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GINME > Week 8: Adrenal Hyperfunction > Flashcards

Week 8: Adrenal Hyperfunction Flashcards

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

A
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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
Q

Cortisone binding properties of albumin

A
  • Low affinity
  • High capacity
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26
Q

What is CBG?

A

Corticosteroid-binding globulin

Binds cortisone in the blood for transport

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27
Q

Where is the cortisol receptor expressed?

A

Nearly every cell in the body

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28
Q

What kind of receptor is the glucocorticoid (cortisol) receptor?

A

member of the nuclear receptor superfamily of ligand-dependent transcription factors

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29
Q

What genes are affected by the glucocorticoid receptor?

A

induces or represses the transcription of target genes that comprise 10-20% of the human genome

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30
Q

What is the defect in Cushing’s Syndrome?

A

Excess endogenous cortisol secretion

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31
Q

Etiologies of Cushing’s Syndrome

4 listed

A

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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32
Q

What is the most common cause of Cushing’s Syndrome

A

Pituitary (Cushing’s Disease) is the most common endogenous cause

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33
Q

Etiologies of ectopic Cushing’s Syndrome

A
  • Small cell lung cancer
  • Bronchial carcinoid
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34
Q
A
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35
Q

Epidemiology of Cushing’s Syndrome

A
  • Female predominance
  • Onset common in the first decade of life as well as 40-50 years old
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36
Q

Signs and symptoms of Cushing’s Syndrome

18 listed

A
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37
Q

Lab tests for Cushing’s Syndrome

3 listed

A
  • 24 hour urine cortisol
  • salivary cortisol
  • Dexamethasone suppression test
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38
Q

Diagnostic criteria of Cushing’s Syndrome

A

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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39
Q

How to determine the source of cortisol excess in Cushing’s Syndrome

A

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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40
Q

Diagnostic approach to Cushing’s Syndrome

A
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41
Q

List of catecholamines

A

dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline)—and histamine and serotonin

42
Q

Imaging for Cushing’s Syndrome

A
  • Pituitary (MRI)
  • Adrenals (CT or MRI)
  • Ectopic (CT of Chest/Abd/pelvis, PET scan)
43
Q

What to do if Cushing’s Syndrome is Dx

A

Refer to Endocrinology

44
Q

Treatment of Cushing’s Syndrome

A

Surgical Treatments

  • Adrenalectomy for adrenal tumors
  • Transsphenoidal resection for pituitary tumors
  • Tumor resection of ectopic tumors when possible

Medical Treatments

  • Ketoconazole
  • Mifepristone
  • Pasireotide
45
Q

Ketoconazole MOA

A
46
Q

Mifepristone MOA

A
47
Q

Describe catecholamine synthesis

A
48
Q

Describe catecholamine metabolism

A
49
Q

What are the catecholamines?

A

catecholamines—dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline)—and histamine and serotonin

50
Q

What are the actions of catecholamines on glucose levels?

A
  • 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
Q

Actions of catecholamines effects on the cardiovascular system

A

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
Q

Actions of catecholamines on blood pressure

A

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
Q

What is pheochromocytoma?

A

Adrenal medulla tumor of chromaffin cells which secretes epinephrine, norepinephrine and dopamine

54
Q

Pheochromocytoma derived from?

A

Chromaffin cells of the adrenal medulla

55
Q

Epidemiology of pheochromocytoma

A

Most common tumor of the adrenal medulla in adults

56
Q

Pheochromocytoma rule of 10’s

A
  • 10% malignant
  • 10% bilateral
  • 10% extra-adrenal
  • 10% calcify
  • 10% occur in children
57
Q

Pheochromocytoma associations

A

up to 25% of cases occur with various syndromes

  • MEN2A and 2B
  • Neurofibromatosis
  • Von Hippel-Lindau Disease
58
Q

Clinical presentation of Pheochromocytoma

A

Spells of

  • HTN
  • Headaches
  • Diaphoresis
  • Palpitations
  • Pallor

or

Asymptomatic

59
Q

Evaluation of Pheochromocytoma

A
  • Plasma metanephrines if suspicion for Pheochromocytoma is high
  • 24-hour urine metanephrines and catecholamines
  • Imaging
    • CT or MRI of adrenals
    • MIBG/PET scan
60
Q

What is an MIBG scan?

A

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
Q

What is this depicting?

A

CT of abdomen with Pheochromocytoma

62
Q

Treatment of Pheochromocytoma

A
63
Q

Actions of aldosterone

A

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
Q

Main defect in Primary Aldosteronism

A

Hypersecretion of aldosterone

65
Q

Primary Aldosteronism etiologies

A
  • Unilateral adenoma
    • Tumors are small
  • Bilateral adrenal hyperplasia
66
Q

Primary Aldosteronism epidemiology

A

Occurs between ages 30-50

67
Q

Primary Aldosteronism associations

A

Present in 5-15% of Hypertensive patients

68
Q

What is this depicting?

A

Primary aldosteronism by H&E stain

69
Q

Aldosterone effects on endothelium

A

↓ NO (Nitric oxide) availability

↓ fibrinolysis

  • decreased compliance
  • microvascular dysfunction
  • perivascular fibrosis
  • Systemic vasoconstriction
70
Q

Aldosterone effects on the heart

A

Fibrosis

apoptosis

inflammation

hypertrophy

coronary vasoconstriction

↓ ionoptropy

71
Q

Aldosterone effects on the kidneys

A
  • Electrolyte imbalance
  • ↓K+
  • ↓Mg++
  • Na+ and H2O retention
  • Proteinuria
  • Glomerular injury
  • Renal vasoconstriction
72
Q

Aldosterone effects on the CNS/PNS

A

↑ local RAAS

↑ SNS

Autonomic dysfunction

73
Q

Primary Aldosteronism clinical presentation

A
  • 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
Q

Evaluation of Primary Aldosteronism

A
  • 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
Q

What is this depicting?

A

CT of adrenal adenoma in the setting of Primary Aldosteronism

76
Q

Treatment of unilateral adenoma in the setting of Primary Aldosteronism

A
  • Surgical resection (laproscopic)
  • Experienced surgeon (urology)
77
Q

Treatment of bilateral adenoma in the setting of Primary Aldosteronism

A
  • Aldosterone receptor antagonist
    • Spironolactone
    • Eplerenone
78
Q

What is this?

A

Adrenal Adenoma in primary aldosteronism

79
Q

Adrenal carcinoma epidemiology

A
  • 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
Q

Adrenal carcinoma etiology

A

Majority of cases are sporadic

  • TP53 tumor suppressor gene
81
Q

Adrenal carcinoma associations

A

Hereditary cancer syndromes

  • Li-Fraumeni Syndrome
  • Beckwith-Wiedemann syndrome
  • Multiple endocrine neoplasia type 1 (MEN1)
82
Q

Li-Fraumeni Syndrome description

A
  • breast cancer, soft tissue and bone sarcoma also brain tumors
83
Q

Li-Fraumeni Syndrome Etiology

A

Inactivating mutations of the TP53

84
Q

Beckwith-Wiedemann Syndrome Description

A
  • Wilm’s tumor
  • neuroblastoma
  • hepatoblastoma
85
Q

Beckwith-Wiedemann Syndrome etiology

A

Abnormalities in 11p15

86
Q

Multiple endocrine neoplasia type 1 description

A
  • 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
87
Q

Multiple endocrine neoplasia type 1 etiologies

A

Inactivating mutations of the MEN1 gene

88
Q

Clinical presentation of Adrenal carcinoma

A
  • 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
89
Q

Evaluation of Adrenal carcinoma

A
  • History and Physical
  • adrenal androgens
    • dehydroepiandrosterone sulfate (DHEAS)
    • Testosterone
90
Q

Adrenal carcinoma imaging

A
  • CT/MRI of abdomen
  • PET scan
91
Q

What is this depicting?

A

Adrenal carcinoma

92
Q

Prognosis of adrenal carcinoma

A
  • 5 year survival 45-60% for early-stage disease
  • 10-25% for advanced-stage disease
93
Q

Treatment of Adrenal carcinoma

A
  • Adrenalectomy (open)
  • Mitotane
  • Chemotherapy
    • cisplatin and etoposide
    • Mitotane + Streptozotocin
  • Radiation therapy
94
Q

Mitotane MOA

A
95
Q

Mitotane effects

A
  • Cytotoxic effect on adrenal tissue
    • normal adrenals and in adrenocortical tumors
      • mitochondrial destruction and necrosis of adrenocortical cells
96
Q

Adrenal incidentaloma epidemiology

A
  • prevalence of 4.4%
    • 10% in older patients
97
Q

What is this?

A

Adrenal incidentaloma on Abd CT

98
Q

Imaging characteristics of adrenal tumors

A
99
Q

Evaluation of Adrenal incidentaloma

A
100
Q

Adrenal incidentaloma features

A

doesn’t say malignant or benign or secretory vs non-secretory

GINME (63 decks)

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