PV3 Week 2

in the sella turcia (bony cavity at the base of the brain)

hypophysis

• anterior (adeno)
• posterior (neuro)
• -separated by the pars intermedia (almost absent in humans)

by the hypophysial stalk

maintains homeostasis (BP, wt, thirst, temp regulation, sleep / wake cycle, energy expenditure)

By interaction with the pituitary gland

• 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)

• *ACTH
• *GH
• also TSH, LH, FSH, prolactin

• -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

• somatotropin
• protein

• -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)

• -GH causes release of FA from adipose
• -GH enhances conversion of FA to acetyl CoA (this is then used for energy)

• -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

• -decreased glucose uptake into skeletal muscle and fat
• -increased glucose production by the liver
• -increased insulin secretion

• -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)

-they are opposite

• -adequate insulin
• -CHO
• (the growth process requires energy)

• -bone growth (increased bone length at epiphyseal cartilages if they are not sealed)
• -stimulates osteoblasts (deposition of new bone)
• -increased bone thickness

• -release decreases after adolescence
• -in old age GH release is 25% of what it was during adolescence

• -starvation (acutely hypoglycemia is a potent stimulator, chronically protein depletion is a potent stimulator)
• -decreased FA concentration (in the blood)
• -exercise
• -excitement
• -trauma
• -1st 2 hours of deep sleep

• -hyperglycemia
• -increased FA levels
• -aging
• -obesity
• -somatostatin (GHIH)
• -exogenous GH
• -insulin-like growth factors

• -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

• -catecholamines
• -dopamine
• -serotonin

• -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

• -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

-hoarseness or stridor (could have thickened VC or paralysis of the recurrent laryngeal nerve due to stretching)

• -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

• -ADH (AKA pitressin or vasopressin)
• -oxytocin (AKA pitocin)

-peptide 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

in the supraoptic and paraventricular nuclei of the hypothalamus

In response to decreased blood volume and increased osmolarity (hypothalamus has osmoreceptors)

• -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)

increased vascular rx

T

PPV, beta adrenergic drugs, histamine

• 60% in males
• 50% in females

• 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

-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

• -head trauma
• -neurosurgery
• -usually transient in these cases

• -congenital
• -acquired (chronic renal disease, SCD, hypokalemia and hypocalcemia)

• -large quantities of dilute urine
• -polydipsia in the absence of hyperglycemia

DDAVP (ADH replacement)

fluid replacement and treatment of the underlying cause

• excess ADH
• -excess water is reabsorbed

• -intracranial tumors
• -hypothyroidism
• -porphyria
• -carcinoma of the lung 
• -major surgery

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)
• -demeclocycline

• -complication of replacing Na+ too fast
• -fatal

0.5 meq/L/hr or 12 meq/L/ 24 hours

• -ADH secretion increases 50X normal
• -BP and SVR are increased

• -sit on top of the kidneys
• -2

• cortex (outer) 80%
• medulla (inner) 20%

F, the adrenal medulla is considered an SNS ganglion

• -zona glomerulosa (outermost part)
• -zona fasciulata (middle and largest layer)
• -zona reticularis (deepest layer)

zona glomerulosa

zona fasciulata

ACTH (AdrenoCorticoTropic Hormone)

• -adrogens (DHEA)
• -small amounts of estrogens and glucocorticoids via ACTH

protein (epi and NE are catecholAMINES)

corticosteroid hormones

• No, it only affects the zone glomerulosa, so only aldosterone is released.
• Similarly, the release of ACTH does not affect aldosterone release.

• -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

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.

• -increased K+
• -increased RAAS activity (due to decreased ECF volume)

slight decrease in aldosterone secretion

Yes, but it does not control the rate of 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

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

• cortisol
• 20 mg secreted / day

• Prednisone (4x as potent as cortisol)
• Cortisone (almost as potent)
• Methylprednisone (5X as potent)
• Dexamethasone (30X as potent)

• -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

• -increased insulin and BG levels
• -decreased glucose utilization by the cells
• -stimulates gluconeogenesis
• -increased glycogen storage

• -decreased synthesis
• -increased catabolism
• -muscle weakness
• -increased liver and plasma proteins
• -increased AA and transport to hepatic cells

• -mobilization of FA
• -increased FA in plasma
• -central obesity

• -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

• -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

• -HTN
• -hypervolemia
• -muscle weakness (due to hypokalemia)
• -metabolic alkalosis 
• -hyperglycemia
• -polyuria (due to hypernatremia)
• -tetany (due to decreased ionized Ca++)

• -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

• -atrophy or destruction of adrenals (multiple hormones involved, not just adrenals)
• -unilateral adrenalectomy
• -DM
• -heparin therapy

• -hyponatremia
• -hypovolemia and hypotension
• -hyperkalemia (cardiac toxicity)
• -metabolic acidosis (K+ and H+ ions are not secreted in exchange for Na+ reabsorption)

give exogenous hormone (fludrocortisone)

• -due to excess cortisol
• -Cushing's syndrome (corticotropin dependent vs. independent)

• -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)

-due to excess ACTH (due to a pituitary tumor or excess CRH from hypothalamus)

corticotropin dependent

F, it's a form of hyperadrenalism

• 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

• -N/V
• -anorexia
• -weakness (lack of cortisol decreases mobilization of proteins and fats so metabolic functions are depressed)
• -skin hyper pigmentation
• -hypovolemia and hypotension
• -hyponatremia
• -hyperkalemia
• -acidotic saliva causing tooth decay

< 20 mcg/ dl????

• -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

• -correct lytes and BG
• -replace volume
• -exogenous steroids

150 mg/ day

• -magnitude of surgery
• -duration of steroid use
• -steroid dose

-pt has been on steroids for > 1-2 weeks over the past 6-12 months

Etomidate as it causes transient depression of cortisol synthesis

epi (80%), NE (20%), dopamine

Effects are similar but AM stimulation lasts 5-10x longer than SNS stimulation

• -catecholamine secreting tumor
• -10-15% are malignant
• -90% are in the AM

30-50 years

Paroxysmal HTN, diaphoresis, H/A, palpitations, weight loss, hypovolemia

• -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)

• -surgical excision
• -phenoxybenzamine
• -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

• -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

• -autosomal dominant multiglandular disorder
• -can produce pheo, thyroid issues, etc.