• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

161 Cards in this Set

  • Front
  • Back
Homeostasis is maintained by these 2 systems
1 nervous system
2 endocrine system
_____ glands secrete more than 20 major hormones directly into the bloodstream (ductless) and not through glands.
List some of the effects of hormones
- stim or inhibition of growth
- mood swings
- induction or suppression of apoptosis
- activation or inhibition of the immune system
- regulation of metabolism
- preparation of body for mating, fighting, fleeing, and other activity
- preparation for puberty, child birth, menopause
- control of reproductive cycle
- hunger cravings
- sexual arousal
List the major endocrine glands
hypothalamus, pituitary, thyroid, parathyroid, adrenals, pineal, reproductive glands, pancreas
Hormones are classified according to chemical structure, into these 3 groups:
peptides, amino acid derivatives, steroids
These hormones are synthesized as prehormones and stored in the cells. Stimulation causes vesicle release into circulation. They are composed of amino acids.
insulin, GH, DDAVP, and ACTH are all examples of
peptide hormones
These hormones, like epinephrine, are derived from amino acids (Especially tyrosine)
amino acid derivatives
These hormones are lipids made from cholesterol
A ____ binds to a cell surface receptor, it does not enter the cell. The resulting complex activates an enzyme that catalyzes the synthesis of cAMP from ATP. cAMP activates other enzymes that are inactive.
peptide hormone
When peptide hormones bind to a cell surface receptor to cause intracellular activities, cAMP is a ____ messenger and the hormone on the outside of the cell is the ____ messenger.
second, first
What are the 2 groups of hormones derived from the amino acid tyrosine?
thyroid hormones and catecholamines
_____ are basically a double tyrosine with the critical incorporation of 3 or 4 iodine atoms.
Thyroid hormones
catecholamines include epinephrine and norepinephrine, which are used as both _______ and ______.
hormones and neurotransmitters
Steroid hormones enter the cell and bind to receptors in the _____. The hormone-receptor complex enters the _____ where it binds with _____ to activate specific genes. Genes (DNA) contain info to produce protein. When genes are active, protein is produced.
cytoplasm, nucleus, chromatin
What are the 5 mechanisms of regulation of hormone secretion?
1. neural control (pain, stress)
2. other hormones (Stimulating/releasing)
3. plasma concentrations of ions/nutrients
4. rate of delivery -- blood flow to a target organ
5. negative feedback loop
Most hormones are broken down in the ____ And ____.
liver and kidneys
Why do hormones bound to proteins have a longer duration?
because proteins protect them from metabolism
The "master gland", under control of the hypothalamus
pituitary gland
The anterior pituitary (adenohypophysis) regulates the activity of....
thyroid, adrenals and reproductive glands

secrete growth hormone (GH), gonadotropins, thyroid-stim hormone (TSH), cortisol production, follice-stim hormone (FSH)
The anterior pituitary secretes Leutinizing hormone (LH) which regulates _____, and prolactin (PRL) which regulates ______.
LH- ovulation
PRL- mammary development
FSH, LH, ACTH, and TSH are under ______ control.
negative feedback
The posterior pituitary (neurohypophysis) secretes....
antidiuretic hormone (ADH, vasopressin) and oxytocin
The hypothalamus secretes ____ and _____ hormones that control the anterior pituitary. It also synthesizes ____ and ____ which travel to the posterior pituitary.
releasing and inhibiting hormones, vasopressin adn oxytocin
List the 9 I's that cause pituitary gland dysfunction:
1. invasive: pituitary adenomas can grow large enough to cause hypopituitarism (craniopharyngioma)
2. injury: head trauma
3. infiltrative: abnormal cells (mets, granulomas) or substances (Fe+) infiltrate, replace, and destroy hypothalamus and/or pituitary tissues
4. immunologic: autoimmune destruction (Hashimotos thyroiditis, lymphocytic hypophysitis, autoimmune adrenalitis)
5. iatrogenic: physician induced hypopituitarism because of sx or radiation therapy
6. infections: TB, HIV
7. idiopathic: unknown cause
8. isolated: isolated defect in secretion of one pituitary hormone
9. infarction: ischemic damage (Cell death due to loss of blood supply)
This is hypopituitarism resulting from ischemic necrosis in hypotensive post-partum women.
Sheehan's syndrome
This hormone peaks during childhood and declines w age. It has no target receptor and affect all tissues. It stimulates bone growth, and increases blood glucose by decreasing sensitivity to insulin.
Growth hormone
Hyposecretion of growth hormone leads to
Hypersecretion of growth hormone leads to

massive bone growth, incr soft tissue (large lips, tongue, epiglottis), osteoarthritis, glucose intolerance, skeletal muscle weakness, CV/CAD/HTN, decreased corticosteroids
What are the anesthesia implications of acromegaly?
- difficult mask fit due to facial anatomy distortion
- difficult mask ventilation
- difficult to intubate due to size of airway
- may require awake FOB
- prone to subglottic stenosis
This type of DI results from an inability to secrete ADH causing water loss.
What are the causes of neurogenic DI?
TBI, tumors, transient DI after pituitary sx
This type of DI results from nonfunctioning receptors in renal collecting ducts, leading to water loss.
Nephrogenic DI
What are the causes of nephrogenic DI?
genetic, hypercalcemia, hypokalemia, med nephrotoxicity, ETOH
What are the anesthesia implications of DI?
electrolyte evaluation, volume status (if low, do slow restoration over 24-48 hrs)
Syndrome of inappropriate diuretic hormone (SIADH) results from high serum ____ levels, and leads to ____ and ____.
ADH, hyponatremia, plasma hypotonicity
Clinical signs of SIADH
hyponatremia, cerebral edema, lethargy, headaches, N/V, seizures, coma
What are the anesthesia considerations of SIADH?
1. fluid restriction
2. Na <115 may require aggressive tx: hypertonic saline correcting 0.5-0.7 mEq/hr
This is the permanent neuro damage resulting from rapid correction of SIADH hyponatremia.
central pontine demyelination syndrome
During the anterior pituitary surgical approach, the surgeon accesses the brain structures via ______ approach in the _____ position. There is potentially large blood loss and post op nasal packing. It is important for _____ wake up for post op neuro exam.
transphenoidal approach, half-sitting position, smooth/rapid wake up
Adults secrete ____ units/day of insulin from the ____ cells in the islets of langerhans.
50, beta cells
Insulin secretion leads to ___ And __ entry into adipose and muscle cells.
glucose, potassium
Insulin secretion increases ___ , ____, and ___ synthesis.
glucogen, protein, and fatty acid
Insulin decreases ______, (the conversion of glycogen to glucose), ______ (production of new glucose), ______ (break down glucose to fatty acids), lipolysis and protein catabolism
glycogenolysis, gluconeogenesis, ketogenesis
This hormone increases blood glucose
This is the impairment of carbohydrate metabolism caused by a deficiency of insulin activity.
DM is diagnosed with a fasting plasma glucose > _____ or a blood glucose > _____.
140, 126
What are the long term health consequences of DM?
HTN, MI, peripheral and cerebral vascular disease, neuropathies, renal fx
What are the 3 life-threatening acute complications of DM?
DKA, hyperosmolar nonketotic coma, hypoglycemia
DKA is an ______ metabolic acidosis.
This is the difference in the measured cations and the measured anions in serum, plasma or urine.
anion gap
What are the s/s of DKA?
dyspnea, abdominal pain, N/V, mental status changes
How is DKA treated?
correct hypovolemia, hyperglycemia, and total body K+ with insulin gtt, K+, and isotonic fluid

do not give LR because when it breaks down lactate creates more sugar, which you want to avoid
The goal of DKA treatment is....
to decr blood glucose by 75-100 per hr or 10%/hr
Why isnt there any ketoacidosis in hyperosmolar nonketotic coma?
there is enough insuiln available
What are the 2 main results of hyperosmolar nonketotic coma?
-dehydration: leads to renal failure, lactic acidosis, and predisposition to form intravasc thromboses
-hyperosmolarity: exceeding 360 mOsm/L alters cerebral H20 balance causing mental status change and seizure
How is hyperosmolar nonketotic coma treated?
fluid resuscitation and small amts of insulin
This is the result of excess insulin relative to carb intake (<50 mg/dL)
What happens if hypoglycemia goes untreated?
mental status changes, faintness, confusion, convulsions, permanent coma
Hypoglycemia is treated with _____ IV. Each mL of this will increase blood glucose of a 70 kg pt by approx ____ mg/dL.
50% glucose IV, 2 mg/dL
What are the anesthetic considerations of hypoglycemia?
- ST and T wave changes
- possible diabetic autonomic neuropathy
- delayed gastric emptying due to autonomic dysfunction
- renal dysfunction
- incr infection
- limited mobility joint syndrome
The primary goal intraoperatively is to avoid hypoglycemia, because it leads to
brain damage
Giving intraoperative insulin, 1 unit results in a decr in glucose by ____ mg/dL
How do you calculate insulin gtt infusion rate?
units per hr = plasma glucose/150
Post-operatively, it is important to closely monitor blood glucose after intervention during anesthesia due to...
variation in onset and duration of insulins.
Why does glucose rise 24-48 hrs post op after using LR as the IVF?
liver converts lactae to glucose
The ____ gland regulates metabolism.
Thyroid hormone contains_____(absorbed by GI tract) which is needed to manufacture necessary hormones.
What two hormones arise from the bond between iodine and amino acid tyrosine?
triiodothyronine (T3)
thyroxine (T4)
Excess TSH secreted to the thyroid gland results in hypertrophy called
Grave's disease, toxic multinodular goiter, thyroiditis, thyroid stim hormone secreting pituitary tumors, functioning thyroid adenomas, and OD of thyroid replacement hormone all cause....
Weight loss, heat intolerance, muscle weakness, diarrhea, hyperactive reflexes, nervousness, Afib, and CHF are all manifestations of which thyroid disorder?
How is hyperthyroid treated?
- drugs to inhibit hormone synthesis (propylthiouracil, methimazole), prevent hormone release, or mask signs of adrenergic overactivity (propranolol)
- B adrenergic antagonists to decr peripheral conversion of T4 to T3
- radioactive iodine
- subtotal thyroidectomy reserved for large toxic multinodular goiters or solitary toxic adenomas
What are the preop goals for hyperthyroid?
euthyroid w medical treatment, normal thyroid tests, resting HR < 85
What are the intraoperative considerations for hyperthyroid pts?
- monitor CV fcn and body temp
- protect eyes, exopthalmus
- HOB 15-20
- avoid ketamine (incr HR and BP), pancuronium (long acting and incr HR and BP), and indirect-acting adrenergic agonist
- thiopental induction agent of choice
- adequate anesthetic depth
- caution w NMBs
This is the most serious threat of hyperthyroid pts, manifesting w hyperpyrexia, tachycardia, altered mental status and hypotension. The onset is 6-24 hrs post op.
thyroid storm
Treatment for thyroid storm?
hydration, cooling, esmolol/propranolol
What are the complications of subtotal thyroidectomy?
- recurrent laryngeal nerve palsy --> hoarseness, aphonia, stridor
- hematoma formation, may cause airway compromise from tracheal collapse
- hypoparathyroidism: unintentional removal of parathyroid, acute hypocalcemia within 24-72 hrs
- unintentional pneumothorax
What are the causes of hypothyroid?
autoimmune disease (Hashimotos thyroiditis), thyroidectomy, radioactive iodine, antithyroid meds, iodine deficiency
What are the clinical signs of hypothyroid?
cretinism, weight gain, cold intolerace, hypoactive reflexes/lethargy, depr, decr HR/myocardial contractility/SV/CO, dull facial expressions, pleural/abdominl/pericardial effusions, low T4 level, incr TSH, myxedema coma, muscle fatigue, constipation
What are the pre-op concerns for hypothyroid pts?
prone to drug induced resp depression
careful w histamine H2 antagonists and reglan (due to slow gastric emptying time)
euthyroid state is ideal, but not an absolute contraind.
What are the intraop techniques for hypothyroid pts?
-ketamine recommended
-decr CO
-difficulty during intubation
What are the post-op concerns for hypothyroid pts?
-recovery may be delayed due to hypothermia, resp depr, or slowed drug biotransformation
-toradol good post op pain choice
____ glands are the principal regulators of Ca homeostasis
Parathyroid glands incr serum Ca by...
- promoting bone resorption
- limiting renal excretion
- indirectly enhancing GI absorption by its effect on Vit D metabolism
Parathyroid glands decr serum Phos by...
incr renal excretion
____% of Ca is bound to proteins and ___% is ionized.
40% bound, 60% ionized
_____ inhibits osteoclasts, decr blood Ca level.
____ promotes resorption of Ca from bone matrix into blood and retards loss of Ca in urine, incr blood Ca levels
Parathyroid Hormone
PTH stimulates the kidney to release _____, which in turn stimulates incr absorption of Ca from foods, incr blood Ca levels.
What are the primary and secondary causes of hyperparathyroidism?
Primary: adenoma, carcinoma, hyperpasia of parathyroid gland
Secondary: renal failure, intestinal malabsorption syndromes, ectopic hyperthyroidism due to production of PTH by rare tumors outside parathyroid gland
Clinical signs of hyperparathyroidism
most due to hypercalcemia (bone mets, Vit D intoxication, milk-alkali syndrome, sarcoidosis, prolonged immobilization), HTN, EKG changes, N/V, PUD, osteoporosis, mental changes
What is the treatment of parathyroid hyperplasia causing hyperparathyroidism?
removal of all 4 glands
What are the anesthesia considerations of a hyperparathyroid pt?
- assess vol status to avoid hypotension
- avoid hypovent.
- cardiac dysrhythmias
- adjust non depol NMBs due to pre-existing muscle weakness
- bone fractures
- vertebral compression
This is seen in a hypocalcemia caused by renal failure, hypomagnesemia, Vit D deficiency, or acute pancreatitis
In hypoparathyroidism, corresponding hypoalbuminemia will decrease ___ Ca levels but ___ Ca levels remain unchanged.
total serum Ca decr,
ionized Ca unchanged
S/S of hypoparathyroidism
hypotension, CHF, EKG changes, muscle cramps, weakness, irritability, + chvosteks sign, + trousseau's sign
This is ipsilateral twitching when tapping facial nerve at the angle of the jaw
chvosteks sign
This is inflation of BP cuff causing aggravation of muscle leading to irritability and spasm at the wrist.
Trousseau's sign
What are the anesthesia considerations for hypoparathyroid pts?
- normal Ca in pts w cardiac manifestations of low Ca
- avoid myocardium depressing anesthetics
- avoid alkalosis
- avoid 5% albumin - binds Ca further and lowers serum levels
- consider NDMR sensitivity
The adrenal glands are divided into ____ and _____.
adrenal cortex and adrenal medulla
This area secretes androgens, mineralocorticoids (aldosterone) and glucocorticoids (cortisol)
adrenal cortex
This area secretes catecholamines (epi, norepi, dopamine)
adrenal medulla
80% of catecholamines are secreted in the form of ___ and release is regulated by cholinergic preganglionic fibers.
This is the most superficial layer of adrenal cortex, and makes mineralcorticoids (aldosterone)
zona glomerulosa
This is the middle cortical layer of the adrenal cortex, and makes glucocorticoids (cortisol)
zona fasciculata
This is the deepest cortical layer of the adrenal cortex, and makes weak androgens (adrenosterone, dehydroepiandrosterone)
zona reticularis
Aldosterone is chiefly involved w _____ and ____ balance.
fluid and electrolyte
Aldosterone causes sodium to be reabsorbed in ______ in exchange for ____ and ___ ions. This leads to an expansion in extracellular fluid volume, decr in plasma K, and metabolic alkalosis.
distal renal tubule, K and H ions
Aldosterone secretion is stimulated by the _____ system.
Aldosterone is elevated in the following circumstances
hypovolemia, hypotension, CHF, surgery
_____ enhances gluconeogenesis and inhibition of peripheral glucose utilization to raise blood glucose and worsen diabetic control.
Glucocorticoids are required for vascular and bronchial smooth muscle to be responsive to _____.
Since glucocorticoids are structurally related to aldosterone, they tend to promote ____ retention and ____ excretion.
sodium retention and K excretion
This glucocorticoid is given for PONV at the beginning of the case.
Decadron 8 mg IV
____ from the anterior pituitary is the principal regulator of glucocorticoid secretion.
The most important endogenous glucorticoid is ____, which avgs production of 20 mg/day.
____ from the pituitary gland stimulates the adrenal glands to make ____.
ACTH from pituitary, make cortisol.
As ____ level rises, it turns down the amt of ____ made by the pituitary gland.
cortisol, ACTH
This is a disease of mineralocorticoid excess, resulting from unilateral adenoma, bilateral hyperplasia, or carcinoma in the adrenal gland.
Conn's Disease
This is the result of mineralocorticoid excess where aldosterone secretion affects RAAS, such as in CHF, hepatic cirrhosis, ascites, nephrotic syndrome, or renal artery stenosis.
Seconary aldosteronism
Mineralocorticoid excess syndromes have these clinical manifestations
incr BP, hypervolemia, prolonged hypokalemia (renal concentrating defect and polyuria), muscle weakness, metabolic alkalosis (lower ionized Ca, tetany), normal serum Na
In pts w high aldosterone level disorders, anesthesia concerns include...
supplemental K, use of spironolactone (K sparing diuretic w antihypertensive properties), assess intravasc volume (Cardiac filling pressures)
Unilateral adrenalectomy, DM, or heparing therapy can all cause _____.
hypoaldosteronism (mineralocorticoid deficiency)
Clinical signs of hypoaldosteronism include
hyperK, acidosis, hypotension
How do you treat hyperaldosteronism?
exogenous mineralocorticoid (fludrocortisone)
What causes glucocorticoid excess?
- steroid hormone meds
- intrinsic hyperfunction of adrenals (adrenocortical adenoma)
- ACTH production by non-pituitary tumor
- hypersecretion by pituitary tumor (Cushings)
Glucocorticoid (cortisol) excess results in these clinical signs:
muscle wasting/weakness, osteoporosis, central obesity w skinny extrem, abdominal striae, glucose intolerance, HTN, mental status changes, incr infection susceptibility, fat deposits on face, shoulders, boobies, bruises, amenorrhea, hirsutism, incr GI acid, edema (Na/fluid retention), hyperglycemia
What are the anesthesia techniques for glucocorticoid (cortisol) excess?
- correct volume overload and hypoK metabolic alkalosis w admin of K and spironolactone
- positioning caution w osteoporosis pts
- weak already, caution w NMBs
This is the destruction of the adrenal gland resulting in combined mineralocorticoid and glucocorticoid deficiency.
Addison's Disease (pimary adrenal insufficiency)
S/S of addison's disease
hypoNa, hypovolemia, decr BP, decr K, metabolic acidosis, cortisol deficiency (Weak, fatigue, hypoglycemia, hypotension, weight loss)
Long term _____ therapy can lead to significant glucocorticoid deficiency via ALA synthetase inhibition.
This is the inadequate ACTH secretion by the pituitary, most commonly caused by giving glucocorticoid meds and then abruptly discontinuing them or mismanaging dosing.
Secondary adrenal insufficiency
_____ can develop in pts who do not recieve incr glucocort. doses during stress, resulting in circulatory collapse, fever, hypoglycemia, and depr mentation.
Addisonian Crisis
This is the destruction of the adrenal gland resulting in combined mineralocorticoid and glucocorticoid deficiency.
Addison's Disease (pimary adrenal insufficiency)
S/S of addison's disease
hypoNa, hypovolemia, decr BP, decr K, metabolic acidosis, cortisol deficiency (Weak, fatigue, hypoglycemia, hypotension, weight loss)
Long term _____ therapy can lead to significant glucocorticoid deficiency via ALA synthetase inhibition.
This is the inadequate ACTH secretion by the pituitary, most commonly caused by giving glucocorticoid meds and then abruptly discontinuing them or mismanaging dosing.
Secondary adrenal insufficiency
_____ can develop in pts who do not recieve incr glucocort. doses during stress, resulting in circulatory collapse, fever, hypoglycemia, and depr mentation.
Addisonian Crisis
What are the anesthesia techniques used for glucocorticoid deficiency?
- ensure adequate steroid replacement therapy
- stress dose required in pts receiving prednisone 5 mg/day > 2 wks in the past 12 months (cannot respond appropriately to surgical stress)
Catecholamine excess from catecholamine-secreting tumor made from chromaffin tissue results in this disease. The tumor is usually benign and localized to a single adrenal gland. (although 10-15% are malignant)

0.1% of all HTN cases
S/S of pheochromocytoma
1. triad: diaphoresis, tachycardia, HTN
2. HTN most common symptom
3. palpitations, tremors, weight loss
4 alpha > Beta adrenergic effects
By giving 10-14 days of ______ therapy to pheochromocytoma pts, you reduce mortality from 50% to 3%.
alpha antagonist therapy
Antihypertensive treatment of pheochromocytoma pts includes
- Ca channel blockers
- phenoxybenzamine is alpha agonist of choice (presynaptic alpha 2 and post synaptic alpha 1)
What are the pre-op strategies for pheochromocytoma pts?
1. volume replacement
2. beta blockade for incr HR only after alpha blockade initiated-- if beta given first causes reflexive HTN, decr CO
3. no reglan (bc stimulates catecholamines)
4. pre-op sedation to decr anxiety
What are the intraop anesthesia techniques for pheochromocytoma pts?
1. avoid SNS stim
2. no ephedrine
3. no atropine
4. hypercarbia and hypoxia may incr SNS stim
5. after tumor ligation and resection may be hypotensive -- persistent adrenergic blockade and intol to high levels of endogenous catecholamines
6. monitor I/Os, CVP, A-line, glucose, labs
7. may need to use adrenergic agonists (phenylephrine or norepi)
8. large bore IVs
9. maint w/ iso or sevo
10. hypotension responds to fluid
11. MgSO4 inhibits catecholamine release
What are the key events that can stimulate SNS in pheochromocytoma pts?
1. intubation (no ketamine, avoid incr HR and BP)
2. surgical tumor manipulation
3. ligation of venous drainage (sudden decr in available catecholamines)
Post op, pheochromocytoma pts return to normal BP within ___ days, ___% of the time.
10 days, 75% of the time
BMI > 30 kg/m2
weight (kg)/ height (M2)
Extreme obesity
> 40 kg/m2
Men w waist measurement > ___ inches and women w waist measurement > ___ inches are at incr health risk.
40 men, 35 women
What diseases are commonly associated w obesity?
DM, HTN, CAD, cholelithiasis
Respiratory effects of obesity
incr O2 demand, incr CO2 production, incr alveolar ventilation, excess adipose decr chest wall compliance, lung volumes suggestive of restrictive lung disease, decr FRC
This is the obesity hypoventilation syndrome characterized by hypercapnia, cyanosis induced polycythemia, R heart failure, somnolence, snoring, OSA
pickwickian syndrome
CV effects of obesity
incr CO, incr blood volume, incr BP, LV hypertrophy
GI effects of obesity
possible hiatal hernia, GERD, poor gastric emptying, fatty liver infiltrates
Airway concerns in obesity
possible difficult airway mgmt during induction, upper airway obstruction during recovery should be anticipated
Pre-op strategies for obese pts
1. pretreat w H2 antagonists and reglan
2. consider holding resp depressive drugs
3. assess CP reserve (EKG, CXR, pulm fcn tests, ABGs
4. ramp bed for good position
5. if difficult airway, have glidescope, FOB or bougie handy
What are the intraoperative techniques for obese pts?
1. controlled ventilation, large TV
2. prevent hypoxia
3. large fat stores provide incr VD for lipid-soluble drugs (some drugs based on ideal body weight)
4. regional: require 20-25% less local due to epidural fat and distended epidural veins; high level of blockade can easily result in resp distress
What are the post op concerns for obese pts?
-Resp failure is major post op problem of extremely obese pts
-delay extubation until fully awake and NMB completely reversed
-45 degree modified sitting position unloads diaphragm and improves vent/oxygenation
-wound infection, DVT and PE incr risks