endocrine Flashcards by Sydney Elmore

endocrine

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

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paracrine

cell releases a substance that acts on adjacent cells

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autocrine

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

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anterior pituitary releases which hormones (6)

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

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what does hypothalamus communicate with

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

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where does the pituitary gland reside

sella turcica.

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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

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hormones not affected by negative feedback

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

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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

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when compared to T4, T3 has

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

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

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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

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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

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how does hyperthyroidism affect BMR, O2 consumption, CO2

increased BMI, O2 consumption, and CO2 production

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

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hyperthyroidism etiologies

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

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hypothyroidism etiologies

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

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hyperthyroidism
dx
cv sx
pulm sx
general findings

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hypothyroidism
dx
cv sx
pulm sx
general findings

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when is thyroid storm most likely to happen

16-18 hours after surgery

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what is etiology of myxedema coma

hypothyroidism

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define cretinism

neonatal hypothyroidism that results in limited physical and mental development

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

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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

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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

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

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

analog of cortisol used to tx addisons

prednisone

3 steroid that do not have mineralcorticoid effects

1. dexamethasone 2. betamethasone 3. 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

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

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

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