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N935 Advanced Pathophysiology > endocrine pituitary gland > Flashcards

endocrine pituitary gland Flashcards

1
Q

endocrine glands secrete

A

hormones directly into the surrounding ECF

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2
Q

exocrine glands secrete

A

products through ducts

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3
Q

examples of exocrine glands

A

salivary and sweat glands

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4
Q

examples of endocrine glands

A

pituitary, thyroid, parathyroid, pancreas, adrenal, ovaries, testes, placenta

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5
Q

endocrine glands control

A

growth, behavior, metabolism, reproduction

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6
Q

hormones are

A

chemical messengers that transport info from one set of cells to another (endocrine cells to target cells)

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7
Q

binding to a target cell receptor is the primary event that initiates

A

a response to a hormone

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8
Q

the hormone receptor has high

A

specificity and affinity for the correct hormone

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9
Q

the synthesis and secretion of hormones by endocrine glands are regulated by

A

neural control, biorhythms, and feedback mechanisms

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10
Q

neural control of hormone secretion

A

can suppress or stimulate secretion

stimuli: pain, smell, touch, stress, sight, taste

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11
Q

hormones under neural control include

A

catecholamines, ADH, cortisol

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12
Q

biorhythms are

A

genetically encoded or acquired

can be circadian, weekly, or seasonal and vary with stages of life

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13
Q

pituitary function

A

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

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14
Q

the pituitary and hypothalamus don’t have a

A

blood brain barrier to allow for feedback products to have a potent effect on them

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15
Q

the anterior lobe of the pituitary

A

adenohypophysis

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16
Q

the posterior lobe of the pituitary

A

neurohypophysis

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17
Q

blood supply to the pituitary is via

A

the superior and inferior hypophyseal arteries

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18
Q

the anterior pituitary secretes which hormones

A

6 hormones:

growth hormone, adrenocorticotropic, thyroid stimulating, follicle stimulating hormone, luteinizing hormone, prolactin

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19
Q

Thyrotropin releasing hormone pathway

A

released by hypothalamus to anterior pituitary that will release thyroid stimulating hormone to the thyroid glands

primary peripheral feedback hormone: triiodothyronine

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20
Q

Corticotropin releasing hormone pathway

A

released by hypothalamus to anterior pituitary to release adrenocorticotropic hormone (ACTH) to adrenal cortex

primary feedback: cortisol

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21
Q

gonadotropin releasing hormone pathway

A

released from hypothalamus to anterior pituitary to release follicle stimulating and luteinizing hormones to the gonads

primary feedback: estrogen, progesterone, testosterone

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22
Q

what are the hormones of the anterior pituitary that can be releasing or inhibiting

A

prolactin, growth hormone

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23
Q

primary pituitary disorder

A

defect to the peripheral endocrine gland (target gland)

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24
Q

secondary pituitary disorder

A

defect to the pituitary gland (ex. tumor)

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25
Q

tertiary pituitary disorder

A

defect to the hypothalamus (not common)

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26
Q

anterior pituitary HYPOsecretion causes

A

nonfunctioning tumors, hypophysectomy, postpartum shock, irradiation, trauma, infiltrative disorders (sarcoidosis)

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27
Q

signs and symptoms with anterior pit HYPOsecretion

A

visual changes (optic nerve near pit and can be compressed), papilloedema, increased ICP

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28
Q

anterior pituitary HYPERsecretion caused by

A

caused by benign adenomas usually

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29
Q

3 most common hormones that are secreted with anterior pit HYPERsecretion

A

prolactin, ACTH, and GH

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30
Q

growth hormone increases during

A

during stress, hypoglycemia, exercise, and deep sleep

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31
Q

major target for GH is the

A

liver, stimulates production of insulin like growth factor type 1 which mediates many of the effects of GH

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32
Q

GH hypersecretion

A

caused by growth hormone secreting pituitary adenoma
in adults - acromegaly
gigantism

33
Q

acromegaly

A

sustained hypersecretion of GH after adolescence

34
Q

gigantism

A

hypersecretion of GH prior to puberty (before closure of growth plates)

35
Q

common features of acromegaly

A 
skeletal and soft tissue overgrowth
visceromegaly
osteoarthritis
glucose intolerance
skeletal muscle weakness
extrasellar tumor extension
peripheral neuropathy
36
Q

comorbities with acromegaly

A

HTN, cardiomyopathy, ischemic heart disease, diabetes, osteoarthritis, skeletal muscle weakness, increased lung volumes, sleep apnea, increased liver, spleen, kidneys, heart

37
Q

acromegaly treatment

A 
restore normal GH levels
microsurgical removal of the tumor with preservation of the gland
transsphenoidal approach - small
intracranial approach - large
irradiation
supressant drug therapy
38
Q

airway management considerations for acromegaly

A

enlarged tongue, lips, epiglottis, nasal turbinates, overgrowth of mandible, vocal cord dysfunction/narrowing
prone to upper airway obstruction, difficult mask, impaired visualization of cords, subglottic narrowing, dyspnea/hoarseness

39
Q

aline considerations for acromegaly

A

check collateral circulation because there may be hypertrophy of the carpal tunnel ligament which can impede ulnar artery flow

40
Q

transsphenoidal approach considerations for acromegaly

A 
HOB 15 degrees
aline
lumbar drain maybe
monitor for VAE
treat intraop HoTN with hydrocortisone 50-100 mg IV
minimal blood loss
41
Q

venous air embolism s/s

A

drop in etco2
bradycardia/heart block
millwheel heart sound (heard with precordial or doppler)

42
Q

complications with transsphenoidal approach

A

cranial nerve damage, epistaxis, hyponatremia, cerebral spinal fluid leak, DI

43
Q

diabetes insipidus results in

A

insufficient ADH

44
Q

diabetes insipidus diagnosis and treatment

A

diagnosis: low urine osmolarity, high serum osmolarity, hypernatremia
treat: monitor urine and electrolytes, DDAVP, restrict Na+ intake, fluid replacement

45
Q

patient education getting transsphenoidal

A

there will be packing in their nose and they will need to breathe through their mouth when they wake up from surgery

46
Q

posterior pituitary secretes

A

ADH and oxytocin

47
Q

ADH controls

A

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

48
Q

Oxytocin stimulates

A

uterine contractions, breast milk ejection, induce labor, decrease postpartum bleeding

49
Q

posterior pituitary hormones synthesis/pathway

A

So, oxytocin and ADH are synthesized in the hypothalamus and travel via neurons on the hypothalamic-hypophyseal tract to the posterior pituitary where they are stored in axon terminals, they then are released into the blood when hypothalamic neurons fire

50
Q

3 types of vasopressin receptors

A

v1 - mediates vasoconstriction
v2 - mediates water reabsorption in the renal collecting ducts
v3 - found in CNS and stimulate modulation of corticotrophin secretion

51
Q

what stimulates ADH release

A

increased plasma sodium, increased serum osmolality, decreased blood volume, smoking, pain, stress, nausea, vasovagal reaction, angII, PPV

52
Q

neurogenic or central DI caused by

A

caused by inadequate release of ADH from head trauma, brain tumors, neurosurgery, infiltrating pituitary lesions

53
Q

nephrogenic DI caused by

A

renal tubular resistance to ADH

54
Q

nephrogenic DI may be associated with

A

hypokalemia, hyperkalemia, genetic mutations, hypercalcemia, medication induced nephrotoxicity

55
Q

inhibitors of ADH action or release

A

ethanol, demeclocyline, phenytoin, chlorpromazine, lithium

56
Q

symptoms of ADH deficiency

A

polyuria (hallmark sign), dilute urine, dehydration, hypernatremia, low urine osmolarity <300, urine specific gravity <1.010, urine volume >2mL/kg/hr, serum osmolarity >290, sodium >145
hyperreflexia, weakness, lethargy, seizures, coma

57
Q

major mechanism for controlling DI in awake patients

A

thirst

58
Q

mild DI or incomplete DI treatment

A

meds that augment or release ADH or increase receptor sensitivity
carbamazepine, clofibrate

59
Q

severe DI or complete DI treatment (plasma osmolarity >290)

A

DDAVP 1-2 mcg IV/SQ q12 hours or 5-40 mcg intranasal spray BID
aqueous vasopressin 5-10 units IM/SQ q8-12 hours

60
Q

DDAVP

A

selective V2 agonist
DOA: 8-12 hours
less vasopressor activity
dose: 5-40 mcg/kg nasally, 0.5-2 mcg/day BID SQ
increases vwb factor (give 30 minutes prior to surgery)

61
Q

perioperative administration of vasopressin is not necessary for incomplete DI because

A

the stress of surgery increases ADH secretion

62
Q

ADH can cause ____ due to ___ and caution is necessary in patients with CAD

A

hypertension; arterial vasoconstriction

63
Q

if plasma osmolarity rises above 290 what should be administered

A

D5W (free water)

64
Q

hypersecretion of ADH can lead to

A

SIADH (syndrome of inappropriate ADH)

65
Q

SIADH

A

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

66
Q

ADH secretion causes the kidneys to ___ in SIADH

A

continue to reabsorb water

67
Q

the urine is ___ relative to plasma and urine output is ___ in SIADH

A

hypertonic; low

68
Q

SIADH vs DI

A

SIADH - serum osmolarity, sodium, and urine volume are low, urine osmolarity is hypertonic, treat with fluid restriction and hypertonic saline

DI - serum osmolarity, sodium, and urine volume are high, urine osmolarity is hypotonic, treat with DDAVP or vasopressin

69
Q

clinical features of SIADH

A 
water intoxication
dilutional hyponatremia 
brain edema (lethargy, HA, nausea, confusion, seizures, coma)
70
Q

severity of symptoms of dilutional hyponatremia is related to

A

the degree of hyponatremia and the rate of decrease in serum sodium

71
Q

what procedure can cause dilutional hyponatremia?

A

TURP

72
Q

causes of inappropriate secretion of ADH

A

hypothyroidism, pulmonary infection, lung carcinoma*, head trauma, intracranial tumors, pituitary surgery, meds (carbamazepine, TCAs, chlorpropamide, cyclophosphamide, oxytocin, nicotine, clofibrate)

73
Q

neoplasms, especially small cell carcinomas of the lung are a common cause of

A

SIADH

74
Q

mild SIADH with no symptoms of hyponatremia treatment

A

water restriction of 800-`1000mL/day of NS

75
Q

SIADH with acute,severe hyponatremia (plasma sodium <115-120) or acute neurological symptoms treatment

A

IV hypertonic saline w/ or w/o loop diuretic

76
Q

what can happen if rapidly increase sodium levels

A

central pontine demyelination syndrome = acute loss of brain water and neurological damage

77
Q

plasma concentration of sodium must be replaced slow at a rate not to exceed

A

1-2 mEq/L or 6-12 mEq/L in 24 hours

78
Q

what is something we can easily prevent in patients with SIADH perioperatively

A

prevent nausea!

N935 Advanced Pathophysiology (15 decks)

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