PV3 Week 2
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Where is the pituitary located?
in the sella turcia (bony cavity at the base of the brain)
What's another name for the pituitary?
- anterior (adeno)
- posterior (neuro)
- -separated by the pars intermedia (almost absent in humans)
How is the pituitary connected to the hypothalamus?
by the hypophysial stalk
what roles does the hypothalamus play?
maintains homeostasis (BP, wt, thirst, temp regulation, sleep / wake cycle, energy expenditure)
How does the hypothalamus control homeostasis?
By interaction with the pituitary gland
What's the difference between how the hypothalamus regulates release of hormones from the anterior and posterior pituitary?
- Anterior- hypothalamus releases hormones (blood) that will mediate anterior pituitary hormone release (anterior pituitary releases tropic hormones that affect other organs)
- Posterior- hormones get released and then transported directly to posterior pituitary via the hypophysial stalk (nerve fibers)
What hormones are released by the anterior pituitary?
- also TSH, LH, FSH, prolactin
Major effects of GH
- -Causes growth of all tissues (not just on a target cell)
- -increases cell size and mitosis
- -enhances body protein (increased protein synthesis)
- -increases utilization of FA (fat stores), fat is preferentially used for energy
- -decreases the rate of glucose utilization
What else is GH called? Is it a protein or steroid hormone?
How does GH cause increased protein synthesis?
- -enhanced AA transport thru cell membrane causes increases intracellular AA concentration
- -enhanced RNA transcription causes increased protein synthesis
- -decreased catabolism of protein and AA means FA are used for energy (protein sparing)
How does GH use FA for energy?
- -GH causes release of FA from adipose
- -GH enhances conversion of FA to acetyl CoA (this is then used for energy)
How can GH have a ketogenic effect?
- -with excess GH there is such great mobilization of FA from adipose tissue that acetyl CoA gets converted to acetoacetic acid then to beta hydroxybutiric acid in the liver
- -acetoacetic acid and beta hydroxybutiric acid get released and cause ketosis
GH effects on CHO metabolism
- -decreased glucose uptake into skeletal muscle and fat
- -increased glucose production by the liver
- -increased insulin secretion
How can GH be diabetogenic?
- -there is decreased uptake of glucose into skeletal muscle and fat
- -BG increases
- -insulin secretion also increases due to increased BG
- -insulin rx results (insulin's effects of promoting glucose uptake and inhibiting gluconeogenesis are lessened)
How do GH effects compare to insulin
-they are opposite
For growth hormone to cause growth what must be present?
- -adequate insulin
- (the growth process requires energy)
What effects does GH have on bone and cartilage?
- -bone growth (increased bone length at epiphyseal cartilages if they are not sealed)
- -stimulates osteoblasts (deposition of new bone)
- -increased bone thickness
How does GH release vary throughout the lifespan?
- -release decreases after adolescence
- -in old age GH release is 25% of what it was during adolescence
What factors promote GH secretion?
- -starvation (acutely hypoglycemia is a potent stimulator, chronically protein depletion is a potent stimulator)
- -decreased FA concentration (in the blood)
- -1st 2 hours of deep sleep
What factors inhibit GH secretion?
- -increased FA levels
- -somatostatin (GHIH)
- -exogenous GH
- -insulin-like growth factors
How does the hypothalamus control GH release?
- -By GHRH and GHIH (both secreted by hypothalamus)
- -GHRH has more of an effect
- -negative feedback, increased levels of GH inhibit further secretion of GH
What other hormones secreted by the hypothalamus promote GH secretion?
- -decreased decreased of all anterior pituitary hormones, including GH
- -congenital (dwarfism) or acquired (2/2 pituitary tumors that destroy the gland)
- -pt will also have hypothyroidism, decreased glucocorticoid (cortisol) and gonadotropin production (impotence or ammenorrhea)
- -replace affected hormones
- -peri-op stress steroids
- -lethargic (lack of thyroid hormones)
- -wt gain (lack of fat mobilization by GH, adrenocorticotropic, adrenocortical, and TH)
- -loss of sexual functions
- -GH excess before epiphyses fuse
- -growth up to 8 ft tall
- -usually due to a pituitary adenoma, growth continues until the gland itself is destroyed (due to compression) leading to panhypopituitarism
-radiation or surgical removal of the tumor
- -excess GH secretion after epiphyses fuse
- -bones get thicker, but not longer (enlargement of head, nose, mandible, and vertebrae are common)
- -overgrowth of soft tissues (larynx, tongue)
- -also due to pituitary adenoma
S/sx GH excess
- -increased incidence of HTN, ischemic HD, osteoporosis, increased lung volume causing V/Q mismatch
- -hyperglycemia due to beta cell hyperactivity causing beta cell degeneration which leads to DM2
Clues that a pt with acromegaly has laryngeal involvement
-hoarseness or stridor (could have thickened VC or paralysis of the recurrent laryngeal nerve due to stretching)
Why do pts with acromegaly have difficult airways?
- -difficult to mask due to distorted facial anatomy
- -enlarged tongue
- -possible involvement of VC or larynx
- -look large on outside, but actually small inside
- -prepare for awake FOI and small ETT
What hormones are released by the neurohypophysis (posterior pituitary)? Are they steroid or peptide hormones?
- -ADH (AKA pitressin or vasopressin)
- -oxytocin (AKA pitocin)
How does the posterior pituitary release hormones?
The posterior pituitary does not make hormones itself, the hormones are made in the hypothalamus and travel in the pituitary stalk, where they get released by the posterior pituitary
Where is vasopressin made?
in the supraoptic and paraventricular nuclei of the hypothalamus
Why is vasopressin secreted?
In response to decreased blood volume and increased osmolarity (hypothalamus has osmoreceptors)
What major effect does ADH have?
- -insertion of aquaporins in the cell membrane
- -increased permeability of the collecting ducts and tubules to water
- -result: increased water reabsorption (small amount of and more concentrated urine)
How does vasopressin affect vascular resistance?
increased vascular rx
T or F, there are stretch receptors in the LA and pulmonary veins that sense changes in blood volume and can trigger ADH release?
What are other stimulators for ADH release?
PPV, beta adrenergic drugs, histamine
What percent of body weight is water?
- 60% in males
- 50% in females
What percent of body weight is ICF and ECF?
- ICF- 40%
- ECF- 60%
- -intravascular 5%
- -interstitial 15%
number of moles of solute / L solution
number of osmoles (number of moles that contribute to osmotic pressure of a solution) / L
number of osmoles / kg
- absence of ADH
- -water is not reabsorbed
2 types of DI
-nephrogenic- there's enough ADH but the renal tubules do not respond to it
-central (neurogenic)- not enough ADH is secreted by the posterior pituitary
Causes of central DI
- -head trauma
- -usually transient in these cases
Causes of nephrogenic DI
- -acquired (chronic renal disease, SCD, hypokalemia and hypocalcemia)
- -large quantities of dilute urine
- -polydipsia in the absence of hyperglycemia
Treatment of central DI
DDAVP (ADH replacement)
Treatment of nephrogenic DI
fluid replacement and treatment of the underlying cause
- excess ADH
- -excess water is reabsorbed
Causes of SIADH
- -intracranial tumors
- -carcinoma of the lung
- -major surgery
What drugs can cause increased ADH release?
Morphine, barbiturates, beta agonists
- -concentrated urine (high Na+ and osm in urine)
- -low UO
- -hyponatremia (dilutional)
- -weight gain (water reabsorption)
- -skeletal muscle weakness
- -MS changes, confusion, convulsions
- -fluid rx (500-800 ml / day)
- -IV NS (hypertonic if neuro symptoms, otherwise isotonic)
central pontine myolinolysis
- -complication of replacing Na+ too fast
guideline for correction of hyponatremia
0.5 meq/L/hr or 12 meq/L/ 24 hours
What happens to ADH secretion with a 15-25% reduction in blood volume?
- -ADH secretion increases 50X normal
- -BP and SVR are increased
Where are the adrenal glands located? How many are there?
- -sit on top of the kidneys
Parts of the adrenal gland
- cortex (outer) 80%
- medulla (inner) 20%
T or F, functionally, the adrenal cortex is considered an SNS ganglion
F, the adrenal medulla is considered an SNS ganglion
3 parts of the adrenal cortex
- -zona glomerulosa (outermost part)
- -zona fasciulata (middle and largest layer)
- -zona reticularis (deepest layer)
What part of the adrenal gland secretes aldosterone?
What part of the adrenal gland secretes cortisol?
What stimulates cortisol secretion?
ACTH (AdrenoCorticoTropic Hormone)
What is secreted by the zona reticularis?
- -adrogens (DHEA)
- -small amounts of estrogens and glucocorticoids via ACTH
Does the AM secrete steroid or protein hormones?
protein (epi and NE are catecholAMINES)
Does the adrenal cortex secrete steroid or protein hormones?
Does angiotensin 2 affect all areas of the adrenal cortex?
- No, it only affects the zone glomerulosa, so only aldosterone is released.
- Similarly, the release of ACTH does not affect aldosterone release.
Major mineralocorticoid secreted by the adrenal cortex? What is it derived from?
- -aldosterone (cortisol also secreted but has only minor mineralocorticoid activity)
- -derived from cholesterol
- -increases Na+ reabsorption (and hence water)
- -promotes K+ excretion by the renal tubules
- -causes increased ECF volume and increased BP
As BP increases 15-25 mmHg due to aldosterone pressure diuresis and naturesis occur leading to excretion of Na+ and water
How can excess aldosterone cause alkalosis
K+ is excreted as Na+ is reabsorbed, in exchange for Na+, H+ ions are secreted. The H+ ion concentration in the ECF decreases causing metabolic alkalosis.
What are triggers for aldosterone release?
- -increased K+
- -increased RAAS activity (due to decreased ECF volume)
What effect does increased ECF Na+ concentration have on aldosterone secretion?
slight decrease in aldosterone secretion
Is ACTH necessary for aldosterone secretion?
Yes, but it does not control the rate of secretion
Explain how the RAAS causes aldosterone secretion
- -decreased blood volume causes decreased renal perfusion pressure
- -renin is released, this catalyzes angiotensinogen to angiotensin I
- -angio I to angio II
- -angio II causes vasoconstriction and aldosterone secretion
Where is ACTH released from?
The anterior pituitary
- -hypothalamic-pituitary-adrenal axis
- -corticotropin releasing factor (CRF) is produced and released by hypothalamus, this stimulates release of ACTH by anterior pituitary
- -ACTH stimulates synthesis of glucocorticoids by the adrenal cortex
- -glucocorticoids provide negative feedback for both CRF and ACTH
What is the major glucocorticoid that's secreted by the adrenal cortex? How much is secreted daily
- 20 mg secreted / day
What are examples of synthetic glucocorticoids?
- Prednisone (4x as potent as cortisol)
- Cortisone (almost as potent)
- Methylprednisone (5X as potent)
- Dexamethasone (30X as potent)
When is most cortisol released?
- -During early waking hours and decreases as the day progresses
- -cortisol release is sensitive to light, stress, disease, and sleep
- -release is pulsatile and follows a circadian rhythm
What effect does cortisol (a glucocorticoid) have on CHO metabolism?
- -increased insulin and BG levels
- -decreased glucose utilization by the cells
- -stimulates gluconeogenesis
- -increased glycogen storage
What effect does cortisol have on protein metabolism?
- -decreased synthesis
- -increased catabolism
- -muscle weakness
- -increased liver and plasma proteins
- -increased AA and transport to hepatic cells
What effect does cortisol have on fat metabolism?
- -mobilization of FA
- -increased FA in plasma
- -central obesity
How does stress cause cortisol release?
- -Stress causes ACTH release by the anterior pituitary
- -ACTH causes cortisol to be released by the adrenal cortex
- -proteins are mobilized and broken down into AA to synthesize substances required to sustain life
What effect does cortisol have on the immune system?
- -blocks early stages of the inflammatory response (stabilizes lysosomal membranes, decreases capillary permeability, decreases WBC migration and phagocytosis, suppresses the immune system)
- -causes rapid resolution of any inflammation that has developed
- -mineralocorticoid excess
- -Conn's syndrome / hyperaldosteronism
- -due to a tumor
- -stimulation of aldosterone secretion by affecting the RAAS
- -things that would cause hypotension (such as CHF, decreased blood volume, cirrhosis, renal artery hypertension) activate RAAS and hence aldosterone
S/sx of mineralocorticoid excess
- -muscle weakness (due to hypokalemia)
- -metabolic alkalosis
- -polyuria (due to hypernatremia)
- -tetany (due to decreased ionized Ca++)
Anesthesia implications of mineralocorticoid excess
- -correct lyte abnormalities (hypernatremia, hypokalemia, hyperglycemia)
- -decreased gastric pH (give H2 blocker)
- -hypokalemia may potentiate NMB and prolong emergence from anesthesia
- -avoid hyperventilation as metabolic alkalosis is a side effect
Causes of mineralocorticoid deficiency
- -atrophy or destruction of adrenals (multiple hormones involved, not just adrenals)
- -unilateral adrenalectomy
- -heparin therapy
S/sx of mineralocorticoid deficiency
- -hypovolemia and hypotension
- -hyperkalemia (cardiac toxicity)
- -metabolic acidosis (K+ and H+ ions are not secreted in exchange for Na+ reabsorption)
Treatment of aldosterone deficiency
give exogenous hormone (fludrocortisone)
Causes glucocorticoid excess
- -due to excess cortisol
- -Cushing's syndrome (corticotropin dependent vs. independent)
What is corticotropin independent glucocorticoid excess?
- -due to abnormalities of the adrenal cortex (adenoma of the adrenal cortex causing increased production of cortisol)
- -also may be due to exogenous glucocorticoid administration
- -not dependent on ACTH levels (may have low or undetectable levels of ACTH)
What is glucocorticoid dependent cortisol excess
-due to excess ACTH (due to a pituitary tumor or excess CRH from hypothalamus)
Is Cushing's disease usually corticotropin dependent or independent?
T or F, cushing's syndrome is a form of hyperaldosteronism?
F, it's a form of hyperadrenalism
Causes of glucocorticoid deficiency
- primary (addison's disease), rare
- -autoimmune destruction of adrenals
- -deficiency in glucocorticoids, mineralocorticoids, and androgens
- secondary due to decreased secretion of CRH or ACTH (CRH released by hypothalamus stimulates ACTH release by anterior pituitary)
- -often due to chronic steroid use causing suppression of HPA axis
- -can be due to radiation or pituitary surgery
Addison's disease s/sx
- -weakness (lack of cortisol decreases mobilization of proteins and fats so metabolic functions are depressed)
- -skin hyper pigmentation
- -hypovolemia and hypotension
- -acidotic saliva causing tooth decay
What cortisol level is considered cortisol deficiency?
< 20 mcg/ dl????
Anesthetic implication of a pt on chronic steroid use
- -pt likely has suppressed HPA axis
- -due to stress of surgery pt will likely need more cortisol
- -pt unable to make cortisol due to HPA axis so we need to give them exogenous steroids
Anesthesia implications of glucocorticoid deficiency
- -correct lytes and BG
- -replace volume
- -exogenous steroids
Maximum amount of cortisol the body can produce
150 mg/ day
Factors to consider when giving a pt exogenous steroids (due to HPA axis depression)
- -magnitude of surgery
- -duration of steroid use
- -steroid dose
General recommendation for what pts need stress dose steroids for surgery
-pt has been on steroids for > 1-2 weeks over the past 6-12 months
What induction agent should be avoided for pts with adrenal insufficiency?
Etomidate as it causes transient depression of cortisol synthesis
What 3 hormones are produced by the adrenal medulla?
epi (80%), NE (20%), dopamine
How does stimulation of the SNS compare to AM stimulation?
Effects are similar but AM stimulation lasts 5-10x longer than SNS stimulation
What is pheochromocytoma?
- -catecholamine secreting tumor
- -10-15% are malignant
- -90% are in the AM
Usual age of presentation of pheo?
Paroxysmal HTN, diaphoresis, H/A, palpitations, weight loss, hypovolemia
Triad of pheo symptoms
- -H/A, tachycardia, diaphoresis in a HTNive pt
- -absence of the triad means pheo is unlikely
- -24 hour urine for free epi and NE and metabolite VMA
- -clonidine suppression test (clonidine will suppress catecholamine levels in essential HTN but not in pheo)
Pheo treatment and anesthesia considerations
- -surgical excision
- -avoid SNS stimulating drugs
- -avoid volatiles that sensitive the myocardium to epi (halothane)
- -careful monitoring especially with tumor manipulation
- -causes irreversible alpha blockade (alpha1 > alpha 2)
- -causes VD
- -used with pheo pts pre-op to control BP
With pheo pts why do you want to alpha block before beta blocking?
- -want to VD the pt (remember with chronic HTN pts are hypovolemic by nature) then correct volume
- -if beta block the pt first, the beta blocked heart may not be able to eject against increased SVR
multiple endocrine neoplasia
- -autosomal dominant multiglandular disorder
- -can produce pheo, thyroid issues, etc.
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