Final Exam Review Flashcards

1
Q

___ glands are organs that secrete hormones

A

Endocrine

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2
Q

What are (4) types of hormones?

A
  • Peptide/protein hormones
  • Catecholamines
  • Steroid hormones
  • Thyroid hormones
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3
Q

What is the most common type of hormone in the body? Examples of this type of hormone include insulin, growth hormone, and antidiuretic hormone

A

Peptide/protein hormones

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4
Q

___ hormone > 100 amino acids

A

Protein

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5
Q

___ hormone < 100 amino acids

A

Peptide

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6
Q

This type of hormone is produced by the adrenal medulla; examples = adrenaline, norepinephrine

A

Catecholamines

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7
Q

This type of hormone is secreted by the adrenal cortex; examples = cortisol, aldosterone, ovaries/testes

A

Steroid hormones

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8
Q

This type of hormone is anything derived from tyrosine; examples = T3, T4

A

Thyroid hormones

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9
Q

Peptide/protein hormones and catecholamines are ___ soluble

A

Water soluble

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10
Q

Steroid and thyroid hormones are ___ soluble

A

Fat soluble

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11
Q

___ feedback loop = the hormone itself sends the signal to STOP production/release of hormone when there is enough

A

Negative feedback loop

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12
Q

Example of a positive feedback loop = ___ hormone

A

Lutenizing hormone

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13
Q

LH and positive feedback—LH acts on the ovaries to cause secretion of ___; ___ (more/less) LH is secreted to secrete more estrogen

A

Secretion of estrogen; more LH is secreted to secrete more estrogen

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14
Q

___ = all of the chemical reactions in the body

A

Metabolism

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15
Q

___ = energy during resting conditions

A

Basal metabolic rate

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16
Q

Basal metabolic rate accounts for ___-___% of daily energy expenditure

A

50-70%

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17
Q

Basal metabolic rate ___ (increases/decreases) with age

A

Decreases

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18
Q

___ is the end product of almost all the energy released in the body

A

Heat

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19
Q

Metabolic rate is quantitatively measured in ___

A

Calories

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20
Q

The following factors ___ (increase/decrease) metabolic rate: thyroxine, testosterone, growth hormone, fever

A

Increase

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21
Q

The following factors ___ (increase/decrease) metabolic rate: inadequate thyroxine (hypothyroidism), sleep, malnutrition

A

Decrease

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22
Q

___ is responsible for temperature regulation

A

Hypothalamus

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23
Q

What specific part of the hypothalamus controls temperature regulation?* KNOW FOR BOARDS

A

Anterior hypothalamus—preoptic nuclei

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24
Q

Shivering increases O2 consumption up to ___%

A

Up to 300%

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25
Q

Hypothermia—PVR ___ (increases/decreases)

A

Increases

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26
Q

Hypothermia—renal effects = ___ = ___ (increased/decreased) plasma volume

A

Diuresis = decreased plasma volume

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27
Q

Hypothermia—cerebral O2 consumption ___ (increases/decreases); MAC ___ (increases/decreases)

A

Decreases; decreases

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28
Q

Hypothermia causes MAC to decrease ___-___% per degree C

A

5-7%

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29
Q

Hypothermia results in delayed ___

A

Emergence

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30
Q

Hypothermia ___ (increases/decreases) clotting factors/platelets

A

Decreases

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31
Q

Hypothermia ___ (increases/decreases) metabolism; ___ NMB; ___ emergence

A

Decreases metabolism; prolongs NMB; delays emergence

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32
Q

Hypothermia ___ healing; risk for infection is ___ (increased/decreased)

A

Delays healing; risk for infection is increased

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33
Q

What are the two body compartments?

A

Peripheral compartment and core compartment

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34
Q

___ compartment = limbs, skin, subcutaneous tissue; ___ of body’s heat content

A

Peripheral compartment; 1/3 of body’s heat content

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35
Q

___ compartment = major thoracic and abdominal organs + brain; ___ of body’s heat content

A

Core compartment; 2/3 of body’s heat content

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36
Q

Vasoconstriction during anesthesia will cause periphery to go down to 30-32 C to maintain core temp at 37 C—T/F?

A

True

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37
Q

___ = principle byproduct of metabolism

A

Heat

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38
Q

Shivering can increase heat production by ___%

A

300%

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39
Q

Body heat is preserved by peripheral vaso___

A

Vasoconstriction

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40
Q

What are (4) mechanisms of heat loss? (in order from greatest amount of heat loss to least)

A
  • Radiation (40%…ppt says 60%)
  • Convection (30%)
  • Conduction (20%)
  • Evaporation (10%)
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41
Q

What type of heat loss is this?—greatest amount of heat loss; amount of heat loss is determined by the difference in temperature between body/surroundings

A

Radiation

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42
Q

What type of heat loss is this?—heat loss via air currents; degree of heat loss depends on amount of body surface area exposed/airflow

A

Convection

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43
Q

What type of heat loss is this?—heat loss via direct contact (i.e.: OR table)

A

Conduction

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44
Q

What type of heat loss is this?—skin prep, open abdominal cavities, respiration

A

Evaporation

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45
Q

Anesthesia (both general and regional) inhibits peripheral vasoconstriction—T/F?

A

True

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46
Q

Biggest drop in body temperature is during the first hour after induction; there is a 1-2 degree C decrease in core temperature because of peripheral vasodilation—T/F?

A

True

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47
Q

Most heat loss occurs in proportion to exposed ___

A

Exposed body surface area

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48
Q

General anesthesia promotes vaso___, ___ (increases/decreases) metabolic rate/heat production, and ___ (increases/decreases) hypothalamic responsiveness to hypothermia

A

Vasodilation, decreases metabolic rate/heat production, and decreases hypothalamic responsiveness to hypothermia

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49
Q

NMBs prevent shivering—T/F?

A

True

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50
Q

Heat loss is more pronounced with ___ and ___ patients (think age extremes)

A

Elderly and neonatal

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51
Q

Neonatal patients have a ___ (lower/higher) body surface area based on their weight, which causes ___ (more/less) heat loss

A

Higher body surface area, causes more heat loss

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52
Q

Sweating leads to heat loss/cooling and must be prevented—T/F?

A

True

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53
Q

What is the most commonly used drug to treat post-op shivering?

A

Demerol

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54
Q

What disorder is this?—rare, usually inherited disorder of skeletal muscle; results in a hypercatabolic state…tachycardia, hypercapnia, muscle rigidity, tachyarrhythmias, metabolic acidosis

A

Malignant hyperthermia

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55
Q

Drug/dose to treat malignant hyperthermia = ___

A

Dantrolene 2.5 mg/kg every 5 minutes until symptoms subside

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56
Q

Max dose of dantrolene = ___

A

10 mg/kg

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57
Q

Even if patient had a previous uneventful surgery, they can still develop MH in the future—T/F?

A

True

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58
Q

MH triggers = ___

A

All inhalation agents + succs

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59
Q

Nitrous oxide can cause MH—T/F?

A

False! Nitrous is safe

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60
Q

Locals, propofol, non-depolarizing NMBs, benzos, and barbituates are all safe to use in patients with a history of MH—T/F?

A

True

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61
Q

___ gland = the “master gland”

A

Pituitary

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62
Q

___ = the coordinating center of the endocrine system

A

Hypothalamus

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63
Q

This organ delivers signals to the pituitary gland, and the pituitary gland releases hormones that influence other endocrine systems

A

Hypothalamus

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64
Q

Hypothalamus + pituitary gland = ___ axis

A

Hypothalamic-pituitary adrenal (HPA) axis

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65
Q

The HPA axis lives inside the BBB—T/F?

A

False—HPA axis lives OUTSIDE the BBB

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66
Q

What are the (6) main hormones secreted from the anterior pituitary gland? (FLAT PIG)

A
  • Follicle stimulating hormone
  • Lutenizing hormone
  • Adrenocorticotropic hormone
  • Thyroid stimulating hormone
  • Prolactin
  • I—ignore
  • Growth hormone
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67
Q

Pituitary gland rests in the ___ bone in area called the ___

A

Sphenoid bone in area called the sella turcica

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68
Q

What are (4) divisions of the pituitary gland?

A
  • Adenohypophysis
  • Pars intermedius
  • Pars tubularis
  • Neurohypophysis
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69
Q

Adenohypophysis = ___ pituitary; ___ (smallest/largest) part of the pituitary gland

A

Anterior pituitary; largest part of the pituitary gland

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70
Q

Pars intermedius = gone after ___

A

Fetal development

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71
Q

Pars tubularis = highly ___, no known hormones secreted

A

Vascular

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72
Q

Neurohypophysis = ___ pituitary

A

Posterior

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73
Q

Anterior vs. posterior pituitary—anterior pituitary is more of a ___ connection

A

Vascular/glandular connection

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74
Q

Anterior vs. posterior pituitary—posterior pituitary is more of a ___ system connection

A

Nervous system/glial connection

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75
Q

Posterior pituitary only secretes ___ and ___ ONLY

A

Oxytocin and antidiuretic hormone ONLY

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76
Q

Hormones secreted by the posterior pituitary are produced by the ___, transfer down nerve fibers, and are stored/released from the ___

A

Produced by the hypothalamus and stored/released from the posterior pituitary

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77
Q

Anterior pituitary is also called the ___

A

Adenohypophysis

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78
Q

Anterior pituitary is connected to the hypothalamus via a ___ network

A

Portal venous network

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79
Q

___ = capillary beds connected; this is how signals are transferred from the hypothalamus down to the anterior pituitary gland

A

Portal venous network

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80
Q

(5) anterior pituitary cell types (in order of percentage in the body):

A
  • Somatotropes (30-40%)
  • Corticotropes (20%)
  • Thyrotropes (3-5%)
  • Gonadotropes (3-5%)
  • Lactotropes (3-5%)
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81
Q

Somatotropes—___-___%; secrete ___

A

30-40% MOST ABUNDANT***; secrete growth hormone

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82
Q

Corticotropes—___%; secrete ___

A

20%; secrete ACTH

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83
Q

Thyrotropes—___-___%; secrete ___

A

3-5%; secrete TSH

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84
Q

Gonadotropes—___-___%; secrete ___ and ___

A

3-5%; secrete LH and FSH

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85
Q

Lactotropes—___-___%; secrete ___

A

3-5%; secrete prolactin

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86
Q

Posterior pituitary is AKA ___

A

Neurohypophysis

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87
Q

Posterior pituitary produces only ___ hormones

A

2

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88
Q

Posterior pituitary produces ___ and ___

A

Oxytocin and vasopressin (AKA ADH—antidiuretic hormone)…regulate uterine contractions/water balance

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89
Q

Blood supply of hypothalamus/pituitary gland—___ is supplied by the superior hypophyseal artery

A

Hypothalamus

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90
Q

Blood supply of hypothalamus/pituitary gland—___ is venous by the way of long portal vessels

A

Anterior pituitary

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91
Q

Blood supply of hypothalamus/pituitary gland—___ is supplied by the inferior hypophyseal artery

A

Posterior pituitary

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92
Q

What are two nuclei in the posterior pituitary?

A
  • Paraventricular nucleus

- Supraoptic nucleus

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93
Q

What nucleus is this?—lies above the third ventricle of the brain; produces and transports oxytocin via nerve fibers to the posterior pituitary

A

Paraventricular nucleus

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94
Q

What nucleus is this?—lies above the optic chiasm/nucleus; produces and transports ADH (vasopressin) via nerve fibers to the posterior pituitary

A

Supraoptic nucleus

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95
Q

This hormone is synthesized in the supraoptic nucleus; increases permeability of collecting ducts, increasing free water absorption

A

Vasopressin (ADH)

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96
Q

Vasopressin (ADH)—___ (increases/decreases) urine osmolality; ___ (increases/decreases) plasma osmolality; ___ (increases/decreases) ECF volume

A

Increases urine osmolality; decreases plasma osmolality; increases ECF volume

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97
Q

Vasopressin (ADH) causes contraction of vascular smooth muscle, producing a vasoconstrictive pressor effect (more prevalent in large doses)—T/F?

A

True

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98
Q

Vasopressin (ADH) acts on what (2) receptors?

A
  • V1 receptor

- V2 receptor

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99
Q

___ receptor = pressor effect; vasoconstriction; direct effect on increasing arterial BP; prevalent with extreme increases in circulating levels, i.e.: hemorrhage

A

V1

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100
Q

___ receptor = ADH effect (reabsorption of water); indirect way of increasing BP by increasing blood volume

A

V2

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101
Q

Would see an increase in vasopressin/ADH from: ___ II; ___ stimulation; ___osmolarity; ___volemia; ___tension

A

Angiotensin II (RAAS system); sympathetic stimulation; hyperosmolarity; hypovolemia; hypotension

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102
Q

Stimulus for vasopressin/ADH release: osmoreceptor in hypothalamus is activated by plasma osmolality > ___ mosm/L

A

> 290 mosm/L

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103
Q

Normal plasma osmolality = ___-___

A

285-290

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104
Q

Once plasma osmolality > 290, hypothalamus sends signals of ___

A

Thirst

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105
Q

Vasopressin release—___ (increased/decreased) ECF volume

A

Decreased

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106
Q

Vasopressin release—___ (increased/decreased) Na

A

Increased

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107
Q

Vasopressin release—___ (increased/decreased) BP

A

Decreased

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108
Q

Nicotine stimulates vasopressin release—T/F?

A

True—sympathetic stimulation

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109
Q

Nausea, pain, and stress can cause vasopressin release—T/F?

A

True

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110
Q

Positive pressure ventilation can cause vasopressin release—T/F?

A

True

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111
Q

Without ADH, urine output is ___

A

Excessive

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112
Q

Diabetes insipidus (DI)—___ thirst, ___ urine

A

Excessive thirst, dilute urine

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113
Q

___ deficiency causes DI

A

ADH deficiency

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114
Q

Two types of DI:

A
  • Central/neurogenic DI

- Nephrogenic DI

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115
Q

What type of DI is most common?

A

Central/neurogenic DI

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116
Q

___ DI is common post head injury or pituitary surgery

A

Central/neurogenic DI

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117
Q

___ DI results from the inability of the kidney to respond to ADH (i.e.: chronic renal disease, lithium toxicity, hypercalcemia, hypokalemia)

A

Nephrogenic DI

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118
Q

DI results in excretion of large amounts of ___osmotic urine with ___osmotic plasma and ___dipsia, ___uria, without hyperglycemia

A

Large amounts of hypoosmotic urine with hyperosmotic plasma and polydipsia, polyuria without hyperglycemia

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119
Q

Treatment of DI = limit ___ intake and give ___

A

Limit sodium intake and give synthetic ADH (DDAVP)

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120
Q

DI can cause ___natremia d/t excessive water loss

A

Hypernatremia

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121
Q

Hypernatremia from DI ___ (increases/decreases) MAC

A

Increases

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122
Q

Hypovolemia from DI requires ___ (increased/decreased) doses of IV agents

A

Decreased

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123
Q

Postpone elective surgery for Na > ___

A

150

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124
Q

Symptoms of ___natremia = restlessness, lethargy, hyperreflexia; can proceed to seizures, coma, death

A

Hypernatremia

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125
Q

Rapid correction of hypernatremia results in seizures, brain edema, permanent neurologic damage, and death—T/F?

A

True

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126
Q

SIADH =

A

Syndrome of inappropriate antidiuretic hormone…ADH overload

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127
Q

SIADH—autonomous release from pituitary (or tumor) causes water ___, ___natremia, ___ urine, ___osmolar plasma

A

Water retention, hyponatremia, concentrated urine, hypoosmolar (dilute) plasma

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128
Q

Causes of SIADH = CNS disorders/head trauma, SCC of lung, pulmonary infection, pituitary surgery—T/F?

A

True

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129
Q

Signs of SIADH = water ___, ___ hyponatremia, ___ edema causing CNS effects—lethargy, seizures, coma

A

Water intoxication, dilutional hyponatremia, brain edema

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130
Q

Treatment of SIADH = treat ___, fluid ___

A

The underlying cause, fluid restriction

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131
Q

What tetracycline antibiotic can be used to treat SIADH?

A

Demeclocycline—decreases the body’s responsiveness to ADH

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132
Q

Hyponatremia—usually asymptomatic until at a sodium level of ___ meq/L

A

125

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133
Q

Serious symptoms of hyponatremia result at levels below ___ meq/L

A

Below 120

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134
Q

Na > ___ safe for elective procedures

A

> 130

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135
Q

Na < ___ may lead to cerebral edema

A

< 130

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136
Q

Intraoperatively, hyponatremia causes a ___ (increase/decrease) in MAC

A

Decrease

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137
Q

Postoperatively, hyponatremia can cause ___, ___, ___ (think neuro symptoms)

A

Agitation, confusion, somnolence

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138
Q

Treatment of hyponatremia = ___% saline, ___ (sometimes used)

A

Hypertonic 3% saline, lasix sometimes used

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139
Q

Hyponatremia must be corrected slowly—recommended correction is 1-2 meq/L/hr or < 12 meq/L in 24 hours—T/F?

A

True

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140
Q

Rapid correction of hyponatremia can result in central ___

A

Central pontine myelinolysis

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141
Q

Monitor serum Na+ every ___ hours during treatment of hyponatremia

A

1-2 hours

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142
Q

Oxytocin (pitocin) is secreted from the ___ nucleus of the posterior pituitary

A

Paraventricular

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143
Q

Oxytocin (pitocin) causes ___ of the uterus during labor (and can be used to contract uterus to decrease blood loss after birth)

A

Contraction

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144
Q

Oxytocin also causes contraction of the myoepithelial cells of the ___

A

Lactating breast

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145
Q

Oxytocin/milk release is an example of a ___ loop

A

Positive-feedback

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146
Q

Pituitary tumors are often found as a result of compression on adjacent structures, such as visual changes with impingement of the optic chiasm—T/F?

A

True

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147
Q

Compression of optic chiasm from pituitary tumor can result in bitemoral hemianopsia, which is loss of ___ in both eyes

A

Peripheral vision

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148
Q

Patients undergoing pituitary resection should undergo evaluation of their hormonal function to detect either ___ or ___

A

Hypersecretion or panhypopituitarism

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149
Q

Pituitary tumors = hypersecretion of ___, ___, ___

A

GH, TSH, ACTH

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150
Q

Panhypopituitarism = ___ (high/low) levels of hormones, have to provide ___

A

Low levels of hormones, have to provide hormone replacement

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151
Q

Acromegaly = too much ___; difficult ___, ___

A

Too much GH; difficult mask, intubation

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152
Q

Hyperthyroid = too much ___; ___cardia, ___ loss

A

Too much TSH; tachycardia, weight loss

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153
Q

Cushing’s disease = too much ___; difficult ___ and ___

A

Too much ACTH; difficult airway and access

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154
Q

Panhypopituitarism = need hormone replacement with ___, ___, ___

A

Cortisol, levothyroxine, DDAVP

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155
Q

Most pituitary resection are done with ___ approach

A

Trans phenomenal

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156
Q

Patients may develop ___ d/t loss of ADH from pituitary tumor surgery; may be temporary or permanent; may be evident intraop or postop

A

DI

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157
Q

Suspect DI in patients after pituitary tumor resection with ___ urine output; confirm with urine specific gravity < ___

A

High urine output; confirm with urine specific gravity < 1.005

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158
Q

Treat DI with ___ and ___ replacement

A

DDAVP and volume replacement

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159
Q

Acromegaly = ___ hypersecretion after adolescence

A

Somatotropin/growth hormone

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160
Q

Patients with acromegaly will be difficult ___/___, have ___ (small/large) tongue and epiglottis, ___ mandible, ___ facial features

A

Difficult mask/intubation, have large tongue and epiglottis, enlarged mandible, distorted facial features

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161
Q

Patients with acromegaly will have ___ narrowing and vocal cord ___

A

Sub glottic narrowing and vocal cord enlargement

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162
Q

Patients with acromegaly, may consider downsizing ETT by ___

A

0.5

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163
Q

___ is common in patients with acromegaly

A

OSA

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164
Q

REVIEW posterior pituitary—___ secretes hormones that are transferred and stored in ___ and released when needed; only 2 hormones secreted by posterior pituitary = ___ and ___

A

Hypothalamus secretes hormones that are transferred and stored in posterior pituitary and released when needed

Only 2 hormones secreted by posterior pituitary = oxytocin and ADH (vasopressin)

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165
Q

REVIEW anterior pituitary—___ sends either releasing or inhibitor signals to anterior pituitary; AP has ___ different cell types that can release ___ different hormones in response to signals sent from hypothalamus

A

Hypothalamus; 5 different cell types; release 6 different hormones

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166
Q

Adrenal glands are located on top of the ___

A

kidneys

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167
Q

Adrenal glands are AKA the ___ glands

A

suprarenal

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168
Q

Two parts of the adrenal glands = ___ and ___

A

cortex and medulla

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169
Q

Adrenal cortex = ___ layer; makes up ___-___% of the adrenal gland; synthesizes more than ___ different types of ___ hormones

A

outer layer; makes up 80-90% of the adrenal gland; synthesizes more than 30 different types of steroid hormones (corticosteroids)

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170
Q

Adrenal medulla = ___ or ___ region; makes up ___-___% of the adrenal gland

A

core or inner region; makes up 10-20% of the adrenal gland

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171
Q

What are the (3) layers of the adrenal cortex?

A
  • Zona glomerulosa
  • Zona fasciculata
  • Zona reticularis
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172
Q

Zona glomerulosa = ___ layer

A

outermost

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173
Q

Zona fasciculata = ___ layer

A

middle layer

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174
Q

Zona reticularis = ___ layer

A

inner layer

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175
Q

Zona glomerulosa produces ___

A

mineralocorticoids, i.e.: aldosterone

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176
Q

Zona fasciculata produces ___

A

glucocorticoids, i.e.: cortisol

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177
Q

Zona reticularis produces ___

A

androgens, i.e.: DHEAS (dehydroepiandrosterone)–has similar effects to testosterone

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178
Q

Adrenal medulla lies underneath the adrenal ___; secretes ___–___% epinephrine, ___% norepinephrine

A

underneath the adrenal cortex; secretes catecholamines; secretes 80% epinephrine, 20% norepinephrine

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179
Q

Adrenal cortex mediates the stress response via the production of substances known as ___ and ___

A

mineralocorticoids and glucocorticoids

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180
Q

This zone of the adrenal cortex produces mineralocorticoids like aldosterone

A

zona glomerulosa

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181
Q

This zone of the adrenal cortex produces glucocorticoids like cortisol

A

zona fasciculata

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182
Q

This zone of the adrenal cortex produces androgens like DHEAS; it is a secondary site of androgen synthesis

A

zona reticularis

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183
Q

Aldosterone, cortisone, and testosterone are all ___ hormones; all are synthesized from ___

A

steroid hormones; all are synthesized from cholesterol

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184
Q

Mineralocorticoids = ___

A

aldosterone

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185
Q

Mineralocorticoids control minerals, AKA ___

A

electrolytes–sodium and potassium

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186
Q

Primary mineralocorticoid is ___

A

aldosterone–90%

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187
Q

Aldosterone affects ___ balance, which regulates blood pressure

A

salt/water balance

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188
Q

RAAS review–kidneys release ___ in response to hypovolemia&raquo_space; ___ is released by the liver and converts renin into ___&raquo_space; ___ is converted to ___ by ACE (which is released from the lungs)&raquo_space; ___ [potent vasoconstrictor] stimulates release of ___ from the adrenal gland&raquo_space; ___ causes retention of sodium and water, excretion of potassium, and increases BP

A

kidneys release renin in response to hypovolemia&raquo_space; angiotensinogen is released by the liver and converts renin into angiotensin I&raquo_space; angiotensin I is converted to angiotensin II by ACE (which is released from the lungs)&raquo_space; angiotensin II [potent vasoconstrictor] stimulates release of aldosterone from the adrenal gland&raquo_space; aldosterone causes retention of sodium and water, excretion of potassium, and increases BP

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189
Q

Anything that causes a drop in ECF (i.e.: hemorrhage) will cause release of ___ from the kidneys and thus kick off the ___ system

A

release of renin from the kidneys and thus kick off the RAAS system

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190
Q

Aldosterone primarily affects the principle cells of the ___ and collecting ducts of the kidneys

A

distal convoluted tubule

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191
Q

Aldosterone causes the retention of ___ and ___; excretion of ___ and ___

A

retention of sodium and water; excretion of K+ and H+

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192
Q

When aldosterone is unopposed, it leads to ___tension, extracellular fluid ___, ___kalemia, ___osis

A

hypertension (d/t sodium and water retention), extracellular fluid expansion (d/t sodium and water retention), hypokalemia (d/t K+ excretion), alkalosis (d/t H+ excretion)

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193
Q

What are two potent controllers of aldosterone secretion?–serum ___ and ___

A

serum potassium and angiotensin II

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194
Q

Primary hyperaldosteronism is AKA ___ syndrome

A

Conn’s syndrome

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195
Q

Conn’s syndrome is caused by ___ secreting tumors or hyperplasias

A

aldosterone secreting tumors or hyperplasias

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196
Q

Treatment of Conn’s syndrome is successful for tumors because they are usually unilateral–once you remove the tumor, patient is cured–T/F?

A

True

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197
Q

Patients with adrenal hyperplasia usually require pharmacological intervention with medications such as spironolactone–K+ sparing diuretic–T/F?

A

True because the excess aldosterone causes K+ excretion

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198
Q

Conn’s syndrome effects [think too much aldosterone]–___ (increased/decreased) ECF volume; ___tension; K+ ___; metabolic ___osis

A

increased ECF volume; hypertension; K+ depletion; metabolic alkalosis

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199
Q

Diagnosis of conn’s syndrome = ___ (high/low) renin from negative feedback

A

low renin–kidneys stop secreting renin in response to high levels of aldosterone

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200
Q

Treatment of conn’s syndrome = ___ or ___ management

A

surgical or medical management

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201
Q

Secondary hyperaldosteronism = excess of aldosterone ___ of the adrenal gland

A

OUTSIDE of the adrenal gland (i.e.: abdominal tumor outside of the adrenal gland)

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202
Q

In secondary hyperaldosteronism, ECF is lost to the ___; intravascularly, patients are ___ despite total volume ___; this triggers release of ___ by kidneys; release of ___ exacerbates fluid/sodium retention

A

ECF is lost to the extravascular space; intravascularly, patients are volume depleted despite total volume overload; this triggers release of renin by kidneys; release of renin exacerbates fluid/sodium retention

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203
Q

In primary and secondary hyperaldosteronism, want to restrict ___ and ___

A

fluids and sodium

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204
Q

___ (low/high) potassium levels in primary and secondary hyperaldosteronism can cause muscle weakness and ___ (increase/decrease) sensitivity to NMBs

A

low potassium levels in primary and secondary hyperaldosteronism can cause muscle weakness and increase sensitivity to NMBs

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205
Q

Hypoaldosteronism = adrenal ___

A

insufficiency

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206
Q

Hypoaldosteronism–___ lost in the urine, ___ retained; plasma volume ___ (increases/decreases); ___tension and ___kalemia may lead to circulatory collapse

A

Na+ lost in the urine, K+ retained; plasma volume decreases; hypotension and hyperkalemia may lead to circulatory collapse

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207
Q

Glucocorticoids = ___

A

cortisol

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208
Q

Cortisol is also called ___

A

hydrocortisone

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209
Q

___ is the principle glucocorticoid (95%) and is produced in the zona ___

A

cortisol is the principle glucocorticoid and is produced in the zona fasciculata

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210
Q

HPA axis and release of cortisol–hypothalamus sends ___ releasing hormone to the ___; ___ pituitary releases ___ to stimulate the adrenal glands to release ___ during stress; when levels are high, the negative feedback loop sends signals back to the hypothalamus to suppress its release

A

hypothalamus sends corticotropin-releasing hormone to the anterior pituitary; anterior pituitary releases ACTH to stimulate the adrenal glands to release cortisol during stress

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211
Q

___ hormone stimulates cortisol secretion almost entirely

A

adrenocorticotropic hormone (ACTH)

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212
Q

ACTH release is controlled by ___ releasing hormone from the ___

A

corticotropin releasing hormone from the hypothalamus

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213
Q

Physiologic stress causes release of both ___ and ___

A

ACTH and CRH

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214
Q

High cortisol levels cause ___ of ACTH and CRH release (negative feedback)

A

inhibition

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215
Q

CRH, ACTH, and cortisol are released in relation to circadian rhythms, with highest levels in the morning to change from a sleep to waking period–T/F?

A

True

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216
Q

Effects of glucocorticoids [cortisol]–stimulate ___neogenesis; ___ (increases/decreases) glucose utilization by cells; ___ (increases/decreases) blood glucose concentration

A

stimulate gluconeogenesis; decreases glucose utilization by cells; increases blood glucose concentration

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217
Q

High levels of cortisol have ___ effects

A

anti-inflammatory

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218
Q

Cortisol ___ healing and is useful in ___ processes, ___ reactions, ___, and organ ___

A

cortisol enhances healing and is useful in autoimmune processes (i.e.: lupus, RA, inflammatory bowel diseases like Crohn’s), allergic reactions, asthma, and organ transplant

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219
Q

Very high doses of cortisol are often used to assist in preventing organ rejection–T/F?

A

True

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220
Q

Almost any stress (physical or neurogenic) can cause an immediate release of ACTH by the anterior pituitary gland, followed by greatly increased secretion of cortisol–T/F?

A

True

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221
Q

The adrenal medulla is ___ connected to the sympathetic nervous system via ___ nerve fibers

A

directly connected to the SNS via ventral nerve fibers

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222
Q

Short-term stress response is a very ___ response; adrenal ___ releases catecholamines

A

very rapid response; adrenal medulla releases catecholamines–epi and norepi

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223
Q

Long-term stress response is a ___ response; adrenal ___ releases ___corticoids and ___corticoids

A

slower response; adrenal cortex release mineralocorticoids (aldosterone) and glucocorticoids (cortisol)

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224
Q

Short-term stress response–___ (increased/decreased) heart rate; ___ (increased/decreased) BP; liver converts glycogen to ___ and releases it into blood; ___ of bronchioles; ___ (increased/decreased) digestive system activity/urine output; ___ (increased/decreased) metabolic rate

A

increased heart rate; increased BP; liver converts glycogen to glucose and releases it into blood; dilation of bronchioles; decreased digestive system activity/urine output; increased metabolic rate

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225
Q

Long-term stress response–retention of ___ and ___ by kidneys; ___ (increased/decreased) blood volume and BP; proteins/fats converted to ___ or broken down for energy; ___ (increased/decreased) blood glucose; ___ of immune system

A

retention of sodium and water by kidneys; increased blood volume and BP; proteins/fats converted to glucose or broken down for energy; increased blood glucose; suppression of immune system

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226
Q

Cushing’s syndrome–caused by excessive ___ secretion

A

cortisol

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227
Q

Cushing’s syndrome causes can be ___ dependent or ___ dependent

A

ACTH dependent or non-ACTH dependent

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228
Q

Causes of Cushing’s syndrome–ACTH secreting ectopic tumor (most often located in the ___ as ___); overactive hypothalamic secretion of ___; primary glucocorticoid secreting ___ tumor

A
  • ACTH secreting ectopic tumor (most often located in the lung as SCC)
  • overactive hypothalamic secretion of corticotropin-releasing hormone
  • primary glucocorticoid secreting adrenal tumor
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229
Q

What is the most common cause of Cushing’s syndrome?

A

Iatrogenic–from chronic administration of glucocorticoids

230
Q

Cushing’s syndrome may make patient more sensitive to ___, so use conservative approach

A

NMBs

231
Q

___tension is very common in Cushing’s syndrome

A

Hypertension

232
Q

Cushing’s syndrome and anesthesia considerations–___ is common in these patients

A

OSA

233
Q

Cushing’s syndrome and anesthesia considerations–___ is often difficult d/t excess fat deposits not only on the head/neck, but also on the upper back

A

intubation

234
Q

Cushing’s syndrome and anesthesia considerations–___ becomes difficult d/t fat deposits on upper back

A

positioning

235
Q

Cushing’s syndrome and anesthesia considerations–patients often have ___ skin/___ bones–careful positioning is imperative to prevent skin breakdown and pathologic fractures with any mild trauma

A

patients often have frail skin/brittle bones

236
Q

Cushing disease is caused by ACTH secreting tumor of the ___ gland

A

pituitary gland

237
Q

In Cushing disease, ___ is the primary cause

A

pituitary

238
Q

The term Cushing’s syndrome is used to describe all causes of cortisol excess, while Cushing disease specifically relates to the ___ as the primary cause

A

pituitary–pituitary tumor is releasing too much ACTH

239
Q

Addison’s disease results from failure to produce ___ hormones

A

adrenocortical hormones–glucocorticoids and mineralocorticoids

240
Q

Primary Addison’s disease = ___ non-function, destruction of the ___ gland, mostly auto___

A

adrenal non-function, destruction of the adrenal gland, mostly autoimmune

241
Q

What are (3) of the most common causes of primary Addison’s disease?

A
  • TB
  • AIDS
  • Fungal infections
242
Q

Treatment of primary Addison’s disease = replace ___ deficiency

A

replace glucocorticoid/mineralocorticoid deficiency

243
Q

In primary Addison’s disease, the pituitary-adrenal axis stays intact–T/F?

A

True

244
Q

Secondary Addison’s disease is caused by ___ or ___ dysfunction

A

hypothalamic or pituitary dysfunction (d/t chronic glucocorticoid therapy or removal of pituitary tumor)

245
Q

Nearly 100% of patients with glucocorticoid deficiency will experience ___

A

anorexia

246
Q

Symptoms of glucocorticoid deficiency in Addison’s disease: ___glycemia; ___; ___ness; weight ___; ___pigmentation (primarily from increased ACTH); severe ___ in response to stress

A

hypoglycemia; fatigue; weakness; weight loss; hyperpigmentation; severe deterioration in response to stress

247
Q

Symptoms of mineralocorticoid deficiency in Addison’s disease: ___hydration; ___uria; ___tension; ___ Na; ___ K; metabolic ___osis

A

dehydration; polyuria; hypotension; low Na; high K; metabolic acidosis

248
Q

Addisonian crisis = ___ collapse

A

CV collapse

249
Q

Treat addisonian crisis with ___

A

cortisol

250
Q

If addisonian crisis is left untreated, death may result in 4 days to 2 weeks–T/F?

A

True

251
Q

Treatment of Addison’s disease, primary or secondary = ___ + ___

A

glucocorticoids + mineralocorticoids

252
Q

Patients who are on chronic steroids need a dose before surgery; periop shock or death can occur if steroids are not given d/t adrenal insufficiency–T/F?

A

True

253
Q

Patients on chronic steroids can’t increase their cortisol release in response to stress (i.e.: hypotension during surgery), and CV collapse can occur–T/F?

A

True

254
Q

Minor surgery requires stress dose steroids–T/F?

A

False–minor surgery typically does NOT require stress dose steroids

255
Q

Moderate surgeries often receive ___ mg ___

A

50 mg hydrocortisone

256
Q

Major surgeries receive ___ mg ___ with tapering

A

100 mg hydrocortisone with tapering

257
Q

Etomidate is an induction drug used for hemodynamically ___ patients

A

hemodynamically unstable

258
Q

Etomidate causes profound suppression of ___ for at least 24 hours and can contribute to ___ and resultant ___tension

A

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

259
Q

Because etomidate can cause adrenal insufficiency, it should be used sparingly in patients with ___

A

septic shock

260
Q

The adrenal medulla is connected ___ to the sympathetic nervous system via nerves; the ___ portion of the spinal cord goes directly into the adrenal medulla to stimulate the release of epi/norepi

A

directly; ventral portion

261
Q

The adrenal medulla bridges the ___ and ___ nervous systems

A

endocrine and sympathetic nervous systems

262
Q

Catecholamines are made by ___ cells in the adrenal medulla

A

chromaffin cells

263
Q

All catecholamines are derived from ___

A

tyrosine

264
Q

The synthesis of norepinephrine begins with hydroxylation of ___ to ___

A

tyrosine to dopa

265
Q

___ is the principle product of the adrenal medulla

A

Epinephrine

266
Q

Epinephrine is only made in the ___

A

adrenal medulla

267
Q

Epinephrine accounts for nearly ___% of the adrenal medulla’s output; the other 20% is ___

A

80%; other 20% is norepinephrine

268
Q

The enzyme Phenylethanolamine N-Methyltransferase (PNMT) is the enzyme responsible for the transformation of ___ into ___

A

transformation of norepinephrine into epinephrine

269
Q

Adrenal medulla = modified ___ ganglion

A

modified sympathetic ganglion

270
Q

Preganglionic sympathetic neuron [in the sympathetic nervous system/spinal cord] is directly connected to the ___

A

adrenal medulla

271
Q

The ___ neuron is located directly inside the adrenal medulla

A

postganglionic neuron

272
Q

Adrenal medulla houses the ___ nerve

A

postganglionic nerve

273
Q

Epinephrine and norepinephrine both have strong ___ effects, which results in arterial vasoconstriction

A

strong alpha-1 effects

274
Q

Epinephrine has stronger ___ effects, which increases ___ and ___ more

A

stronger beta-1 effects, which increases heart rate and contractility

275
Q

Epi affects every alpha/beta receptor–alpha-1, alpha-2, beta-1, beta-2–T/F?

A

True

276
Q

Norepi has minimal effects on ___ receptors

A

beta-2 receptors

277
Q

___ is the enzyme necessary for conversion of norepinephrine to epinephrine

A

PNMT–phenylethanolamine N-methyltransferase

278
Q

PNMT expression is influenced by ___, which helps account for their role in affecting blood pressure

A

glucocorticoids (cortisone)

279
Q

___ is the only important endocrine disease associated with the adrenal medulla

A

pheochromocytoma

280
Q

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

A

pheochromocytoma

281
Q

Pheochromocytoma is a tumor that makes ___ in an unregulated fashion

A

catecholamines

282
Q

Symptoms of pheochromocytoma–paroxysmal ___

A

paroxysmal hypertension

283
Q

Paroxysmal hypertension = ___ and ___ high blood pressure

A

episodic and volatile high BP

284
Q

Most of the time with pheochromocytoma, HTN is ___, but it can exist paroxysmally

A

HTN is constant

285
Q

During true paroxysmal HTN, BP can increase to extremely high levels, potentially causing stroke or MI–T/F?

A

True

286
Q

Most tumors in pheochromocytoma are solitary tumors localized to a single adrenal gland (mostly to the right)–T/F?

A

True

287
Q

Of pheochromocytoma tumors that are extra-adrenal (10%), 95% are in the ___

A

abdomen

288
Q

Urinary ___ levels help to make the diagnosis of pheochromocytoma, as both ___ and ___ are degraded to this

A

Urinary Vannilylmandelic acid (VMA), as both epi and norepi are degraded to this

289
Q

What enzyme breaks down catecholamines epi and norepi to VMA?

A

COMT–catechol-O-methyltransferase

290
Q

What is the other enzyme that breaks down epi/norepi, but is less important than COMT?

A

MOA–monoamine oxidase

291
Q

Management of pheochromocytoma–establish ___ block before ___ block to prevent ___

A

alpha block before beta block to prevent unopposed alpha mediated vasoconstriction/accelerated HTN

292
Q

Alpha blockers (phenoxybenzamine or prazosin) should be started ___-___ days prior to surgery to normalize BP

A

10-14 days

293
Q

Phenoxybenzamine is a ___-acting alpha blocker (lasts for ___-___ hours) and is ___-selective (blocks alpha 1 and 2)

A

long-acting alpha blocker (lasts for 24-48 hours) and is non-selective

294
Q

Prazosin is a ___ alpha blocker

A

selective–blocks alpha 1 only

295
Q

If you beta block before alpha block is established, it can lead to immediate ___ shock, so always give alpha blockade before beta blockade

A

immediate cardiogenic shock

296
Q

If patient comes into ER with pheochromocytoma and alpha blocking therapy isn’t possible, ___ can be used during induction of anesthesia; ___ such as Cardene have also been used and titrated to effect

A

nitroprusside can be used; calcium channel blockers such as Cardene have also been used

297
Q

___-acting vasoactive agents are desirable during adrenalectomy, as paroxysms of both hypotension and hypertension are common when the tumor is manipulated or removed

A

Short-acting

298
Q

Avoid ___-releasing agents, ___, and ___ because these agents provoke pheochromocytoma

A

histamine-releasing agents, metoclopramide, and glucagon

299
Q

Pheochromocytoma–when the tumor is removed, abrupt ___ may occur

A

hypotension

300
Q

When tumor is removed, treat hypotension with ___ and ___

A

IVF and vasopressors

301
Q

Adrenalectomy–catecholamine levels return to normal several days after surgery, and approximately 75% of patients become normotensive within ___ days postop

A

10 days

302
Q

Medullary hyposecretion–physiologic effect is not a serious problem; the sympathetic nervous system compensates for CV regulation; and other regulatory hormones compensate for metabolic effects–T/F?

A

True

303
Q

___ = glands secreting digestive juices into the duodenum

A

Acini

304
Q

(4) cell types in the islet of langerhans:

A
  • Alpha cells
  • Beta cells
  • Delta cells
  • Pancreatic polypeptide cells
305
Q

___ cells secrete glucagon

A

alpha

306
Q

___ cells secrete insulin

A

beta

307
Q

__ cells secrete somatostatin

A

delta

308
Q

___ is a hormone associated with energy abundance and storage of this excess energy

A

Insulin

309
Q

Insulin causes carbohydrates to be stored as ___ in muscle and liver; excess carbs that cannot be converted to glycogen are converted to ___ and are stored in ___; insulin promotes uptake of amino acids and their conversion to ___

A

carbs to be stored as glycogen in muscle and liver; excess carbs that cannot be converted to glycogen are converted to fat and are stored in adipose; insulin promotes uptake of amino acids and their conversion to protein

310
Q

Insulin release is stimulated by ___ (low/high) blood glucose, amino acids, beta-keto acids, glucagon, acetylcholine, intestinal hormones, beta agonists

A

high blood glucose

311
Q

Insulin release is inhibited by ___ (low/high) blood glucose, fasting, glucagon, cortisol, catecholamines (alpha-agonists), growth hormone, somatostatin

A

low blood glucose

312
Q

Catecolamines ___ (stimulate/inhibit) insulin release

A

inhibit

313
Q

Plasma half-life of insulin is ___ to ___ minutes

A

6 to 7 minutes

314
Q

Neurons are ___ to glucose

A

permeable

315
Q

___ is the body’s key hormone controlling plasma glucose removal

A

insulin

316
Q

Insulin is released when energy intake exceeds ___ requirements

A

usage

317
Q

Insulin allows energy from glucose to be stored as ___, ___, and ___

A

glycogen, structural proteins, and fat

318
Q

Insulin release begins at ___ mg/dl; max response at ___-___ mg/dl

A

100 mg/dl; max response at 400-600 mg/dl

319
Q

Rapid rise in insulin released is matched by rapid turn-off of insulin once glucose is reduced–T/F?

A

True

320
Q

___ is secreted by alpha cells of the islets of Langerhans when blood glucose levels fall

A

glucagon

321
Q

Glucagon has effects that oppose the effects of ___

A

insulin

322
Q

Glucagon ___ (increases/decreases) blood glucose concentration and can cause ___glycemia

A

increases blood glucose concentration and can cause hyperglycemia

323
Q

Glucagon enhances ___ strength

A

heart

324
Q

Glucagon release is stimulated by ___glycemia, beta-adrenergic ___, ___

A

fasting hypoglycemia, beta-adrenergic stimulation, exercise

325
Q

Exercise causes release of glucagon not d/t ___glycemia, but as a response to increased circulating ___

A

not d/t hypoglycemia, but as a response to increased circulating amino acids

326
Q

Glucagon release is stimulated by ___kinin, ___in, and ___ol

A

cholecystokinin, gastrin, cortisol

327
Q

Surgery stimulates the release of ___

A

glucagon

328
Q

Glucagon is inhibited by ___ (low/high) glucose levels, ___statin, ___ acids, ___ones, and ___

A

high glucose levels, somatostatin, free fatty acids, ketones, and insulin

329
Q

Antidote for beta blocker overdose = ___

A

glucagon–has been used to improve cardiac isotropy to overcome a beta blocked heart; basically overpowers beta receptors

330
Q

What is this?–disorder of metabolism causing excessive thirst and the production of large quantities of urine

A

Diabetes

331
Q

What is this?–a syndrome of impaired carbohydrate, fat, and protein metabolism caused by either a lack of insulin or a decreased sensitivity of tissues to insulin

A

Diabetes

332
Q

Type ___ diabetes is caused by a lack of insulin secretion

A

I

333
Q

Type ___ diabetes is caused by decreased sensitivity of the tissues to insulin (insulin resistance)

A

II

334
Q

Insulin insufficiency leads to ___glycemia from decreased cell entry, ___ (increased/decreased) gluconeogenesis, and ___ release from the liver

A

hyperglycemia, increased gluconeogenesis, and glucose release from the liver

335
Q

Glucose is reabsorbed by the kidney until about ___ mg/dl

A

180

336
Q

Acute symptoms of diabetes–___uria, ___dipsia, ___phagia and weight ___, CNS ___/___, visual ___

A

polyuria, polydipsia, polyphagia and weight loss, CNS irritability/confusion, visual disturbances

337
Q

Type 1 DM is caused by destruction of ___ islet cells, resulting in loss of insulin release

A

destruction of beta islet cells

338
Q

Type 1 DM can be caused by ___ infections or ___ disorders

A

viral infections or autoimmune disorders

339
Q

Type 1 DM–___ plays a role in determining susceptibility of beta cells to insults

A

heredity

340
Q

Type 2 DM is caused by greatly diminished sensitivity of target tissues to metabolic effects of ___

A

insulin

341
Q

High levels of keto acids are NOT usually present in type ___ diabetes

A

2

342
Q

Plasma insulin is ___ in type 2 DM

A

elevated–levels still insufficient for regulation, beta-cells become exhausted in some patients

343
Q

Most patients with type 2 DM are ___ (80%), ___

A

obese–80%, sedentary

344
Q

DM diagnosis–A1C >/= ___

A

> /= 6.5%

345
Q

DM diagnosis–fasting plasma glucose (FPG) >/= ___ mg/dl

A

> /= 126 mg/dl

346
Q

DM diagnosis–2-hr plasma glucose > ___ mg/dl during oral glucose tolerance test

A

> 200 mg/dl

347
Q

DM diagnosis–random plasma glucose >/= ___ mg/dl in patient with symptoms of ___glycemia or ___glycemic crisis

A

> /= 200 mg/dl in patient with symptoms of hyperglycemia or hyperglycemic crisis

348
Q

___ is commonly used to diagnose DM

A

Hgb A1C

349
Q

___ is used to gauge how well managed a person’s diabetes is

A

Hgb A1C

350
Q

Hgb A1C reflects average blood sugar level over approximately ___ months (RBC lifespan)

A

3

351
Q

Normal Hgb A1C levels are between ___-___%

A

4-5.6%

352
Q

The higher the Hgb A1C, the ___ (lower/higher) the risks of developing complications related to diabetes

A

higher

353
Q

Consensus–BS > ___ should be treated

A

> 200

354
Q

Plan surgery in diabetics as ___ case of the day to prevent prolonged fasting

A

1st

355
Q

Oral hypoglycemics are held day of surgery to prevent hypoglycemia until oral intake is restarted–T/F?

A

True

356
Q

Insulin therapy should balance adequate glucose control with the avoidance of hypoglycemia–T/F?

A

True

357
Q

Type 1 diabetics ___ (should/should not) continue basal insulin administration to avoid ketoacidosis

A

should continue

358
Q

Patients on insulin pumps may be managed by continuing the pump for short operations or changing over to ___

A

IV insulin infusions

359
Q

Oral hypoglycemic agents are used as adjuncts to ___ therapy and ___ for treating Type 2 diabetics

A

diet therapy and exercise

360
Q

Type 2 diabetics target A1C < ___% or < ___% in older adults without hypoglycemia

A

< 7% or < 8%

361
Q

These drugs decrease hepatic glucose production, increase peripheral insulin uptake; example = metformin (glucophage)

A

Biguanides

362
Q

Biguanides can cause lactic ___ in surgical patients, especially patients with liver/kidney disease and/or CHF; biguanides can be used to treat ___ disease

A

lactic acidosis in surgical patients; can be used to treat polycystic ovarian disease

363
Q

___ have a hypoglycemia risk because they increase insulin secretion from the pancreas; examples = glimepiride, glipizide, glyburide

A

sulfonylureas

364
Q

___ are similar to sulfonylureas in that they increase insulin production and thus carry a hypoglycemia risk; example = repaglinide (prancing)

A

Meglitinides

365
Q

Thiazolidinediones (i.e.: tazone, pioglitazone) decrease glucose production in liver, decrease insulin resistance; there was a 2010 CHF black box warning that has been lifted; if patient has class III or IV CHF, probably shouldn’t give it–T/F?

A

True

366
Q

Alpha-glucosidase inhibitors (i.e.: acarbose) slow ___ and ___ of carbs from GI tract; these should be avoided in ___ diseases

A

slow digestion and absorption of carbs from GI tract; these should be avoided in intestinal diseases

367
Q

___ insulin is most often used for IV

A

regular insulin

368
Q

Long-acting insulin should be ___% day of surgery

A

50%

369
Q

Hold ___-acting and ___-acting insulin day of surgery

A

short-acting and regular-acting

370
Q

Greatest risk with insulin given day of surgery is ___

A

hypoglycemia

371
Q

___ is added to some insulins to prolong their effect

A

Protamine

372
Q

Must be cautious when giving ___ to reverse heparin; monitor patient for ___ reaction

A

must be cautious when giving protamine to reverse heparin; monitor patient for hypersensitivity reaction

373
Q

DKA occurs in type ___ diabetics with ___ insulin levels

A

occurs in type 1 diabetics with profoundly low insulin levels

374
Q

Primary features of DKA = ___hydration, ___osis, ___ depletion

A

dehydration, acidosis, electrolyte depletion

375
Q

In DKA, blood glucose ___ (increases/decreases) without effective insulin, leading to osmotic ___ and lyte ___

A

blood glucose increases without effective insulin, leading to osmotic diuresis and lyte losses

376
Q

DKA–dehydration up to ___-___ L

A

4-6L

377
Q

DKA–loss of up to ___% body K+

A

10%

378
Q

Symptoms of DKA–___/___; ___uria; ___dipsia; ___phagia; ___exia; ___ changes; ___ breathing; ___ halitosis

A

nausea/vomiting; polyuria; polydipsia; polyphagia; anorexia; orthostatic changes; Kussmaul breathing; acetone halitosis

379
Q

LOC in DKA is related to patient’s ___, not acidosis

A

osmolality

380
Q

Treatment of DKA = massive ___, ___ replacement, ___ therapy

A

massive fluid resuscitation, electrolyte replacement, insulin therapy

381
Q

Patients with DKA will often present with severe ___kalemia

A

hyperkalemia

382
Q

Nonketotic hyperosmolar state occurs in type ___ diabetics; same precipitating events as DKA with very high blood ___

A

type 2; very high blood glucose

383
Q

Primary features of nonketotic hyperosmolar state–severe ___glycemia; ___hydration; severe ___osmolar state (Na down 1.6/100 glucose); and lack of ___

A

severe hyperglycemia; dehydration; severe hyperosmolar state; and lack of ketoacidosis

384
Q

Symptoms of nonketotic hyperosmolar state–___osis from ___viscosity; neuro signs–___, ___, ___

A

thrombosis from hyper viscosity; neuro signs–confusion, seizures, coma

385
Q

Treatment of nonketotic hyperosmolar state = ___ resuscitation; add ___ to IVF when BG ~250 to avoid precipitous drop and cerebral edema; K+, phosphate, insulin if needed

A

fluid resuscitation; add glucose to IVF

386
Q

Hypoglycemia has profound effects on ___

A

CNS–confusion, convulsions, coma

387
Q

Early response to hypoglycemia–liver ___ breakdown

A

liver glycogen breakdown

388
Q

Late response to hypoglycemia–___ stimulation, ___ release

A

sympathetic stimulation, epi release

389
Q

Very late response to hypoglycemia–___ and ___ secreted

A

growth hormone and cortisol secreted

390
Q

___ = beta cell adenoma

A

insulinoma

391
Q

Insulin shock = coma under ___ mg/dl

A

20 mg/dl

392
Q

Treatment of insulin shock = ___

A

glucose, glucagon, epi

393
Q

Hypoglycemic shock develops in range of ___-___ mg/dl

A

20-50 mg/dl

394
Q

Hypoglycemic shock–progressive nervous irritability leads to ___, ___, and ___

A

fainting, seizures, and coma

395
Q

Hypoglycemic shock–brain uses glucose only if available, but can use ___ with difficulty in times of stress

A

fats/ketones

396
Q

Treat hypoglycemic shock with ___ and infusion of ___

A

D50 and infusion of D5

397
Q

Prolonged hypoglycemia leads to brain cell death and apoptosis–T/F?

A

True

398
Q

Thyroid gland regulates ___

A

metabolic rate

399
Q

Thyroid blood supply comes from ___ and ___ thyroid arteries

A

superior and inferior

400
Q

The thyroid is a very ___ organ

A

vascular

401
Q

Thyroid is ___ shaped

A

butterfly

402
Q

Thyroid is one of the ___ endocrine glands

A

largest

403
Q

Thyroid consists of two ___ and an ___

A

two lobes and an isthmus–isthmus connects the R and L thyroid glands/lobes

404
Q

Thyroid produces what (3) thyroid hormones:

A
  • Thyroxine (T4)
  • Triiodothyronine (T3)
  • Reverse T3 (rT3)–inactive
405
Q

1 mg of iodine is required each week to form normal amounts of thyroid hormone–T/F?

A

True

406
Q

___ is absorbed from our diets and then converted to iodide before it is used by the thyroid

A

Iodine

407
Q

When adequate iodine is not available, the thyroid ___ produce the hormones

A

cannot

408
Q

___ is the functional unit of the thyroid

A

follicle

409
Q

___ is where thyroid hormone is stored; stores enough thyroid hormone to last ___-___ months

A

colloid; stores enough thyroid hormone to last 2-3 months

410
Q

Since the colloid stores enough thyroid hormone to last 2-3 months, if you had a complete loss of thyroid hormone production, the physiologic effects wouldn’t be seen for several months–T/F?

A

True

411
Q

TSH is secreted from the ___ pituitary and attaches itself to the ___ of the follicle

A

TSH is secreted from the anterior pituitary; attaches itself to the outside of the follicle

412
Q

___ is very important for the thyroid to create its hormones and convert ___ (active) to ___ (inactive)

A

Iodine; convert T4 (active) to T3 (inactive)

413
Q

T4 = ___

A

thyroxine

414
Q

T3 = ___

A

triiodothyronine

415
Q

___ and ___ are the most important thyroid hormones for metabolic control

A

T4 and T3

416
Q

The secretion of T4 from the thyroid is ___-___ mcg/day

A

80-100 mcg/day

417
Q

The thyroid secretes ___% thyroxine (T4) and ___% triiodothyronine (T3)

A

93% T4, 7% T3

418
Q

Nearly all T4 is deiodinated to T3 in the tissues–T/F?

A

True

419
Q

T3 is ___x more potent than T4 but is more ___ and cleared more ___ (less protein bound)

A

T3 is 4x more potent than T4 but is more scarce and cleared more rapidly (less protein bound)

420
Q

The thyroid directly secretes ___, which is converted to ___

A

secretes T4, which is converted to T3

421
Q

___ mostly acts as a hormone precursor or vehicle for ___

A

T4 mostly acts as a hormone precursor or vehicle for T3

422
Q

Most of the thyroid hormone effects come from ___

A

T3

423
Q

Synthroid = synthetic ___

A

T4

424
Q

___ is heavily protein-bound; 99% bound to plasma proteins (i.e.: albumin); has a very ___ half-life

A

T4; has a very long half-life

425
Q

___ has a much shorter half-life and controls most of the effects of the thyroid hormones

A

T3

426
Q

TRH is released by the ___

A

hypothalamus

427
Q

TRH causes release of ___ by the anterior pituitary

A

thyroid-stimulating hormone

428
Q

TSH causes release of ___ hormones (both ___ and ___) from the thyroid gland

A

thyroid hormones (both T3 and T4)

429
Q

Only ___ thyroid hormone is active

A

free

430
Q

Over ___% of thyroid hormone is bound to protein–thyroid binding globulin (TBG) or lesser extent albumin

A

99%

431
Q

___ is more metabolically active

A

T3

432
Q

Physiologic effects of the thyroid come from ___

A

T3

433
Q

Because of the high amount of protein binding and slow release into cells, T4 half-life is ___-___ days, T3 half-life is ~___ hours

A

T4 half-life is 6-7 days, T3 half-life is ~24 hours

434
Q

It is likely that all cells in the body are targets for thyroid hormones–T/F?

A

True

435
Q

Thyroid hormone net effect is a widespread increase in ___ activity, ___ production, and ___ consumption in nearly all cells

A

increase in metabolic activity, heat production, and oxygen consumption

436
Q

Thyroid hormone causes vaso___ from ___ (increased/decreased) cellular O2 consumption; ___ (increases/decreases) blood flow to most tissues

A

causes vasodilation from increased cellular O2 consumption; increases blood flow to most tissues

437
Q

Muscles can become weak when thyroid hormone is excessive d/t protein catabolism–T/F

A

True

438
Q

___ is a condition where the thyroid cannot make adequate TH; it is the most common thyroid disorder; women>men

A

Hypothyroidism

439
Q

Primary hypothyroidism–___% of most cases

A

95%

440
Q

Primary hypothyroidism–___ TSH, yet T3 and T4 are ___ because of problems with the thyroid gland

A

elevated TSH, yet T3 and T4 are not produced because of problems with the thyroid gland

441
Q

Primary hypothyroidism is most commonly due to ___; most often occurs in ___; can be associated with other auto-immune disorders

A

most commonly due to autoimmune Hashimoto’s thyroiditis; most often occurs in middle-aged females

442
Q

___ inhibits the release of TH and can cause hypothyroid

A

Lithium

443
Q

Secondary hypothyroidism–___% of cases; inadequate T3, T4 due to ___ not being released from the pituitary

A

5% of cases; inadequate T3 and T4 due to TSH not being released from the pituitary

444
Q

Tertiary hypothyroidism–

A

< 5% of cases; inadequate T3, T4 due to thyrotropin releasing hormone (TRH) from hypothalamus

445
Q

Hypothyroidism that occurs in infancy leads to ___ and ___ (cretinism)

A

mental retardation and growth deficits (cretinism)

446
Q

The most severe form of hypothyroidism is ___

A

myxedema coma

447
Q

Myxedma coma is triggered by ___, ___, exposure to ___, ___

A

illness, infection, exposure to cold, medicines

448
Q

Symptoms of myxedema coma include ___, ___ (increased/decreased) breathing, ___ (increased/decreased) blood sugar, ___ (increased/decreased) blood pressure, and ___ (increased/decreased) temperature

A

coma, decreased breathing, decreased blood sugar, decreased blood pressure, and decreased temperature

449
Q

___ is the standard test for thyroid gland function

A

Serum T4 assay

450
Q

Total T4 is ___ in 90% of people with hyperthyroidism

A

elevated

451
Q

Total T4 is ___ in 85% of people with hypothyroidism

A

low

452
Q

Blood levels of TSH are ___ in primary hypothyroidism

A

high

453
Q

Treatment of hypothyroid centers on replacing ___ until thyroid hormone levels normalize

A

replacing the thyroid hormone that is lacking until thyroid hormone levels normalize

454
Q

___ is the most commonly used medicine to treat hypothyroid

A

Levothyroxine (Synthroid)–synthetic T4

455
Q

Elective surgery should be postponed until ___ state is achieved, but this is not always done

A

euthyroid

456
Q

Hypothyroid and anesthesia–be aware of the ___ possibility

A

“crash on induction”

457
Q

Want to give ___ for induction for patients with hypothyroid

A

sympathomimetics

458
Q

___ is frequently used on induction for patients with hypothyroid; helps prevent drops in BP

A

Ketamine

459
Q

___ agents not recommended in patients with hypothyroidism d/t the sensitivity of the myocardium to depression

A

Volatile

460
Q

___onium/___onium have vagolytic/sympathomimetic effects

A

Pancuronium/rocuronium

461
Q

___ is a condition of thyroid gland overactivity

A

Hyperthyroidism

462
Q

___ is inflammation of the thyroid which causes release of excessive hormone but not increased production

A

Thyroiditis

463
Q

___ is an oversupply of thyroid hormones on peripheral tissues (another name for hyperthyroidism)

A

Thyrotoxicosis

464
Q

Staring gaze in hyperthyroidism = ___

A

exophthalmos

465
Q

Most common cause of hyperthyroidism is ___ (60-90% of cases), which is an autoimmune disease

A

Grave’s disease

466
Q

Grave’s disease–autoantibodies activate the ___ receptor, causes mutlinodular ___

A

TSH, causes multi nodular goiter

467
Q

Treatment of hyperthyroidism involves initial temporary use of ___ and possibly late use of permanent ___ or ___ therapy

A

initial temporary use of suppressive medicines and possibly late use of permanent surgical or radioisotope therapy

468
Q

Two antithyroid drugs that inhibit production of TH–___ and ___

A

methimazole and propylthiouracil (PTU)

469
Q

Antithyroid drugs inhibit ___ of thyroglobulin and prevent conversion of ___ to ___

A

inhibit iodination of thyroglobulin and prevent conversion of T4 to T3

470
Q

Propranolol for hyperthyroidism–L-isomer causes ___

A

beta blockade–treats tachycardia, tremor, palpitations, anxiety, and heat intolerance

471
Q

Propranolol for hyperthyroidism–D-isomer inhibits the conversion of ___ to ___

A

T4 to T3

472
Q

Radioactive iodine for hyperthyroidism–one time dose in ___ form, results in ___ of thyroid tissue

A

one time dose in pill form, results in destruction of thyroid tissue

473
Q

Surgery for hyperthyroidism–___ or ___ thyroidectomy

A

partial or total thyroidectomy

474
Q

Surgery for hyperthyroidism is used extensively–T/F? Why?

A

False–is NOT used extensively in the absence of cancer as meds are effective and there are risks of removing parathyroids or recurrent laryngeal nerve

475
Q

___ = extreme form of hyperthyroidism

A

Thyroid storm

476
Q

Thyroid storm occurs within ___-___ hours postop

A

6-18 hours

477
Q

80% of patients who experience thyroid storm are not suspected of having ___

A

thyroid problems

478
Q

S/S of thyroid storm–___thermia, ___cardia, ___rhythmias, ___, ___

A

hyperthermia, tachycardia, dysrhythmias, CHF, shock

479
Q

Symptoms of thyroid storm may resemble ___, ___, ___

A

MH, pheochromocytoma, neuroleptic malignant syndrome

480
Q

Because thyroid storm may resemble many other things, it is important to obtain a ___ diagnosis

A

differential

i.e.: MH usually occurs intraoperatively with elevated CO2; thyroid storm typically occurs postoperatively

481
Q

Treatment of hyperthyroidism before surgery–sodium iodide and propranolol lead to euthyroidism in about ___ days

A

10 days

482
Q

Treatment of hyperthyroidism before surgery–antithyroid drugs ___-___ weeks before surgery (i.e.: methimazole, PTU)

A

6-8 weeks

483
Q

Patients with hyperthyroidism–check airway for goiter, wheezing, obstruction; goiter can be ___/___sternal and might not be so obvious; may have to do an ___ intubation on these patients if they have symptoms of airway compromise

A

goiter can be sub/retrosternal and might not be so obvious; may have to do an awake fiberoptic intubation

484
Q

Goiter means ___

A

enlargement

485
Q

Goiter results from chronic stimulation by ___

A

TSH

486
Q

In an emergency, administer antithyroid drugs–sodium ___; ___–blocks peripheral conversion of T4 to T3, making rT3 instead; and ___

A

sodium iodide; cortisol; PTU

487
Q

Avoid ___ [volatile agent] and ___ [ACLS drug] in hyperthyroid patients

A

halothane and atropine

488
Q

Neuro monitoring with him tube = wires placed at the level of the ___ to monitor the ___ and ___ during thyroidectomy

A

wires placed at the level of the vocal cords to monitor the RLN and SLN during thyroidectomy

489
Q

Unilateral RLN damage = ___

A

hoarseness

490
Q

Bilateral RLN damage = ___, ___, ___

A

aphonia, stridor, aspiration

491
Q

SLN damage = ___ voice in upper registers

A

abnormal

492
Q

Hematoma/bleed during thyroidectomy = airway ___ requiring decompression and rapid ___ before airway compromise

A

airway emergency requiring decompression and rapid intubation before airway compromise

493
Q

___calcemia results from inadvertent removal of the parathyroid glands; signs = ___ness, ___ny, and ___spasm 24-72 hours later

A

Hypocalcemia; signs = weakness, tetany, and laryngospasm 24-72 hours later

494
Q

Hypocalcemia can end with ___ collapse

A

CV collapse

495
Q

___ = tracheal softening, causes airway collapse with inspiration

A

tracheomalacia

496
Q

Why is calcium important?–___ conduction, ___ formation, ___ function, blood ___, ___ and ___ function, capillary ___, cell ___ and ___, ___transmitter action

A

nerve conduction, bone formation, muscle function, blood coagulation, cerebral and cardiac function, capillary permeability, cell growth and division, neurotransmitter action

497
Q

Body contains ___-___kg of calcium

A

1-2 kg

498
Q

___% of calcium is in the skeleton, ___% is in the plasma, and ___% is in the ECF, ___% in cells

A

98% in skeleton

  1. 03% in plasma
  2. 1% in ECF

1% in cells

499
Q

Plasma calcium–___% ionized, active form

A

50%

500
Q

Ionized calcium is most important for calcium functions on ___, the ___ system, and ___ formation

A

the heart, the nervous system, and bone formation

501
Q

___% of calcium is protein bound, primarily bound to albumin

A

41%

502
Q

___calcemia = nervous system excitement

A

hypocalcemia

503
Q

Signs of hypocalcemia = ___ny, ___ures, ___ QT interval

A

tetany, seizures, longer QT interval

504
Q

Hypocalcemia–inflate BP cuff and hand spasms = ___ sign

A

Trousseau’s sign

505
Q

Hypocalcemia–tapping facial nerve leads to twitching = ___ sign

A

Chvostek’s sign

506
Q

Hypercalcemia–chief manifestation = skeletal muscle ___

A

weakness

507
Q

Other signs of hypercalcemia = nervous system ___; ___ QT; ___ PR interval; ___ [think GI]; ___xia

A

nervous system depression; short QT; long PR interval; constipation; anorexia

508
Q

Treatment of hypercalcemia–maintain ___, ___ate, administer ___ (antibiotic) in severe cases

A

maintain UOP, hydrate, administer mithramycin (antibiotic) in severe cases

509
Q

Body contains ___ kg of phosphorus

A

1

510
Q

Phosphorus–___% skeletal, ___% muscle/tissue, ___% ECF

A

85% skeletal, 15% muscle/tissue, 1% ECF

511
Q

Phosphorus levels fluctuate significantly more than Ca levels because phosphorus moves between ECF and ___ as well as between ECF and ___

A

between ECF and bone as well as between ECF and ICF

512
Q

Phosphorus is easily absorbed via the ___ tract

A

GI

513
Q

Major control site of phosphorus is the ___

A

kidney–urinary excretion balances GI intake

514
Q

PTH ___ (increases/decreases) urinary excretion of phosphorus

A

increases

515
Q

GI absorption of phosphorus is increased by ___

A

1,25 D3

516
Q

1,25 D3 = ___

A

active metabolite of vitamin D

517
Q

Parathyroid consists of ___ glands

A

4

518
Q

Parathyroid glands contain mainly ___ cells and ___ cells

A

chief cells and oxyphil cells

519
Q

Chief cells secrete ___ hormone

A

parathyroid hormone

520
Q

Synthesis and secretion of parathyroid hormone is related to ___ concentrations in the blood

A

calcium

521
Q

Parathyroid glands can become enlarged from prolonged ___, ___nancy, ___tation

A

prolonged stimulation, pregnancy, lactation

522
Q

Decreases in calcium concentration in the ECF ___ (increases/decreases) secretion of PTH

A

increases

523
Q

Increases in calcium concentration in the ECF ___ (increases/decreases) secretion of PTH

A

decreases

524
Q

When PTH is secreted, it ___ (increases/decreases) bone reabsorption to mobilize calcium and phosphate–resorption = process by which osteoclasts break down bone and release calcium from bone fluid to blood

A

increases

525
Q

PTH ___ (increases/decreases) reabsorption of Ca in the kidney’s distal tubules

A

increases

526
Q

PTH ___ (increases/decreases) reabsorption of phosphate in the renal tubules

A

decreases

527
Q

PTH ___ (increases/decreases) the production of 1,25 D3 which ___ (enhances/inhibits) intestinal Ca absorption

A

PTH increases the production of 1,25 D3 which enhances intestinal Ca absorption

528
Q

Major stimulus for PTH is ___ serum Ca level

A

low

529
Q

Increased PTH results in serum: ___ calcium, ___ phosphate

A

increased calcium, decreased phosphate

530
Q

Increased PTH results in urine: ___ calcium, ___ phosphate

A

decreased calcium, increased phosphate

531
Q

PTH increases the ___ of phosphate, potassium, and sodium by increasing the ___ of calcium, magnesium, and hydrogen

A

excretion, reabsorption

532
Q

Excretion/reabsorption largely takes place in the distal tubules/collecting ducts–T/F?

A

True

533
Q

___ is produced in the parafollicular (clear or C cells) of the thyroid; in general, it has the opposite effect of parathyroid hormone

A

Calcitonin

534
Q

Calcitonin ___ (increases/decreases) calcium by ___ bone resorption and ___ urinary excretion of calcium

A

calcitonin decreases calcium by inhibiting bone resorption and increasing urinary excretion of calcium

535
Q

Calcitonin–serum calcium and phosphate are ___

A

decreased

536
Q

Calcitonin–urine calcium and phosphate are ___

A

increased (d/t increased excretion)

537
Q

Secretion of calcitonin is controlled by serum ___ level

A

calcium

538
Q

___ (increased/decreased) calcium leads to increased calcitonin secretion

A

increased

539
Q

___ has a potent effect to increase calcium absorption from the intestinal tract

A

Vitamin D

540
Q

Vitamin D has important effects on both bone ___ and bone ___

A

bone deposition and bone absorption

541
Q

Vitamin D is not an ___ substance

A

active

542
Q

Vitamin D must be converted to its active product ___

A

1,25 D3 (dihydroxycholecalciferol)

543
Q

Vitamin D3 is formed in the ___ by exposure to ___

A

formed in the skin by exposure to sunlight

544
Q

Vitamin D3 is converted to 1,25 D3 by the ___

A

liver

545
Q

GI absorption of calcium is ___ (increased/decreased) by vitamin D

A

increased

546
Q

Urinary excretion of calcium is ___ (increased/decreased) by PTH and ___ (increased/decreased) by calcitonin

A

decreased by PTH and increased by calcitonin

547
Q

Bone resorption of calcium is ___ (increased/decreased) by PTH and ___ (increased/decreased) by calcitonin

A

increased by PTH and decreased by calcitonin

548
Q

Hypoparathyroidism is usually a result of damage to the gland during ___

A

thyroid surgery

549
Q

Hypoparathyroidism–calcium levels fall below normal in ___-___ hours, which results in: ___ny, muscle ___, ___ seizures, CV ___

A

24-72 hours, which results in: tetany, muscle cramps, grand mal seizures, CV collapse

550
Q

Treatment of hypoparathyroidism = high ___ and ___ intake

A

calcium and vitamin D intake

551
Q

PTH could be used to treat hypoparathyroidism, but it is ___ and has a ___ half-life

A

expensive and has a short half-life

552
Q

Occasionally, ___ is necessary for treatment of hypoparathyroidism

A

Vitamin D3 (1/25-D3)

553
Q

___magnesemia can cause hypocalcemia that is resistant to calcium–so treat first with ___

A

Hypomagnesemia–so treat first with magnesium

554
Q

Magnesium suppresses the release of ___

A

PTH

555
Q

Primary hyperparathyroidism = inappropriate hyper secretion of ___, resulting in hypercalcemia

A

PTH

556
Q

Primary hyperparathyroidism results in ___calcemia, ___calciuria, ___phosphatemia

A

hypercalcemia, hypercalciuria, hypophosphatemia

557
Q

Primary hyperparathyroidism (too much calcium) = ___ QT interval, ___ cardiac relaxation

A

shortens QT interval, depresses cardiac relaxation

558
Q

Primary hyperparathyroidism causes ___ formation as calcium mobilized from bone must eventually be excreted by kidneys

A

kidney stone formation

559
Q

Most common cause of hyperparathyroidism is parathyroid ___ or ___

A

parathyroid hyperplasia or parathyroid tumor

560
Q

___ may stimulate the parathyroids

A

Pregnancy

561
Q

Secondary hyperparathyroidism results from hypersecretion of ___ in response to a ___calcemic stress–i.e.: vitamin D deficiency, chronic renal disease

A

PTH in response to a hypocalcemia stress

562
Q

Secondary hyperparathyroidism results in ___, d/t inadequate mineralization of the bones

A

osteomalacia

563
Q

Vitamin D deficiency results from inadequate ___

A

dietary intake–often d/t fat malabsorption syndrome

564
Q

Vitamin D deficiency can result from inadequate ___

A

sunlight

565
Q

Vitamin D deficiency–___ (increased/decreased) absorption of calcium and phosphate, ___ (increased/decreased) serum calcium and phosphate, ___ (increased/decreased) PTH and ___ (increased/decreased) bone resorption

A

decreased absorption of calcium and phosphate, decreased serum calcium and phosphate, increased PTH and increased bone resorption

566
Q

Vitamin D deficiency results in ___ in adults

A

osteomalacia

567
Q

Vitamin D deficiency results in ___ in children

A

rickets–bones fail to mineralize, epiphyses fail to fuse, epiphyseal plates widen and bowing and fractures occur

568
Q

1 gm of calcium chloride = ___ gm of calcium gluconate

A

3 gm

569
Q

Calcium is indicated for treatment of ___kalemia induced EKG changes because of its cell membrane stabilizing effects

A

hyperkalemia

570
Q

Calcium is indicated in patients with ___ associated with either calcium channel blockers or beta adrenergic blockers

A

hypotension

571
Q

Calcium is indicated in cases of ___ toxicity, as may occur in parturients being treated for preeclampsia

A

magnesium

572
Q

Calcium is contraindicated in patients with ___ toxicity, as it may cause lethal arrhythmias

A

digoxin