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Endocrine > Adrenal Glands > Flashcards

Adrenal Glands Flashcards

1
Q

In order to sythesize cortisol in the adrenal cells, _ must be taken into the adrenal cells and processed

A

In order to sythesize cortisol in the adrenal cells, LDL must be taken into the adrenal cells and processed

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2
Q

Once LDL is transported into adrenal cells (for cortisol synthesis) the LDL is broken down into cholesterol esters within the _

A

Once LDL is transported into adrenal cells (for cortisol synthesis) the LDL is broken down into cholesterol esters within the lysosome
* Cholesterol esters are further hydrolyzed into cholesterol

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3
Q

_ is the protein which transfers cholesterol into the mitochondria (rate limiting step of steroid production)

A

Steroidogenic acute regulatory protein (StAR) is the protein which transfers cholesterol into the mitochondria (rate limiting step of steroid production)

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4
Q

Cholesterol is converted into _ inside the mitrochondria by the enzyme cholesterol desmolase

A

Cholesterol is converted into pregnenolone inside the mitrochondria by the enzyme cholesterol desmolase
* Pregnenolone –> progesterone (SER)
* Later 11 deoxycortisol –> cortisol (mitochondria)

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5
Q

Cortisol is (hydrophilic/lipophilic) and travels freely in the bloodstream

A

Cortisol is lipophilic and travels freely in the bloodstream

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6
Q

The vast majority of cortisol will be (free/bound)

A

The vast majority of cortisol will be bound
* 90% will be bound to corticosteroid-binding globulin/ transcortin

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7
Q

Only _ cortisol can enter cells and activate the receptor

A

Only free cortisol can enter cells and activate the receptor

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8
Q

Glucocorticoid receptors are found in the _

A

Glucocorticoid receptors are found in the cytosol of virtually every nucleated cell

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9
Q

The response to cortisol takes hours to days because cortisol acts by affecting _

A

The response to cortisol takes hours to days because cortisol acts by affecting gene expression, which in turn will affect protein synthesis

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10
Q

Cortisol (increases/decreases) GLUT4 transporter expression

A

Cortisol decreases GLUT4 transporter expression
* Glucocorticoids decrease glucose utilization to maintain availability

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11
Q

Cortisol acts on the pancreas to _ insulin and _ glucagon secretion

A

Cortisol acts on the pancreas to decrease insulin and increase glucagon secretion
* Cushing syndrome can cause a person to develop insulin resistant diabetes

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12
Q

Cortisol increases lipolysis to generate _ , which can be used for energy in times of stress

A

Cortisol increases lipolysis to generate glycerol, which can be used for energy in times of stress

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13
Q

Cortisol _ protein synthesis and _ peripheral amino acid uptake in muscles

A

Cortisol inhibits protein synthesis and decreases peripheral amino acid uptake in muscles
* Can cause muscle wasting in patients with excess

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14
Q

The way that cortisol maintains a normal blood pressure is by _

A

The way that cortisol maintains a normal blood pressure is by upregulating the number of alpha1 receptors on arterioles
* This increases the sensitivity to NE and E

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15
Q

Cortisol decreases inflammation by inhibiting the production of _

A

Cortisol decreases inflammation by inhibiting the production of proinflammatory mediators like leukotrienes, prostaglandins, IL-2, IFN-gamma, IFN-a, TNF-alpha

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16
Q

Cortisol can increase the total number of neutrophils on WBC via _

A

Cortisol can increase the total number of neutrophils on WBC via inhibiting the adhesion of WBCs to blood vessel walls, shifting the neutrophils from vessel wall to the circulation

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17
Q

Cortisol causes _ in fibroblast activity

A

Cortisol causes decreased fibroblast activity
* Leads to decreased collagen synthesis and diminished wound healing

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18
Q

Decreased fibroblast activity caused by cortisol can manifest as _

A

Decreased fibroblast activity caused by cortisol can manifest as striae

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19
Q

Cortisol _ osteoblast activity

A

Cortisol decreases osteoblast activity
* Patients on glucocorticoids are at risk of osteoporosis

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20
Q

Why are glucocorticoids given to mothers who go into labor prematurely?

A

Glucocorticoids are very important to the maturation of lungs and to the production of surfactant

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21
Q

The hypothalamus releases CRH in a _ fashion

A

The hypothalamus releases CRH in a pulsatile fashion
* We always have a basal level of cortisol, ACTH, CRH
* The HPA axis is responsible for cortisol regulation

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22
Q

The cell bodies that produce CRH are located in the _

A

The cell bodies that produce CRH are located in the paraventricular nucleus of the hypothalamus

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23
Q

Aldosterone is lipophilic and freely travels in the bloodstream; however the majority will be bound to _

A

Aldosterone is lipophilic and freely travels in the bloodstream; however the majority will be bound to albumin or transcortin, cortisol, progesterone

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24
Q

MR receptors have equal affinity for mineralocorticoids and cortisol; what is the consequence of this

A

High levels of cortisol can stimulate MR receptors and cause effects similar to hyperaldosteronism

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25
Q

The adrenal cortex originates from _ embryologic structure

A

The adrenal cortex originates from mesoderm

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26
Q

The adrenal medulla originates from _ embryologic structure

A

The adrenal medulla originates from neural crest

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27
Q

The superior adrenal artery branches off of the _

A

The superior adrenal artery branches off of the inferior phrenic artery

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28
Q

The middle adrenal artery branches off of the _

A

The middle adrenal artery branches off of the abdominal aorta

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29
Q

The inferior adrenal artery branches off of the _

A

The inferior adrenal artery branches off of the renal artery

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30
Q

The right suprarenal vein drains into the _

A

The right suprarenal vein drains into the IVC, directly

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31
Q

The left suprarenal vein drains into the _

A

The left suprarenal vein drains into the left renal vein –> IVC

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32
Q

The (right/left) renal vein crossses over the aorta

A

The left renal vein crosses over the aorta

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33
Q

The (right/left) renal vein is longer

A

The left renal vein is longer than the right

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34
Q

_ is a condition in which the SMA compresses the left renal vein and causes hematuria, flank pain, pelvic congestion

A

Nutcracker syndrome is a condition in which the SMA compresses the left renal vein and causes hematuria, flank pain, pelvic congestion

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35
Q

A patient with hematuria, flank pain, and pelvic congestion may have compression of the renal vein via the _

A

A patient with hematuria, flank pain, and pelvic congestion may have compression of the renal vein via the superior mesenteric artery (or sometimes the aorta)

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36
Q

Why might nutcracker syndrome cause pelvic congestion in a female?

A

The gonadal vein can’t drain

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37
Q

The adrenal cortex produces _ while the adrenal medulla produces _

A

The adrenal cortex produces steroid hormones (mineralocorticoids, glucocorticoids, androgens) while the adrenal medulla produces stress hormones (epi, norepi)

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38
Q

The zona glomerulosa produces _

A

The zona glomerulosa produces mineralocorticoids

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39
Q

The zona reticularis produces _

A

The zona reticularis produces androgens

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40
Q

The zona fasciculata produces _

A

The zona fasciculata produces glucocorticoids

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41
Q

_ cells secrete neurohormones epinephrine and norepinephrine; they are found in the adrenal medulla or celiac ganglion

A

Chromaffin cells secrete neurohormones epinephrine and norepinephrine; they are found in the adrenal medulla or celiac ganglion

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42
Q

Glucocorticoids (aka cortisol) have three important roles:

A

Glucocorticoids (aka cortisol) have three important roles:
1. Maintains BP (can inc RAAS and act on MR)
2. Increases glucose in the bloodstream
3. Anti-inflammatory effects

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43
Q

Clinical manifestations of glucocorticoid deficiency include:

A

Clinical manifestations of glucocorticoid deficiency include:
* Weakness, fatigue, muscle aches
* Orthostatic hypotension, hypoglycemia
* GI symptoms, weight loss

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44
Q

Mineralocorticoid (aka aldosterone) functions to _

A

Mineralocorticoid (aka aldosterone) functions to increase Na+ retention, excrete K+

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45
Q

Consequences of aldosterone deficiency:

A

Consequences of aldosterone deficiency:
* Hyperkalemia (palpitations, chest pain, N/V)
* Type IV RTA
* Normal Na+

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46
Q

Aldosterone deficiency can cause a hyperkalemic, hypercholeremic non-AG metabolic acidosis; explain

A

Aldosterone deficiency can cause a hyperkalemic, hypercholeremic non-AG metabolic acidosis due to hyperkalemia –> inhibits ammonium excretion

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47
Q

Androgens have roles in _ physiology

A

Androgens have a role in regulating energy, concentration, mood, menses, libido

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48
Q

Decreased androgens can manifest as _

A

Decreased androgens can manifest as depressed mood, poor energy, decreased concentration, irregular menses, erectile dysfunction

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49
Q

Primary adrenal insufficiency causes ADH secretion to (increase/decrease)

A

Primary adrenal insufficiency causes ADH secretion to increase

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50
Q

Increased ADH secretion in primary AI is two-fold; explain

A

Increased ADH secretion in primary AI is two-fold:
1. CRH increases ADH and primary AI will increase CRH levels
2. Cortisol normally opposes ADH secretion so during AI, ADH is left unopposed

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51
Q

Causes of primary adrenal insufficiency:

A

Causes of primary adrenal insufficiency:
* Adrenalectomy
* Autoimmune conditions
* HIV
* Disseminated TB
* Fungal infections
* Waterhouse-Friderichsen
* Addison’s disease
* Drugs (azoles, rifampin)

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52
Q

Waterhouse-Friderichsen syndrome is caused by septicemia from _ infection that leads to adrenal hemorrhage

A

Waterhouse-Friderichsen syndrome is caused by septicemia from N. meningitidis infection that leads to adrenal hemorrhage

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53
Q

Chronic primary adrenal insufficiency is commonly caused by _ in developed countries and _ in developing countries

A

Chronic primary adrenal insufficiency is commonly caused by Addison’s disease in developed countries and TB in developing countries

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54
Q

Someone with a primary adrenal insufficiency will have
_ morning cortisol
_ morning ACTH
_ ACTH stimulation test
_ lab findings

A

Someone with a primary adrenal insufficiency will have
low morning cortisol
high morning ACTH
no response on ACTH stimulation test
low aldosterone, high K+ , low glucose, high eosinophils

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55
Q

New onset eosinophilia may be an indicator of _ due to the lack of cortisol and the high ACTH

A

New onset eosinophilia may be an indicator of adrenal insufficiency due to the lack of cortisol and the high ACTH

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56
Q

Only (primary/secondary) adrenal insufficiency will present with signs of mineralocorticoid deficiency

A

Only primary adrenal insufficiency will present with signs of mineralocorticoid deficiency
* Primary = problem with the adrenals themselves
* Secondary = problem with anterior pituitary (RAAS controls aldosterone not ACTH)

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57
Q

Explain the causes and pathophysiology of secondary adrenal insufficiency

A

Decreased anterior pituitary function –> low ACTH –> low adrenal cortex activity –> low cortisol
* Often involves damage to anterior pituitary from mechanical, infectious, infiltrative causes
* Mechanical: TBI, surgery, stroke, sheehan
* Infectious: TB, syphilis
* Infiltrative: hemochromatosis, sarcoidosis

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58
Q

Diagnostics expected with secondary AI:

A

Diagnostics expected with secondary AI:
* Low ACTH, low cortisol, normal aldosterone, normal K+
* Low morning cortisol
* Low morning ACTH
* ACTH stimulation test increases cortisol

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59
Q

A very common cause of “tertiary” adrenal insufficiency is _

A

A very common cause of “tertiary” adrenal insufficiency is abrupt cessation of exogenous steroid use

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60
Q

What happens if exogenous steroids (like prednisone) are suddenly stopped and not tappered?

A

Hypothalamic dysfunction –> low CRH –> low ACTH –> low cortisol

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61
Q

What are the next diagnostic steps after finding a low AM ACTH?

A

Low ACTH –> do a CRH stimulation test
* No response? secondary
* Increases ACTH? tertiary

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62
Q

If ACTH stimulation test increases cortisol, the adrenal insufficiency is either _ or _

A

If ACTH stimulation test increases cortisol, the adrenal insufficiency is either secondary or tertiary

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63
Q

Cushing syndrome is _ , cushing disease is _

A

Cushing syndrome is hypercortisolism , cushing disease is hypercortisolism from pituitary tumor

64
Q

Things like adrenal adenoma or adrenal carcinoma cause increased cortisol from (unilateral/bilateral) adrenal atrophy

A

Things like adrenal adenoma or adrenal carcinoma cause increased cortisol from unilateral adrenal atrophy

65
Q

Exogenous corticosteroid use (prednisone) can lead to decreased CRH, decreased ACTH and (bilateral/unilateral) adrenal hyperplasia

A

Exogenous corticosteroid use (prednisone) can lead to decreased CRH, decreased ACTH and bilateral adrenal hyperplasia

66
Q

Clinical presentation of hypercortisolism:

A

Clinical presentation of hypercortisolism:
* Moon facies
* Weight gain
* Hyperglycemia/insulin resistance
* Abdominal obesity
* Dorsocervical fat pad
* Purple striae/skin thinning
* Amenorrhea, hirsutism, osteoporosis

67
Q

Hypercortisolism is associated with:
_ 24-hr urine free cortisol
_ late night salivary cortisol
_ ACTH

A

Hypercortisolism is associated with:
increased 24-hr urine free cortisol
increased late night salivary cortisol
? ACTH (increased from cushings or paraneoplastic, decreased if exogenous cause)

68
Q

If a patient has cushing disease, high dose dexamethasone suppression test will show _

A

If a patient has cushing disease, high dose dexamethasone suppression test will show adequate suppression

69
Q

If a high-dose dexamethasone test shows no suppression, the cause is likely _

A

If a high-dose dexamethasone test shows no suppression, the cause is likely exogenous
* If the source is pituitary, cortisol should decrease

70
Q

If CRH stimulation test reveals increased ACTH and increased cortisol, the cause is (cushing/paraneoplastic)

A

If CRH stimulation test reveals increased ACTH and increased cortisol, the cause is Cushing disease
* Paraneoplastic will show no increase in ACTH or cortisol

71
Q

Describe the pathway of normal aldosterone secretion

A

Low BP or low renal perfusion –> increase renin –> RAAS activation –> increases angiotensin II –> signals to the zona glomerulosa –> increase aldosterone

72
Q

Primary hyperaldosteronism is caused by _

A

Primary hyperaldosteronism is caused by hyperplasia of zona glomerulosa
* Unilateral adrenal adenoma- Conn’s
* Bilateral adrenal hyperplasia

73
Q

Secondary hyperaldosteronism is caused by _

A

Secondary hyperaldosteronism is caused by increased RAAS/renin release
* CHF, liver failure, renal artery stenosis

74
Q

Low K+ levels can lead to ADH desensitization and _

A

Low K+ levels can lead to ADH desensitization and nephrogenic DI –> polyuria, polydipsia

75
Q

Hyperaldosteronism may present with _ clinical signs

A

Hyperaldosteronism may present with secondary HTN, headache, muscle weakness, palpitations, cardiac arrhythmia

76
Q

Na+ levels may be high or even normal in a patient with hyperaldosteronism, why?

A

Aldosterone escape –> adequate Na+ excretion in the urine (natriuresis) –> no edema

77
Q

Hyperaldosteronism is associated with metabolic _

A

Hyperaldosteronism is associated with metabolic alkalosis

78
Q

Primary hyperaldosteronism is associated with _ renin levels

A

Primary hyperaldosteronism is associated with low renin

79
Q

_ is a drug that can be used in the treatment of hyperaldosteronism

A

Spironolactone is a drug that can be used in the treatment of hyperaldosteronism

80
Q

The most common tumor of the adrenal medulla in children is _

A

The most common tumor of the adrenal medulla in children is neuroblastoma

81
Q

The most common tumor of the adrenal medulla in adults is _

A

The most common tumor of the adrenal medulla in adults is pheochromocytoma

82
Q

Pheochromocytoma involves abnormal proliferation of _ cells

A

Pheochromocytoma involves abnormal proliferation of chromaffin cells
* Increases production of epi, norepi, dopamine

83
Q

Pheochromocytoma involves a proliferation of cells that are derived from _ embryologic structure

A

Pheochromocytoma involves a proliferation of cells that are derived from neural crest

84
Q

Pheochromocytomas are associated with _ genetic markers

A

Pheochromocytomas are associated with:
* NF-1
* VHL
* MEN2a, 2b

85
Q

Pheochromocytomas are associated with which MEN syndromes?

A

MEN2A, MEN2B

86
Q

In addition to increased catecholamines, pheochromocytomas can be diagnosed by the presense of _ in the urine and plasma

A

In addition to increased catecholamines, pheochromocytomas can be diagnosed by the presense of metanephrines in the urine and plasma

87
Q

Pheochromocytomas will have positive _ and _ neuroendocrine cell markers

A

Pheochromocytomas will have positive chromogranin and synaptophysin

88
Q

How do we manage pheochromocytomas?

A

alpha antagonists –> beta blockers –> tumor resection

89
Q

Why do alpha antagonists need to be given before beta blockers?

A

Don’t leave alpha unopposed –> could result in hypertensive crisis (drop HR with beta blockers can cause BP to shoot up)

90
Q

Neuroblastoma is associated with the amplification of _ oncogene

A

Neuroblastoma is associated with the amplification of N-myc

91
Q

Neuroblastomas result in a tumor along the _

A

Neuroblastomas result in a tumor along the sympathetic chain

92
Q

The classic presentation of a neuroblastoma is a child with _

A

The classic presentation of a neuroblastoma is a child with abdominal distension and a firm mass that crosses the midline, may also have jerky movements of the eyes and feet (opsoclonus-myoclonus)

93
Q

Neuroblastoma is associated with two markers, _ and _

A

Neuroblastoma is associated with two markers, +NSE and +Bombesin

94
Q

Neuroblastoma will present with increased urine _

A

Neuroblastoma will present with increased urine VMA, HVA

95
Q

Neuroblastoma has a characteristic _ on histology

A

Neuroblastoma has a characteristic homer-wright rosette on histology

96
Q

Neuroblastomas are treated with _

A

Neuroblastomas are treated with resection, chemotherapy, and radiation

97
Q

Adrenal carcinoma is _

A

Adrenal carcinoma is a tumor of the adrenal cortex
* May secrete glucocorticoids, mineralocorticoids, androgens, estrogens

98
Q

Adrenal carcinoma will present clinically with _

A

Adrenal carcinoma will present clinically with abdominal/back pain, abdominal mass and sx of high cortisol, aldosterone, androgens, and estrogens

99
Q

Adrenal carcinoma will have _ response to dexamethasone suppression test

A

Adrenal carcinoma will have no response to dexamethasone suppression test

100
Q

Aromatase is present in _ tissue; it converts testosterone –> estrogen

A

Aromatase is present in adipose tissue; it converts testosterone –> estrogen
* Increased adipose = increased aromatase

101
Q

_ is responsible for internal virilization in males

A

Testosterone is responsible for internal virilization in males

102
Q

_ is responsible for external virilization in males

A

DHT is responsible for external virilization in males

103
Q

If the enzyme (11,17,21) begins with 1, then its deficiency causes _

A

If the enzyme (11,17,21) begins with 1, then its deficiency causes HTN

104
Q

If the enzyme (11,17,21) ends with 1, then its deficiency causes

A

If the enzyme (11,17,21) ends with 1, then its deficiency causes female virilization

105
Q

The adrenal cortex is derived from the _

A

The adrenal cortex is derived from the mesoderm

106
Q

The adrenal medulla is derived from the _

A

The adrenal medulla is derived from the neural crest (ectoderm)

107
Q

The _ is composed of post-ganglionic sympathetic cells aka the chromaffin cells

A

The adrenal medulla is composed of post-ganglionic sympathetic cells aka the chromaffin cells

108
Q

Pheochromocytoma and neuroblastoma are two neoplasms in the _ region

A

Pheochromocytoma and neuroblastoma are two neoplasms in the adrenal medulla

109
Q

Neoplasms in the adrenal cortex are either _ or _

A

Neoplasms in the adrenal cortex are either carcinomas or adenomas

110
Q

Presentation of pheochromocytoma:

A

Presentation of pheochromocytoma:
* Secondary HTN
* Episodes of sweating, headache, palpitations
* Paroxysmal hypertensive crisis
* Arrythmias, sudden death, heart failure

111
Q

Pheochromocytomas are usually (benign/malignant) and (unilateral/bilateral)

A

Pheochromocytomas are usually benign and unilateral

112
Q
A

Pheochromocytoma: well circumscribed, red-brown/dusty

113
Q
A

Pheochromocytoma:
* Polygonal/spindle cells
* Nests with vascular network
* Round nuclei, nucleoli
* Red-purple cytoplasm

114
Q

Pheochromocytoma may present with elevated urine/ plasma _

A

Pheochromocytoma may present with elevated urine/ plasma metanephrines (HVA, MVA)

115
Q

Before pheochromocytoma surgery we pretreat with _ and _

A

Before pheochromocytoma surgery we pretreat with phenoxybenzamine (alpha antagonist) and metoprolol (beta blocker)

116
Q

Pheochromocytoma and neuroblastomas are both neoplasms of the medulla but pheos are derived from _ cells and neuroblastomas are derived from _

A

Pheochromocytoma and neuroblastomas are both neoplasms of the medulla but pheos are derived from chromaffin cells and neuroblastomas are derived from neural crest cells (primitive cells)

117
Q

Complications of neuroblastomas include:

A

Complications of neuroblastomas include:
* Metastasis
* Hypertension
* Opsoclonus-Myoclonus
* Constipation
* Spinal cord compression

118
Q
A

Neuroblastoma: hereogeneous, necrosis, irregular border

119
Q
A

Neuroblastoma
* Classic homer-wright rosettes

120
Q

Of the adrenal hormones, _ and _ are regulated by ACTH

A

Of the adrenal hormones, cortisol and androgens are regulated by ACTH
* Aldosterone is regulated by renin and angiotensin

121
Q

The one adrenal hormone that is not significantly affected in secondary AI is _

A

The one adrenal hormone that is not significantly affected in secondary AI is aldosterone

122
Q

Hyperpigmentation is a sign of _ AI

A

Hyperpigmentation is a sign of primary AI (ACTH is high)

123
Q

_ is an emergency that is triggered by a stressor and causes severe weakness, fatigue, weight loss, nausea, hypotension, hyponatremia, and hypoglycemia

A

Adrenal crisis is an emergency that is triggered by a stressor and causes severe weakness, fatigue, weight loss, nausea, hypotension, hyponatremia, and hypoglycemia

124
Q

In primary AI, hyponatremia is two fold; _ and _

A

In primary AI, hyponatremia is two-fold
1. Low aldosterone
2. Low cortisol

125
Q

Low cortisol causes hyponatremia through _

A

Low cortisol causes hyponatremia through excess secretion of ADH

126
Q

In secondary AI, hyponatremia is caused by _ alone

A

In secondary AI, hyponatremia is caused by low cortisol –> high ADH alone (aldosterone is preserved by RAAS)

127
Q

The most common cause of secondary AI is _

A

The most common cause of secondary AI is withdrawal of chronic glucocorticoids

128
Q

Treatment for primary AI

A

Treatment for primary AI: glucocorticoids and mineralocorticoids

129
Q

Treatment for secondary AI

A

Treatment for secondary AI: glucocorticoids (aldosterone will be normal bc of RAAS)

130
Q

How do we treat adrenal crisis?

A

Isotonic fluids, glucocorticoids, dextrose

131
Q

Congenital adrenal hyperplasia are disorders caused by _

A

Congenital adrenal hyperplasia are disorders caused by enzyme deficiencies in adrenal steroid synthesis pathway

132
Q

All congenital adrenal hyperplasia conditions are _ inheritence pattern

A

All congenital adrenal hyperplasia conditions are autosomal recessive

133
Q

Females with androgen excess may present with _

A

Females with androgen excess may present with ambiguous genitalia, clitoromegaly, irregular infertility, hirsuitism

134
Q

The gene mutation associated with 21-hydroxylase deficiency is _

A

The gene mutation associated with 21-hydroxylase deficiency is CYP21A

135
Q

The gene mutation associated with 11B-hydroxylase deficiency is

A

The gene mutation associated with 11B-hydroxylase deficiency is CYP11B1

136
Q

The gene mutation associated with 17a-hydroxylase deficiency is

A

The gene mutation associated with 17a-hydroxylase deficiency is CYP17A1

137
Q

21-hydroxylase deficiency is associated with:
_ cortisol
_ aldosterone
_ androgens

A

21-hydroxylase deficiency is associated with:
Low cortisol (deficient)
Low aldosterone (deficient)
High androgens

138
Q

21-hydroxylase deficiency can be diagnosed with _ 17-OH-progesterone and _ DHEA

A

21-hydroxylase deficiency can be diagnosed with high 17-OH-progesterone and high DHEA, along with low cortisol and high ACTH

139
Q

What are the hormone deficiencies/excesses seen in 11B-hydroxylase deficiency?

A

Cortisol and aldosterone = deficient
Androgen and 11-deoxycorticosterone = excess

140
Q

17a-hydroxylase is associated with which hormone def/excesses?

A

Mineralocorticoid excess
Androgen deficiency

141
Q
A
142
Q

The hallmark of CAH is excess _ which causes adrenal hyperplasia

A

The hallmark of CAH is excess ACTH which causes adrenal hyperplasia

143
Q

All CAH have low _

A

All CAH have low cortisol

144
Q

Severe hypokalemia can cause muscle weakness or _ changes on EKG

A

Severe hypokalemia can cause muscle weakness or T wave inversions on EKG

145
Q
A

Adrenal adenoma

146
Q
A

Renal artery stenosis

147
Q

_ or _ can be used for an aldosterone suppression test

A

IV saline or oral salt loading can be used for an aldosterone suppression test

148
Q

Ald/Renin > 30 indicates _
Ald/Renin < 30 indicates _

A

Ald/Renin > 30 indicates primary hyperaldosteronism
Ald/Renin < 30 indicates secondary hyperaldosteronism

149
Q

What are the complications associated with cushings?

A
  • Diabetes
  • Hypertension
  • Osteoporosis
  • DVT
  • Infections
  • Cataracts
  • Glaucoma
150
Q

Why does cushing syndrome have signs and sx of mineralocorticoid and adrenal androgen excess?

A

High levels of cortisol can have effects on MR and androgen receptors

151
Q

High dose dexamethasone suppression test will only suppress (cushing disease/ectopic ACTH secretion)

A

High dose dexamethasone suppression test will only suppress cushing disease, not ectopic ACTH

152
Q

The 6 P’s of pheochromocytomas:

A

The 6 P’s of pheochromocytomas:
1. Pain (headaches)
2. Pressure (BP)
3. Palpitations
4. Perspiration
5. Pallor
6. Panic attacks

153
Q

The most common inherited syndrome in a patient with pheochromocytoma is _ and this is associated with a _ gene mutation

A

The most common inherited syndrome in a patient with pheochromocytoma is MEN2 and this is associated with a RET gene mutation
* NF-1 and VHL are less common

154
Q

We can use a _ suppression test to confirm a pheochromocytoma

A

We can use a clonidine suppression test to confirm a pheochromocytoma

155
Q

Ingestion of licorice mimics which hormone excess?

A

Aldosterone

156
Q

The classic triad of pheochromocytoma is _

A

The classic triad of pheochromocytoma is
1. Headache
2. Hypertension
3. Palpitations

Endocrine (8 decks)

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