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N935 Pathophysiology > Pituitary Gland > Flashcards

Pituitary Gland Flashcards

1
Q

What are endocrine glands?

A

cells that secrete hormone directly into the surrounding ECF

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2
Q

How are exocrine glands products expelled?

A

through ducts

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3
Q

What are seven endocrine glands?

A 
Thyroid
Parathyroid
Pituitary
Pancreas
Adrenal
Placenta
Ovaries and Testes
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4
Q

What are the mediators of the endocrine system?

A

hormones

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5
Q

What are hormones?

A

chemical messengers that transport information (a message) from one set of cells (endocrine cells) to another (target cells)

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6
Q

What is an example of an endocrine function?

A

pituitary gland to thyroid gland

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7
Q

What causes a response to a hormone?

A

primarily, the binding of hormone to its target cell receptor

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8
Q

What characteristics of the hormone receptor help with hormone receptor binding?

A

high specificity and affinity

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9
Q

Where is the receptor found?

A

location of the receptor directs the hormone to the correct target organ or target cell

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10
Q

What is an example of a hormone that has numerous target sites?

A

insulin

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11
Q

What is an example of a hormone that has one target tissue?

A

TSH

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12
Q

What are three processes that regulate hormone secretion?

A

neural control
biorhythms
feedback mechanisms

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13
Q

What hromones are under neural control?

A

ADH, catecholamines, cortisol

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14
Q

How can neural control influence hormone secretion?

A

suppress or stimulate secretion

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15
Q

What are types of stimulus for neural influence over hormones?

A

smell, touch, stress, sight, taste, pain

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16
Q

What are biorhythms?

A

intrinsic hormonal oscillations may be circadian, weekly or seasonal
vary in stages of life

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17
Q

What is the role of the pituitary?

A

collects and integrates information from almost everywhere in the body & uses information to control the secretion of vital pituitary hormones

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18
Q

What is the pituitary gland regulated by?

A

feedback control from peripheral target organ hormones or other target products

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19
Q

Do the pituitary and hypothalamus have a BBB?

A

No

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20
Q

Why do the pituitary and hypothalamus lack a BBB?

A

allows for feedback to have a potent effect on the two structures

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21
Q

Where is the pituitary gland located?

A

sella turcica at base of the brain

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22
Q

What is the anterior lobe of the pituitary?

A

adenohypophysis

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23
Q

What is the posterior lobe of the pituitary?

A

neurophypophysis

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24
Q

What is blood supply to the pituitary?

A

superior and inferior hypophyseal arteries

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25
Q

What are the six hormones secreted by the anterior pituitary?

A 
growth hormone
adrenocorticotrophic hormone
thyroid-stimulating hormone
follicle-stimulating hormone
luteinizing hormone
prolactin
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26
Q

What is the anterior pituitary target cell type for thyrotropin-releasing hormone?

A

thyrotroph

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27
Q

What is the anterior pituitary target cell type for corticotropin-releasing hormone?

A

corticotroph

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28
Q

What is the anterior pituitary target cell type for gonadotropin-releasing hormone?

A

gonadotroph

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29
Q

What is the anterior pituitary target cell type for prolactin-releasing hormone?

A

lactotroph

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30
Q

What is the anterior pituitary target cell type for prolactin-inhibiting hormone?

A

lactotroph

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31
Q

What is the anterior pituitary target cell type for growth hormone releasing hormone?

A

somatotroph

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32
Q

What is the anterior pituitary target cell type for growth hormone inhibitory factor hormone?

A

somatotroph

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33
Q

What is the anterior pituitary hormone release when thyrotroph is targeted?

A

thyroid stimulating hormone (TSH)

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34
Q

What is the target of TSH

A

thyroid gland

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35
Q

What is the primary peripheral feedback hormone for TRH?

A

T3

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36
Q

What is the anterior pituitary hormone released from corticotrophs

A

adrenocorticotropic hormone (ACTH, corticotropin)

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37
Q

What is the hormone target site of ACTH?

A

zona fasciculata & zona reticularis of adrenal cortex

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38
Q

What is the primary peripheral feedback hormone of CRH?

A

cortisol

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39
Q

What anterior pituitary hormone is released from gonadotrophs?

A

follicle-stimulating hormone lutenizing hormone

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40
Q

What are the target sites of LH and FSH

A

gonads (testes and ovaries)

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41
Q

What is the primary peripheral feedback hormone for GRH?

A

estrogen
progesterone
testosterone

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42
Q

What hormone does a lactotroph release?

A

prolactin

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43
Q

What is the target site of prolactin?

A

breast

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44
Q

Is there a primary feedback loop for prolactin secretion?

A

no

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45
Q

What is released from a somatotroph?

A

growth hormone

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46
Q

What is the target of growth hormone?

A

all tissues

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47
Q

What is the primary peripheral feedback hormone of somatotroph?

A

growth hormone, insulin, growth factor 1

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48
Q

What is a primary pituitary disorder?

A

defect to the peripheral endocrine gland

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49
Q

What is a secondary pituitary disorder?

A

defect to the pituitary

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50
Q

What is a tertiary disorder?

A

defect to the hypothalamus

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51
Q

What is panhypopituitarism?

A

generalized pituitary hypofunction

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52
Q

What causes anterior pituitary hyposecretion?

A 
nonfunctioning tumors compress and destroy normal pituitary tissue
hypophysectomy
postpartum shock
irradiation
trauma
infiltrative disorders
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53
Q

What may be required if the tumor or pituitary gland causing hypopituitarism is removed?

A

thyroid hormone
glucocorticoids
vasopressin

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54
Q

what does removing the tumor or pituitary gland causing hypopituitarism do?

A

decompress or removes the tumor

to control bleeding

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55
Q

What is anterior pituitary hypersecretion caused by?

A

bengin adenomas

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56
Q

What are the three most common tumors found in ant pituitary hypersecretion?

A

prolactin
ACTH
GH

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57
Q

what the symptoms of hyper-prolactin?

A

amenorrhea, infertility, decreased libido and impotence

58
Q

what the symptoms of hyper-ACTH?

A

cushing’s disease

59
Q

what the symptoms pf hyper-growth hormone?

A

promotes growth of all tissues capable of growing

60
Q

What type of tumors are very rare in hyper-secretion of the anterior pituitary?

A

thyrotropin and gonadotropin

61
Q

What does growth hormone release reflect?

A

pulsatile fluctuations of GH releasing hormone and growth hormone regulate synthesis throughout the day

62
Q

When do GH secretion increase?

A

stress, hypoglycemia, exercise adn deep sleep

63
Q

Where does GH effect?

A

almost every part of the body

64
Q

What is the major GH target?

A

liver

65
Q

Why is the liver the major target of GH?

A

stimulates production of insulin-like growth factor type 1 (IGF-1) which mediates many of the effects of GH

66
Q

What does GH and IGF1 cause?

A

skeletal muscle, heart, skin and visceral organs undergo hypertrophy and hyperplasia

67
Q

How is hypersecretion of GH caused?

A

growth hormone secreting adenoma

68
Q

What is hypersecretion of GH called in adults?

A

acromegaly

sustained hypersecretion of GH after adolescence

69
Q

What is hypersecretion of GH called prior to puberty?

A

gigantism

hypersecretion of GH prior to the closure of growth plates

70
Q

What are features of acromegaly?

A 
skeletal overgrowth
soft tissue overgrowth
visceromegaly
osteoarthritis
glucose intolerance
skeletal muscle weakness
extrasellar tumor extension
peripheral neuropathy
71
Q

What are comorbidities associated with acromegaly?

A 
HTN
cardiomyopathy
ischemic heart disease
diabetes
osteoarthritis
skeletal muscle weakness/fatigue
increased lung volumes
sleep apnea
increased liver, spleen, kidneys and heart
72
Q

What is the treatment for acromegaly?

A

restore normal GH levels
preferred initial treatment is microsurgical removal of the tumor with preservation of the gland
irradiation and/or suppressant drug therapy are adjunctive treatments or for non-surgical candidates

73
Q

How are small GH tumors removed?

A

with a transphenoidal approach

74
Q

How are larger GH tumors removed?

A

with an intracranial approach

75
Q

What are options for nonsurgical candidates of acromegaly?

A

irradiation and/or suppressant drug therapy

76
Q

Describe airway management for patients with acromegaly

A 
enlarged tongue, lips and epiglottis,nasal turbinates
overgrowth of mandible
vocal cord dysfunction
upper airway obstruction
difficult mask fit
impaired visualization of cords
subglottic narrowing
dyspnea/ hoarsenes (larynx involved)
77
Q

What percent of acromegaly patients have OSA?

A

60%

78
Q

What happens post-operatively for surgical acromegaly patients?

A

postoperative respiratory obstruction or failure

79
Q

What are anesthesia management considerations for acromegaly?

A 
systemic HTN
ischemic heart disease
arrhythmias
skeletal muscle weakness
Hyperglycemia (glucose intolerance)
entrapment neuropathies common
80
Q

If preanesthetic assessment (in acromegaly) reveals adrenal or thyroid axis impairment should be administered?

A

stress level glucocorticoid therapy and thyroid replacement

81
Q

What does an entrapment neuropathy indicate?

A

perform allen’s test prior to placing arterial line; confirm collateral blood flow
hypertrophy of carpal tunnel ligament may impede ulnar artery flow

82
Q

What is necessary for pituitary surgery and preoperative preparation?

A

thorough medical history and physical

concentrate of symptoms associated with acromegaly

83
Q

What labs are needed pre-operatively for pituitary surgery?

A

electrolytes
glucose
hormone levels

84
Q

What is the purpose of looking at images pre-operatively for pituitary surgery?

A

determine the extent of the tumor invasion

85
Q

What can be seen on an EKG pre-operatively for pituitary surgery?

A

Left ventricular hypertrophy and arrhythmias
consider echocardiogram if the patient has cardiac dysfunction
optimize cardiac function prior to surgery

86
Q

What are considerations for trans-sphenoidal approach?

A

head of bed is elevated 15
arterial line si usually inserted for BP monitoring
a lumbar drain is placed
consider monitoring for VAE (if tumor is large and invading large sinus and/or in steep head up position)
not a lot of blood loss
use of submuscosal injection of Epi containing solutions or use of topical vasoconstrictors can result in HTN
anesthestic technique should allow for muscle relaxation, smooth extubation and rapid neurologic assessment
intraoperative hypotension (maybe due to inaddequate cortisol secretion) requires replacement of hydrocortison 50-100mg IV
blood loss minimal; potential for large amounts of blood loss if a large cavernous sinus is inadevertly entered
DI
cranial nerve damage, epitaxis, hyponatremia, cerebral spinal fluid leaks
adequate fluid replacement

87
Q

What are DI considerations?

A

can occur intra or postoperatively because of surgical trauma to the posterior pituitary (trauma reversible)
results in insufficient ADH

88
Q

What is the diagnosis for DI?

A

diagnosis with serum electrolytes, plasma osmolarity and urine osmolarity

89
Q

How do you treat DI?

A

intranasal desmopressin or restrict Na intake

90
Q

What does the posterior pituitary secrete?

A

oxytocin

antidiuretic hormone

91
Q

Role of ADH

A

control renal water excretion and reabsorption and is a major regulator of serum osmolarity

92
Q

Role of oxytocin

A

powerfully stimulates uterine contractions, stimulates myeopithelia cells of breast for milk ejection during lactation, is used for inducing labor and decreasing postpartum bleeding

93
Q

What are the types of vasopressin receptors?

A

V1- mediates vasoconstriction
V2- mediates water reabsorption in renal collecting ducts
V3- found in the CNS and stimulate modulation of corticotrophin secretion

94
Q

What are the ten stimuli for ADH release?

A 
increased plasma sodium
increased sodium osmolality
decreased blood volume
smoking (nicotine)
pain
stress
nausea
vasovagal reaction
angiotensin 2
positive pressure ventilation
95
Q

What occurs in ADH deficiency?

A

diabetes insipidus (DI)

96
Q

what are the two types of DI

A

neurogenic and nephrogenic

97
Q

What is neurogenic DI?

A

caused by inadequate release of ADH

98
Q

What is nephrogenic DI?

A

renal tubular resistance to ADH

99
Q

What are causes of neurogenic DI?

A

head trauma
brain tumors
neurosurgery
infiltrating pituitary leisons

100
Q

What is associated with nephrogenic DI?

A 
hypokalemia
hyperkalemia
genetic mutations
hypercalcemia
medication induced nephrotoxicity
101
Q

What are inhibitors of ADH action or release?

A 
ethanol
demeclocycline
phenytoin
chlorpromazine
lithium
102
Q

What are symptoms of ADH deficiency?

A 
polyuria
inability to produce concentrated urine
dehydration
hypernatremia
low urine osmolarity <300mOsm/L
urine specific gravity <1.010
urine volume > 2ml/kg/hr
Serum osmolarity > 290mOsm/L and sodium >145mEq/L
neurologic symptoms of hyperreflexia, weakness lethargy seizures and coma
103
Q

What is the most common symptoms of ADH deficiency?

A

polyuria

104
Q

What is the major mechanism for controlling DI in awake patients?

A

thirst

105
Q

What is the treatment for mild/moderate DI?

A

medications that augment the release of ADH or increase receptor sensitivity
chlorpropramide (sulyfonurea hypoglycemia agent)
carbamazepine- anticonvulsant
clofibrate- hypolipidemic agent

106
Q

What is the treatment for significant DI?

A

DDVAP

107
Q

What is considered significant DI?

A

plasma osmolarity >290mOsm/L

108
Q

What is DDAVP?

A

selective V2 agonist
less vasopressor activity
enhanced antidiuretic properties
administered SubQ, intranasal, IV

109
Q

What is the DOA of vasopressin?

A

8-12 hours

110
Q

What is the dose range for ADH?

A

5-40mcg/day nasally

0.5-2mcg/day BID SQ

111
Q

What should be assessed in posterior pituitary pre-operative assessments?

A

careful assessment of plasma electrolytes, renal function and plasma osmolarity
dehydrate makes the patients very sensitive to the hypotensive effect of GA
intravascular volume should be replaced with isotonic fluids over 24-48hours

112
Q

What is the pre-operative treatment for ADH deficiency?

A

Vasopressin is not alway recommended because surgical stress increases ADH secretion
measurement of plasma osmolarity, UOP and serum sodium during the intraopertive and immediate postoperative period
isotonic fluids during the intraoperative period & if the plasma osmolarity rises above 290 mOSm/L D5W should be administered (hypotonic solution shifts fluid into cells for the cell to swell)

113
Q

What is the treatment for complete DI?

A

desmopressin 1-2mcg/kg IV/SQ intranasal spray BID

aqueous vasopressin 5-10 unites IM/SQ q 8-12 hours

114
Q

When should caution be used in DDAVP administration for complete DI?

A

if patient has CAD

ADH substitutes like ADH causing hypertension due to arterial constriction

115
Q

What is SIADH?

A

syndrome of inappropriate antidiuretic hormone

116
Q

Describe SIADH

A

disorder characterized by high circulating levels of ADH relative to plasma osmolarity & serum sodium concentration

117
Q

What does ADH secretion cause in the kidneys in SIADH?

A

kidneys will reabsorb water and despite the presence of hyponatremia and plasma hypotonicity

118
Q

What occurs at a cellular level in SIADH?

A

expanison of ICF and ECF as well as hemodilution and weight gain

119
Q

What is difference in the urine and plasma in SIADH

A

urine is hypertonic compared to plasma

urine output is low

120
Q

Serum osmolarity in SIADH

A

<270mOsm/L

121
Q

Serum osmolarity in DI

A

> 290mOsm/L

122
Q

Serum sodium in SIADH

A

<130mEq/L

123
Q

Serum sodium in DI

A

> 145mEq/L

124
Q

Urine Volume in SIADH

A

low

125
Q

Urine Volume in DI

A

high > 2ml/kg/hr

126
Q

Urine osmolarity in SIADH

A

hypertonic urine relative to plasmA

127
Q

urine osmolarity in DI

A

hypotonic urine relative to plasma

128
Q

Treatment of SIADH (chart)

A

fluid restriction

if patient is symptomatic or serum sodium <115-120mEq/L consider hypertonic saline

129
Q

Treatment of DI

A

DDVAP or vasopressin

130
Q

What is the difference between desmopressin and vasopressin?

A

desmopressin has less vasoconstrictor effects then vasopressin

131
Q

what are the three main clinical features of SIADH?

A

water intoxification
dilutional hyponatremia
brain edema

132
Q

What are the severity of symptoms in SIADH determined by?

A

the degree of hyponatremia and rate of decrease in serum sodium

133
Q

What are s/s of brain edema?

A 
lethargy
headache
nausea
mental confusion
seizures
coma
134
Q

What are causes of SIADH?

A 
hypothyroidism
pulmonary infection
lung carcinoma
head trauma
intracranial tumors
pituitary surgery
135
Q

What are medications that can cause SIADH?

A 
carbamazepine
tricyclic antidepressants
chlorpropamide
cyclophosphamide
oxytocin
nicotine
clofibrate
136
Q

What are intracranial tumors that cause SIADH?

A

neoplasm (especially small cell carcinomas of the lung are common)
ADH produced by these tumors are identical to that produced by the hypothalamus

137
Q

How do you treat mild SIADH with no symptoms of hyponatremia?

A

treat with water restriction of 800-1000ml/day of NS

138
Q

What is the treatment to SIADH with acute, severe hyponatremia with plasma sodium concentration of <115-120 emq/l or acute neurological symptoms

A

IV hypertonic saline with or without loop diuretic

139
Q

How frequent should serum sodium be checked when treating SIADH?

A

2 hours

140
Q

What are pre-operative evaluation for SIADH?

A

careful status evaluation
perioperative fluid management (fluid restriction that involves use of isotonic solution)
CVP can help with guiding volume replacement
frequent measures of urine output, urine osmolarity, plasma osmolarity, and serum sodium concentrations
prevent nausea because it is potent for releasing ADH

N935 Pathophysiology (6 decks)

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