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Endocrine - Summer 2019 > Adrenal > Flashcards

Adrenal Flashcards

1
Q

Adrenal glands AKA

A

suprarenal glands

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2
Q

The adrenals are responsible for releasing ________ hormones

A

stress

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3
Q

The adrenal has a cortex and medulla. Cortex means ________ and medulla means _______

A

outer / inner

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4
Q

The adrenal medulla is connected directly to the _____ via nerves

A

SNS

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5
Q

The adrenal medulla bridges the endocrine and ______

A

SNS

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6
Q

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

A

catecholamines

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7
Q

Catecholamines are made by _______ cells in the adrenal medulla and are all derived from ________

A

chromaffin / tyrosine

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8
Q

What are the 4 catecholamines

A

DOPA, Dopamine, Norepinephrine, epinephrine

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9
Q

Catecholamines activate the stress, or ______ response

A

fight or flight

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10
Q

__________ is the principal product of the adrenal medulla and is made only in the medulla

A

epineprhine

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11
Q

Epinephrine accounts for nearly ____% of the adrenal medulla’s output, the other _____% is norepinephrine, and a scant amount of dopamine also made here

A

80% / 20%

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12
Q

The fight or flight response demonstrates ______ control of adrenal medullary function

A

central

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13
Q

Epinephrine and norepi are released and act as hormones causing _______ activation

A

sympathetic

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14
Q

Sympathetic activation is mobilization of needed resources including increased ____ and ____ as well as ___________.

A

BP, HR and bronchodilation

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15
Q

The fight or flight response happens in response to

A

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

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16
Q

The FOF response acts by increasing CO to ____ and ______

A

heart and skeletal muscle

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17
Q

The FOF response decreases blood flow to the ____, ____ and _____

A

kidneys, skin and mucosa

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18
Q

The FOF utilizes ______ and _____ mobilization for energy

A

glucose and fatty acid

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19
Q

What happens to respirations during FOF?

A

increased

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20
Q

Epi and norepi differ in which ________ receptors they stimulate

A

adrenergic

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21
Q

Epi and norepi both have strong _______ effects which result in ARTERIAL vasosconstriction

A

alpha-1

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22
Q

Epinephrine has stronger _______ effects which increases HR and contractility more

A

beta-1

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23
Q

___________ is an enzyme necessary for conversion of norepinephrine to epinephrine

A

Phenylethanolamine Methyltransferase (PNMT)

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24
Q

PNMT expression is regulated by _________, which helps account for __________ role in affecting BP.

A

glucocorticoids (cortisone) / glucocorticoids

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25
Q

_________ is a tumor either caused by adrenal medullary hyperplasia or extra-adrenal chromaffin tissue. These tumors make _______ in an unregulated fashion.

A

pheocromocytoma / catecholamines

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26
Q

Symptons of Pheocromocytoma

A

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

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27
Q

Most tumors (85-90%) are solitary tumors localized to a single _____ _______

A

adrenal gland (mostly RIGHT)

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28
Q

10% of tumors are extramedullary, of these 95% are in the _______

A

abdomen

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29
Q

Dx of pheocromocytoma

A

strong clinical symptoms, then biochemical testing, then imaging

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30
Q

______ ____ ______ levels help to make the diagnosis as both epinephrine and norepi are degraded into this

A

Urinary Vanillylmandelic acid (VMA)

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31
Q

Anesthetic considerations for someone with a pheocromocytoma have helped decrease perioperative mortality from 45% to __ -__%

A

0-3%

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32
Q

The introduction of ___ ________ ______ preoperatively reduces the incidence of periop BP fluctuations, MI, CHF, dysrhythmias and CVA associated with pheocromocytoma

A

alpha adrenergic anatagonists

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33
Q

The alpha blockers ______ or _______ should be started 10-14 days prior to surgery to normalize BP in someone with pheocromocytoma

A

phenoxybenzamine / prazosin

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34
Q

With pheocromocytoma, once adequate alpha blockade is established, ______ ________ can begin. _____ blockade is delayed because of the risk of unopposed alpha mediated vasoconstriction.

A

beta blockade / beta

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35
Q

When arteries relax, _______ expansion is necessary

A

volume

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36
Q

Anesthetic plan for someone with pheocromocytoma typically includes _______ with arterial line and central venous access.

A

GETA

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37
Q

PHEOCROMOCYTOMA Anesthetic considerations - Short acting vasocative agents are desirable as paroxysms of both _____ and ______ are common when the tumor is manipulated

A

hypotension / hypertension

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38
Q

What agents provoke pheocromocytomas, awaken the beast, and should be avoided?

A

histamine releasing drugs, metoclopramide, glucagon

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39
Q

What can happen when a pheo tumor is removed? What is the treatment?

A

abrupt hypotension / 1st fluids then vasopressors if needed

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40
Q

For pheocromocytoma, catecholamine levels return to normal several days after surgery and approximately ___% of patients become normotensive within ____ days postop.

A

75% / 10 days

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41
Q

T/F The physiologic effect of Medullary HYPOsecretion is not a serious problem

A

TRUE

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42
Q

Medullary hyposecretion is not a serious problem because the _______ compensates for CARDIOVASCULAR regulation and other regulatory hormones compensate for ________ effects

A

SNS / metabolic

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43
Q

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

A

mineralcorticoid / glucocorticoid / androgen

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44
Q

What are the 3 zones of the adrenal cortex

A

zona glomerulosa, zona fasciculata, zona reticularis

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45
Q

The zona glomerulosa produces ________

A

mineralcortcoids

46
Q

The zona fasciculata produces ________

A

glucocorticoids

47
Q

The zona reticularis produces __________

A

androgens

48
Q

The primary mineralcorticoid is _________

A

aldosterone

49
Q

The primary glucocorticoid is ________

A

cortisol

50
Q

The primary androgen is ________

A

androstendedione

51
Q

All of the streroid hormones (aldosterone, cortisol, androstendedione) are syntesized from ______

A

cholesterol

52
Q

Mineralcorticoids are named so because they control ________ also known as the electrolytes Na and K.

A

minerals

53
Q

Aldosterone efffects ______ and _______ balalnce and therby effect _____ _____ regulation of BP

A

salt and water / long-term

54
Q

Aldosterone effects the ______and _____ of the kidneys and causes retention of _____ and _____ and excretion of ______ and ______.

A

DCT / Collecting Ducts / sodium and water / potassium and hydrogen

55
Q

If unopposed, __________ leads to HTN, ECF expansion, hypokalemia, alkalosis

A

aldosterone

56
Q

Aldosterone works with the _______ for BP control

A

RAAS

57
Q

RAAS - in brief

A

Hypovolemia triggers kidneys to secrete renin. Through a series of steps Angiotensin II is prodcued. Angiotensin II is a potent vasoconstrictor and also stimulates secretion of aldosterone. Aldosterone causes retention of sodium and water and excretion of potassium, and also increases BP.

58
Q

Aldosterone is regulated primarily by what?

A

RAAS and potassium levels

59
Q

T/F Adreanlcorticotropic Hormone (ACTH) and sodium levels do not exert much control over the release of aldosterone?

A

TRUE

60
Q

Primary Hyperaldosteronsim AKA

A

Conn’s Syndrome

61
Q

Conn’s syndrome causes

A

Caused by aldosterone secreting tymors or hyperplasias

62
Q

Effects of Conn’s syndrome

A

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

63
Q

Diagnosis of Conn’s syndrome is made by?

A

low renin from negative feedback

64
Q

Treatment for Conn’s syndrome

A

surgically remove the tumor

65
Q

Secondary hyperaldosteronism is caused by what?

A

CHF, cirrhosis with ascites, and nephrosis

66
Q

In secondary hyperaldosteronism, ECF is lost to the extravascular space. They will be intravascularly ______ _______ despite total body volume overload, which triggers release of ______ from the kidneys. This exacerbates fluid and Na retention.

A

volume depleted / renin

67
Q

Hypoaldosteronism is from ________ insufficiency. What is this noted by?

A

adrenal / Na lost in urine and K retained.

68
Q

With adrenal insufficiency (hypoalsdosteronism), plasma volume _________ and hypotension/hyperkalemia may lead to ________ ______

A

depletion / circulatory collapse

69
Q

Glucocorticoids are named because of their effects on _____ _______

A

glucose metabolism

70
Q

Cortisol is AKA

A

hydrocortisone

71
Q

_______ is the principal glucocorticoid and is prodcued in the zona ________

A

cortisol / fasciculata

72
Q

T/F Cortisol is essential for life and regulates a variety of cardiovascular, metabolic, immunologic, and homeostatic functions

A

TRUE

73
Q

Glucocorticoids stimulate gluconeogensis. This causes formation of carbohydrate from protein by the ________. It also causes mobilization of amino acids from muscle. Muscles can become _______ in great cortisol excess.

A

liver/ weak

74
Q

Glucocorticoids ________ glucose utilization by cells and ________ blood glucose concentration

A

decrease / elevates

75
Q

The elevation of blood glucose by glucocorticoids is caused by what?

A

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

76
Q

Almost any stress (physical of nuerogenic) can cause an immediate release of ______ by the ANTERIOR PITUITARY gland followed by greatly increased secretion of ______

A

ACTH / Cortisol

77
Q

Examples that can cause ACTH release

A

trauma, infection, heat/cold, surgery, catecholamine injection

78
Q

It is unclear what benefit cortisol provides in stressful situations but is probably related to ______ of resources for immediate availability

A

mobilization

79
Q

High levels of cortisol of have ________ effects

A

anti-inflammatory

80
Q

Cortisol prevents the development of inflammation by stabilizing _______, decreasing capillary permeability, decreasing migration of WBCs into inflamed areas, and other effects. Cortisol also causes __________ of inflammation within hours to days.

A

lysosomes / resolution

81
Q

ACTH stimulates _______ secretion almost entirely

A

cortisol

82
Q

ACTH release is controlled by _______ from the _______

A

corticotropin releasing hormone (CRH) / hypothalmus

83
Q

Physiologic stress causes release of both ____ and _____

A

ACTH and CRH

84
Q

High cortisol levels cause ________ of ACTH and CRH release

A

inhibition

85
Q

Cortisol release is caused by the __________ when it senses stress

A

hypothalmus

86
Q

Cortisol helps to relieve the damaging nature of the _________ state

A

stressful

87
Q

Cortisol provides direct ______ _______ to decrease its release

A

negative feedback

88
Q

CRF, ACTH, and cortisol are released in relation to circadian rhythms with high levels in the _____________

A

morning

89
Q

ACTH secreting tumor of the pituitary

A

Cushings Disease

90
Q

caused by excessive cortisol secretion

A

cushings syndrome

91
Q

Causes for Cushing’s syndrome

A

ACTH secreting ectopic tumor, overactive hypothalamic secretion of CRH, primary glucocorticoid secreting adrenal tumor, Iatrogenic (chronic administration)

92
Q

Effect of Cushing’s syndrome on connective tissue

A

thin skin, easy bruising, stria, poor healing/collagen formation and inhibition of fibroblasts

93
Q

Effect of Cushing’s syndrome on Bone

A

inhibition of GI Ca++ absorption, decreased serum Ca++, increased PTH, decreased bone formation, increased bone resorption leading to osteoporosis

94
Q

Cushing’s effect on muscle

A

wasting, weakness, fatigability

95
Q

Cushing’s effect on Fat

A

Truncal obesity, moon faces, buffalo hump

96
Q

Cushing’s effect on Skin

A

Hirsutisim, acne from increased adrenal androgen secretion

97
Q

Cushing’s effect on Endocrine

A

impaired glucose tolerance, amenorrhea

98
Q

Cushing’s effect on Renal

A

salt/water retention, hypokalemia from mineralcorticoid activity of excess glucocorticoids

99
Q

Cushing’s effect on cardiovascular

A

HTN

100
Q

Cushing’s effect on CNS

A

euphoria, irritability, emotional lability, depression

101
Q

This results from failure to produce adrenocortical hormones (glucocorticoids and mineralcorticoids)

A

Addison’s disease

102
Q

Primary Addison’s

A

adrenal nonfunction - mostly autoimmune

103
Q

Secondary Addison’s

A

hypothalamic or pituitary nonfunction

104
Q

Causes of secondary Addison’s

A

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

105
Q

Symptoms of Addison’s dz (glucocorticoid deficiency)

A

hypoglycemia, fatigue, weakness, wt loss, anorexia, hyperpigmentation (primarily by increased ACTH), severe deteroiration to stress

106
Q

What is addisonian crisis and how is it treated?

A

Cardiovascular collapse and treated with cortisol

107
Q

Symptoms of Addison’s dz (mineralcorticoid deficiency)

A

dehydration, polyuria, hypotension, low Na, Retention of K, metabolic acidosis

108
Q

How soon can one die from Addison’s dz if untreated

A

4 days to 2 weeks

109
Q

________ doses of glucocorticoids are given in the perioperative period to patients who take chronic steroids

A

larger

110
Q

What would you give to a patient who takes chronic steroids?

A

Hydrocortisone 50-100 mg IV (adults)

111
Q

Etomidate causes profound suppression of cortisol for at least 24 hrs and can contribute to adrenal insufficiency and resultant _________. Etomidate should be used sparingly in patients with ______ shock for this reason. Etomidate has not been shown to increase mortality when used for RSI.

A

hypotension / septic / RSI

Endocrine - Summer 2019 (7 decks)

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