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Endocrinology > Adrenal Disorders > Flashcards

Adrenal Disorders Flashcards

1
Q

What percentage of cardiac output do the adrenal glands receive?

A

0.14% of the cardiac output for approximately 0.02% of total body weight

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2
Q

What are the arterial supplies of the adrenal glands?

A
  • superior suprarenal (adrenal) arteries
  • middle suprarenal arteries
  • inferior suprarenal arteries
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3
Q

What is the venous drainage for the right adrenal gland?

A

right suprarenal vein

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4
Q

What is the venous drainage for the left adrenal gland?

A

suprarenal vein

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5
Q

What are the three zones of the adrenal cortex?

A
  • zona glomerulosa
  • zona fasciculata
  • zona reticularis
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6
Q

What hormones are produced by the zona glomerulosa?

A

Mineralocorticoids (aldosterone)

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7
Q

What is the primary function of aldosterone?

A

Reabsorption of sodium

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8
Q

What hormones are produced by the zona fasciculata?

A

Glucocorticoids (cortisol)

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9
Q

What are the functions of cortisol?

A
  • Glucose metabolism
  • Inflammation
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10
Q

What hormones are produced by the zona reticularis?

A

Androgens (DHEA, DHEAS)

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11
Q

What is the primary product of the adrenal medulla?

A

Catecholamines (Epinephrine)

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12
Q

What is the cellular organization of the adrenal cortex?

A
  • Glomerulosa: clusters of small round cells
  • Fasciculata: large polyhedral cells arranged in bundles
  • Reticularis: smaller cells arranged in cords
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13
Q

What provides blood directly to the adrenal medulla?

A

Medullary arterioles

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14
Q

What drains steroid hormones from the adrenal cortex?

A

Cortical plexuses and sinusoids

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15
Q

What are the effects of aldosterone?

A
  • Na+ and water reabsorption
  • K+ excretion
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16
Q

What are the target organs for aldosterone?

A
  • kidney
  • colon
  • salivary glands
  • sweat glands
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17
Q

What regulates aldosterone synthesis?

A
  • Angiotensin II
  • Extracellular K+
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18
Q

What is the role of principal cells in aldosterone action?

A

Increase the activity of ENaC, ROMK, KCC, and Maxi-K

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19
Q

What is the primary mechanism of Na+ reabsorption and K+ excretion?

A

Aldosterone increases Na+/K+ ATPase activity

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20
Q

What regulates glucocorticoids in the body?

A

HPA axis
External stimuli: stress & circadian rhythm

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21
Q

What is the precursor to adrenocorticotropic peptide?

A

Pro-opiomelanocortin (POMC)

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22
Q

What essential enzymes are involved in cortisol synthesis?

A
  • 17α-hydroxylase
  • 21α-hydroxylase
  • 11β-hydroxylase
  • 3β-hydroxysteroid dehydrogenase
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23
Q

What percentage of cortisol is transported bound to corticosteroid-binding globulin (CBG)?

A

~90% of the cortisol

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24
Q

Fill in the blank: Only _______ of the circulating cortisol is free.

A

3% to 4%

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25
Q

What is the function of 11β-HSD I?

A

Catalyzes a reversible oxidation of cortisol to inactive cortisone and can reactivate cortisone to cortisol

11β-HSD I plays a dual role in cortisol metabolism, facilitating both inactivation and reactivation.

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26
Q

What does 11β-HSD II do?

A

Catalyzes only the oxidation reaction inactivating cortisol

11β-HSD II exclusively converts cortisol to cortisone, preventing cortisol’s effects.

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27
Q

List the metabolic effects of cortisol.

A
  • Increases plasma glucose
  • Increases free fatty acid
  • Increases protein catabolism
  • Increased food intake

These effects contribute to cortisol’s role in energy mobilization during stress.

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28
Q

What immune effects does cortisol have?

A
  • Decreased production of interleukins 1 and 6 (IL-1 and IL-6)
  • T-cell suppression
  • Anti-inflammatory effects
  • Decreases in capillary permeability
  • Decreases prostaglandin and leukotriene synthesis

These actions help modulate the immune response and reduce inflammation.

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29
Q

How does cortisol affect the musculoskeletal system?

A
  • Increases bone resorption
  • Muscle loss
  • Decreases collagen formation
  • Weakness & fatigue

These changes can lead to osteoporosis and muscle wasting.

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30
Q

What renal and GI effects does cortisol have?

A
  • Decreases Ca2+ reabsorption from the kidney
  • Decreases Ca2+ absorption from the GI tract

These effects can lead to altered calcium metabolism.

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31
Q

What cardiovascular effects are associated with cortisol?

A
  • Stimulates red blood cell production
  • Potentiates vasoconstriction
  • Increases catecholamine actions

These effects can influence blood pressure and overall cardiovascular health.

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32
Q

What is the role of zona reticularis in adrenal androgen synthesis?

A
  • Produces DHEA
  • Produces androstenedione
  • Produces DHEA sulfate (DHEA-S)

The zona reticularis is crucial for the synthesis of adrenal androgens, especially during adrenarche.

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33
Q

What is adrenarche?

A

Pre-pubertal surge of adrenal androgens

Adrenarche marks the onset of increased adrenal androgen production, leading to physical changes.

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34
Q

What enzymes are involved in peripheral synthesis of sex steroids?

A
  • Sulfatase
  • 3β-hydroxysterol dehydrogenase
  • 17β-hydroxysterol dehydrogenase
  • P450 aromatase

These enzymes convert DHEAS into active sex steroids like testosterone and estradiol.

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35
Q

What is the major precursor for sex steroid synthesis?

A

DHEAS

DHEAS is stable and inactive in blood, serving as a reservoir for sex steroid synthesis.

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36
Q

What is the role of cholesterol in steroidogenesis?

A
  • Obtained from LDL or HDL
  • Synthesized de novo

Cholesterol is essential for the synthesis of all steroid hormones.

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37
Q

What does the steroid acute regulatory (StAR) protein do?

A

Transports cholesterol to the inner mitochondrial membrane

StAR is crucial for initiating steroid hormone synthesis.

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38
Q

What enzyme catalyzes the synthesis of pregnenolone?

A

Cholesterol side-chain cleavage enzyme (CYP11A1)

CYP11A1 is the first step in the steroidogenesis pathway.

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39
Q

What is the incidence of classic 21-hydroxylase deficiency?

A

1:15,000

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40
Q

What is the incidence of classic 11β-hydroxylase deficiency?

A

1:100,000

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41
Q

What is the incidence of 17α-hydroxylase deficiency?

A

1:50,000

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42
Q

Which gene is associated with 21-hydroxylase deficiency?

A

CYP21

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43
Q

Which gene is associated with 11β-hydroxylase deficiency?

A

CYP11B1

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44
Q

Which gene is associated with 17α-hydroxylase deficiency?

A

CYP17

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45
Q

What is the effect of 21-hydroxylase deficiency on cortisol levels?

A

↓

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46
Q

What is the effect of 11β-hydroxylase deficiency on mineralocorticoids?

A

↑

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47
Q

What is the effect of 17α-hydroxylase deficiency on sodium levels?

A

↑

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48
Q

What happens to potassium levels in 21-hydroxylase deficiency?

A

↑

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49
Q

Does 21-hydroxylase deficiency cause hypertension?

A

no; this CAH vairent causes hypoaldosteronism which exhibits hypotensive effects

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50
Q

Does 11β-hydroxylase deficiency cause hypertension?

A

yes

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51
Q

What is the effect of 17α-hydroxylase deficiency on androgens?

A

↓

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52
Q

What is the sexual development outcome in XX females with 21-hydroxylase deficiency?

A

Atypical

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53
Q

What is the sexual development outcome in XY males with 17α-hydroxylase deficiency?

A

Atypical; undescended testicles

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54
Q

What condition is associated with congenital adrenal hyperplasia (CAH)?

A

Steroidogenesis

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55
Q

What is the structure and histology of the adrenal medulla?

A

~10% of the mass of the adrenal gland

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56
Q

What type of cells are chromaffin cells?

A

Structural and functional equivalents of postganglionic neurons in the sympathetic nervous system

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57
Q

From which embryological layer do chromaffin cells arise?

A

Neuroectoderm

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58
Q

What stimulates chromaffin cells?

A

Acetylcholine

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59
Q

What is the primary hormone secreted by chromaffin cells?

A

Epinephrine (~80%)

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60
Q

What is the secondary hormone secreted by chromaffin cells?

A

Norepinephrine (~20%)

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61
Q

What enzyme is uniquely expressed in adrenal medulla epinephrine-secreting cells?

A

Phenylethanolamin-N-methyltransferase (PNMT)

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62
Q

What stimulates the expression of PNMT?

A

Cortisol draining from the adrenal cortex

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63
Q

What role does the adrenal medulla play in the sympathetic response to stress?

A

Amplifies the sympathetic response

64
Q

Fill in the blank: Catecholamines are degraded by _______.

A

Catechol-O-methyltransferase (COMT)

65
Q

Which organs are involved in the degradation of catecholamines?

A
  • Endothelial cells
  • Heart
  • Liver
  • Kidneys
66
Q

What is the half-life of catecholamines?

A

Short (seconds)

67
Q

What metabolites are excreted in the urine after catecholamine degradation?

A

Vanillylmandelic acid (VMA) sulfates or glucuronides

68
Q

T or F: Aldosterone regulates BP

A

False
it regulates extracellular volume which contributes to BP maintenance

69
Q

T or F: DHEA-S is ;high during fetal development and diminishes after birth

70
Q

DHEA-S gradual increase as it comes closer & closer to puberty. How does DHEA-S contribute to puberty

A

stimulates pubic & axillary hair growth

71
Q

What are the adrenal glands?

A

Complex structures required for maintenance of life, triangular shaped organs located above each kidney.

72
Q

What is the size and weight of the adrenal glands?

A

Measure between 2 and 5 cm and weigh 4-5 grams each.

73
Q

What can happen without adrenal hormones?

A

Electrolyte abnormalities, circulatory collapse, and death.

74
Q

What type of hormones are produced by the adrenal cortex?

75
Q

What are the three major categories of adrenal steroid hormones?

A
  • Mineralocorticoids
  • Glucocorticoids
  • Androgens
76
Q

What is the main mineralocorticoid hormone?

A

Aldosterone.

77
Q

What is the primary function of aldosterone?

A

Maintains the balance of sodium and potassium.

78
Q

What is the main glucocorticoid hormone?

79
Q

What are the primary effects of cortisol?

A
  • Helps the body with stress
  • Increases blood sugar
  • Suppresses the immune system
80
Q

What is the main androgen hormone produced by the adrenal glands?

81
Q

What are the three zones of the adrenal cortex and their functions?

A
  • Zona Glomerulosa: produces mineralocorticoids
  • Zona Fasciculata: produces glucocorticoids
  • Zona Reticularis: produces androgens
82
Q

What regulates aldosterone production?

A

Angiotensin II as part of the renin-angiotensin-aldosterone system (RAAS).

83
Q

What condition is characterized by excess aldosterone?

A

Primary aldosteronism or Conn’s Syndrome.

84
Q

What are the common causes of hyperaldosteronism?

A
  • Unilateral Adrenal Adenoma: 60%
  • Bilateral Adrenal Hyperplasia: 20-60%
  • Unilateral adrenal hyperplasia: 2%
  • Adrenocortical carcinoma: <1%
  • Familial aldosteronism type I, II, III: <1%
85
Q

What is a common symptom of elevated aldosterone levels?

A

High blood pressure.

86
Q

What groups should be screened for hyperaldosteronism?

A
  • Sustained BP above 150/100
  • Elevated BP on 3 antihypertensive medications
  • Controlled hypertension on 4 or more medications
  • High BP and low potassium
  • Hypertension with adrenal incidentaloma
  • Hypertension and sleep apnea
  • First degree relatives of patients with primary hyperaldosteronism
  • Hypertension with early onset high BP or stroke before age 40
87
Q

What does the diagnostic work-up for hyperaldosteronism include?

A
  • Screening with plasma aldosterone and renin levels
  • Confirmatory testing
  • Determining the type of PA
88
Q

What is the primary treatment for primary aldosteronism?

A

Curative surgical adrenalectomy.

89
Q

What is a common medical therapy for hyperaldosteronism?

A

Mineralocorticoid receptor antagonists like Spironolactone.

90
Q

What is Cushing’s Syndrome?

A

A condition caused by excess cortisol.

91
Q

What are the two main types of Cushing’s Syndrome?

A
  • ACTH dependent
  • ACTH independent
92
Q

What tests are used to screen for Cushing’s Syndrome?

A
  • 1 mg Dexamethasone Suppression Test
  • 24 Hour Urine for Cortisol
  • Midnight Salivary Cortisol Level
93
Q

What is the treatment for Cushing’s Syndrome?

A

Surgical removal of the growth producing excess cortisol or medication that blocks cortisol production.

94
Q

What is adrenal insufficiency?

A

A rare but potentially life-threatening condition requiring steroid replacement.

95
Q

How is adrenal insufficiency diagnosed?

A

Based on clinical and laboratory levels.

96
Q

What are the two types of adrenal insufficiency?

A
  • Primary disease
  • Secondary disease
97
Q

What is primary adrenal insufficiency also known as?

A

Addison’s disease

Addison’s disease is characterized by a disorder affecting the adrenal gland.

98
Q

What are the cortisol and ACTH levels in primary adrenal insufficiency?

A

Cortisol level is low and ACTH level is high

Both cortisol and aldosterone are deficient in primary adrenal insufficiency.

99
Q

What are the most common causes of primary adrenal insufficiency?

A
  • Autoimmune Addison’s disease
  • Infections like Tuberculosis and AIDS
  • Infiltrative disorders like Sarcoidosis, Lymphoma, and Metastases
  • Bilateral adrenal hemorrhage
  • Genetic disorders like congenital adrenal hyperplasia

These causes contribute to the dysfunction of the adrenal gland.

100
Q

What is a notable symptom associated with primary adrenal insufficiency?

A

Hyperpigmentation

Caused by high levels of circulating ACTH and alpha melanocyte stimulating hormone.

101
Q

What are the cortisol and ACTH levels in secondary adrenal insufficiency?

A

Cortisol level is low and ACTH level is normal or low

Only cortisol is deficient in secondary adrenal insufficiency.

102
Q

What are the most common causes of secondary adrenal insufficiency?

A
  • Chronic use of glucocorticoids
  • Pituitary adenoma
  • Head trauma
  • Infection
  • Isolated ACTH deficiency

These causes affect the hypothalamus and/or pituitary gland.

103
Q

What are signs and symptoms caused by glucocorticoid deficiency?

A
  • Weakness
  • Fatigue
  • Loss of appetite
  • Weight loss
  • Myalgia
  • Normochromic anemia
  • Lymphocytosis
  • Eosinophilia
  • Hypoglycemia
  • Hyponatremia

These symptoms can lead to chronic ill health.

104
Q

What are signs and symptoms caused by mineralocorticoid deficiency?

A
  • Dizziness and postural hypotension
  • Abdominal pain
  • Salt craving
  • Hyponatremia
  • Hyperkalemia

Symptoms can be vague leading to adrenal crisis.

105
Q

What are the electrolyte abnormalities seen in primary adrenal insufficiency?

A
  • Hyponatremia
  • Hyperkalemia

These electrolyte imbalances are significant in diagnosing adrenal insufficiency.

106
Q

When should cortisol be sampled for adrenal insufficiency diagnosis?

A

Between 8 and 9 am

A cortisol level of less than 3 ug/dL makes adrenal insufficiency likely.

107
Q

What is the ACTH level typically in primary adrenal insufficiency?

A

Usually greater than 100 pg/mL

This helps differentiate primary from secondary adrenal insufficiency.

108
Q

What is the treatment for primary adrenal insufficiency?

A
  • Cortisol
  • Aldosterone

DHEAS is also recommended for women experiencing low energy and libido after steroid replacement.

109
Q

What is the usual dose of hydrocortisone for adrenal insufficiency?

A

20 mg divided into 1 to 3 times daily

Hydrocortisone is preferred due to its mineralocorticoid effect.

110
Q

What is congenital adrenal hyperplasia (CAH)?

A

A group of autosomal recessive disorders caused by mutations in genes encoding enzymes for cortisol biosynthesis

The most common cause is a mutation in CYP21A2.

111
Q

What is the most common cause of CAH?

A

Mutation in CYP21A2

This accounts for 95% of CAH cases.

112
Q

What can overproduction of adrenal androgens in CAH lead to in females?

A

In utero virilization of external genitalia

This can range from mild labial fusion to complete masculinization.

113
Q

What is the treatment for congenital adrenal hyperplasia?

A
  • Hormone replacement with a steroid
  • Fludrocortisone

These treatments address hormone deficiencies.

114
Q

What is pheochromocytoma?

A

A neuroendocrine tumor originating predominantly in the adrenal medulla

It is functionally indistinguishable from paragangliomas.

115
Q

What are common signs and symptoms of pheochromocytoma?

A
  • Paroxysmal profuse sweating
  • Pallor
  • Tremor
  • Tachycardia
  • Episodic hypertension

Testing is recommended for individuals with these symptoms.

116
Q

What catecholamines does the adrenal medulla produce?

A
  • Epinephrine
  • Norepinephrine
  • Dopamine

The secretion is dependent on the phenotype of the tumor.

117
Q

What is the best screening test for pheochromocytoma if there is low suspicion?

A

Measuring urinary fractionated metanephrines

This test has higher specificity.

118
Q

What is the preferred test for pheochromocytoma if there is high suspicion?

A

Plasma metanephrines

This test has higher sensitivity.

119
Q

What are catecholamine metabolites called?

A

Metanephrines

Metanephrines can be measured in plasma or urine.

120
Q

Why are 24-hour urine collections recommended for quantitation of catecholamines and metanephrines?

A

Plasma catecholamines have short half-lives and their secretion may be episodic.

121
Q

Which test is the best screening test if there is low suspicion of pheochromocytoma?

A

Measuring urinary fractionated metanephrines.

122
Q

What is preferred if there is high suspicion of pheochromocytoma?

A

Plasma metanephrines.

123
Q

What percentage of the general population has nonspecific anatomic adrenal abnormalities?

A

Approximately 3%–7%.

124
Q

When is radiologic screening advisable for pheochromocytoma?

A

When biochemical screening tests reveal abnormal catecholamine release.

125
Q

What is the best imaging test to localize a pheochromocytoma?

A

CT of the abdomen with and without contrast.

126
Q

What Hounsfield Unit density is typically observed in pheochromocytoma?

A

Greater than 10.

127
Q

How do pheochromocytomas appear on MRI?

A

Very bright with high signal on T2 sequence.

128
Q

What test may be used if a pheochromocytoma cannot be visualized?

A

MIBG Scintigraphy.

129
Q

What is the optimal treatment for pheochromocytoma?

A

Removal of the tumor as soon as possible.

130
Q

What team is usually involved in the treatment of pheochromocytoma?

A

Endocrinologist, anesthesiologist, and surgeon.

131
Q

What is important to normalize before surgery for pheochromocytoma?

A

Blood pressure, heart rate, and restore volume.

132
Q

What is the preferred first medication to start for pheochromocytoma?

A

Phenoxybenzamine.

133
Q

Why should beta blockers not be used alone in pheochromocytoma treatment?

A

They can lead to unopposed alpha stimulation, causing hypertensive crisis.

134
Q

When can a beta adrenoreceptor blocker be added to treatment?

A

After at least 7 days of alpha blockade if tachycardia is present.

135
Q

What should be done if blood pressure remains high after initial treatment?

A

Add calcium channel blocker.

136
Q

What is a treatment option for metastatic pheochromocytoma?

A

MIBG radiation or chemotherapy.

137
Q

What symptoms did the 47-year-old man in the case study present with?

A

Episodic headaches, sweating, heart palpitations, and tremor.

138
Q

What was the urinary metanephrines level in the case study patient?

A

1300 µg/24 hours (normal range: 45-290 µg/24 hours).

139
Q

What did the CT of the abdomen reveal in the case study patient?

A

A 3 cm left adrenal adenoma.

140
Q

What are the two main components of the adrenal gland?

A

Adrenal cortex and medulla.

141
Q

What does the adrenal cortex produce?

A

Mineralocorticoids, glucocorticoids, and androgens.

142
Q

What does the adrenal medulla produce?

A

Epinephrine and norepinephrine.

143
Q

What condition is caused by overproduction of aldosterone?

A

Conn’s Syndrome.

144
Q

What condition is caused by overproduction of cortisol?

A

Cushing’s Syndrome.

145
Q

What leads to pheochromocytoma and paragangliomas?

A

Overproduction of epinephrine and norepinephrine.

146
Q

aldosterone secretion is stimulated by what conditions?

A

low blood osmolality, low salt intake, and laying down

147
Q

T or F: mineralocorticoids are regulated by the HPA axis.

A

False
aldosterone is regulated by the RAAS axis

148
Q

List effects of glucocorticoids

A

stimulates gluconeogenesis to raise blood sugar
increases protein catabolism
fat redistribution
inhibits host response to infection

149
Q

high levels of glucocorticoids and low levels of ACTH are indicative of what

A

primary ACTH-independent Hypercortisolism

150
Q

How can cushing’s disease be distinguished from cushing’s syndrome?

A

Under normal physiological conditions, ACTH and cortisol levels share a positive correlation

If ACTH is low in the presence of elevated cortisol, this indicates cortisol is being secreted independently of ACTH; hence, the adrenal gland is what is dysfunctioning: Cushing’s syndrome

Let’s say ACTH and cortisol are both high. this indicates cortisol secretion is dependent on ACTH secretion; hence, the pituitary is what is dysfunctioning: cushing’s disease

151
Q

T or F: secondary AI affects all adrenal hormones? Explain your reasoning

A

False
only the zona fasciculata is affected b/c ACTH secretion from the anterior pituitary is what is impaired

152
Q

For primary AI, all adrenal zonae are affected. List some of the main clinical presentations of each.

A

Glucocorticoid deficiency: hyponatremia, hyperkalemia induced myalgia w/ flaccid paralysis, salt cravings, hypoglycemia, heighted senses, hyperpigmentation

mineralocorticoid deficiency: dizziness w/ orthostatic hypotension, syncope, hypovolemia

sex hormone deficiency: decreased libido, impotences, ovarian failure

153
Q

what are the most important complications of hyperaldosteronism

A

HTN, hypokalemia induced alkalosis, edema, cardiac arrhythmias, muscle wasting

154
Q

what is the most common cause of secondary hyperaldosteronism

A

decreased renal blood flow and perfusion

155
Q

CKD can lead to what long-term complication?

A

hypoaldosteronism

156
Q

what are causes of adrenal hyperplasia?

A

decreased production of cortisol via enzymatic defects increases ACTH production

157
Q

Compare and Contrast the presentational differences b/t congenital adrenal hyperplasia and adrenal insufficiency

A

Both:
increased ACTH secretion causing hyperpigmentation, myalgias & hypoglycemia
decreased cortisol production leads to salt-wasting, hyperkalemia, and hypotension

Different:
AI: sex hormone deficiency: amenorrhea, hypogonadism
CAH: sex hormone EXCESS: virilization, hirsutism, precocious pseudopuberty

Endocrinology (9 decks)

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