endocrine Flashcards
endocrine
cell releases a substance that travels through the blood stream before it acts on different cells
paracrine
cell releases a substance that acts on adjacent cells
autocrine
cell releases a substance that acts on the surface of the same cell
anterior pituitary releases which hormones (6)
follicle stimulating hormone
leutinizing hormone
adrenocorticotropin
thyroid stimulating hormone
prolactin
growth hormone
what does hypothalamus communicate with
pituitary gland. hypothalamus monitors hormone levels and instructs pituitary gland accordingly
where does the pituitary gland reside
sella turcica.
systemic hormones affected by negative feedback systems
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
hormones not affected by negative feedback
oxytocin (positive feedback only)
prolactin (under neural control, increased DA increases prolactin release ex: metoclopramide)
anesthetic considerations for acromegaly
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
when compared to T4, T3 has
higher potency
shorter t1/2
less protein bound
smaller concentration in blood
compare and contrast SIADH and ADH
associated conditions
presentation
plasma
urine
tx
anesthetic considerations for acromegaly
-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
in the patient with hypoactive thyroid, how is TSH affected
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
how does hyperthyroidism affect BMR, O2 consumption, CO2
increased BMI, O2 consumption, and CO2 production
review s/sx of hyperthyroidism
CV
resp
MAC
GI
cellular metabolism
MSK
growth
hyperthyroidism etiologies
graves (most common)
MG
multimodal goiter
carcinoma
pregnancy
pituitary adenoma
amiodarone (less common)
hypothyroidism etiologies
hashimotos (most common)
iodine deficiency
hypothalamic pituitary dysfunction
neck radiation
thyroidectomy
amiodarone (more common)
hyperthyroidism
dx
cv sx
pulm sx
general findings
hypothyroidism
dx
cv sx
pulm sx
general findings
when is thyroid storm most likely to happen
16-18 hours after surgery
what is etiology of myxedema coma
hypothyroidism
define cretinism
neonatal hypothyroidism that results in limited physical and mental development
hyperthyroidism anesthetic considerations: drugs to utilize, MOA, and key points (4)
hyperthyroidism emergency surgery considerations: management
-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
RLN injury during thyroid surgery
is laryngospasm in the immediate postoperative period with a hyperthyroid patient due to hypocalcemia
no because that complication occurs 24-48h after surgery
s/sx thyroid storm
-fever >38.5
-tachycardia
-HTN
-CHF
-shock
-confusion and agitation
-n/v
management thyroid storm (four B’s and other considerations)
-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
is inhalation induction faster or slower with myxedema coma patients
faster (CO is POO)
sensitivity to NDNMB’s in hypothyroid patients
increased due to muscle weakness
how does MAC change with thyroid issues
it doesn’t, hoe
how to combat hyponatremia r/t hypothyroidism
D5NS- impaired clearance of free water is combatted with this
compare and contrast PTH and calcitonin
site of production
site of release
stimulator for release
physiologic effect
mechanism
most common cause of hypercalcemia
primary hyperparathyroidism
most common cause of primary hyperparathyridism
parathyroid adenoma
presentation of patient with primary hyperparathyroidism
increased PTH levels, hypercalcemia, hypophosphatemia
most common cause of secondary hyperparathyroidism
CKD
what is the SE of secondary hyperparathyroidism r/t CKD
renal osteodystrophy
secondly hyperparathyroidism and PTH output
something stimulates parathyroid glands to increase PTH output
tx of primary hypoparathyroidism (most commonly from surgical removal)
supplemental Ca2+, vitD, mag
hyperparathyroidism and effects:
CV
neuro
MSK
GI
GU
hypoparathyroidism and effects:
CV
neuro
MSK
GI
list 4 ways body responds to decreased calcium
- parathyroid releases PTH
- osteoclasts in bone release calcium
- calcium is reabsorbed in kidneys
- calcium reabsorption in gut increases presence of vitamin D
adrenal zones and what it releases
salt, sugar, sex
RAAS overview
aldosterone release is increased by (3)
RAAS activation
increased K
decreased Na
does aldosterone regulate sodium concentration or osmolarity
no.
when Na is reabsorbed into peritubular capillaries, water follows. Na concentration does not change
osmolarity is controlled via ADH
does ADH increase reabsorption of water and sodium
yes, water but NO sodium
how does aldosterone affect renal function
increases Na/water reabsorption
increases K/H excretion
what are the hemodynamic effects of cortisol
increases sensitivity of beta receptors on myocardium and necessary for vasoconstrictive effects of catecholamines
does aldosterone have glucocorticoid effects
no
analog of cortisol used to tx addisons
prednisone
3 steroid that do not have mineralcorticoid effects
- dexamethasone
- betamethasone
- triamcinilone
does cortisol have glucocorticoid and mineralcorticoid effects
yes 1:1
what steroid has the greatest mineralcorticoid effect
aldosterone- 3,000 times more potent than cortisol
conns syndrome etiology (primary and secondary)
clinical features of conns syndrome (mineralcorticoid excess)
HTN (Na and water retention)
hypokalemia (K wasting)
metabolic alkalosis (H wasting)
tx of conns syndrome (mineralcorticoid excess)
removal of aldosterone secreting tumor
aldosterone antagonists- spironolactone or eplerenone
K supplementation
Na restriction
cushings disease is a result of excess
ACTH
clinical features of cushings (remember cortisol has mineralcorticoid glucocorticoid and androgenic effects)
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)
tx of cushings
transphenoidal resection of ptuitary
pituitary radiation
adrenalectomy (if adrenal tumor)
cushings anesthetic implications
-special attention to aseptic technique
-careful with positioning
-consider postop steroid supplementation
-DI (transient) following pituitary resection
-include hypoaldosteronism considerations
adrenal insufficiency (addisons) characterized by
destruction of all cortical zones
etiology of adrenal insufficiency
clinical features of adrenal insufficiency
muscle weakness/fatigue
HoTN
Hoglycemia
hyponatremia
hyperkalemia
metabolic acidosis
n/v
hyperpigmentation
clinical features of acute adrenal crisis
hemodynamic instability/collapse
fever
hypoglycemia
impaired mental status
tx of adrenal insufficiency (addisons)
steroid replacement therapy (15-30mg cortisol/day)
tx of acute adrenal crisis
steroid replacement therapy (hydrocortisone 100mg and 100-200mg q24h)
ECF volume expansion (D5NS)
hemodynamic supportr
is there a risk of HPA suppression?
yes if (prednisone dose, stress dose?)
maybe if
no if
should patients receive a steroid dose if
superficial surgery
minor surgery
moderate surgery
major surgery
and how much if so
what do alpha, beta, delta, and polypeptide cells produce in the pancreas
why do we give insulin and D50 for hyperkalemia
stimulation of Na/K/ATPase via insulin decreases serum K
hormones that stimulate insulin release
glucagon
GH
catecholamines
cortisol
drug category that increases insulin release
Beta agonists
drug categories that decrease insulin release
BB, volatiles
things that stimulate glucagon release
hypoglycemia
stress
trauma
sepsis
beta agonists
things that decrease glucagon release
somatostatin (GHIH)
how does glucagon affect the heart
increases myocardial contractility, HR, and AV conduction by increasing intracellular production of cAMP
(1-5mg IV)
somatostatin inhibits
insulin and glucose release, inhibits splanchnic BF, gastric motility, gallbladder contraction
pancreatic polypeptide inhibits
pancreatic exocrine secretion, gallbladder contraction, gastric acid secretion, gastric motility
DM dx criteria
dx criteria for metabolic syndrome is at least 3 of the following
DKA (gap acidosis and hyperglycemia) overview
HHS overview
classic triad of sx for DM
polyuria
dehydration
polydipsia
do DM patients have increased risk of diarrhea and constipation
yeh
do DM patients have trouble regulating temp
yeah, at increased risk of hypothermia
what does this mean
prayer sign in DM patients- decreased ROM of AO joint
can HCTZ mask sx of intraop hypoglycemia
no
which insulin’s dont have a peak
glargine (long acting)
degludec (ultra long acting)
drugs that enhance hypoglycemic effects of insulin
MAOI’s
salicylates
tetracyclines
carcinoid syndrome etiology
secretion of vasoactive substances from enterochromaffin cells
carcinoid syndrome can also occur in these two instances
- hepatic fx is normal but the amount of hormone produced by the tumor exceeds the livers ability to clear it
- tumor resides in a location where BF bypasses liver such as the lungs
most common signs of carcinoid syndrome (2)
flushing and diarrhea
sx of carcinoid hormones (3)
carcinoid syndrome and concurrent cardiac diseases include
pulmonic stenosis and tricuspid regurg
carcinoid syndrome: protect RV by
avoiding conditions that increase PVR (hypoxia, hypercarbia, N2O, light anesthesia, acidosis)
s/sx carcinoid crisis
tachycardia
hyper or hypotension
intense flushing
abdominal pain
diarrhea
drugs to give when patient has carcinoid syndrome
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
drugs to AVOID when patient has carcinoid syndrome
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
