in the sella turcia (bony cavity at the base of the brain)
What's another name for the pituitary?
hypophysis
pituitary divisions
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?
*ACTH
*GH
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?
somatotropin
protein
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
-CHO
(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)
-exercise
-excitement
-trauma
-1st 2 hours of deep sleep
What factors inhibit GH secretion?
-hyperglycemia
-increased FA levels
-aging
-obesity
-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?
-catecholamines
-dopamine
-serotonin
Panhypopituitarism
-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)
Panhypopituitarism tx
-replace affected hormones
-peri-op stress steroids
Panhypopituitarism s/sx
-lethargic (lack of thyroid hormones)
-wt gain (lack of fat mobilization by GH, adrenocorticotropic, adrenocortical, and TH)
-loss of sexual functions
Gigantism
-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
Gigantism tx
-radiation or surgical removal of the tumor
Acromegaly
-excess GH secretion after epiphyses fuse
-bones get thicker, but not longer (enlargement of head, nose, mandible, and vertebrae are common)
-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)
-peptide hormones
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?
T
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%
Molarity
number of moles of solute / L solution
Osmolarity
number of osmoles (number of moles that contribute to osmotic pressure of a solution) / L
Osmolality
number of osmoles / kg
DI
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
-neurosurgery
-usually transient in these cases
Causes of nephrogenic DI
-congenital
-acquired (chronic renal disease, SCD, hypokalemia and hypocalcemia)
DI s/sx
-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
SIADH
excess ADH
-excess water is reabsorbed
Causes of SIADH
-intracranial tumors
-hypothyroidism
-porphyria
-carcinoma of the lung
-major surgery
What drugs can cause increased ADH release?
Morphine, barbiturates, beta agonists
SIADH s/sx
-concentrated urine (high Na+ and osm in urine)
-low UO
-hyponatremia (dilutional)
-weight gain (water reabsorption)
-skeletal muscle weakness
-MS changes, confusion, convulsions
SIADH treatment
-fluid rx (500-800 ml / day)
-IV NS (hypertonic if neuro symptoms, otherwise isotonic)
-demeclocycline
central pontine myolinolysis
-complication of replacing Na+ too fast
-fatal
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
-2
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?
zona glomerulosa
What part of the adrenal gland secretes cortisol?
zona fasciulata
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?
corticosteroid 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
Aldosterone effects
-increases Na+ reabsorption (and hence water)
-promotes K+ excretion by the renal tubules
-causes increased ECF volume and increased BP
Aldosterone escape
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
-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
HPA axis
-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
cortisol
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
primary aldosteronism
-mineralocorticoid excess
-Conn's syndrome / hyperaldosteronism
-due to a tumor
secondary aldosteronism
-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
-HTN
-hypervolemia
-muscle weakness (due to hypokalemia)
-metabolic alkalosis
-hyperglycemia
-polyuria (due to hypernatremia)
-tetany (due to decreased ionized Ca++)
Anesthesia implications of mineralocorticoid excess