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APEX > Unit 10 - Endocrine > Flashcards

Unit 10 - Endocrine Flashcards

1
Q

negative feedback loop

A

The response is negative (opposite) the initiating stimulus, which returns the parameter to a set point to maintain stability (homeostasis).

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2
Q

positive feedback loop

A

Provides an unstable cycle in which the system responds in a way that increases the magnitude of the response.

This results in the amplification of the original signal instead of stabilization

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3
Q

what 2 major systems maintain homeostasis in the body

A

nervous system
endocrine system

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4
Q

hormones released by the posterior pituitary

A

ADH
oxytocin

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5
Q

hormones released by the anterior pituitary

A

Follicle-stimulating hormone
Luteinizing hormone
Adrenocorticotropic hormone
Thyroid-stimulating hormone
Prolactin
Growth hormone

“FLAT PiG”
i = ignore

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6
Q

function of hypothalamus in the endocrine system

A
  • monitors hormone concentrations in the systemic circulation
  • instructs the pituitary to increase or decrease hormone release (usually through negative feedback)
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7
Q

function of FSH

A

germ cell maturation
ovarian follicle growth (females)

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8
Q

function of Luteinizing hormone

A

testosterone (males)
ovulation (females)

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9
Q

function of ACTH

A

adrenal hormone release

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10
Q

function of prolactin

A

lactation

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11
Q

where are inhibiting and releasing hormones released from

A

hypothalamus into hypophysial portal vessels

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12
Q

where is ADH primarily formed

A

in supraoptic nuclei of hypothalamus

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13
Q

where is oxytocin primarily formed

A

paraventricular nuclei

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14
Q

where does pituitary gland reside

A

sella turcica

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15
Q

how is the pituitary connected to the hypothalamus

A

via pituitary stalk

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16
Q

another name for anterior pituitary

A

adenohypophysis

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17
Q

another name for posterior pituitary gland

A

neurohypophysis

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18
Q

what results from FSH hyper hypo-secretion

A

hyper = early puberty
hypo = infertility

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19
Q

what results from LH hyper and hypo-secretion

A

hypo = early puberty
hyper = infertility

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20
Q

result of ACTH hyper and hypo-secretion

A

hyper = Cushing’s
hypo = Addison’s disease

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21
Q

result of TSH hyper and hypo-secretion

A

hyper = hyperthyroidism
hypo = hypothyroidism, Cretinism

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22
Q

result of prolactin hyper and hypo-secretion

A

hyper = infertility
hypo = menstrual dysfunctoin

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23
Q

result of growth hormone hyper and hypo-secretion

A

hyper = acromegaly, gigantism
hypo = dwarfism

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24
Q

result of ADH hyper and hypo-secretion

A

hyper = SIADH
hypo = diabetes insipidus

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25
Q

result of oxytocin hyposecretion

A

hypo = uterine atony

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26
Q

regulates TRH release

A

Triiodothyronine (T3)

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27
Q

regulates CRH release

A

cortisol

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28
Q

regulate LHRH release

A

testosterone
estrogen
progesterone

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29
Q

regulate GHRH and GHIG release

A

growth hormone
insulin growth factor-1

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30
Q

5 systemic hormones affected by negative feedback

A
  1. TRH
  2. CRH
  3. LHRH
  4. GHRH
  5. GHIH
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31
Q

2 hormones not affected by negative feedback

A

oxytoxin
prolactin

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32
Q

hormone that is part of a positive feedback loop

A

oxytocin

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33
Q

how is oxytocin release stimulated

A

uterine contraction

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34
Q

how is prolactin release controlled

A

under neural control, where increased dopamine decreases prolactin release

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35
Q

why can metoclopramide caue hyperprolactinemia

A

increased dopamine decreases prolactin release

metoclopramide is a dopamine antagonist

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36
Q

conditions assoc. with SIADH

A
  • TBI (most common)
  • cancer (small-cell lung carcinoma)
  • noncancerous lung disease
  • carbamazepine
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37
Q

most common cause of SIADH

A

TBI

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38
Q

electrolyte abnormality with SIADH

A

hyponatremia

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39
Q

plasma volume, osmolarity, and sodium in SIADH

A
  • Volume = euvolemic or hypervolemic
  • Osmolarity = hypotonic (< 275 mOsm/L)
  • Sodium = low (< 135 mEq/L)
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40
Q

urine volume, osmolarity, and sodium in SIADH

A
  • Volume = low
  • Osmolarity = higher than plasma
  • Sodium = high
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41
Q

treatment of SIADH

A
  • fluid restriction
  • demeclocycline
  • +/- treat hyponatremia
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42
Q

use of demeclocycline in SAIDH

A

decreases responsiveness to ADH

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43
Q

when should sodium be corrected in pt with SIADH

A

if pt is symptomatic or Na+ < 120 mEq/L, give hypertonic NS

Don’t correct hyponatremia > 1 mEq/L/hr

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44
Q

when should sodium be corrected in pt with SIADH

A

if pt is symptomatic or Na+ < 120 mEq/L, give hypertonic NS

Don’t correct hyponatremia > 1 mEq/L/hr

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45
Q

conditions assoc with DI

A
  • pituitary surgery (most common)
  • TBI
  • subarachnoid hemorrhage
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46
Q

most common cause of DI

A

pituitary surgery

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47
Q

presentation of DI

A

polyuria

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48
Q

plasma volume, osmolariy, and sodium in DI

A
  • Volume = euvolemic or hypovolemic
  • Osmolarity = hypertonic (> 290 mOsm/L)
  • Sodium = high (> 145 mEq/L)
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49
Q

urine volume, osmolarity, and sodium in DI

A
  • Volume = high
  • Osmolarity = lower than plasma
  • Sodium = normal
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50
Q

DI treatment

A

supportive, DDAVP or vasopressin

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51
Q

what is acromegaly

A

Results from oversecretion of GH after adolescence

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52
Q

cause of nearly all cases of acromegaly

A

pituitary adenoma

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53
Q

what causes gigantism

A

increased GH output before puberty

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54
Q

why are pts with acromegaly at risk for difficult mask ventilation and DL

A

mask: distorted facial features, poor seal
DL: large tongue, teeth, and epiglottis

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55
Q

why should you use a smaller ETT in a pt with acromegaly

A

subglottic narrowing & vocal cord enlargement

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56
Q

why should nasal intubation be avoided in pts with acromegaly

A

risk epistaxis d/t turbinate enlargement

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57
Q

common comorbidities with acromegaly

A
  • OSA
  • HTN
  • CAD
  • rhythm disturbances
  • glucose intolerance
  • skeletal muscle weakness
  • entrapment neuropathies
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58
Q

source of T4

A

Directly released from thyroid

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59
Q

source of T3

A

Mostly extrathyroid conversion of T4 to T3

Small amount released from thyroid

60
Q

where is concentration of T4 the highest

A

In the blood

61
Q

where is the concentrtion of T3 the highest

A

In the target cell

T4 converted to T3

62
Q

where is the concentrtion of T3 the highest

A

In the target cell

T4 converted to T3

63
Q

which is more protein bound - T4 or T3

A

T4

64
Q

which is more potent - T4 or T3

A

T4

65
Q

half-life of T3

A

1 day

66
Q

half life of T4

A

7 days

67
Q

TSH release from anterior pituitary affects the thyroid gland in 2 key ways:

A

1) Tells the thyroid gland to produce T3 & T4 (requires iodine)
2) Tells follicular tissue to produce thyroglobulin colloid (does not require iodine)

68
Q

TSH release from anterior pituitary affects the thyroid gland in 2 key ways:

A

1) Tells the thyroid gland to produce T3 & T4 (requires iodine)
2) Tells follicular tissue to produce thyroglobulin colloid (does not require iodine)

69
Q

substrate thyroid requires to synthesize T3 & T4

A

iodine

70
Q

TSH in pt with hypoactive thyroid

A

chronically elevated

there isn’t enough thyroid hormone to suppress TSH

71
Q

TSH in pt with hypoactive thyroid

A

chronically elevated

there isn’t enough thyroid hormone to suppress TSH

72
Q

stimulates follicles to make thyroglobulin colloid

A

TSH

73
Q

required for follicles to make thyroglobulin colloid

A

iodine

74
Q

what causes goiter in hypoactive thyroid

A

Since TSH is chronically elevated, follicles continue to produce thyroglobulin colloid - causes thyroid gland to increase in size

75
Q

3 hormones stored and released by the thyroid gland

A
  1. T4 = thyroxine
  2. T3 = Triiodothyronine
  3. calcitonin
76
Q

nerve at risk for injury in thyroid or parathyroid surgery

A

RLN

77
Q

how does thyroid hormone affect VO2 & CO2 consumption

A

both increased

78
Q

effects of increased thyroid hormone on ANS

A
  • ↑ number & sensitivity of # receptors
  • ↓ number of cardiac muscarinic receptors
79
Q

CV effects of increased thyroid hormone

A
  • Increased myocardial performance independent of the ANS
  • ↑ chronotropy, contractility, lusitropy
  • ↓ SVR
80
Q

respiratory effects of increased thyroid hornone

A

↑ BMR = ↑ CO2 production = ↑ Vm (↑ Vt & RR)

81
Q

increased thyroid hormone = increased O2 consumption in all tissues except:

A

CNS

82
Q

how does thyroid hormone affect MAC

A

hyper- and hypothyroidism do NOT affect MAC

O2 consumption increased in all tissues except CNS

83
Q

how does thyroid hormone affect MAC

A

hyper- and hypothyroidism do NOT affect MAC

O2 consumption increased in all tissues except CNS

84
Q

GI effects of increased thyroid hormone

A

intestineal hypermotility, diarrhea

85
Q

how does increased thyroid hormone affect fat

A

↑ utilization of fat stores = weight loss

86
Q

how does increased thyroid hormone affect protein

A

↑ catabolism = skeletal muscle weakness

87
Q

effect of thyroid hormone on carbohydrates

A

↑ gluconeogenesis, ↑ insulin release, ↑ glucose uptake

88
Q

what causes tremors with increased thyroid hormone

A

↑ sensitivity of neuronal synapses in the spinal cord

89
Q

etiologies of hyperthyroidism

A
  • Grave’s (autoimmune - most common)
  • myasthenia gravis
  • multimodal goiter
  • carcinoma
  • pregnancy
  • pituitary adenoma
  • amiodarone (less common)
90
Q

TSH, T3, & T4 in hyperthyroidism

A

low TSH + high T3 & T4

91
Q

CV s/s of hyperthyroidism

A

HTN
Tachyarrhythmias
Atrial fibrillation

92
Q

pulmonary s/s hyperthyroidism

A

Increased minute ventilation

93
Q

electrolyte imbalance associated with hyperthyroidism

A

hypercalcemia

94
Q

medical management of hyperthyroidism

A

Thionamides
Beta blockers
potassium iodide
radioactive iodine

95
Q

mechanism of thionamides

A

Inhibits thyroid synthesis by blocking iodine addition to tyrosine residues on thyroglobulin

96
Q

meds that inhibit peripheral conversion of T4 to T3

A

PTU
Propranolol
glucocorticoids
thiopental

97
Q

how long does it take to achieve a euthyroid state with thionamides

A

6-7 weeks

98
Q

available routes of thionamides

A

Only available PO

99
Q

serious side effects of thionamides

A

hepatitis
agranulocytosis

100
Q

mechanism of potassium iodide in management of hyperthyroidism

A

Reduces thyroid hormone synthesis and release

101
Q

when should potassium iodide be given in relation to surgery time

A

Administer 10 days before surgery

102
Q

mechanism of radioactive iodine in hyperthyroidism

A

destroys thyroid tissue

103
Q

surgical management of hyperthyroidism

A

subtotal or total thyroidectomy

104
Q

complications of thyroidectomy

A
  • hypothyroidism
  • hemorrhage (tracheal compression)
  • RLN injury
  • hypocalcemia
105
Q

etiologies of hypothyroidism

A
  • Hashimoto’s thyroiditis (autoimmune – most common)
  • iodine deficiency
  • hypothalamic-pituitary dysfunction
  • neck radiation
  • thyroidectomy
  • amiodarone (more common)
106
Q

TSH, T3, & T4 in hypothyroidism

A

high TSH + low T3 & T4

107
Q

CV s/s of hypothyroidism

A

Peripheral vasoconstriction
Decreased HR & contractility
Decreased CO
Heart failure
Pericardial effusion

108
Q

pulmonary s/s hypothyroidism

A

Decreased minute ventilation
Reduced response to hypoxia
Reduced response to hypercarbia
Pleural effusion

109
Q

GI effects of hypothyroidism

A

delayed gastric emptying, constipation

110
Q

medical management of hypothyroidism

A

synthetic T4 (levothyroxine)

111
Q

initial response to levothyroxine therapy

A

natriuresis & decreased TSH

112
Q

complication of neonatal hypothyroidism that leads to limited physical and mental development

A

Cretinism

113
Q

airway complications of hypothyroidism

A

Airway obstruction due to large tongue, swollen vocal cords, and/or goiter

Goiter = awake intubation

114
Q

how does hypothyroidism affect circulation

A

Hypodynamic circulation: ↓ HR, SV, contractility, CO, and baroreceptor responsiveness

115
Q

best way to support hemodynamics in hypothyroidism

A

sympathomimetics that improve myocardial performance (not neo)

116
Q

management of hypotension unresponsive to catecholamines in pts with hypothyroidism

A

corticosteroids

Decreased adrenal function is common

117
Q

management of hypotension unresponsive to catecholamines in pts with hypothyroidism

A

corticosteroids

Decreased adrenal function is common

118
Q

when is thyroid storm most likely to happen

A

6-18 hours after surgery

Can occur in hyper- and euthyroid patients

119
Q

when is thyroid storm most likely to happen

A

6-18 hours after surgery

Can occur in hyper- and euthyroid patients

120
Q

s/s thyroid storm

A
  • fever
  • tachycardia/tachyarrhythmias
  • HTN
  • CHF
  • shock
  • confusion & agitation
  • N/V
121
Q

4 B’s of thyroid storm management

A
  • Block synthesis
  • Block release
  • Block T4 to T3 conversion
  • Block beta receptors
122
Q

meds that block synthesis of thyroid hormone

A
  • methimazole
  • carbimazole
  • PTU
  • potassium iodide
123
Q

meds that block release of thyroid hormone

A
  • radioactive iodine
  • potassium iodide
124
Q

beta blockers used in treatment of thyroid storm

A

esmolol
propranolol

125
Q

use of glucocorticoids in thyroid storm treatment

A

blocks conversion of T4 to T3 and supports stress response

hypermetabolism consumes endogenous steroids

126
Q

why should aspirin be avoided in thyroid storm

A

can dislodge T4 from plasma proteins and ↑ free fraction of T4

127
Q

preparing for a hyperthyroid patient needing emergency surgery

A
  • administration of a beta-blocker, potassium iodide, and glucocorticoids
  • PTU should be started
128
Q

how long may medical management of hyperthyroidism take to be euthyroid

A

6-8 weeks

129
Q

airway management in a patient with goiter

A

1 - awake intubation

Next bet - technique that maintains spontaneous ventilation

130
Q

meds to avoid in hyperthyroidism

A
  • sympathomimetics
  • anticholinergics
  • ketamine
  • pancuronium
131
Q

why might pts with hyperthyroid be at higher risk for corneal abrasion

A

exopthalmos

132
Q

why is positioning important with hyperthyroid pts

A

increased bone turnover increases risk of osteoporosis

133
Q

s/s unilateral RLN injury

A

hoarseness

ipsilateral vocal cord is positioned midline on inspiration

134
Q

s/s unilateral RLN injury

A

hoarseness

ipsilateral vocal cord is positioned midline on inspiration

135
Q

s/s bilateral RLN injury

A

airway obstruction

both cords are positioned midline on inspiration

136
Q

s/s bilateral RLN injury

A

airway obstruction

both cords are positioned midline on inspiration

137
Q

cause of hypocalcemia after thyroid surgery

A

resection of parathyroid glands

138
Q

how is thyroxine synthesized

A

from tyrosine

139
Q

why should NMBs be used carefully in hyperthyroid pts

A

increased incidence of myasthenia gravis and myopathy

140
Q

things thyroid storm can mimic under GA

A
  1. MH
  2. pheochromocytoma
  3. neuroleptic malignant syndrome
  4. light anesthesia
141
Q

Chvostek’s sign

A

tapping on anlge of jaw (facial n./masseter muscle) = ipsilateral facial contraction

142
Q

Trousseau’s sign

A

upper extremity BP cuff inflated above SBP for 3 min = dec blood flow accentuates neuromuscular irritability = muscle spasm of hand and forearm

143
Q

2 CV side effects of hypocalcemia

A

hypotension
prolonged QT

144
Q

when does hypocalcemia most commonly occur after thyroid surgery

A

24-48 hrs postop

If it happens to occur sooner, it’s typically no earlier than 6- 12 hours after surgery

145
Q

common electrolyte abnormality in a pt with myxedema

A

dilutional hyponatremia

146
Q

–left off on page 7–

A

APEX (54 decks)

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