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Endocrine - Troutmanm > Adrenal > Flashcards

Adrenal Flashcards

1
Q

Where are the adrenal glands located?

A

atop the kidneys

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2
Q

What are the adrenal glands also called?

A

suprarenal glands

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3
Q

What shape are the adrenal glands?

A

triangular or semilunar shaped

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4
Q

T/F: adrenal glands contain distinct zones which produce different hormones

A

True

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5
Q

What type of hormones are the adrenal glands responsible for releasing?

A

Stress hormones

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6
Q

A/P: The adrenal gland has both a _____ & _____

A

cortex and a medulla

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7
Q

What does cortex mean?

What does medulla mean?

A

outer layer

inner region

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8
Q

*** The adrenal medulla is connected directly to the sympathetic nervous system via

A

nerves

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9
Q

What does the adrenal medulla bridge?

A

bridges the endocrine and sympathetic nervous system

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10
Q

The adrenal medulla releases substances known as ________ which enter the circulation and act on ________ like other hormones

A

catecholamines

distal tissues

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11
Q

What are catecholamines made by?

A

Catecholamines are made by chromaffin cells in the adrenal medulla

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12
Q

What are all catecholamines derived from?

A

tyrosine

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13
Q

*** What are the 4 catecholamines?

A

DOPA, Dopamine, Norepinephrine, and Epinephrine

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14
Q

What do catecholamines activate?

A

the stress or “fight or flight” response

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15
Q

What is the principle product of the adrenal medulla?

A

epinephrine

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16
Q

Where is epinephrine made?

A

Epinephrine is made ONLY in the adrenal medulla

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17
Q

What percentage of epi and norepinephrine are made in the adrenal medulla?

A

Epi accounts for 80%
Norepi accounts for 20%
Scant amount of dopamine also made here

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18
Q

What does the fight or flight response demonstrate control of?

A

adrenal medullary function

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19
Q

Epi and norepi are released and act as hormones causing

A

sympathetic activation

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20
Q

Sympathetic activation is a mobilization of needed resources including

A

increased blood pressure, heart rate, blood glucose, and brochodilation

Dowshifting of less needed resources also occurs.

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21
Q

What is the F or F response activated by?

A

pain, fear, hemorrhage, cold, hypoglycemia, hypotension, heat, exercise

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22
Q

What does the F or F response increase CO to?

A

heart and skeletal muscle

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23
Q

What does the F or F response decrease CO to?

A

kidneys, skin and mucosa

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24
Q

What does the F or F response mobilize for energy?

A

glucose and fatty acid

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25
Q

Is respiration increased or decreased d/t F or F?

A

increased

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26
Q

T/F: Epinephrine and norepineprine are similar but differ in important ways

A

true

Differences occur in which adrenergic receptors they stimulate

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27
Q

Epinenephrine and Norepinephrine both have ______ effects which result in arterial _______

A

strong alpha-1

vasoconstriction

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28
Q

Which catecholamine has a stronger beta 1 effect?

A

Epinephrine has stronger beta-1 effects which increases heart rate and contractility more

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29
Q

*** What enzyme is necessary for the conversion of norepinephrine to epi?

A

Phenylethanolamine N-Methyltransferase (PNMT)

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30
Q

*** What is PNMT expression regulated by?

A

glucocorticoids (cortisone), which helps to account for glucocorticoids role in affecting blood pressure

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31
Q

What is pheochromocytoma?

A

a tumor either caused by adrenal medullary hyperplasia or extra-adrenal chromaffin tissue

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32
Q

How does a pheochromocytoma tumor effect catecholamines?

A

These tumors make catecholamines in an unregulated fashion.

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33
Q

*** What are symptoms of pheochromocytoma?

A

paroxysmal hypertension, tachycardia, headache, sweating, anxiety, tremor, and glucose intolerance

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34
Q

How are most pheochromocytoma tumors localized?

A

Most tumors (85-90%) are solitary tumors localized to a single adrenal gland (mostly the right)

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35
Q

Where are 10% of pheochromocytoma tumors located?

A

10% of tumors are extra-medullary, of these 95% are in the abdomen

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36
Q

How is pheochromocytoma diagnosed?

A

Diagnosis is made with first a strong clinical suspicion based on symptoms, then through biochemical testing, then imaging

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37
Q

What lab helps make a diagnosis of pheochromocytoma and how?

A

Urinary Vanillylmandelic acid (VMA) levels help to make the diagnosis as both epinephrine and norepinephrine are degraded to this

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38
Q

what type of imaging is useful for diagnosis of a pheochromocytoma tumor?

A

Ultrasound and MRI are useful in locating tumors and have decreased need for surgical localization

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39
Q

T/F: Anesthetic considerations have helped decrease perioperative mortality from a high of 45% to 0-3%

A

true

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40
Q

The introduction of __________ preoperatively reduces the incidence of periop blood pressure fluctuations, MI, CHF, dysrhythmias, and CVA

A

alpha adrengergic antagonist

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41
Q

The alpha blockers _____ or _____ should be started 10-14 days prior to surgery to normalize BP

A

phenoxybenzamine or prazosin

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42
Q

For pheochromocytoma, what type of blockade must happen first?

A

Once adequate alpha blockade is established, beta blockade can begin
Beta blockade is delayed because of the risk of unopposed alpha mediated vasoconstriction

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43
Q

For pheochromocytoma, when arteries do relax after alpha and beta blockade - what will they need?

A

volume expansion

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44
Q

What does the typical anesthetic plan for pheochromocytoma include?

A

typically includes GETA with arterial line, and central venous access

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45
Q

Why are short acting agents desired during pheochromocytoma surgery?

A

paroxysms of both hypotension and hypertension are common when the tumor is manipulated or removed

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46
Q

What agents should be AVOIDED in pheochromocytoma surgery?

A

Avoidance of histamine releasing agents, metoclopramide, and glucagon (these agents provoke pheochromocytomas)

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47
Q

What my happen when the pheochromocytoma tumor is removed?

A

abrupt hypotension

48
Q

What is the initial treatment for abrupt hypotension after the pheochromocytoma is removed?

A

Restitution of intravascular fluid deficits is initial treatment, but vasopressors are sometimes needed

49
Q

When do catecholamine levels return to normal after pheochromocytoma surgery?

When does BP return to normal?

A

Catecholamine levels return to normal several days after surgery and approximately 75% of patients become normotensive within 10 days postop

50
Q

Is medullary hypo secretion a serious problem?

A

NO

the sympathetic nervous system compensates for cardiovascular regulation

other regulatory hormones compensate for metabolic effects

51
Q

The adrenal cortex mediates the stress response via the production of substances known as _______ & _______, it also is a secondary site of _______ synthesis

A

mineralocorticoids and glucocorticoids

androgen

52
Q

How many zones is the adrenal cortex divided into? What are they?

A

3
the zona glomerulosa
the zona fasciculata
the zona reticularis

53
Q

*** What does the zone glomerulosa produce?

A

mineralocorticoids

54
Q

*** What does the zone fasiculata produce?

A

glucocorticoids

55
Q

*** What does the zone reticularis produce?

A

androgens

56
Q

*** What is the primary mineralocorticoid produced?

A

aldosterone

57
Q

*** What is the primary glucocorticoid produced?

A

cortisol

58
Q

*** What is the primary androgen produced?

A

androstenedione

59
Q

*** All of these are STEROID HORMONES (aldosterone, cortisol, androstenedione), and ALL are synthesized from ______

A

cholesterol

60
Q

Why are mineralocorticoids named so?

A

because they control “minerals” also known as the electrolytes sodium (Na+) and potassium (K+)

61
Q

*** What is the primary mineralocorticoid?

A

aldosterone

62
Q

How does aldosterone work?

A

Aldosterone effects salt and water balance and thereby effect long term regulation of blood pressure

63
Q

What part of the kidney does aldosterone effect?

A

distal convoluted tubule and collecting ducts of the kidneys

64
Q

What does aldosterone cause retention and excretion of?

A

causes retention of sodium and water and excretion of potassium and hydrogen

65
Q

*** aldosterone is unopposed, what does it lead to?

A

If unopposed, aldosterone leads to hypertension, extracellular fluid expansion, hypokalemia, and alkalosis

66
Q

What does aldosterone work with for BP control?

A

renin-angiotensin system

67
Q

Briefly describe the RAAS

A

Hypovolemia triggers kidneys to secrete renin

Through a series of steps angiotensin II is produced

Angiotensin II is a potent vasoconstrictor and also stimulates the secretion of aldosterone

Aldosterone causes retention of water and sodium and secretion of potassium, and also increases blood pressure

68
Q

What is aldosterone primarily regulated by?

A

Aldosterone is regulated primarily by renin-angiotensin system and by potassium levels

69
Q

Do adrenalcorticotropic Hormone (ACTH) and sodium levels exert much control over the release of aldosterone

A

NO

70
Q

*** What is primary hyperaldosteronism also known as?

A

Conns syndrome

71
Q

*** What is Conns Syndrome caused by?

A

Caused by aldosterone secreting tumors or hyperplasias

72
Q

*** What are the effects of Conns Syndrome?

A

increased ECF volume, hypertension, K+ depletion and metabolic alkalosis

73
Q

*** What is the diagnosis and treatment for Conns Syndrome?

A

Low Renin from negative feedback

Surgical

74
Q

What is the term for adrenal insufficiency?

A

hypoaldosteronism

75
Q

What happens with Na and K in hypoaldosteronism?

A

Na is lost in urine, K is retained

Plasma volume decreases and hypotension/ hyperkalemia may lead to circulatory collapse

76
Q

How did glucocorticoids get their name?

A

because of there effects on glucose metabolism

77
Q

What is another name for cortisol

A

hydrocortisone (they are the same thing!)

78
Q

*** What is the principle glucocorticoid and where is it produced?

A

Cortisol is the principal glucocorticoid and is produced in the zona fasciculata

79
Q

Cortisol is essential for life, and regulates a variety of what type of functions functions

A

cardiovascular, metabolic, immunologic, and homeostatic

80
Q

What does glucocorticoids stimulate?

A

Gluconeogenesis

81
Q

What is gluconeogenesis?

A

Formation of carbohydrate from protein by the liver

Causes mobilization of amino acids from muscle

82
Q

What happens to muscles in great cortisol excess?

A

muscle weakness

83
Q

Does glucocorticoids increase or decrease glucose utilization by cells

A

decrease

84
Q

Does glucocorticoids increase or decrease blood glucose levels?

A

increase

Caused by both increased formation of glucose by the liver and decreased utilization of glucose by tissue

85
Q

Almost any stress (physical or neurogenic) can cause an immediate release of ____ by the _______ gland followed by greatly increased secretion of cortisol

  • Trauma
  • Infection
  • Heat/Cold
  • Surgery
  • Catecholamine injection
A

ACTH

ANTERIOR pituitary

Unclear what benefit cortisol provides in stressful situations, probably related to mobilization of resources for immediate availability

86
Q

High levels of cortisol have what type of effect?

A

anti-inflammatory effects

87
Q

How does cortisol prevent development of inflammation?

A

by stabilizing lysosomes, decreasing capillary permeability, decreasing migration of WBC’s into inflamed areas, and other effects

88
Q

Cortisol also causes resolution of inflammation within what time frame?

A

hours to days

Mechanism unclear
May be due to mobilization of energy resources for quicker repair
May be due to inactivation and removal of inflammatory products
Healing is enhanced
Useful in autoimmune processes, allergic reactions

89
Q

What stimulates cortisol secretion?

A

Adrenocorticotropic Hormone (ACTH) stimulates cortisol secretion almost entirely

90
Q

What is ACTH controlled by? and where does it come from?

A

ACTH release is controlled by Corticotropin-Releasing Factor (CRH) from the hypothalamus.

91
Q

What causes a release of both ACTH and CRH?

A

physiologic stress

92
Q

What causes inhibition of ACTH and CRH release

A

High levels of cortisol

93
Q

Cortisol release is caused by the _____ when it senses stress

Cortisol helps relieve the damaging nature of the stressful state

Cortisol provides direct _______ to decrease its release

A

hypothalamus

negative feedback

94
Q

CRH, ACTH, and cortisol are released in relation to _________ with high levels in the morning

A

circadian rhythms

95
Q

What is Cushings DISEASE

A

ACTH secreting tumor of the pituitary

96
Q

What is Cushings SYNDROME?

A

caused by excessive cortisol secretion

97
Q

What are 4 ways Cushing Syndrome can happen?

A

ACTH secreting ectopic tumor

Overactive Hypothalamic secretion of CRH

Primary glucocorticoid secreting adrenal tumor

Iatrogenic (chronic administration)

98
Q

What happens to bone and muscle in Cushings Syndrome?

A

osteoporosis

Muscle wasting, weakness, fatigability

(These are the ones he specifically went over - look at slide 33!)

99
Q

Cushing Syndrome: Fat changes

A

Truncal obesity, moon facies, buffalo hump

100
Q

Cushing Syndrome: Renal changes

A

Salt/ water retention, HYPOkalemia from mineralocorticoid activity of excess glucocorticoids

101
Q

Cushing Syndrome: CV

A

hypertension

102
Q

Cushing Syndrome: Endocrine

A

Impaired glucose tolerance, amenorrhea

103
Q

What does Addisons disease result from?

A

Results from failure to produce adrenocortical hormones (glucocorticoids and mineralocorticoids)

104
Q

What is primary Addisons disease?

A

Adrenal nonfunction-mostly autoimmune

105
Q

What is secondary Addisons disease?

A

Hypothalamic or pituitary nonfunction

106
Q

What are causes of secondary Addisons disease?

A

Adrenal atrophy, metastatic tumor, TB, Iatrogenic/acute withdrawal of glucocorticoid treatment or removal of cortisol secreting tumor

107
Q

What are symptoms are glucocorticoid deficiency?

A

Hypoglycemia, fatigue, weakness, weight loss, anorexia

Hyperpigmentation (primarily by increased ACTH)

Severe deterioration to stress

108
Q

How do you treat an Addisonian Crisis?

A

treat crisis with cortisol

109
Q

symptoms of mineralocorticoid deficiency

A 
Dehydration
Polyuria
Hypotension
Low Na+
Retention of K+
Metabolic acidosis
110
Q

In what time frame will death occur if Addisonian Crisis is not treated?

A

Death in 4 days to 2 weeks if untreated

111
Q

How do you treat an Addisons Disease?

A

Treat with glucocorticoids and mineralocorticoids (need both)

112
Q

What can happen to a patient who takes chronic steroids when these medications where held periop?

A

Case reports of patients who take chronic steroids having periop shock or death when these medicines were held, presumably from acute adenal insufficiency

113
Q

Are larger or smaller doses of glucocorticoids given to patients in the periop period who have Addisons?

A

larger

Little evidence to support definitive guidelines for who, when, and how much to give

oftentimes hydrocortisone 50-100mg IV given to adult patients

114
Q

*** Why should you NOT use etomidate in this patient population?

A

Etomidate causes profound suppression of cortisol for at least 24 hours and can contribute to adrenal insufficiency and resultant hypotension

Etomidate should be used sparingly (or never) in patients with septic shock for this reason

115
Q

T/F: Etomidate has not been shown to increase mortality when used for rapid sequence induction

A

True

Endocrine - Troutmanm (7 decks)

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