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APEX-KLE > KLE-Endocrine modules 1-9 > Flashcards

KLE-Endocrine modules 1-9 Flashcards

1
Q

What are the messengers of the endocrine system

A

hormones

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2
Q

Define endocrine

A

a cell releases a substance that travels through the bloodstream before acting on different cells

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3
Q

Define paracrine

A

Cell releases a substance that acts on adjacent cells

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4
Q

Define autocrine

A

Cell releases a substance that acts on the surface of the same cell

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5
Q

Define negative feedback

A

Response is negative (opposite) the initiating stimulus

Returns the parameter to a set point to maintain stability

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6
Q

Define positive feedback

A

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

Results is amplification of the original signal

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7
Q

What is the function of the hypothalamus

A

Links the CNS to the endocrine system by monitoring hormone concentrations in circulation then influencing output from pituitary gland

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8
Q

How is the hypothalamus able to monitor hormone concentration in circulation

A

It resides outside the BBB

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9
Q

How does the hypothalamus communicate with the anterior pituitary

A

Releasing and inhibiting hormones are released from the hypothalamus into the hypophyseal portal vessels, traveling along the pituitary stalk

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10
Q

Where is ADH produce

A

Primarily in supraoptic nuclei of hypothalamus

secondary = paraventricular nuclei

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11
Q

Where is oxytocin produced

A

primarily in paraventricular nuclei of the hypothalamus

Secondary = supraoptic nuclei

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12
Q

How are posterior pituitary hormones transported from the hypothalamus

A

Via axonal transport along the pituitary stalk

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13
Q

What are 7 hypothalamic hormones

A
  1. Luteinizing hormone-releasing hormone
  2. Corticotropin-releasing hormone
  3. Thyrotropin-releasing hormone
  4. Prolactin-releasing factor
  5. Prolactin-inhibiting factor
  6. Growth hormone-releasing hormone
  7. Growth hormone-inhibiting hormone
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14
Q

What is the target hormone for luteinizing hormone-releasing hormone
Where

A

In anterior pituitary

  1. Inc follicle-stimulating hormone (FSH)
  2. Inc luteinizing hormone
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15
Q

What is the target hormone for corticotropin-releasing hormone
Where

A

In anterior pituitary

Inc adrenocorticotropic hormone (ACTH)

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16
Q

What is the target hormone for thyrotropin-releasing hormone

Where

A

In anterior pituitary

Inc TSH

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17
Q

What are the target hormones for prolactin-releasing/inhibiting factors
Where

A

In anterior pituitary
Prolactin releasing = INC prolactin
Prolactin inhibiting = DEC prolactin

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18
Q

What are the target hormones for growth hormone-releasing/inhibiting hormone
Where

A

In anterior pituitary
Growth hormone-releasing = INC GH
Growth hormone-inhibiting = DEC GH

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19
Q

What are 6 hormones released from the anterior pituitary

A

FLAT PiG

  1. Follicle-stimulating hormone
  2. Luteinizing hormone
  3. Adrenocorticotropic hormone
  4. Thyroid stimulating hormone
  5. Prolactin
  6. Growth hormone
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20
Q

Where is the pituitary gland located

A

In the sella turcica

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21
Q

What are other names for the anterior and posterior pituitary

A 
Anterior = adenohypophysis
posterior = neurohypophysis
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22
Q 
Follicle-stimulating hormone:
Released from=
Action=
Hyposecretion=
Hypersecretion=
A

Released from= anterior pituitary
Action= germ cell maturation, ovarian follicle growth (fem)
Hypersecretion= early puberty
Hyposecretion= infertility

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23
Q 
Luteinizing hormone:
Released from=
Action=
Hypersecretion=
Hyposecretion=
A

Released from= anterior pituitary
Action= testosterone production (male), ovulation (fem)
Hypersecretion= early puberty
Hyposecretion= infertility

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24
Q 
Adrenocorticotropic hormone:
Released from=
Action=
Hypersecretion=
Hyposecretion=
A

Released from= anterior pituitary
Action= adrenal hormone release
Hypersecretion= Cushing’s disease
Hyposecretion= Addison’s disease

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25
Q 
Thyroid stimulating hormone:
Released from=
Action=
Hypersecretion=
Hyposecretion=
A

Released from= anterior pituitary
Action= thyroid hormone release
Hypersecretion= hyperthyroidism
Hyposecretion= hypothyroidism, cretinism

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26
Q 
Prolactin:
Released from=
Action=
Hypersecretion=
Hyposecretion=
A

Released from= anterior pituitary
Action= lactation
Hypersecretion= infertility
Hyposecretion= menstrual dysfunction

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27
Q 
Growth hormone:
Released from=
Action=
Hypersecretion=
Hyposecretion=
A

Released from= anterior pituitary
Action= cell growth
Hypersecretion= acromegaly, gigantism
Hyposecretion= dwarfism

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28
Q 
Antidiuretic hormone:
Released from=
Action=
Hypersecretion=
Hyposecretion=
A

Released from= posterior pituitary
Action= water retention
Hypersecretion= SIADH
Hyposecretion= Diabetes insipidus

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29
Q 
Oxytocin:
Released from=
Action=
Hypersecretion=
Hyposecretion=
A

Released from= posterior pituitary
Action= uterine contraction, breast feeding
Hypersecretion= nada
Hyposecretion= Uterine atony

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30
Q

What are the negative feedback hormones that regulate the following hormones:
Thyrotropin-releasing hormone=
Luteinizing hormone-releasing hormone=
Corticotropin-releasing hormone=
Growth hormone-releasing/inhibiting hormone=

A

Thyrotropin-releasing hormone= Triiodothyronine (T3)

Luteinizing hormone-releasing hormone= Testosterone, estrogen, progesterone

Corticotropin-releasing hormone= cortisol

Growth hormone-releasing/inhibiting hormone= Growth hormone, insulin growth factor-1

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31
Q

Which hormones are not affected by negative feedback regulation

A

Oxytocin

Prolactin

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32
Q

How is oxytocin release regulated

A

Via positive feedback loop

More oxytocin = more uterine contractions = more oxytocin…

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33
Q

How is prolactin regulated

A

Output is under neural control

Increased dopamine decreases prolactin release

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34
Q

What are 4 associated conditions causing SIADH

A
  1. TBI
  2. Cancer (small-cell lung ca)
  3. Noncancerous lung dz
  4. Carbamazepine
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35
Q

What are 3 associated conditions causing DI

A
  1. Pituitary surgery (most common)
  2. TBI
  3. SAH
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36
Q

Presentation of:
SIADH
DI

A 
SIADH = hyponatremia
DI = polyuria
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37
Q

What is the plasma content of the following in SIADH:
Volume=
Osmolarity=
Sodium=

A 
Volume= euvolemic or hyper
Osmolarity= hypotonic (<275)
Sodium= Low (<135)
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38
Q

What is the plasma content of the following in DI:
Volume=
Osmolarity=
Sodium=

A 
Volume= Euvolemic or hypo
Osmolarity= hypertonic (>290)
Sodium= High (>145)
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39
Q

What is the urine content of the following in SIADH:
Volume=
Osmolarity=
Sodium=

A 
Volume= Low
Osmolarity= Higher than plasma osmo
Sodium= High
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40
Q

What is the urine content of the following in DI:
Volume=
Osmolarity=
Sodium=

A 
Volume= high
Osmolarity= lower than plasma osmo
Sodium= normal
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41
Q

What are 4 treatments for SIADH

A
  1. Fluid restriction
  2. Demeclocycline (decreases responsiveness to ADH)
  3. Hypertonic NaCl if symptomatic
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42
Q

When is hypertonic NaCl indicated in SIADH

How is it corrected

A

Symptomatic Na <120

Don’t exceed correction of Na >1 mEq/L/Hr

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43
Q

What are treatments for DI

A
  1. DDAVP or vasopressin

2. Supportive

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44
Q

What can cause over secretion of growth hormone

A

pituitary adenoma

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45
Q

What are 4 ventilation and intubation considerations for pts with acromegaly

A
  1. Distorted facial features = difficult mask ventilation
  2. Large mouth structures = difficult DL
  3. Subglottic narrowing and VC enlargement = difficult ETT placement, smaller ETT
  4. Enlarge turbinates = Risk of epistaxis with nasal intubation
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46
Q

7 Common comorbid conditions with acromegaly

A
  1. OSA
  2. HTN
  3. CAD
  4. Rhythm disturbances
  5. glucose intolerance
  6. Skeletal muscle weakness
  7. Entrapment neuropathies
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47
Q

Where is the thyroid gland located

A
  1. anterior to trachea
  2. inferior to cricoid cartilage
  3. superior to suprasternal notch
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48
Q

RLN location with respect to thyroid gland

A

Courses along the lateral border of each thyroid lobe

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49
Q

Why is RLN injury increased with thyroid and parathyroid surgery

A

D/t its location running along side of the thyroid gland lateral borders

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50
Q

Thyroxine (T4):
Source=
Highest concentration=
half-life=

A

Source= direct release from thyroid
Highest concentration= in blood
half-life= 7

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51
Q

Triiodothyronine (T3):
Source=
Highest concentration=
half-life=

A

Source= Extrathyroid conversion of T4 to T3
Highest concentration= converted from T4 in target cell
half-life= 1 day

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52
Q

Thyroxin (T4) vs Triiodothyronine (T3):
Protein binding =
Potency =

A

Protein binding = more

Potency = less

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53
Q

Triiodothyronine (T3) vs thyroxine (T4):
Protein binding =
Potency =

A

Protein binding = less

Potency = more

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54
Q

What is TSH action on the thyroid gland

A
  1. stimulates iodide pump so thyroid produces T3 and T4

2. Stimulates follicular tissue to produce thyroglobulin colloid

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55
Q

How is TSH level regulated

A

Negative feedback via T3 and T4 suppressing TSH release

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56
Q

Why is TSH elevated in hypothyroidism

A

There isn’t enough thyroid hormone for T3/T4 production so TSH release isn’t suppressed by the negative feedback loop

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57
Q

How does a goiter form

A

When thyroid hormone is deficient there is too much TSH to stimulate the follicles and make thyroglobulin colloid (which doesn’t require iodine for production)

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58
Q

How does increased thyroid hormone affect metabolism (simple)

A

INC thyroid hormone => INC BMR => INC O2 consumption + INC CO2 production

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59
Q

What are 4 ways increased thyroid hormone affects myocardial performance

A
  1. INC chronotropy
  2. INC contractility
  3. INC Lusitropy
  4. dec SVR (vasodilation)
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60
Q

What are 2 ways increased thyroid hormone affects ANS which is passed to the heart

A
  1. INC number/sensitivity of beta receptors

2. dec number of cardiac muscarinic receptors

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61
Q

How does increased thyroid hormone affect respiratory pattern

A

INC BMR => INC CO2 production => Vm (inc Vt and RR)

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62
Q

How does increased thyroid hormone affect volatile MAC

A

No effect on MAC b/c CNS isn’t affect by INC O2 consumption

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63
Q

How does increased thyroid hormone affect inhaled induction

A

INC CO => INC anesthetic uptake into blood => dec rate of rise of FA/FI => slower induction

64
Q

How does increased thyroid hormone affect GI tract

A

hypermotility = diarrhea

65
Q

What effect does increased thyroid hormone have on cellular metabolism of nutrients
Fat
Protein
CHO

A

Fat: inc utilization of fat stores = weight loss
Protein: inc catabolism = skeletal muscle weakness
CHO: inc gluconeogenesis, inc insulin release, inc glucose intake

66
Q

Why are pts with hyperthyroidism heat intolerant

A

inc O2 consumption => inc CO2 production => vasodilation => heat loss

67
Q

Why do pts with hyperthyroidism experience tremors

A

Inc sensitivity of neuronal synapses in spinal cord

68
Q

What are 7 causes of hyperthyroidism

A
  1. Grave’s disease (autoimmune)
  2. Myasthenia gravis (autoimmune)
  3. Multinodular goiter
  4. Carcinoma
  5. Pregnancy
  6. Pituitary adenoma
  7. Amiodarone
69
Q

What are the most common causes of hyper/hypothyroidism

A

hyper = Grave’s disease
hypo = hashimoto’s thyroiditis
Both autoimmune

70
Q

What are 6 causes of hypothyroidism

A
  1. Hashimoto’s thyroiditis
  2. Iodine deficiency
  3. Hypothalamic-pituitary dysfunction
  4. Neck radiation
  5. thyroidectomy
  6. amiodarone
71
Q

How is hypothyroidism diagnosed

A

High TSH

Low T3/T4

72
Q

How is hyperthyroidism diagnosed

A

Low TSH

High T3/T4

73
Q

What are 3 cardiac manifestations of hyperthyroidism

A
  1. HTN
  2. Tachycardia
  3. A-Fib
74
Q

What are 5 cardiac manifestations of hypothyroidism

A
  1. peripheral vasoconstriction
  2. decreased HR
  3. decreased contractility
  4. heart failure
  5. pericardial effusion
75
Q

What are 4 respiratory manifestations of hypothyroidism

A
  1. decreased Vm
  2. Reduced response to hypoxia
  3. Reduced response to hypercarbia
  4. Pleural effusion
76
Q

What are 8 physical manifestations of hyperthyroidism

A
  1. Goiter
  2. Weight loss
  3. muscle weakness
  4. moist, warm skin
  5. heat intolerance
  6. Fine hair
  7. tremors
  8. exopthalmos
77
Q

What are 8 physical manifestations of hypothyroidism

A
  1. Goiter
  2. Weight gain
  3. muscle fatigue
  4. lethargy
  5. Dry, thick skin
  6. cold intolerance
  7. dry brittle hair
  8. constipation
78
Q

What is thyroid storm

A

Increased thyroid hormone output in response to a stressful event

79
Q

When is thyroid storm most likely to happen in the perioperative period

A

6-18 hours after surgery

80
Q

What is a complication of hypothyroidism

A

Myxedema coma d/t severley impaired thyroid function

81
Q

What is the result of neonatal hypothyroidism

A

Cretinism = limited physical and mental development

82
Q

What medications are used to inhibit thyroid synthesis in hyperthyroidism

A

Thionamides

  • propylthiouracil
  • methimazole
  • carbimazole
83
Q

What is the MOA of thionamides

A

Inhibition of thyroid synthesis by blocking iodine addition to tyrosine on thyroglobulin
PTU inhibits T4 to T3 conversion peripherally

84
Q

How long before euthyroid is achieved once thionamides are initiated for hyperthyroidism

A

6-7 weeks

85
Q

What medications are used to reduce SNS stimulation in hyperthyroidism

A

beta blockers

86
Q

What is unique about the use of propranolol in hyperthyroidism

A

It also inhibits peripheral conversion of T4 to T3

87
Q

What medication reduces thyroid hormone synthesis

A

potassium iodide

88
Q

When should potassium iodide be initiated in perioperative hyperthyroid pt

A

10 days before surgery

89
Q

What medication destroys thyroid tissue

A

radioactive iodine

90
Q

Guidelines for surgery of the hyperthyroid pt

A

Do not proceed to elective surgery until pt is euthyroid

91
Q

What 3 medications should be available to give in hyperthyroid pts that require emergency surgery

A
  1. beta blockers
  2. Potassium iodide
  3. glucocorticoids
92
Q

How does a goiter affect airway manipulation

A

Can cause tracheal deviation and tracheomalacia

93
Q

What type of intubation should be performed in goiter pts

A

Awake intubation

Any method that maintains spontaneous ventilation

94
Q

What 4 medications or classes should be avoided in the hyperthyroid pt

A
  1. sympathomimetics
  2. anticholinergics
  3. ketamine
  4. pancuronium
95
Q

Why is there increased risk for corneal abrasion in hyperthyroid pts

A

Pts may have exopthalmos which increases risk

96
Q

Signs of unilateral RLN injury w/ thyroid surgery

A

ipsilateral VC positioned midline

Hoarseness

97
Q

Signs of bilateral RLN injury w/ thyroid surgery

A

Both VC positioned midline on inspiration

Airway obstruction

98
Q

How can nerve injury be assessed following extubation

A

Have pt say E or moon

99
Q

How is RLN function assessed intraoperatively

A

NIM tube with electrodes positioned between the VC

100
Q

When does hypocalcemia occur with thyroidectomy including parathyroid glands

A

24-48 hrs post surgery

101
Q

8 s/sx of hypocalcemia

A
  1. muscle spasm-tetany
  2. laryngospasm
  3. mental status change
    4 HoTN
  4. prolonged QT
  5. Paresthesias
  6. Chvostek’s sign
  7. trousseau’s sign
102
Q

What are 7 s/sx of thyroid storm

A
  1. Fever >38.5*C
  2. Tachycardia or dysrhythmias
  3. HTN
  4. CHF
  5. Shock
  6. Confusion and agitation
  7. N/V
103
Q

What conditions can thyroid storm mimic while under anesthesia

A
  1. MH
  2. pheochromocytoma
  3. neuroleptic malignant syndrome
  4. light anesthesia
104
Q

What are the 4 main managements for thyroid storm

A
  1. Block synthesis (methimazole, PTU)
  2. Block release (radioactive I)
  3. Block T4/T3 conversion (propranolol, glucocorticoids)
  4. Block beta receptors (beta blockers)
105
Q

Why are glucocorticoids used in hyperthyroidism

A

They block conversion of T4/T3

Support stress response-hypermetabolism consumption of endogenous steroids

106
Q

What are anesthetic management considerations for thyroid storm

A
  1. Cardiopulm support
  2. glucocorticoids
  3. active cooling
  4. Acetaminophen for fever
107
Q

How is hypothyroidism medically managed

A

Levothyroxine

Thyroid hormone is replaced with synthetic T4

108
Q

What are 2 initial responses to initiation of levothyroxine

A
  1. Natriuresis

2. Decreased TSH

109
Q

How is airway manipulation affected in the hypothyroid pt

A

Airway obstruction can be d/t large tongue, swollen VS, and/or goiter

110
Q

Why is there an increased risk of aspiration in hypothyroid pt

A

They have delayed gastric emptying

111
Q

Describe the CV effects of hypothyroidism

A
  1. dec HR
  2. dec SV
  3. dec contractility
  4. dec CO
  5. dec baroreceptor responsiveness
    - inc risk of HoTN
112
Q

Why is inhalation induction faster in hypothyroidism

A

b/c dec CO

113
Q

What vasoactive drugs are best in hypothyroidism

A

sympathomimetics

avoid phenylephrine

114
Q

How is adrenal function affected by hypothyroidism

Anesthetic implications

A

Decreased adrenal function is common

Hotn unresponsive to catecholamines can be treated with corticosteroids

115
Q

How is metabolism and excretion affected by hypothyroidism

A

Hepatic metabolism and renal excretion are slowed

This can prolong drug effects

116
Q

Which fluid may be best in hypothyroid pt and why

A

D5NS

Provides glucose and combats hyponatremia d/t impaired H2O clearance

117
Q

What response can hypothyroid pts have to nondepolarizing NMB

A

They can have increased sensitivity

118
Q

How do osteoblasts affect serum Ca++

A

They reduce iCa++ by promoting Ca++ bone deposition

119
Q

How do osteoclasts affect serum Ca++

A

They increase iCa++ by promoting bone resorption

120
Q

What is the relationship between PTH and calcitonin

A

PTH works to increase Ca++ levels

Calcitonin works to decrease Ca++ levels

121
Q

How do PTH and calcitonin affect serum Ca++ and phosphate levels

A

PTH= inc Ca++, dec phosphate

Calcitonin= dec Ca++, inc phosphate

122
Q

PTH:
site of production=
site of release=
stimulator for release=

A

site of production= chief cells in parathyroid gland
site of release= parathyroid gland
stimulator for release= dec iCa++, inc phosphate

123
Q

PTH:
physiologic effect=
mechanism=

A

physiologic effect= Inc iCa++, dec phosphate

mechanism=

  • inc Ca++ bone resorption
  • inc intestinal Ca++ absorption by upregulating kidney enzymes for calcitrol
  • kidney Ca++ reabsorption inc
  • kidney phosphate elimination inc
124
Q

Calcitonin:
site of production=
site of release=
stimulator for release=

A

site of production= C cells in thyroid gland
site of release= thyroid gland
stimulator for release= inc iCa++

125
Q

Calcitonin:
physiologic effect=
mechanism=

A

physiologic effect= dec iCa++, inc phosphate

mechanism=
-inc Ca++ deposition in bone

126
Q

What is the most common cause of hypercalcemia

A

hyperparathyroidism

127
Q

What is the most common cause of primary hyperparathyroidism

A

Parathyroid adenoma

128
Q

What lab abnormalities are present in the hyperparathyroid pt

A

incr PTH levels
hypercalcemia
hypophosphatemia

129
Q

What is the best treatment for primary hyperparathyroidism

A

resection of PT glands

130
Q

What is the most common cause of secondary hyperparathyroidism

A

kidney disease

131
Q

What is the term for PTH induced bone disease in renal pts

A

renal osteodystrophy

132
Q

What is the treatment for primary hypoparathyroidism

A
  1. Ca++ supplement
  2. Vitamin D
  3. Mg++ supplement
133
Q

What are CV effects of hyperparathyroidism

A
  1. HTN

2. Shortened QT interval

134
Q

What are musculoskeletal effects of hyperparathyroidism

A
  1. bone pain
  2. osteopenia
  3. pathologic fractures
  4. muscle weakness
135
Q

What are GI effects of hyperparathyroidism

A
  1. Anorexia
  2. N/V
  3. abd pain
  4. PUD
  5. Pancreatitis
136
Q

What are GU effects of hyperparathyroidism

A
  1. polyuria
  2. polydipsia
  3. kidney stones
137
Q

What are CV effects of hypoparathyroidism

A
  1. HoTN
  2. myocardial depression
  3. long QT interval
138
Q

What are musculoskeletal effects of hypoparathyroidism

A

muscle spasms

paresthesia

139
Q

4 ways the body responds to hypocalcemia

A
  1. parathyroid gland releases PTH
  2. osteoclasts in bone release Ca++
  3. Ca++ is reabsorbed in the kidneys
  4. Ca++ absorption in gut increases in presence of vitamin D
140
Q

What are the zones of the adrenal cortex

A
  1. Zona glomerulosa
  2. Zona fasciculata
  3. Zona reticularis
141
Q

Which hormones are released from each adrenal cortical zone

A

(G) Glomerulosa = mineralocorticoids (salts)
(F) Fasciculata = glucocorticoids (sugar)
(R) Reticularis = androgens (sex)

142
Q

What is released from the adrenal medulla

A

Catecholamines:
Epinephrine (80%)
Norepinephrine (20%)

143
Q

Example of a mineralocorticoid

A

aldosterone

144
Q

What ions are excreted with aldosterone action on kidneys

A

K+

H+

145
Q

3 reasons aldosterone release is increased

A
  1. RAAS activation
  2. hyperkalemia
  3. Hyponatremia
146
Q

Example of a glucocorticoid

A

cortisol

147
Q

Where is the site of action of cortisol

A

It diffuses through the lipid bilayer and binds with intracellular steroid receptors

148
Q

What is the mechanism of cortisol action

A

Activation or inhibition of DNA transcription, it influences protein synthesis inside the target cell

149
Q

What effect does cortisol have on the hypothalamus and anterior pituitary

A

Inhibition via negative feedback loop

150
Q

What is normal daily cortisol production

A

15-30 mg/day

151
Q

What can increase serum cortisol

A

stress

152
Q

What are the 3 main jobs of cortisol

A
  1. Energy mobilization
  2. Anti-inflammatory effects
  3. Hemodynamics
153
Q

3 ways cortisol affects energy mobilization

A
  1. Gluconeogenesis = converts AA to glucose and increased glucose
  2. Protein catabolism = muscle breakdown to inc AA availability
  3. Fatty acid mobilization = inc FFA oxidation and ability to use fat for energy
154
Q

How does cortisol mitigate anti-inflammatory effects

A

Mitigates the inflammatory cascade by stabilizing lysosomal membranes and reducing cytokine release

155
Q

What 2 types of blood cells are decreased as a result of cortisol

A

Eosinophils

Lymphocytes

156
Q

What effect does cortisol have on myocardial performance

A

Myocardial performance improves by increased number and sensitivity of beta receptors on myocardium

157
Q

Why is exogenous cortisol required for BP management

A

It is required for vasculature to respond to vasoconstrictive effects of catecholamines

APEX-KLE (4 decks)

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