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207 Cards in this Set
- Front
- Back
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Where are the adrenal glands located?
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superior poles of each kidney
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What are the two distinct anatomic and physiologic entities of the adrenal glands?
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Adrenal Medulla
Adrenal Cortex |
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The largest (80%) of the adrenal gland is the _________.
The smaller part (20%) of the adrenal gland is the ________. |
adrenal cortex
adrenal medulla |
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What are the 3 broad classifications of the hormones secreted by the adrenal cortex? What are these hormones referred to collectively?
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mineralcorticoids
glucocorticoids androgenic hormones Corticosteroids |
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What are the 3 catecholamines secreted from the adrenal medulla and percentages of each?
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Epinephrine (80%)
Norepinephrine (20%) Dopamine (minute amts) |
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What are the 3 layers of the adrenal cortex? (Think...GFR from the outside in)
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Zona Glomerulosa
Zona Fasciculata Zona Reticularis |
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Which area is are mineralocorticoids secreted from and what is the primary one?
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Zona Glomerulosa
Aldosterone |
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What is secreted from the Zona Fasciculata?
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Glucocorticoids, primarily cortisol
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What is secreted from the Zona Reticularis?
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Androgenic hormones
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Corticosteroids are secreted from the adrenal __________ and have a ___________ structure and share a common_________ ___________.
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cortex
steroidal cholesterol frame |
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ACTH, released from the _____________, controls the release and production of ___________ and _____________ hormones.
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anterior pituitary gland
glucocorticoid androgenic |
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________ stimulates glucocorticoid synthesis by activating the enzyme _________ which converts ________ to __________.
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ACTH
desmolase cholesterol pregnenolone |
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This initial conversion of cholesterol to pregnenolone is stimulated by ________ and occurs where?
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Angiotensin II
Zona Glomerulosa |
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Does ACTH have any real effect on mineralocorticoid secretion?
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No
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What do aldosterone and cortisol have in common in regard to their chemical make up?
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a cholesterol frame
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The Adrenal Cortex synthesizes more than _____ types of hormones.
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30
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What is the main glucocorticoid released from the adrenal cortex and what is it's percentage?
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cortisol (hydrocortisone)
95% |
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Secretion of cortisol, as a glucocorticoid, is largely controlled by what? Where is cortisol secreted from?
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ACTH
adrenal cortex, zona fasciculata |
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What is the most potent regulator of ACTH and why?
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cortisol
negative feedback system |
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What type of feedback system is described by low blood levels causing increased secretion? High blood levels inhibiting further secretion?
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Positive feedback system
Negative feedback system |
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How much cortisol is produced daily?
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15-30mg
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What is the peak time frame for cortisol production?
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5am-9am
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Any type of stress can increase the release of which hormone? How much can it increase?
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Cortisol (cortex...zona fasiculata)
250mg |
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Is most of the cortisol bound or unbound? What is the bound portion attached to?
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bound
attached to a-globulin transcortin |
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Which type of cortisol, bound or unbound exerts biological effects?
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unbound
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What are 2 roles of cortisol that are crucial?
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conversion of norepi to epi
production of angiotensin |
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What are the 8 mechanisms that stimulate secretion of ACTH?
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corticotropin-releasing hormone
sleep-to-waking period stress hypoglycemia sepsis trauma decreased plasma cortisol a-Adrenergic receptor stimulation |
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What is the #1 reason for endogenous anxiety?
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hypoglycemia
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What 2 mechanisms inhibit ACTH secretion?
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elevated plasma cortisol
opioids |
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Which hormone is essential to maintain life? (glucocorticoids, mineralocorticoids, androgenic)
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glucocorticoids
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Which hormone is necessary for the proper use of proteins, carbohydrates, and fats by the body?
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glucocorticoids (cortisol)
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Which hormone mediates the catecholamine effects on the heart and vasculature and how does it do so?
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cortisol
augments catecholamine-induced vasoconstriction |
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In the elderly, does cortisol production increase or decrease? What about plasma levels? Why?
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production decreases
plasma levels remain normal because hepatic and renal clearance also decreases |
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Inadequate secretion of this hormone during critical illness can lead to hypotension, shock, and death. What can you do about it?
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cortisol
administer hydrocortisone |
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___________stimulates _____________ in the liver to enhance production of high energy fuel for metabolism.
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Cortisol
gluconeogenesis |
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How much does gluconeogenesis increase in the presence of cortisol?
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6 to 10 fold
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Which hormone is "diabetogenic"?
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Cortisol
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How long can a single dose of glucocorticoid raise blood glucose?
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12-24 hrs
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What are the 4 effects of cortisol on carbohydrate metabolism? (think fight or flight-what do we need)
|
-Mobilizes amino acids from hepatic tissue for GLUCONEOGENESIS and glycogenolysis
-Moderately decreases the rate of cellular glucose uptake and use in extrahepatic tissue -Promotes appetite -Induces liver enzymes |
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What are the 2 primary affects of cortisol on protein metabolism?
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-decreases protein synthesis
-increases protein catabolism in nearly all tissues (except the liver)--> partially blocked by insulin |
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What causes skeletal muscle to become weak and atrophy from marked protein catabolism?
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excess cortisol
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Name 11 common physical characteristics of excessive cortisol.
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Red cheeks
Moon face Fat pads/Buffalo hump Thin skin High BP Thin arms & legs Bruisability--ecchymoses Red striations Pendulous abdomen Poor wound healing Osteoporosis-compressed vertebrae |
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A patient with Cushing's presents with ankle edema, what are your first thoughts?
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Better figure out why they have ankle edema because it's not from the excessive cortisol!
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What are the 2 primary effects of cortisol on fat metabolism?
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-mobilizes free fatty acids from adipose tissue
-enhances oxidation of fatty acids within the cells |
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What might cause metabolic systems to shift to using FFAs instead of glucose for energy?
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starvation or stress
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Name the 5 reasons that cortisol is useful in asthma, allergic reactions, and inflammatory disorders.
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-diminishes inflammatory responses by suppressing cytokines
-decreases migration of leukocytes to the area of inflammation -stabilizes lysosomal membranes -decreases antibody production -DECREASES NUMBER OF LYMPHOCYTES IN THE BLOOD (NOT FUNCTION) |
|
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How does cortisol cause immunosuppression?
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decreases the number of lymphocytes in the blood (not function)
phagocytic activity does NOT decrease |
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What is the principal mineralocorticoid? Where is it secreted from?
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Aldosterone
Zona Glomerulosa |
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What cytochrome enzyme is involved in the generation of aldosterone?
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aldosterone synthase
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What is the major regulator of ECF?
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aldosterone
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Aldosterone plays a major role in regulation of what 3 things?
|
ECF--MAJOR REGULATOR
Na and K concentrations Promotes total body fluid balance |
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Following secretion, aldosterone circulates bound to plasma proteins to what 3 target sites?
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sweat glands
alimentary tract distal convoluted tube of the kidney |
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Aldosterone acts on the ____________ and ____________ to ________(increase/decrease) reabsorption of Na and _________(increase/decrease) secretion of K.
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distal tubule
collecting duct increase increase (Na comes back in and K goes out) |
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Where does an aldosterone inhibiting diuretic act?
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distal tubule
collecting duct |
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What are the 4 main physiological stimulants of aldosterone release?
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-hyperkalemia
-angiotensin II -hyponatremia -ACTH |
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What is the most potent vasopressor produced in the body?
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Angiotensin II
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What is the activator of the RAS?
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Angiotensin II
|
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What is regulated by the RAS (and K concentration)?
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aldosterone
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Where is renin released?
|
kidney
|
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What 4 factors stimulate the release of renin?
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Hypovolemia
Hypotension Hyponatremia SNS Stimulation |
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What is the role of renin after it's release from the kidney?
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converts Angiotensin to Angiotensin II
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What does Angiotensin II do?
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causes the release of aldosterone from the zona glomerulosa of the adrenal cortex
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What is the sequence of events after aldosterone has been released?
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-Aldosterone causes reabsorption of Na in exchange for secretion of K.
-Water follows Na -ECF expands=increased BP |
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Your patient has lost blood volume and their pressure is dropping.....what's the body going to do to attempt to restore it?
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-Decreased blood volume stimulates renin release from the kidneys.
-Renin converts Angiotensin to Angiotensin II. -Angiotensin II stimulates release of aldosterone. -Aldosterone causes reabsorption of Na in exchange for K. (Na in and K out) -H2O follows Na--->increased ECF--->increased blood volume---->increased BP |
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If aldosterone increases what electrolyte decreases?
If aldosterone decreases what electrolyte increases? What electrolyte has an inverse relationship with aldosterone? What electrolyte has a direct relationship with aldosterone? |
Potassium
Potassium Potassium Sodium |
|
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What 2 glands are under exclusive neuronal control?
|
Adrenal medulla
Posterior Pituitary |
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_______________ fibers bypass the ____________ ganglia and pass directly from the ___________ to the __________________.
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Preganglionic
paravertebral spinal cord adrenal medulla |
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What does the adrenal medulla secrete? What's the 80/20 rule?
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catecholamines
epinephrine (80%) norepinephrine (20%) dopamine (minute amts) |
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What controles the release of catecholamines from the adrenal medulla?
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Ach
|
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Catecholamines are synthesized, stored, and released from what type of cells?
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chromaffin granules
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End products of catecholamine metabolism include:
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VANILLYMANDELIC ACID (80-90%)
METANEPHRINE small amount unchanged (1%) |
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Catecholamine release can be stimulated by emotional reactions or physiologic stimuli such as: (2)
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hypoglycemia
hypotension |
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The effects of Epi and NE are similar to sympathetic stimulation but last how much longer? Why?
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5-10x longer
slow removal of hormones from the blood |
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What kind of receptors does NE stimulate and what is the overall result?
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alpha and beta adrenergic receptors
causes vasoconstriction which increases PVR |
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Epinephrine acts on what receptors and what are the primary actions?
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Greater affinity for beta adrenergic receptors
Actions seen primarily in the heart producing chronotropic and inotropic effects. |
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Epi and NE can increase the metabolism rate by as much as _____% above normal.
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100
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Cushing's Disease and Cushing's Syndrome are often used interchangeable. Which is generally associated with pathology?
Which is generally associated with exogenous glucocorticoid therapy? |
Cushing's Disease
Cushing's Syndrome |
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Hypercortisolism can result from what 4 processes?
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-exogenous steroid administration
- excess ACTH from the pituitary -adrenal hyperplasia -adrenal adenoma or carcinoma |
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What is the most common reason for excessive ACTH secretion that leads to excessive cortisol What physical characteristic may signify excessive ACTH.
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ANTERIOR PITUITARY TUMOR
skin pigmentation |
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Adrenal adenoma and carcinoma is ______% of the cause of hypercortisolism.
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20-25
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Adrenal tumors are usually ___________ and ____% are malignant. Pituitary tumors are ___________.
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unilateral
50 bilateral |
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What are some common symptoms of hypercortisolism?
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HTN
Increased intravascular volume (hypernatremia, hypokalemia) Hyperglycemia Poor wound healing (immunosuppression) Truncal obesity Hypercoagulability Fatigability Abdominal Striae Osteoporosis (impaired Ca absorption) Muscle wasting/weakness Psychological disturbances |
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What is the most common cause of secondary hypercortisolism?
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Iatrogenic administration of exogenous glucocorticoids.
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What are 3 common examples of exogenous glucocorticoids?
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cortisone (hydrocortisone)
prednisone (solumedrol) dexamethasone |
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What is unique about dexamethasone?
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it has no mineralocorticoid (Na retaining) properties
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Extended exogenous treatment with glucocorticoids results in __________ adrenal cortex.
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atrophied
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All patients that have undergone a week of steroid therapy in the past______ should receive_____________. What happens to these patients during surgery if they don't receive therapy?
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year
steroid therapy They are unable to respond to surgical stress. |
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A patient with Cushing's Disease must receive placement with hydrocortisone or Decadron? Why?
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hydrocortisone
Hydrocortisone has the added benefit of mineralocorticoid effect without the need to administer exogenous mineralocorticoid. (Na reaborption) |
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What if your patient has received steroid therapy?
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assess the length of the course and dose and replace with corresponding dose of decadron
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Which drug has the greatest glucocorticoid effect: hydrocortisone or decadron? How much greater is the effect?
|
Decadron
25x greater effect |
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Can you give a patient with Cushings disease/syndrome decadron?
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No, they need hydrocortisone. (they require the mineralocorticoid/extra sodium)
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What 3 lab tests are used to identify Cushing's?
|
plasma cortisol levels
urinary cortisol levels plasma ACTH |
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Simultaneous measurements of plasma/urinary cortisol and ACTH can identify if the is pituitary or adrenal. What would you see with each?
|
Pituitary= increased ACTH
Adrenal= increased cortisol |
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A high dose of decadron
|
depresses cortisol levels in pituitary tumors.
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When performing a dexamethasone suppression test, which tumors will exhibit depression of cortisol? Why?(pituitary adenomas or adrenal tumors)
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Pituitary tumors will show decreased cortisol because they retain some negative feedback.
Adrenal tumors do not. |
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What are the 2 primary characteristics of secondary hypocortisolism?
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low cortisol
normal aldosterone |
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Patients with hypocortisolism have _______ (less/more) problems with severe hypovolemia or electrolyte derangements.
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less
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How would you "tune-up" a patient with hypocortisolism?
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give a dose of hydrocortisone
|
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Which drug can cause intense burning in the groin? What can be done to prevent this?
|
Decadron
Give diluted, slowly, over 5 minutes. |
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Patients with hypocortisolism are extremely _______to drug induced ____________.
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sensitive
myocardial depression |
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In a patient with Cushing's, what are 3 important anesthetic implications related to muscle weakness?
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-conservative administration of muscle relaxant (exaggerated effect)
-extubate awake -good pre-op teaching about the possibility of waking with ETT and mechanical ventilation |
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Characteristic obesity of Cushing's will cause __________ (increased/decreased) airway pressures and __________(increased/decreased) FRC.
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increased
decreased |
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So what's the deal with taping the eyes and ETT in a patient with Cushing's? What are Ann's 2 points?
|
BE VERY CAREFUL WITH EYE AND FACE TAPE
-thin skin can cause bruising, swelling, or skin removal -endeavor to make tape less "sticky" |
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How does Ann describe the type of anesthesia she wants you to use for a patient with Cushing's?
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CONSERVATIVE, "TIGHT" ANESTHESIA
-prudent titration!! -anticipate and take no chances |
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What 2 hormones are insufficient or absent in Addison's disease?
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cortisol
aldosterone |
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What are the 3 causes of Addison's Disease?
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-destruction of adrenal cortex
-prolonged exogenous corticosteroid use -deficiency of ACTH (secondary adrenal insufficiency) |
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Addison's disease does not appear until _____% of the adrenal cortex is destroyed.
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90
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Historically, Addison's was a product of __________; now the major cause is ________________ of the ______________.
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tuberculosis
autoimmune destruction adrenal gland |
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Name 5 possible disease processes that can attribute to Addison's.
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bacterial and fungal infections
advanced HIV metastatic CA sepsis hemorrhage |
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What are some signs/symptoms of Addison's?
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Weight loss
Fatigue Anorexia N/V Abd pain Hyperpigmentation hypotension electrolyte disorders thinning ax/pubic hair |
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What causes hyperpigmentation?
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compensatory increase in ACTH stimulates increase in melanocyte production
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What are 8 signs of symptoms of electrolyte dysfunction?
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hyperchloremia
hyperkalemia hyponatremia (inverse relationship Na/K) hypoglycemia metabolic acidosis loss of ICF (hypovolemia) increased BUN hemoconcentration |
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What famous figure had Addison's Disease?
|
JFK
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What lab tests would identify Addison's?
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-plasma cortisol levels before and after ACTH administration at 30 and 60 minutes
-plasma cortisol would rise -adrenal insufficiency would exhibit little or no effect` |
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Treatment of Addison's Disease includes what 2 points?
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cortisol and aldosterone titrated to meet pt needs
monitor electrolytes |
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What situation is described by relative or absolute deficiency of adrenal corticosteroid hormones resulting in hemodynamic compromise?
|
Addisonian Crisis
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What are 3 possible causes of Addisonian Crisis?
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-abrupt termination of steroid therapy
-recent steroid therapy not supplemented preoperatively -uncompensated stress |
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What 2 cardiovascular situations are typical presentations of Addisonian crisis?
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-hypotension and tachycardia unresponsive to fluids
- arrhythmias secondary to hyperkalemia compounded with hypovolemia secondary to hyponatremia |
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Will a patient with Addisonian's crisis have high or low blood sugar? What GI symptoms will they present with
|
low
vomiting, diarrhea, cramps |
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What are the 4 major treatment modalities of Addisonian's crisis?
|
1. Fluids D5NS (tx hypoglycemia)
2. Steroid replacement (solu cortef/hydrocortisone) 3. Inotropes 4. Electrolyte correction ( |
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What drug should be avoided in patients susceptible to adrenal insufficiency?
|
etomidate; a single dose can cause acute adrenocortical insufficiency
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Typically, a patient with Addison's is an ASA ___.
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3
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What are the 3 important aspects of management of Addison's for an emergent procedure?
|
-treat symptoms; electrolyte/fluid imbalances
-employ steroid treatment ASAP -more rigorous monitoring (A Line/CL) |
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Conn Syndrome is primary or secondary hypoaldosteronism?
|
primary
|
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What are the 3 important points related to Conn Syndrome?
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-excess secretion of aldosterone from a functional TUMOR
-secretion is independent of physiologic stimulus -increased urinary excretion of K |
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What are the 3 important points related to secondary hyperaldosteronism?
|
-no tumor
-stimulus for aldosterone secretion resides outside of the adrenal gland -increased circulating serum concentrations of renin |
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What are the 6 s/sx of hyperaldosteronism?
|
-Hypernatremia (increased ECF volume)
-Hyperkalemia -Hypertension (HA) -Polyuria, Nocturia -Skeletal cramps/weakness -Metabolic Acidosis |
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What are the 4 aspects of treatment for hyperaldosteronism?
|
-Supplemental K slowly
-Spironolactone (aldosterone antagonist) -Tx HTN -Surgical removal of aldosterone secreting tumor (Conn Syndrome) |
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What are the 2 most important points related to management of anesthesia with hyperaldosteronism?
|
-Monitor fluid status (shifts quickly, CVP, or PAC)
-Monitor electrolytes/acid-base (expect hypkalemic metabolic acidosis) |
|
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Who was the first anatomist to give a detailed description of adrenal glands? What did he do and where was he from?
|
Bartholomeus Eustachius (1520-1574)
Professor at Colegio della Sapienza at Rome |
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When did the discovery of adrenal glands receive attention?
|
time of Thomas Addison (1793-1860)
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When and who reported the first case of pheochromocytoma?
|
Felix Frankel 1886
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What does pheochromocytoma mean?
|
dark color tumor
|
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Who may or may not have been the first person to remove a pheochromocytoma?
|
Charles Mayo
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Which 2 glands are under exclusive neuronal control?
|
Adrenal medulla, Posterior pituitary
|
|
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What is secreted from the adrenal medulla and in what percentages?
|
Epi 80%
NE 20% Dopamine-small amts |
|
|
What cells are synthesize, store, and release catecholamines?
|
chromaffin granule cells
|
|
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What are the major end products of catecholamine metabolism?
|
Vanillymandelic acid 80-90%
Metanephrine Small amount of unchanged catecholamine 1% |
|
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What is the significance of the 1% of unchanged catecholamine?
|
it is used as a diagnostic tool in identifying a pheo
|
|
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What is a pheochromocytoma and where can they be found?
|
Pheo's are catecholamine secreting tumors that can be either on the inside or outside of the adrenal medulla.
Pheo's inside are derived from the adrenomedullary chromaffin cells. Pheo's outside arise form the extra-adrenal chromaffin cells. |
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Are pheo's dependent or independent of neurogenic control?
|
independent
|
|
|
Although the effects of Epi and NE are similar to the effects of direct sympathetic stimulation, how much longer do they last and what causes the increase in duration?
|
5-10x longer
secondary to slow removal of hormones from the blood |
|
|
NE stimulates what type of receptors and what is its overall effect?
|
stimulates alpha and beta adrenergic receptors
vasoconstriction and increased PVR |
|
|
What receptors does Epi stimulate and what is the overall effect?
|
greater affinity for beta adrenergic receptors
actions primarily in the heart=chronotropic and inotropic effects |
|
|
Epi and NE can increase metabolism by as much as _____ % above normal.
|
100
|
|
|
What is the only catecholamine that acts on alpha receptors?
|
NE
|
|
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What are 4 actions that occur with alpha 1 receptor stimulation?
|
VASOCONSTRICTION
intestinal relaxation uterine contraction pupillary dilation |
|
|
What are 4 actions that occur with alpha 2 receptor stimulation?
|
decreased presynaptic transmission (auto receptors)
platelet aggregation VASOCONSTRICTION decreased insulin secretion |
|
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What are 3 actions that occur with beta 1 receptor stimulation?
|
increased HR and contractility
increased lipolysis increased renin secretion |
|
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What are 3 actions that occur with beta 2 receptor stimulation?
|
vasodilation
bronchodilation increased glycogenolysis |
|
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What are 2 actions that occur with beta 3 receptor stimulation?
|
increased lipolysis
increased brown fat thermogenesis |
|
|
What may be a sign that brown fat thermogenesis is occurring?
|
ketones in the urine
|
|
|
What percentage of patients with HTN have a pheo?
|
.01-.1%
|
|
|
Is the rate of incidence preferential to males or females? When does it typically present?
|
Equally among males and females
Presents 3rd to 5th decade of life |
|
|
What is an adrenal lesion found on imaging called?
|
incidentaloma
|
|
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What are some signs that may cause you to investigate for a pheo? (5)
|
S/Sx
Severe HTN or HTN crisis Refractory HTN HTN that presents <20 or >50 yrs >50 HTN=sudden, aggressive onset |
|
|
What is the percentage of pheos that are extra adrenal? adrenomedullary?
|
10%
90% |
|
|
What percentage of pheos are benign? malignant?
|
90%
10% |
|
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What percentage of pheos are bilateral/multiple? unilateral?
|
10%
90% |
|
|
What percentage of pheos occur in children? Are familial? Discovered incidentally?
|
10%
|
|
|
What are GI signs and symptoms of pheochromocytoma?
|
N/V
Abd pain Severe constipation (MEGACOLON) WHO? ELVIS |
|
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What are the cardiac signs and symptoms of pheo?
|
chest pain
angina with normal coronaries CHF cardiac dysrhythmias or conduction defects |
|
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What are 2 causes of angina with normal coronaries in pheo?
|
catecholamine induced increased myocardial consumption
coronary vasospasm |
|
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What are the 3 metabolic signs and symptoms of a pheo?
|
hypercalcemia
mild glucose intolerance lipolysis |
|
|
What should I be concerned with related to hypercalcemia?
|
kidney stones from high Ca -->kidney dysfunction --->compounded problem
|
|
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What are 2 side effects of lipolysis? What receptor stimulation generates this?
|
weight loss
ketoacidosis beta 3 |
|
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What are the 5 P's of Pheo?
|
Pressure (HTN)
Pain (Headache) Perspiration (circulating EPI/NE) Palpitation Pallor |
|
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What is the minimum number of signs that you MUST have to be diagnosed with a pheo?
|
3 out of 5
|
|
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The lack of 3 out of 5 signs LITERALLY excludes diagnosis of a pheo to a statistically insignificant number. What's the number?
|
0.000347
|
|
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What's the 6th P?
|
Paroxysms
|
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What the heck is happening during a paroxysm? What is the patient at risk for? What s/sx might they present with?
|
With true paroxysm, BP may rise to alarmingly high levels.
Pt is at risk for cerebrovascular hemorrhage, heart failure, dysrhythmias, or MI. (?maybe hypotension...) HA, palpitations, tremor, profuse sweating, and either pallor or flushing may accompany an attack. |
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How long might a paroxysm last and at what frequency do paroxysms occur?
|
They are spontaneous, last 10-60 minutes, and can occur daily to monthly.
|
|
|
Name 3 things that can precipitate paroxysm.
|
Intra-arterial contrast (not IV)
Drugs (opioids, BB, induction agents, histamine, ACTH, glucagon, metoclopramide) Strenuous exercise |
|
|
What is the most potent vasodilating peptide found in the body?
|
adrenomedullin
|
|
|
What are 3 factors that can attribute to paroxysmal episode presenting with hypotension?
|
ECF volume contraction
loss of postural reflexes secondary to prolonged catecholamine stimulation tumor release of adrenomedullin |
|
|
What is the most likely lab test for diagnosis of a pheo and what are we checking for?
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24 hr urine
Check: creatinine catecholamines vanillymandelic acid dopamine |
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What would give positive results? What might give a false positive?
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3x elevation is positive
False +: MAOi's, labetolol, street drugs, ethanol, and ephedrine cold remedies |
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What test might be useful, particularly after induction, if your lucky enough to be in a hospital that has it available?
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blood draw for plasma catecholamines
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CT and MRI are both useful in identification of a pheo. How sensitive is a CT for the 2 types of pheos? MRI is more sensitive than CT for which kind?
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CT: adrenal pheo 93-100--extra-adrenal 90%
MRI: more sensitive than CT for extra-adrenal |
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What is the cause of a pheo? What is the cause of a carcinoid tumor? What are the leading s/sx for each?
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pheo: catecholamine secreting tumor--PALLOR
Cardinoid: histamine and serotonin secreting tumor--CUTANEOUS FLUSHING |
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What is the treatment for pheo vs the treatment for carcinoid tumor?
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Pheo-A blockade (phenoxybenzamine, phentolamine)
Carcinoid Tumor: octeotride (suppression of hormones)--resection if possible |
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What was the mortality of pheochromocytoma resection before 1951? Now?
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Before 1951-24-50%
Now 0-2.7% |
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What is the first step in managing a patient for pheo resection?
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alpha blockade
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Name the 4 mechanisms that make an alpha blocker effective in managing a pheo.
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stabilizes BP through vasodilation
expands intravascular volume normalizes myocardial performance decreases the incidence of hyperglycemia by facilitating the release of insulin |
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What are the 2 alpha blockers commonly used?
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phenoxybenzamine
phentolamine |
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What do I need to know about phenoxybenzamine?
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long acting a1 and a2 adrenergic blocker
may require 10-14 days pre-op expensive and hard to come by, special order med S/E=orthostatic HTN, reflex tachy (tx w/ BB-propranolol commonly) |
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What do I need to know about phentolamine?
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use day of surgery (bolus/gtt)
non selective a blocker short duration, long half life LA reversal in dentistry |
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What other action should be done to prep the patient pre-operatively in addition to alpha blockade?
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adequate volume expansion
-pre-op weight gain -decreased Hct |
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What would you use to treat HTN, tachycardia, and dysrhythmias?
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beta blocker-decreases myocardial contractility and conduction
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Unopposed alpha stimulation=
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HEART FAILURE
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A heart that is beta blocked cannot respond to __________ in _______caused by the pheo. So what MUST you do prior to beta blocking?
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increases
SVR alpha block (a comes before b) |
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Name the 2 best options to treat arrhythmias during resection of a pheo.
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esmolol (fast on/fast off)
lidocaine |
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In addition to alpha and beta blockade, what might be done to minimize SNS stimulation for resection of a pheo?
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anxiolysis-versed
SNS block-GETTA combo: pre-op epidural w/GETTA, place cath awake and bolus, run infusion during surgery |
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Describe what it means to be "loaded for bear."
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Full monitors and set up, multi-port central, CVP, A line PRIOR to induction, Nipride and Esmolol gtt infusions hung and ready to go
Insulin gtt if necessary |
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What histamine releasing drugs might you avoid?
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Morphine
Droperidol |
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Why might one choose isoflurane as the agent of choice for induction of a pheo?
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decreases sensitivity of the myocardium to catecholamines (miniscule difference from sevo)
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Pheo resection can be done laparoscopically if the tumor is what size? What is the absolute contraindication for this approach?
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<8
malignant behavior |
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Name 3 times of intra-op hazard and what are you expecting at these times.
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1-tracheal intubation--expect HTN--make sure pt is deep
2-manipulation of the tumor--expect hypertension 3-after ligation of the tumor's venous drainage--expect hypotension--have phenylephrine mini gtt ready, decrease inhalational agent, increase fluids, vasopressin |
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What is the principal complication during emergence and post-op after resection of a pheo? What are the other 2 possibilities?
3 H's |
hypotension (down regulation of adrenergic receptors)
hypertension hypoglycemia (insulin release is no longer blocked) |
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It takes several days after pheo resection for catecholamines levels to return to normal. _____% of patients are normotensive in _____days.
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75%
10 days |
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HTN is cured following pheo resection in ___% in 5 years and ____% at 10 years.
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74
45 |
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When a pheo crisis presents, what is your primary goal?
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reduce BP before CVA or other hypertensive sequela
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Is malignant unresectable pheo associate with long term survival? What is the survival rate at approximately 15 years?
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generally yes
50% |
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What 2 treatment modalities seem to have no effect on survival of malignant unresectable pheo? How is it managed long term?
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chemo and radiation
life long alpha blockers and monitoring |
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How is pheo differentiated from PIH or HELPP in pregnancy?
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presence of catecholamines in the urine
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How is a pheo treated in the 1st or 2nd trimester?
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pre-op alpha blockade and resection
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How is a pheo treated int eh 3rd trimester?
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Hospital admission with lines insertion
ICU management and stabilization deliver fetus at viability, the immediate resection |
