Adrenal/Pituitary/DI Flashcards
1
Q
What are the components of each adrenal gland?
A
Cortex and medulla
2
Q
What does the cortex of the adrenal gland synthesize?
A
Glucocorticoids, mineralocorticoids, and androgens
3
Q
What hormone does the hypothalamus send to the anterior pituitary in adrenal gland dysfunction?
A
Corticotropin-releasing hormone (CRH)
4
Q
What does ACTH stimulate in the adrenal cortex?
A
Production of cortisol
5
Q
What does cortisol facilitate in the adrenal medulla?
A
Conversion of NE to EPI
6
Q
What effects does cortisol induce in terms of glucose metabolism?
A
Hyperglycemia, gluconeogenesis, inhibition of glucose uptake by cells
7
Q
What are the combined effects of cortisol and aldosterone?
A
Sodium retention and K+ excretion
8
Q
What are pheochromocytomas?
A
Catecholamine-secreting tumors
9
Q
Where do pheochromocytomas arise from?
A
Chromaffin cells of sympathoadrenal system
10
Q
What can uncontrolled catecholamine release from pheochromocytomas result in?
A
Malignant HTN, CVA, MI
11
Q
What percentage of pheochromocytomas are inherited?
A
10%
12
Q
Where do 80% of pheochromocytomas occur?
A
Adrenal medulla
13
Q
How do malignant pheochromocytomas spread?
A
Through venous & lymph systems
14
Q
What is the typical secretion ratio of NE:EPI in most pheochromocytomas?
A
85:15
15
Q
What do some pheochromocytomas secrete at higher levels?
A
EPI and dopamine
16
Q
What are the symptoms of pheochromocytoma?
A
h/a, pallor, sweating, palpitations, orthostatic HoTN
17
Q
How is pheochromocytoma diagnosed?
A
24h urine collection for metanephrines and catecholamines
18
Q
How can the tumor in pheochromocytoma be localized?
A
CT & MRI imaging, MIBG scintigraphy
19
Q
What is the preoperative treatment for Pheochromocytoma?
A
α blockade with drugs like Phenoxybenzamine
20
Q
Why is α blockade important in Pheochromocytoma preop?
A
To lower BP, decrease intravascular volume, prevent hypertensive episodes
21
Q
What happens if tachycardia occurs after α blockade in Pheochromocytoma?
A
Treat with beta-blockers
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
23
Q
Besides alpha blockers, what other drug class is used to control hypertension in Pheochromocytoma?
A
CCBs
24
Q
What are the 2 forms of Hypercortisolism (Cushing Syndrome)?
A
ACTH dependent and ACTH independent
25
What stimulates the adrenal cortex to produce excessive amounts of cortisol in ACTH-dependent Cushing's syndrome?
Inappropriately high plasma ACTH
26
What is acute ectopic ACTH syndrome often associated with?
Small cell lung carcinoma
27
What is the most common cause of ACTH-independent Cushing syndrome?
Benign or malignant adrenocortical tumors
28
What are the symptoms of hypercortisolism?
Sudden weight gain, central obesity, moon face, ecchymoses, HTN, glucose intolerance, muscle wasting, depression, insomnia
29
How is Cushing's syndrome diagnosed?
24 hr urine cortisol
30
How can you determine if Cushing's is ACTH dependent or independent?
Plasma ACTH measurements
31
What test distinguishes Cushing's from ectopic ACTH syndrome?
High-dose dexamethasone suppression test
32
Are imaging procedures useful for determining adrenal cortex function in Cushing's syndrome?
No
33
What is the treatment of choice for Cushing Syndrome if a microadenoma is resectable?
Transsphenoidal microadenomectomy
34
What is an alternative treatment option for Cushing Syndrome if a microadenoma is not resectable?
85-90% resection of the anterior pituitary
35
When is pituitary irradiation and bilateral total adrenalectomy necessary in patients with Cushing Syndrome?
In some cases
36
What is the treatment for adrenal adenoma or carcinoma in Cushing Syndrome?
Surgical removal of the adrenal gland
37
What should be evaluated and treated preoperatively in patients with Cushing Syndrome?
Blood pressure, electrolyte imbalance, blood glucose
38
What should be considered in positioning due to long-term effects in Cushing Syndrome patients?
Osteoporosis
39
What is primary hyperaldosteronism?
Excess aldosterone from tumor
40
What can primary hyperaldosteronism be occasionally associated with?
Pheochromocytoma, hyperparathyroidism, acromegaly
41
What is secondary hyperaldosteronism characterized by?
Increased renin stimulating aldosterone release
42
What are some symptoms of hyperaldosteronism?
HTN, hypokalemia, metabolic alkalosis
43
What is a highly suggestive sign of hyperaldosteronism?
Spontaneous hypokalemia with systemic hypertension
44
How does plasma renin activity differ between primary and secondary hyperaldosteronism?
Primary: suppressed; Secondary: high
45
What can long-term ingestion of licorice lead to?
Features mimicking hyperaldosteronism (HTN, hypokalemia, RAAS suppression)
46
What are the treatment options for hyperaldosteronism?
Spironolactone, K+ replacement, antihypertensives, diuretics, tumor removal, adrenalectomy
47
What does hyperkalemia in the absence of renal insufficiency suggest?
Hypoaldosteronism
48
How can hyperkalemia be enhanced?
By hyperglycemia
49
What type of metabolic acidosis is common in hypoaldosteronism?
Hyperchloremic
50
What symptoms may be present in hypoaldosteronism besides hyperkalemia?
Heart block, orthostatic HoTN, hyponatremia
51
In what conditions does hyporeninemic hypoaldosteronism typically occur?
In patients >45 with CRF or DM
52
What is a reversible cause of hypoaldosteronism induced by a medication?
Indomethacin-induced prostaglandin deficiency
53
What is the treatment for hypoaldosteronism?
Liberal sodium intake, fludrocortisone
54
What are the 2 types of Adrenal Insufficiency?
Primary and secondary
55
What is the most common cause of primary Adrenal Insufficiency?
Autoimmune adrenal destruction
56
In primary Adrenal Insufficiency, how much of the adrenal glands must be involved before signs appear?
>90%
57
What is the main hormone deficiency in secondary Adrenal Insufficiency?
Only glucocorticoid
58
What is the most common cause of secondary Adrenal Insufficiency?
Iatrogenic (e.g., pituitary surgery, synthetic glucocorticoids)
59
What is a clinical difference between primary and secondary Adrenal Insufficiency?
Cutaneous hyperpigmentation is lacking in secondary AI
60
What is the diagnostic criteria for adrenal insufficiency?
Baseline cortisol < 20 μg/dL and remains <20 μg/dL after ACTH stimulation
61
How is absolute adrenal insufficiency characterized?
Low baseline cortisol level and positive ACTH stimulation test result
62
How is relative adrenal insufficiency indicated?
Higher baseline cortisol level but positive ACTH stimulation test result
63
What is the treatment for adrenal insufficiency?
Steroids
64
Where are the parathyroid glands located?
Behind upper & lower poles of thyroid gland
65
What hormone do the parathyroid glands produce?
PTH
66
How is PTH released into circulation?
Negative feedback dependent on plasma calcium level
67
What stimulates the release of PTH?
Hypocalcemia
68
How does hypercalcemia affect PTH?
Suppresses both synthesis and release
69
What is the role of PTH in maintaining plasma calcium levels?
Promoting calcium movement in GI tract, renal tubules, and bone
70
What is hyperparathyroidism?
Increased PTH secretion
71
How is hyperparathyroidism classified?
Primary, secondary, or ectopic
72
What are the causes of primary hyperparathyroidism?
Adenoma, carcinoma, hyperplasia
73
What are the symptoms of hyperparathyroidism?
Sedation, n/v, weakness, sensation changes, polyuria, renal stones, PUD, cardiac disturbances
74
How is hyperparathyroidism diagnosed?
Plasma calcium, 24 hr urinary calcium
75
What is the treatment for hyperparathyroidism?
Surgical removal of abnormal gland portions
76
What is secondary hyperparathyroidism?
Compensatory response to counteract a separate disease process causing hypocalcemia
77
Why does secondary hyperparathyroidism seldom produce hypercalcemia?
Adaptive response
78
How is secondary hyperparathyroidism treated?
Controlling underlying disease, normalizing serum phosphate concentrations
79
What is hypoparathyroidism?
Deficient PTH or tissue resistance
80
What is pseudohypoparathyroidism?
PTH adequate, kidney resistance
81
How is hypoparathyroidism diagnosed?
Hypocalcemia, ↓PTH, ↑phosphate
82
What are symptoms of chronic hypocalcemia?
Fatigue, cramps, prolonged QT
83
What is the most common cause of chronic hypocalcemia?
CRF
84
How is hypoparathyroidism treated?
Calcium replacement, Vitamin D
85
Where is the pituitary gland located?
Sella turcica at the base of the brain
86
What are the two parts that the pituitary gland consists of?
Anterior pituitary & posterior pituitary
87
What hormones does the anterior pituitary secrete?
6 hormones under the control of the hypothalamus
88
How are vasopressin (ADH) and oxytocin transported and stored?
Synthesized in hypothalamus, then stored in posterior pituitary
89
What senses plasma osmolarity to stimulate the release of certain hormones from the posterior pituitary?
Osmoreceptors in the hypothalamus
90
What condition is often associated with the hypersecretion of ACTH by anterior pituitary adenomas?
Cushing syndrome
91
What is acromegaly?
Excessive growth hormone secretion in adults
92
What is the most common cause of acromegaly?
Adenoma in anterior pituitary gland
93
How can acromegaly be diagnosed?
Elevated serum IGF-1 levels
94
What test can be performed to assess acromegaly?
Oral glucose tolerance test
95
What surgery is the main treatment for acromegaly?
Transsphenoidal excision of pituitary adenoma
96
What is the alternative treatment option for acromegaly if surgery is not feasible?
LA somatostatin analogue
97
What are the anesthesia implications for patients with acromegaly?
Obstructed airway, need for smaller ETT
98
How does acromegaly affect the placement of a face mask during anesthesia?
Interferes due to distorted facial anatomy
99
Why may visualizing the vocal cords be challenging in acromegaly patients during direct laryngoscopy?
Enlarged tongue and epiglottis
100
What does diabetes insipidus (DI) reflect?
Absence of vasopressin (ADH)
101
How is neurogenic DI differentiated from nephrogenic DI?
Response to desmopressin
102
What are the symptoms of diabetes insipidus?
Polydipsia and high output of poorly concentrated urine
103
What is the initial treatment for diabetes insipidus?
IV e-lytes to offset polyuria
104
How is neurogenic DI treated?
DDAVP
105
How is nephrogenic DI treated?
Low-salt, low-protein diet, diuretics, NSAIDs
106
What should be monitored during anesthesia for a patient with DI?
Urine output & serum electrolyte concentrations
107
What diverse pathologies can cause Syndrome of Inappropriate ADH (SIADH)?
Intracranial tumors, hypothyroidism, porphyria, lung carcinoma
108
What is a common occurrence in most patients following major surgeries in relation to ADH levels?
Elevated ADH levels
109
What is highly suggestive of SIADH?
Inappropriately increased urinary sodium and osmolarity with hyponatremia and decreased serum osmolarity
110
What can abrupt decreases in serum sodium concentration lead to?
Cerebral edema and seizures
111
What are the treatments for SIADH?
Fluid restriction, salt tablets, loop diuretics & vasopressin antagonists
112
How should hyponatremia be treated at less than 8 mEq/L within 24 hours?
With hypertonic saline
