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endocrine Flashcards

1
Q

endocrine

A

cell releases a substance that travels through the blood stream before it acts on different cells

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2
Q

paracrine

A

cell releases a substance that acts on adjacent cells

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3
Q

autocrine

A

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

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4
Q

anterior pituitary releases which hormones (6)

A

follicle stimulating hormone
leutinizing hormone
adrenocorticotropin
thyroid stimulating hormone
prolactin
growth hormone

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5
Q

what does hypothalamus communicate with

A

pituitary gland. hypothalamus monitors hormone levels and instructs pituitary gland accordingly

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6
Q

where does the pituitary gland reside

A

sella turcica.

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7
Q

systemic hormones affected by negative feedback systems

A

triiodothyronine (T3) regulates TRH release
cortisol regulates CRH release
testosterone, estrogen, progesterone regulates LHRH release
growth hormone and insulin growth factor 1 regulate GHRH and GHIH release

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8
Q

hormones not affected by negative feedback

A

oxytocin (positive feedback only)
prolactin (under neural control, increased DA increases prolactin release ex: metoclopramide)

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9
Q

anesthetic considerations for acromegaly

A

distorted facial features (difficult mask ventilation)
large tongue, teeth, and epiglottis (difficult laryngoscopy)
subglottic narrowing and vocal cord enlargement
turbinate enlargement (risk of epistaxis, try to avoid nasal intubation if possible)
OSA is common
increased risk of HTN, CAD, rhythm disturbances
glucose intolerance
skeletal muscle weakness
entrapment neuropathies common

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10
Q

when compared to T4, T3 has

A

higher potency
shorter t1/2
less protein bound
smaller concentration in blood

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11
Q

compare and contrast SIADH and ADH
associated conditions
presentation
plasma
urine
tx

A
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12
Q

anesthetic considerations for acromegaly

A

-distorted facial features (difficult mask)
-large tongue, teeth, epiglottis (difficult laryngoscopy)
-subglottic narrowing and vocal cord enlargement (use smaller tube)
-turbinate enlargement (risk of epistaxis- avoid nasal intubations if possible)
-OSA common
-increased HTN CAD and rhythm disturbances
-glucose intolerance
-skeletal muscle weakness
-entrapment neuropathies are common

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13
Q

in the patient with hypoactive thyroid, how is TSH affected

A

theres not enough thyroid hormone to suppress TSH, so it remains chronically elevated
(-TSH stimulates iodide pump to make T4 and T3)
-thyoglobulin colloid is increased as a response to chronically elevated TSH which is why goiter appears

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14
Q

how does hyperthyroidism affect BMR, O2 consumption, CO2

A

increased BMI, O2 consumption, and CO2 production

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15
Q

review s/sx of hyperthyroidism
CV
resp
MAC
GI
cellular metabolism
MSK
growth

A
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16
Q

hyperthyroidism etiologies

A

graves (most common)
MG
multimodal goiter
carcinoma
pregnancy
pituitary adenoma
amiodarone (less common)

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17
Q

hypothyroidism etiologies

A

hashimotos (most common)
iodine deficiency
hypothalamic pituitary dysfunction
neck radiation
thyroidectomy
amiodarone (more common)

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18
Q

hyperthyroidism
dx
cv sx
pulm sx
general findings

A
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19
Q

hypothyroidism
dx
cv sx
pulm sx
general findings

A
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20
Q

when is thyroid storm most likely to happen

A

16-18 hours after surgery

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21
Q

what is etiology of myxedema coma

A

hypothyroidism

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22
Q

define cretinism

A

neonatal hypothyroidism that results in limited physical and mental development

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23
Q

hyperthyroidism anesthetic considerations: drugs to utilize, MOA, and key points (4)

A
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24
Q

hyperthyroidism emergency surgery considerations: management

A

-do not do elective until euthyroid (6-8w)
-emergency surgery warrants BB, potassium iodide, and glucocorticoids. start PTU
-goiter= awake intubation
-avoid sympathomimetics, anticholinergics, ketamine, and pancuronium
-exopthalmos increases risk of corneal abrasion
-titrate NMB’s carefully- increased risk of MG and myopathy
-hypoxia and hypercarbia stimulate SNS
-careful with positioning, increased bone turnover increases risk of osteoporosis

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25
Q

RLN injury during thyroid surgery

A
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26
Q

is laryngospasm in the immediate postoperative period with a hyperthyroid patient due to hypocalcemia

A

no because that complication occurs 24-48h after surgery

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27
Q

s/sx thyroid storm

A

-fever >38.5
-tachycardia
-HTN
-CHF
-shock
-confusion and agitation
-n/v

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28
Q

management thyroid storm (four B’s and other considerations)

A

-block synthesis (methimazole, carbimapezole, PTU, potassium iodide)
-block release (radioactive iodide, potassium iodide)
-block T4-T3 conversion (PTU, propranolol, glucocorticoids)
-block beta receptors (propranolol, esmolol)

-dont give aspirin but give acetaminophen for fever and cool patient
-CV support

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29
Q

is inhalation induction faster or slower with myxedema coma patients

A

faster (CO is POO)

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30
Q

sensitivity to NDNMB’s in hypothyroid patients

A

increased due to muscle weakness

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31
Q

how does MAC change with thyroid issues

A

it doesn’t, hoe

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32
Q

how to combat hyponatremia r/t hypothyroidism

A

D5NS- impaired clearance of free water is combatted with this

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33
Q

compare and contrast PTH and calcitonin
site of production
site of release
stimulator for release
physiologic effect
mechanism

A
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34
Q

most common cause of hypercalcemia

A

primary hyperparathyroidism

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35
Q

most common cause of primary hyperparathyridism

A

parathyroid adenoma

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36
Q

presentation of patient with primary hyperparathyroidism

A

increased PTH levels, hypercalcemia, hypophosphatemia

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37
Q

most common cause of secondary hyperparathyroidism

A

CKD

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38
Q

what is the SE of secondary hyperparathyroidism r/t CKD

A

renal osteodystrophy

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39
Q

secondly hyperparathyroidism and PTH output

A

something stimulates parathyroid glands to increase PTH output

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40
Q

tx of primary hypoparathyroidism (most commonly from surgical removal)

A

supplemental Ca2+, vitD, mag

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41
Q

hyperparathyroidism and effects:
CV
neuro
MSK
GI
GU

A
42
Q

hypoparathyroidism and effects:
CV
neuro
MSK
GI

A
43
Q

list 4 ways body responds to decreased calcium

A
  1. parathyroid releases PTH
  2. osteoclasts in bone release calcium
  3. calcium is reabsorbed in kidneys
  4. calcium reabsorption in gut increases presence of vitamin D
44
Q

adrenal zones and what it releases

A

salt, sugar, sex

45
Q

RAAS overview

A
46
Q

aldosterone release is increased by (3)

A

RAAS activation
increased K
decreased Na

47
Q

does aldosterone regulate sodium concentration or osmolarity

A

no.
when Na is reabsorbed into peritubular capillaries, water follows. Na concentration does not change
osmolarity is controlled via ADH

48
Q

does ADH increase reabsorption of water and sodium

A

yes, water but NO sodium

49
Q

how does aldosterone affect renal function

A

increases Na/water reabsorption
increases K/H excretion

50
Q

what are the hemodynamic effects of cortisol

A

increases sensitivity of beta receptors on myocardium and necessary for vasoconstrictive effects of catecholamines

51
Q

does aldosterone have glucocorticoid effects

A

no

52
Q

analog of cortisol used to tx addisons

A

prednisone

53
Q

3 steroid that do not have mineralcorticoid effects

A
  1. dexamethasone
  2. betamethasone
  3. triamcinilone
54
Q

does cortisol have glucocorticoid and mineralcorticoid effects

A

yes 1:1

55
Q

what steroid has the greatest mineralcorticoid effect

A

aldosterone- 3,000 times more potent than cortisol

56
Q

conns syndrome etiology (primary and secondary)

A
57
Q

clinical features of conns syndrome (mineralcorticoid excess)

A

HTN (Na and water retention)
hypokalemia (K wasting)
metabolic alkalosis (H wasting)

58
Q

tx of conns syndrome (mineralcorticoid excess)

A

removal of aldosterone secreting tumor
aldosterone antagonists- spironolactone or eplerenone
K supplementation
Na restriction

59
Q

cushings disease is a result of excess

A

ACTH

60
Q

clinical features of cushings (remember cortisol has mineralcorticoid glucocorticoid and androgenic effects)

A

glucocorticoid: hyperglycemia
weight gain
increased risk of infection
osteoporosis
muscle weakness
mood DO

mineralcorticoid: HTN, hypokalemia, metabolic alkalosis

androgenic: women become masculinized (hirsutism, hair thinning, acne, amenorrhea)
men become feminized (gynecomastia, impotence)

61
Q

tx of cushings

A

transphenoidal resection of ptuitary
pituitary radiation
adrenalectomy (if adrenal tumor)

62
Q

cushings anesthetic implications

A

-special attention to aseptic technique
-careful with positioning
-consider postop steroid supplementation
-DI (transient) following pituitary resection
-include hypoaldosteronism considerations

63
Q

adrenal insufficiency (addisons) characterized by

A

destruction of all cortical zones

64
Q

etiology of adrenal insufficiency

A
65
Q

clinical features of adrenal insufficiency

A

muscle weakness/fatigue
HoTN
Hoglycemia
hyponatremia
hyperkalemia
metabolic acidosis
n/v
hyperpigmentation

66
Q

clinical features of acute adrenal crisis

A

hemodynamic instability/collapse
fever
hypoglycemia
impaired mental status

67
Q

tx of adrenal insufficiency (addisons)

A

steroid replacement therapy (15-30mg cortisol/day)

68
Q

tx of acute adrenal crisis

A

steroid replacement therapy (hydrocortisone 100mg and 100-200mg q24h)
ECF volume expansion (D5NS)
hemodynamic supportr

69
Q

is there a risk of HPA suppression?
yes if (prednisone dose, stress dose?)
maybe if
no if

A
70
Q

should patients receive a steroid dose if
superficial surgery
minor surgery
moderate surgery
major surgery

and how much if so

A
71
Q

what do alpha, beta, delta, and polypeptide cells produce in the pancreas

A
72
Q

why do we give insulin and D50 for hyperkalemia

A

stimulation of Na/K/ATPase via insulin decreases serum K

73
Q

hormones that stimulate insulin release

A

glucagon
GH
catecholamines
cortisol

74
Q

drug category that increases insulin release

A

Beta agonists

75
Q

drug categories that decrease insulin release

A

BB, volatiles

76
Q

things that stimulate glucagon release

A

hypoglycemia
stress
trauma
sepsis
beta agonists

77
Q

things that decrease glucagon release

A

somatostatin (GHIH)

78
Q

how does glucagon affect the heart

A

increases myocardial contractility, HR, and AV conduction by increasing intracellular production of cAMP
(1-5mg IV)

79
Q

somatostatin inhibits

A

insulin and glucose release, inhibits splanchnic BF, gastric motility, gallbladder contraction

80
Q

pancreatic polypeptide inhibits

A

pancreatic exocrine secretion, gallbladder contraction, gastric acid secretion, gastric motility

81
Q

DM dx criteria

A
82
Q

dx criteria for metabolic syndrome is at least 3 of the following

A
83
Q

DKA (gap acidosis and hyperglycemia) overview

A
84
Q

HHS overview

A
85
Q

classic triad of sx for DM

A

polyuria
dehydration
polydipsia

86
Q

do DM patients have increased risk of diarrhea and constipation

A

yeh

87
Q

do DM patients have trouble regulating temp

A

yeah, at increased risk of hypothermia

88
Q

what does this mean

A

prayer sign in DM patients- decreased ROM of AO joint

89
Q

can HCTZ mask sx of intraop hypoglycemia

A

no

90
Q

which insulin’s dont have a peak

A

glargine (long acting)
degludec (ultra long acting)

91
Q

drugs that enhance hypoglycemic effects of insulin

A

MAOI’s
salicylates
tetracyclines

92
Q

carcinoid syndrome etiology

A

secretion of vasoactive substances from enterochromaffin cells

93
Q

carcinoid syndrome can also occur in these two instances

A
  1. hepatic fx is normal but the amount of hormone produced by the tumor exceeds the livers ability to clear it
  2. tumor resides in a location where BF bypasses liver such as the lungs
94
Q

most common signs of carcinoid syndrome (2)

A

flushing and diarrhea

95
Q

sx of carcinoid hormones (3)

A
96
Q

carcinoid syndrome and concurrent cardiac diseases include

A

pulmonic stenosis and tricuspid regurg

97
Q

carcinoid syndrome: protect RV by

A

avoiding conditions that increase PVR (hypoxia, hypercarbia, N2O, light anesthesia, acidosis)

98
Q

s/sx carcinoid crisis

A

tachycardia
hyper or hypotension
intense flushing
abdominal pain
diarrhea

99
Q

drugs to give when patient has carcinoid syndrome

A

somatostatin (octreotide or lanreotide) inhibits release of vasoactive substances from carcinoid tumors. improves hemodynamic stability
antihistamines (H1 and H2- diphenhydramine and ranitidine or cimetidine)
5HT3 antagonists
steroids
phenylephrine or vaso for HoTN

100
Q

drugs to AVOID when patient has carcinoid syndrome

A

histamine releasing drugs (morphine, meperidine, atracurium, thiopental, succ)
succ induced fasciculations can cause hormone release from tumor
exogenous catecholamines can potentiate hormone release
sympathomimetic agents: ephedrine and ketamine

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