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Week 8: Adrenal Hyperfunction Flashcards

(100 cards)

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1
Q

Identify

A
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2
Q

Identify

A
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3
Q

Describe adrenal steroidogenesis

A
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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
27
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
30
What is the defect in Cushing's Syndrome?
Excess endogenous cortisol secretion
31
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
36
Signs and symptoms of Cushing's Syndrome 18 listed
37
Lab tests for Cushing's Syndrome 3 listed
* 24 hour urine cortisol * salivary cortisol * Dexamethasone suppression test
38
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
41
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
46
Mifepristone MOA
47
Describe catecholamine synthesis
48
Describe catecholamine metabolism
49
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
52
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
53
What is pheochromocytoma?
Adrenal medulla tumor of chromaffin cells which secretes epinephrine, norepinephrine and dopamine
54
Pheochromocytoma derived from?
Chromaffin cells of the adrenal medulla
55
Epidemiology of pheochromocytoma
Most common tumor of the adrenal medulla in adults
56
Pheochromocytoma rule of 10's
* 10% malignant * 10% bilateral * 10% extra-adrenal * 10% calcify * 10% occur in children
57
Pheochromocytoma associations
up to 25% of cases occur with various syndromes * MEN2A and 2B * Neurofibromatosis * Von Hippel-Lindau Disease
58
Clinical presentation of Pheochromocytoma
Spells of * HTN * Headaches * Diaphoresis * Palpitations * Pallor or Asymptomatic
59
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
60
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.
61
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
64
Main defect in Primary Aldosteronism
Hypersecretion of aldosterone
65
Primary Aldosteronism etiologies
* Unilateral adenoma * Tumors are small * Bilateral adrenal hyperplasia
66
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
74
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
75
What is this depicting?
CT of adrenal adenoma in the setting of Primary Aldosteronism
76
Treatment of unilateral adenoma in the setting of Primary Aldosteronism
* Surgical resection (laproscopic) * Experienced surgeon (urology)
77
Treatment of bilateral adenoma in the setting of Primary Aldosteronism
* Aldosterone receptor antagonist * Spironolactone * Eplerenone
78
What is this?
Adrenal Adenoma in primary aldosteronism
79
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 *
80
Adrenal carcinoma etiology
Majority of cases are sporadic * TP53 tumor suppressor gene
81
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
90
Adrenal carcinoma imaging
* CT/MRI of abdomen * PET scan
91
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
96
Adrenal incidentaloma epidemiology
* prevalence of 4.4% * 10% in older patients
97
What is this?
Adrenal incidentaloma on Abd CT
98
Imaging characteristics of adrenal tumors
99
Evaluation of Adrenal incidentaloma
100
Adrenal incidentaloma features
doesn't say malignant or benign or secretory vs non-secretory

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