Adrenal/Pituitary/DI Flashcards

1
Q

What are the components of each adrenal gland?

A

Cortex and medulla

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2
Q

What does the cortex of the adrenal gland synthesize?

A

Glucocorticoids, mineralocorticoids, and androgens

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3
Q

What hormone does the hypothalamus send to the anterior pituitary in adrenal gland dysfunction?

A

Corticotropin-releasing hormone (CRH)

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4
Q

What does ACTH stimulate in the adrenal cortex?

A

Production of cortisol

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5
Q

What does cortisol facilitate in the adrenal medulla?

A

Conversion of NE to EPI

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6
Q

What effects does cortisol induce in terms of glucose metabolism?

A

Hyperglycemia, gluconeogenesis, inhibition of glucose uptake by cells

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7
Q

What are the combined effects of cortisol and aldosterone?

A

Sodium retention and K+ excretion

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8
Q

What are pheochromocytomas?

A

Catecholamine-secreting tumors

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9
Q

Where do pheochromocytomas arise from?

A

Chromaffin cells of sympathoadrenal system

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10
Q

What can uncontrolled catecholamine release from pheochromocytomas result in?

A

Malignant HTN, CVA, MI

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11
Q

What percentage of pheochromocytomas are inherited?

A

10%

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12
Q

Where do 80% of pheochromocytomas occur?

A

Adrenal medulla

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13
Q

How do malignant pheochromocytomas spread?

A

Through venous & lymph systems

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14
Q

What is the typical secretion ratio of NE:EPI in most pheochromocytomas?

A

85:15

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15
Q

What do some pheochromocytomas secrete at higher levels?

A

EPI and dopamine

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16
Q

What are the symptoms of pheochromocytoma?

A

h/a, pallor, sweating, palpitations, orthostatic HoTN

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17
Q

How is pheochromocytoma diagnosed?

A

24h urine collection for metanephrines and catecholamines

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18
Q

How can the tumor in pheochromocytoma be localized?

A

CT & MRI imaging, MIBG scintigraphy

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19
Q

What is the preoperative treatment for Pheochromocytoma?

A

α blockade with drugs like Phenoxybenzamine

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20
Q

Why is α blockade important in Pheochromocytoma preop?

A

To lower BP, decrease intravascular volume, prevent hypertensive episodes

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21
Q

What happens if tachycardia occurs after α blockade in Pheochromocytoma?

A

Treat with beta-blockers

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22
Q

Why should nonselective beta-blockers not be given before α blockers in Pheochromocytoma?

A

May lead to unopposed α agonism and hypertensive crises

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23
Q

Besides alpha blockers, what other drug class is used to control hypertension in Pheochromocytoma?

A

CCBs

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24
Q

What are the 2 forms of Hypercortisolism (Cushing Syndrome)?

A

ACTH dependent and ACTH independent

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25
Q

What stimulates the adrenal cortex to produce excessive amounts of cortisol in ACTH-dependent Cushing’s syndrome?

A

Inappropriately high plasma ACTH

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26
Q

What is acute ectopic ACTH syndrome often associated with?

A

Small cell lung carcinoma

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27
Q

What is the most common cause of ACTH-independent Cushing syndrome?

A

Benign or malignant adrenocortical tumors

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28
Q

What are the symptoms of hypercortisolism?

A

Sudden weight gain, central obesity, moon face, ecchymoses, HTN, glucose intolerance, muscle wasting, depression, insomnia

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29
Q

How is Cushing’s syndrome diagnosed?

A

24 hr urine cortisol

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30
Q

How can you determine if Cushing’s is ACTH dependent or independent?

A

Plasma ACTH measurements

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31
Q

What test distinguishes Cushing’s from ectopic ACTH syndrome?

A

High-dose dexamethasone suppression test

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32
Q

Are imaging procedures useful for determining adrenal cortex function in Cushing’s syndrome?

A

No

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33
Q

What is the treatment of choice for Cushing Syndrome if a microadenoma is resectable?

A

Transsphenoidal microadenomectomy

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34
Q

What is an alternative treatment option for Cushing Syndrome if a microadenoma is not resectable?

A

85-90% resection of the anterior pituitary

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35
Q

When is pituitary irradiation and bilateral total adrenalectomy necessary in patients with Cushing Syndrome?

A

In some cases

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36
Q

What is the treatment for adrenal adenoma or carcinoma in Cushing Syndrome?

A

Surgical removal of the adrenal gland

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37
Q

What should be evaluated and treated preoperatively in patients with Cushing Syndrome?

A

Blood pressure, electrolyte imbalance, blood glucose

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38
Q

What should be considered in positioning due to long-term effects in Cushing Syndrome patients?

A

Osteoporosis

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39
Q

What is primary hyperaldosteronism?

A

Excess aldosterone from tumor

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40
Q

What can primary hyperaldosteronism be occasionally associated with?

A

Pheochromocytoma, hyperparathyroidism, acromegaly

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41
Q

What is secondary hyperaldosteronism characterized by?

A

Increased renin stimulating aldosterone release

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42
Q

What are some symptoms of hyperaldosteronism?

A

HTN, hypokalemia, metabolic alkalosis

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43
Q

What is a highly suggestive sign of hyperaldosteronism?

A

Spontaneous hypokalemia with systemic hypertension

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44
Q

How does plasma renin activity differ between primary and secondary hyperaldosteronism?

A

Primary: suppressed; Secondary: high

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45
Q

What can long-term ingestion of licorice lead to?

A

Features mimicking hyperaldosteronism (HTN, hypokalemia, RAAS suppression)

46
Q

What are the treatment options for hyperaldosteronism?

A

Spironolactone, K+ replacement, antihypertensives, diuretics, tumor removal, adrenalectomy

47
Q

What does hyperkalemia in the absence of renal insufficiency suggest?

A

Hypoaldosteronism

48
Q

How can hyperkalemia be enhanced?

A

By hyperglycemia

49
Q

What type of metabolic acidosis is common in hypoaldosteronism?

A

Hyperchloremic

50
Q

What symptoms may be present in hypoaldosteronism besides hyperkalemia?

A

Heart block, orthostatic HoTN, hyponatremia

51
Q

In what conditions does hyporeninemic hypoaldosteronism typically occur?

A

In patients >45 with CRF or DM

52
Q

What is a reversible cause of hypoaldosteronism induced by a medication?

A

Indomethacin-induced prostaglandin deficiency

53
Q

What is the treatment for hypoaldosteronism?

A

Liberal sodium intake, fludrocortisone

54
Q

What are the 2 types of Adrenal Insufficiency?

A

Primary and secondary

55
Q

What is the most common cause of primary Adrenal Insufficiency?

A

Autoimmune adrenal destruction

56
Q

In primary Adrenal Insufficiency, how much of the adrenal glands must be involved before signs appear?

A

> 90%

57
Q

What is the main hormone deficiency in secondary Adrenal Insufficiency?

A

Only glucocorticoid

58
Q

What is the most common cause of secondary Adrenal Insufficiency?

A

Iatrogenic (e.g., pituitary surgery, synthetic glucocorticoids)

59
Q

What is a clinical difference between primary and secondary Adrenal Insufficiency?

A

Cutaneous hyperpigmentation is lacking in secondary AI

60
Q

What is the diagnostic criteria for adrenal insufficiency?

A

Baseline cortisol < 20 μg/dL and remains <20 μg/dL after ACTH stimulation

61
Q

How is absolute adrenal insufficiency characterized?

A

Low baseline cortisol level and positive ACTH stimulation test result

62
Q

How is relative adrenal insufficiency indicated?

A

Higher baseline cortisol level but positive ACTH stimulation test result

63
Q

What is the treatment for adrenal insufficiency?

A

Steroids

64
Q

Where are the parathyroid glands located?

A

Behind upper & lower poles of thyroid gland

65
Q

What hormone do the parathyroid glands produce?

A

PTH

66
Q

How is PTH released into circulation?

A

Negative feedback dependent on plasma calcium level

67
Q

What stimulates the release of PTH?

A

Hypocalcemia

68
Q

How does hypercalcemia affect PTH?

A

Suppresses both synthesis and release

69
Q

What is the role of PTH in maintaining plasma calcium levels?

A

Promoting calcium movement in GI tract, renal tubules, and bone

70
Q

What is hyperparathyroidism?

A

Increased PTH secretion

71
Q

How is hyperparathyroidism classified?

A

Primary, secondary, or ectopic

72
Q

What are the causes of primary hyperparathyroidism?

A

Adenoma, carcinoma, hyperplasia

73
Q

What are the symptoms of hyperparathyroidism?

A

Sedation, n/v, weakness, sensation changes, polyuria, renal stones, PUD, cardiac disturbances

74
Q

How is hyperparathyroidism diagnosed?

A

Plasma calcium, 24 hr urinary calcium

75
Q

What is the treatment for hyperparathyroidism?

A

Surgical removal of abnormal gland portions

76
Q

What is secondary hyperparathyroidism?

A

Compensatory response to counteract a separate disease process causing hypocalcemia

77
Q

Why does secondary hyperparathyroidism seldom produce hypercalcemia?

A

Adaptive response

78
Q

How is secondary hyperparathyroidism treated?

A

Controlling underlying disease, normalizing serum phosphate concentrations

79
Q

What is hypoparathyroidism?

A

Deficient PTH or tissue resistance

80
Q

What is pseudohypoparathyroidism?

A

PTH adequate, kidney resistance

81
Q

How is hypoparathyroidism diagnosed?

A

Hypocalcemia, ↓PTH, ↑phosphate

82
Q

What are symptoms of chronic hypocalcemia?

A

Fatigue, cramps, prolonged QT

83
Q

What is the most common cause of chronic hypocalcemia?

A

CRF

84
Q

How is hypoparathyroidism treated?

A

Calcium replacement, Vitamin D

85
Q

Where is the pituitary gland located?

A

Sella turcica at the base of the brain

86
Q

What are the two parts that the pituitary gland consists of?

A

Anterior pituitary & posterior pituitary

87
Q

What hormones does the anterior pituitary secrete?

A

6 hormones under the control of the hypothalamus

88
Q

How are vasopressin (ADH) and oxytocin transported and stored?

A

Synthesized in hypothalamus, then stored in posterior pituitary

89
Q

What senses plasma osmolarity to stimulate the release of certain hormones from the posterior pituitary?

A

Osmoreceptors in the hypothalamus

90
Q

What condition is often associated with the hypersecretion of ACTH by anterior pituitary adenomas?

A

Cushing syndrome

91
Q

What is acromegaly?

A

Excessive growth hormone secretion in adults

92
Q

What is the most common cause of acromegaly?

A

Adenoma in anterior pituitary gland

93
Q

How can acromegaly be diagnosed?

A

Elevated serum IGF-1 levels

94
Q

What test can be performed to assess acromegaly?

A

Oral glucose tolerance test

95
Q

What surgery is the main treatment for acromegaly?

A

Transsphenoidal excision of pituitary adenoma

96
Q

What is the alternative treatment option for acromegaly if surgery is not feasible?

A

LA somatostatin analogue

97
Q

What are the anesthesia implications for patients with acromegaly?

A

Obstructed airway, need for smaller ETT

98
Q

How does acromegaly affect the placement of a face mask during anesthesia?

A

Interferes due to distorted facial anatomy

99
Q

Why may visualizing the vocal cords be challenging in acromegaly patients during direct laryngoscopy?

A

Enlarged tongue and epiglottis

100
Q

What does diabetes insipidus (DI) reflect?

A

Absence of vasopressin (ADH)

101
Q

How is neurogenic DI differentiated from nephrogenic DI?

A

Response to desmopressin

102
Q

What are the symptoms of diabetes insipidus?

A

Polydipsia and high output of poorly concentrated urine

103
Q

What is the initial treatment for diabetes insipidus?

A

IV e-lytes to offset polyuria

104
Q

How is neurogenic DI treated?

A

DDAVP

105
Q

How is nephrogenic DI treated?

A

Low-salt, low-protein diet, diuretics, NSAIDs

106
Q

What should be monitored during anesthesia for a patient with DI?

A

Urine output & serum electrolyte concentrations

107
Q

What diverse pathologies can cause Syndrome of Inappropriate ADH (SIADH)?

A

Intracranial tumors, hypothyroidism, porphyria, lung carcinoma

108
Q

What is a common occurrence in most patients following major surgeries in relation to ADH levels?

A

Elevated ADH levels

109
Q

What is highly suggestive of SIADH?

A

Inappropriately increased urinary sodium and osmolarity with hyponatremia and decreased serum osmolarity

110
Q

What can abrupt decreases in serum sodium concentration lead to?

A

Cerebral edema and seizures

111
Q

What are the treatments for SIADH?

A

Fluid restriction, salt tablets, loop diuretics & vasopressin antagonists

112
Q

How should hyponatremia be treated at less than 8 mEq/L within 24 hours?

A

With hypertonic saline