Q

Cortisol effects on bone

A

Induces the destruction of osteoblasts → decreased bone formation

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20
Q

Cortisol effects on the liver

A

Promotes the survival of hepatocytes

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21
Q

Cortisol effects on the heart

A

Promotes the survival of cardiomyocytes

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22
Q

How much cortisol is secreted daily?

A

15-20 mg/day

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23
Q

How does cortisol circulate?

A
  • <5% is free cortisol
  • 95% is protein-bound to CBG (corticosteroid-binding globulin) & Albumin
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24
Q

Cortisone binding properties of CBG

3 listed

A
  • High-affinity
  • low capacity
  • Reduced in areas of inflammation
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25
Cortisone binding properties of albumin
* Low affinity * High capacity
26
What is CBG?
Corticosteroid-binding globulin Binds cortisone in the blood for transport
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Where is the cortisol receptor expressed?
Nearly every cell in the body
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What kind of receptor is the glucocorticoid (cortisol) receptor?
member of the nuclear receptor superfamily of ligand-dependent transcription factors
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What genes are affected by the glucocorticoid receptor?
induces or represses the transcription of target genes that comprise 10-20% of the human genome
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What is the defect in Cushing's Syndrome?
Excess endogenous cortisol secretion
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Etiologies of Cushing's Syndrome 4 listed
Pituitary (Cushing's Disease) Ectopic (Small cell lung cancer or Bronchial carcinoid) Exogenous steroids Excess cortisol secretion from an adrenal tumor (hyperplasia, adenoma or carcinoma)
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What is the most common cause of Cushing's Syndrome
Pituitary (Cushing's Disease) is the most common endogenous cause
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Etiologies of ectopic Cushing's Syndrome
* Small cell lung cancer * Bronchial carcinoid
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Epidemiology of Cushing's Syndrome
* Female predominance * Onset common in the first decade of life as well as 40-50 years old
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Signs and symptoms of Cushing's Syndrome 18 listed
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Lab tests for Cushing's Syndrome 3 listed
* 24 hour urine cortisol * salivary cortisol * Dexamethasone suppression test
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Diagnostic criteria of Cushing's Syndrome
2 tests are needed to confirm the cortisol excess * ACTH to determine the source of cortisol excess * 24-hour urine cortisol * Salivary cortisol * Dexamethasone suppression test
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How to determine the source of cortisol excess in Cushing's Syndrome
ACTH to determine the source of cortisol excess * ACTH is undetectable if the source is adrenal * Elevated ACTH indicates a pituitary or ectopic source
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Diagnostic approach to Cushing's Syndrome
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List of catecholamines
dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline)—and histamine and serotonin
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Imaging for Cushing's Syndrome
* Pituitary (MRI) * Adrenals (CT or MRI) * Ectopic (CT of Chest/Abd/pelvis, PET scan)
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What to do if Cushing's Syndrome is Dx
Refer to Endocrinology
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Treatment of Cushing's Syndrome
Surgical Treatments * Adrenalectomy for adrenal tumors * Transsphenoidal resection for pituitary tumors * Tumor resection of ectopic tumors when possible Medical Treatments * Ketoconazole * Mifepristone * Pasireotide
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Ketoconazole MOA
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Mifepristone MOA
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Describe catecholamine synthesis
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Describe catecholamine metabolism
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What are the catecholamines?
catecholamines—dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline)—and histamine and serotonin
50
What are the actions of catecholamines on glucose levels?
* Increase glucose levels * stimulation of glycogenolysis and gluconeogenesis in the liver * Stimulates glucagon secretion from the α-cells of the pancreas * Inhibition of GLUT4 transporters * Inhibition of insulin secretion from the β-cells of the pancreas`
51
Actions of catecholamines effects on the cardiovascular system
Increases the ionotropic effect → contractility of the cardiac muscle → increasing cardiac output Increases bathmotropic effect → increase excitability of the cardiac muscle → increases cardiac output Increases dromotropic effect → increase AV nodal conduction velocity → heart rate → increases cardiac output Increases chronotropic effect → increases the SA nodal discharge rate → increases cardiac output
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Actions of catecholamines on blood pressure
Alters blood pressure by altering vascular resistance Vasoconstriction - α-adrenergic receptors in the liver, kidney, skin and gut Vasodilation - β-adrenergic receptors in skeletal muscle
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What is pheochromocytoma?
Adrenal medulla tumor of chromaffin cells which secretes epinephrine, norepinephrine and dopamine
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Pheochromocytoma derived from?
Chromaffin cells of the adrenal medulla
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Epidemiology of pheochromocytoma
Most common tumor of the adrenal medulla in adults
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Pheochromocytoma rule of 10's
* 10% malignant * 10% bilateral * 10% extra-adrenal * 10% calcify * 10% occur in children
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Pheochromocytoma associations
up to 25% of cases occur with various syndromes * MEN2A and 2B * Neurofibromatosis * Von Hippel-Lindau Disease
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Clinical presentation of Pheochromocytoma
Spells of * HTN * Headaches * Diaphoresis * Palpitations * Pallor or Asymptomatic
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Evaluation of Pheochromocytoma
* Plasma metanephrines if suspicion for Pheochromocytoma is high * 24-hour urine metanephrines and catecholamines * Imaging * CT or MRI of adrenals * MIBG/PET scan
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What is an MIBG scan?
An MIBG scan is a nuclear medicine imaging test. It combines a small amount of radioactive material with a substance called metaiodobenzylguanidine (MIBG) to find certain types of tumours in the body.
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What is this depicting?
CT of abdomen with Pheochromocytoma
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Treatment of Pheochromocytoma
63
Actions of aldosterone
Regulates extracellular fluid volume and K+ metabolism by the mineralocorticoid receptor in principal cells in the renal cortical collecting duct * Na+ reabsorption * H2O follows Na+ * K+ secretion * H+ secretion
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Main defect in Primary Aldosteronism
Hypersecretion of aldosterone
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Primary Aldosteronism etiologies
* Unilateral adenoma * Tumors are small * Bilateral adrenal hyperplasia
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Primary Aldosteronism epidemiology
Occurs between ages 30-50
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Primary Aldosteronism associations
Present in 5-15% of Hypertensive patients
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What is this depicting?
Primary aldosteronism by H&E stain
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Aldosterone effects on endothelium
↓ NO (Nitric oxide) availability ↓ fibrinolysis * decreased compliance * microvascular dysfunction * perivascular fibrosis * Systemic vasoconstriction
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Aldosterone effects on the heart
Fibrosis apoptosis inflammation hypertrophy coronary vasoconstriction ↓ ionoptropy
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Aldosterone effects on the kidneys
* Electrolyte imbalance * ↓K+ * ↓Mg++ * Na+ and H2O retention * Proteinuria * Glomerular injury * Renal vasoconstriction
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Aldosterone effects on the CNS/PNS
↑ local RAAS ↑ SNS Autonomic dysfunction
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Primary Aldosteronism clinical presentation
* HTN * headaches * Hypokalemia * muscle weakness * fatigue * Hypernatremia * Metabolic alkalosis * No edema * Aldosterone escape mechanism * ↑ renal perfusion pressure → volume expansion → ↓ proximal Na+ reabsorption and ↑ Na+ delivery to the distal nephron * overrides aldosterone stimulated Na+ reabsorption * Volume expansion also ↑ plasma natriuretic hormone → inhibitory effect on Na+ reabsorption in the collecting duct
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Evaluation of Primary Aldosteronism
* Serum aldosterone and plasma renin activity * High aldosterone to Renin ratio \> 20 * Confirmatory testing with oral salt loading or saline infusion * CT/MRI of the abdomen * Adrenal vein sampling
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What is this depicting?
CT of adrenal adenoma in the setting of Primary Aldosteronism
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Treatment of unilateral adenoma in the setting of Primary Aldosteronism
* Surgical resection (laproscopic) * Experienced surgeon (urology)
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Treatment of bilateral adenoma in the setting of Primary Aldosteronism
* Aldosterone receptor antagonist * Spironolactone * Eplerenone
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What is this?
Adrenal Adenoma in primary aldosteronism
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Adrenal carcinoma epidemiology
* 1-2 per million population per year * Peaks before the age of five and in the 4th to 5th decade of life * Female predominance *
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Adrenal carcinoma etiology
Majority of cases are sporadic * TP53 tumor suppressor gene
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Adrenal carcinoma associations
Hereditary cancer syndromes * Li-Fraumeni Syndrome * Beckwith-Wiedemann syndrome * Multiple endocrine neoplasia type 1 (MEN1)
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Li-Fraumeni Syndrome description
* breast cancer, soft tissue and bone sarcoma also brain tumors
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Li-Fraumeni Syndrome Etiology
Inactivating mutations of the TP53
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Beckwith-Wiedemann Syndrome Description
* Wilm's tumor * neuroblastoma * hepatoblastoma
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Beckwith-Wiedemann Syndrome etiology
Abnormalities in 11p15
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Multiple endocrine neoplasia type 1 description
* Parathyroid, pituitary and pancreatic neuroendocrine tumors * adrenal adenoma/carcinoma * Unilateral or bilateral adrenal tumors can be found in 20-40% of patients with MEN1 * majority are benign tumors usually nonfunctional * can present with excess production of aldosterone or cortisol
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Multiple endocrine neoplasia type 1 etiologies
Inactivating mutations of the MEN1 gene
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Clinical presentation of Adrenal carcinoma
* 60% secretory * 45% Cushing's Syndrome alone * 25% mixed Cushing's Syndrome and Virilization syndrome * overproduction of both glucocorticoids and androgens * \<10% present with virilization alone
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Evaluation of Adrenal carcinoma
* History and Physical * adrenal androgens * dehydroepiandrosterone sulfate (DHEAS) * Testosterone
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Adrenal carcinoma imaging
* CT/MRI of abdomen * PET scan
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What is this depicting?
Adrenal carcinoma
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Prognosis of adrenal carcinoma
* 5 year survival 45-60% for early-stage disease * 10-25% for advanced-stage disease
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Treatment of Adrenal carcinoma
* Adrenalectomy (open) * Mitotane * Chemotherapy * cisplatin and etoposide * Mitotane + Streptozotocin * Radiation therapy
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Mitotane MOA
95
Mitotane effects
* Cytotoxic effect on adrenal tissue * normal adrenals and in adrenocortical tumors * mitochondrial destruction and necrosis of adrenocortical cells
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Adrenal incidentaloma epidemiology
* prevalence of 4.4% * 10% in older patients
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What is this?
Adrenal incidentaloma on Abd CT
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Imaging characteristics of adrenal tumors
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Evaluation of Adrenal incidentaloma
100
Adrenal incidentaloma features
doesn't say malignant or benign or secretory vs non-secretory
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