Phys Chapter 77: Adrenocortical Hormones
The adrenals are on top of the kidneys
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Each gland is made of 2 parts: the adrenal medulla and the adrenal cortex
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The adrenal medulla is the center of the gland
o It’s function is related to the symp nervous system
o The medulla secretes catecholamines epinephrine and norepinephrine in response to
symp stimulation
 These hormones cause almost the same effects as direct stimulation from the
symp nerves
The adrenal cortex secretes corticosteroids
o Corticosteroids are all made from cholesterol
o The two major adrenocortical hormones are mineralocorticoids and glucocorticoids
 Mineralocorticoids- called that because they especially affect the electrolytes
(minerals) of the ECF, especially sodium and postassium
 Main mineralocorticoid is aldosterone
 Glucocorticoids- called that because they can increase blood glucose
concentration
 Main glucocorticoid is cortisol
o Also, a small amount of sex hormones are secreted, especially androgens, which have
about the same effect on the body as testosterone
 They’re normally only of slight importance, but problems with the cortex can
cause extreme amounts to be secreted and cause masculinizing effects
o The adrenal cortex has 3 layers:
 Zona glomerulosa- outer, thin layer of cells just beneath the capsule
 The cells here are the only cells in the adrenals that can make significant
amounts of aldosterone, because they have aldosterone synthase
 Secretion from these cells is controlled mainly by ECF levels of
angiotensin 2 and potassium, which both stimulate aldosterone release
 Zona fasciculata- middle layer that makes up ¾ of the cortex
 Secretes glucocorticoids cortisol and corticosterone, and some adrenal
androgens and estrogens
 Secretion from these cells is controlled by adrenocortocotropic
hormone (ACTH) from the anterior pituitary
 Zona reticularis- innermost layer of the cortex
 Secretes dehydroepiandrosterone (DHEA) and androstenedione, and
some estrogens and glucocorticoids
 Secretion from cells is controlled by ACTH and cortical androgenstimulating hormone
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When a layer hypertrophies from excessive work, it doesn’t affect secretion from the
other two layers
Adrenocortical hormones are steroids made from cholesterol
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All steroids are made from cholesterol
Although the cells of the adrenal cortex can make a little cholesterol on the spot, most of the
cholesterol the adrenal cortex uses is brought by LDL
o The LDL diffuses from the plasma into the interstitial fluid and bind to receptors in
clathrin-coated pits on the adrenocortical cell membrane
o The clathrin-coated pits then get endocytosed into the cell to form vesicles that fuse
with lysosomes, which release the cholesterol, to be used to make adrenal steroids
How much cholesterol enters the cell is regulated by feedback
o ACTH increases LDL receptors so that the adrenal glands take in more cholesterol, and
also increases the activity of the enzymes that free cholesterol from LDL
Once cholesterol enters the cell, it’s taken to the mitochondria, where it’s cleaved by
cholesterol desmolase into pregnalone
o This is the rate-limiting step in steroid making
o In all 3 zones, this step is stimulated to make aldosterone, cortisol, and androgens
o Ex: both ACTH and angiotensin 2 increase the conversion of cholesterol to pregnalone
Adrenal steroid making happens in the mitochondria and the ER
In addition to aldosterone and cortisol, other steroids having glucocorticoid or mineralocorticoid
properties, or properties of both, are secreted in small amounts by the adrenal cortex
Mineralocorticoids:
o Aldosterone- very potent and does most mineralocorticoid action in the body
o Deoxycorticosterone- less potent and not as much is made
o Corticosterone, cortisol, and cortisone all have slight mineralocorticoid activity
o 9α-fluorocortisol- synthetic and slightly more potent than aldosterone
Glucocorticoids:
o Cortisol- very potent and does most of the glucocorticoid activity in the body
o Corticosterone- less potent and does most of the activity not already done by cortisol
o Prednisone, methylprednisone, and dexamethasone- synthetic and much more potent
than cortisol
Some of these hormones have both glucocorticoid and mineralocorticoid effects
o Especially cortisol having some mineralocorticoid ability
 Syndromes of excess cortisol will show significant mineralocorticoid effects to
go along with the excessive glucocorticoid effects
Dexamethasone has pretty much no mineralocorticoid ability, and is an important drug that’s
very potent at stimulating glucocorticoid activity
Adrenocortical hormones bind to plasma proteins
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Most (90-95%) of the cortisol released to plasma binds to plasma proteins, especially cortisolbinding globulin aka transcortin, and albumin
Binding to plasma proteins slows elimination of the hormone, and gives it a long half-life
So cortisol has a long half-life of an hour to an hour and a half
A little over half (60%) of aldosterone binds to plasma proteins
o So aldosterone has a shorter half life of about 20 minutes
Binding to plasma proteins provides a reservoir of hormone
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The adrenal steroids are degraded mainly in the liver and get conjugated into mostly glucoronic acid,
and a little bit of sulfates
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Glucoronic acid and sulfates are inactive and have no hormone activity
¼ of the conjugates go into bile to be excreted in feces
The other ¾ are water soluble and go into the blood, where they don’t bind to proteins and get
filtered by the kidneys to be excreted in urine
So liver disease makes it so that it can’t inactivate adrenal hormones, and kidney disease
decreases excretion of conjugates
Mineralocorticoids:
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Loss of adrenocortical secretion leads to death within days to weeks
o Without mineralocorticoids, potassium levels in the ECF increase, sodium and chloride
is lost from the body quickly, and the fluid volume and blood volume are greatly
decreased
o The person will then have decreased cardiac output, leading to shock, and then death
Aldosterone is the major mineralocorticoid
Aldosterone does most of the mineralocorticoid activity, but cortisol does a little bit of it
o Aldosterone is way more potent, but there’s way more cortisol in the body
Cortisol can bind to mineralocorticoid receptors with high affinity
Kidney epithelial cells have 11β-hydroxysteroid dehydrogenase type 2, which converts cortisol
to cortisone
o Since cortisone doesn’t really bind mineralocorticoid receptors, cortisol doesn’t
normally have much of a mineralocorticoid effect
o If a person has a deficiency in 11β-hydroxysteroid dehydrogenase type 2, cortisol could
have a significant mineralocorticoid effect
 Called apparent mineralocorticoid excess syndrome (AME)
 Patient has all the problems a person with excess aldosterone has, except the
plasma aldosterone levels are low
 Licorice has a glycyrrhetinic acid that can also cause AME by blocking 11βhydroxysteroid dehydrogenase type 2
Aldosterone increases renal tubular reabsorption of sodium, and secretion of potassium
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Especially in the principal cells of the collecting tubules, and a little in the distal tubules
and collecting ducts
o So aldosterone in the blood causes more sodium in the blood and less potassium in the
blood, while lack of aldosterone causes the opposite
Excess aldosterone increases ECF volume and arterial pressure, but only a small effect on plasma
sodium levels
o Even though aldosterone is potent at preventing sodium excretion, it only increases the
sodium in the ECF a little bit when it does this
 This is because when sodium is reabsorbed by the tubules, there’s simultaneous
osmotic absorption of an equal amount of water
 Also, sodium increases in the plasma stimulate thirst and makes you drink more
water
 So the fluid volume increases almost as much as the retained sodium, and
doesn’t change the sodium concentration much
o When excess sodium is being lost, aldosterone only has a transient (temporary) effect
on retaining sodium
 Aldosterone-caused increases in ECF volume that last more than a day or two
increase the arterial pressure
 The increased arterial pressure increases kidney excretion of salt and water,
called pressure natriuresis (the salt loss) and pressure diuresis (the water loss)
 This system of returning to normal salt and water excretion when there’s excess
aldosterone is called aldosterone escape
 Once this happens, no more salt and water will be taken in than what is
excreted, despite the excess aldosterone
 This gives the person hypertension, which will be there for as long as there’s
excess aldosterone
o When no aldosterone is secreted, lots of salt is lost in the urine, which decreases sodium
chloride in the ECF, and decreases fluid volume
 Cause dehydration and low blood volume, leading to circulatory shock that
can lead to death
Excess aldosterone causes hypokalemia and muscle weakness, while too little aldosterone
causes hyperkalemia and heart toxicity
o Excess aldosterone not only causes loss of potassium from the ECF into the urine, but
also stimulates movement of potassium from the ECF into most cells of the body
 Causes a big decrease in plasma potassium, called hypokalemia
o When plasma potassium is about half normal, it causes severe muscle weakness
 Due to change in the electrical excitability of nerve and muscle membranes,
preventing normal action potentials
o When there is too little aldosterone, the ECF potassium increases and can cause heart
toxicity, including weak heart contraction, arrhythmia, and heart failure
Excess aldosterone increases kidney loss of hydrogen ions
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So aldosterone not only causes potassium to be secreted into the tubules in exchange
for sodium reabsorption in the principal cells of the renal collecting tubules, but also
causes secretion of hydrogen ions in exchange for sodium in the intercalated cells of the
collecting tubules, causing metabolic alkalosis
Aldosterone stimulates sodium and potassium transport in sweat glands, salivary glands, and
intestinal epithelial cells
o Both glands form a primary secretion that has lots of sodium chloride, but much of the
sodium and chloride get reabsorbed as it goes through the excretory ducts
o Potassium and bicarb get secreted into the ducts
o Aldosterone increases the reabsorption of sodium chloride and secretion of potassium
in the ducts
o Aldosterone is important in the sweat ducts to conserve salt in hot environments
o Aldosterone is important in the saliva to conserve salt when excess saliva is lost
Aldosterone also increases sodium absorption by the intestines, especially at the colon,
preventing loss into the stool
o No aldosterone can lead to failure to reabsorb sodium chloride, causing less water to be
reabsorbed, causing diarrhea, which causes more loss of salt from the body
How aldosterone works:
o Aldosterone is lipid soluble and diffuses to the interior of the tubular epithelial cells
o In the cytoplasm of the tubular cells, aldosterone combines with a mineralocorticoid
receptor protein
 The mineralocorticoid receptor can also bind cortisol, but most of the cortisol
has been converted by 11β-hydroxysteroid dehydrogenase type 2 to cortisone,
which doesn’t bind to mineralocorticoid receptors
o The aldosterone-receptor complex then diffuses into the nucleus, where it causes DNA
to make mRNA for sodium and potassium transport
o The mRNA then diffuses back into the cytoplasm, where it finds ribosomes and
translates proteins
o One of the enzymes made is sodium-potassium adenosine triphosphatase (ATPase),
which is the most important part of the sodium-potassium pump that causes exchange
at the basolateral membrane of renal tubular cells
o Another protein made is epithelial sodium channel (ENaC) proteins that get put on the
luminal membrane of the tubular cell to allow diffusion of sodium into the cell
 Whatever sodium doesn’t diffuse through gets pumped by the sodiumpotassium pump into the cell
o So aldosterone’s effect on sodium transport doesn’t happen right away and takes a bit
Regulating aldosterone secretion:
o Aldosterone regulation is separate from other adrenal hormones
o Four important factors in regulating aldosterone:
 Increased potassium in the ECF increases aldosterone secretion
 Increased angiotensin 2 in the ECF increases aldosterone secretion
 Increased sodium in the ECF slightly decreases aldosterone secretion
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ACTH is needed to secrete aldosterone, but doesn’t do much to control the rate
of secretion
Potassium and the renin-angiotensin system are the most potent at regulating
aldosterone
 Renin-angiotensin is triggered by decreased blood flow to the kidneys or
sodium loss, and causes aldosterone release
 The aldosterone then increases excretion of potassium by the kidneys, and
increases the blood volume and arterial pressure, getting levels back to normal
 ACE inhibitors inhibit angiotensin 2, and therefore aldosterone
Doesn’t take much release of ACTH to allow whatever amount of aldosterone release
you need
Glucocorticoids:
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Almost all glucocorticoid activity is done by cortisol, aka hydrocortisone
o Tiny bit of activity is from corticosterone
Glucocorticoids effect on carb metabolism – increases glucose making, but decreases its use,
to increase blood glucose
o Glucocorticoids stimulate gluconeogenesis
 Gluconeogenesis- making carbs from proteins or another substance
 Cortisol increases the enzymes you need to convert amino acids into glucose in
the liver
 Glucocorticoids activate DNA transcription in the liver cell nuclei to
make mRNA that leads to enzymes for gluconeogenesis
 Cortisol causes the movement of amino acids from the extrahepatic tissues,
mainly the muscle
 So more amino acids are available in the plasma for use by the liver in
gluconeogenesis
 This allows other glycolytic hormones, like epinephrine and glucagon, to
mobilze glucose in times of need like in between meals
o Cortisol also causes a decrease in the rate of glucose use by most cells
 Thought to be because cortisol depresses oxidation of NADH to form NAD+, so
you inhibit glycolysis (increased ratio)
o Both the increased rate of gluconeogenesis and the decreased rate of glucose use
causes the blood glucose to increase
 Increased blood glucose causes release of insulin
 For a reason we don’t know, glucocorticoids decrease the sensitivity of cells to
insulin and therefore glucose uptake and use
 Especially skeletal muscle and adipose
 Thought to be because the lots of fatty acids from glucocorticoids
mobilizing them, inhibit insulin’s effect
 Blood glucose can increase enough to cause adrenal diabetes
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Giving people with adrenal diabetes insulin only decreases the person’s blood
glucose somewhat, and nowhere near what it does in pancreatic diabetes
 Because the tissues are resistant to the effects of insulin
Glucocorticoids effect on proteins:
o One of the main effects of cortisol is to decrease protein stores in most body cells
 Except the liver
 Caused by decreased protein synthesis and increased protein breakdown in the
cells
 If there’s enough cortisol, the muscles can get very weak, and immunity can
also be weakened
o Cortisol increases liver and plasma proteins
 So even though protein is decreased elsewhere in the body, proteins are
increased in the liver
 The liver then can release proteins into the plasma, increasing plasma proteins
o Cortisol increases blood amino acids, increases their movement into the liver cells,
and decreases their movement into nonliver cells
 Especially decreases movement into muscle cells
 Decreased amino acids into cells decreases their [amino acid], which decreases
protein making
 As this happens, proteins are being broken down and released into plasma to
increase the plasma amino acid levels
 So cortisol mobilizes amino acids from nonliver tissues and decreases the
amount of protein in the tissues
 All the plasma amino acids are used by the liver for making proteins and glucose
 So gluconeogenesis is increased and uses the amino acids, and proteins
are made from them as well
Glucocorticoids effect on fat metabolism:
o Cortisol promotes fatty acid mobilization from adipose tissue
o This increases the levels of free fatty acids in the plasma, which increases their use for
energy
o Cortisol also increase the oxidation of fatty acids in cells
o A reason for all these fat effects could be the decreased transport of glucose into fat
cells
 Glucose is needed to make α-glycerophosphate, which is needed for depositing
and maintaining trigylcerides in adipose
 So no α-glycerophosphate from no glucose leads to release of fatty acids
o So cortisol causes the cells to shift from using glucose for energy to using fatty acids
for energy at times of starvation or other stress
 Takes hours to make the shift, unlike decreased insulin which does this quicker
 Needed to conserve glucose and glycogen
Many people with excess glucocorticoids get specific kind of obesity, with excess fat
deposition in the chest and head, giving a “buffalo-like” torso and a rounded “moon face”
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Cortisol is important in resisting stress and inflammation
o Almost any stress, physical or mental, causes an immediate increase in ACTH secretion
from the anterior pituitary, followed in minutes by increased adrenal cortex secretion
of cortisol
o One reason why could be all the movement of amino acids and fatty acids from storage
to the liver for energy
o Usually any time there’s tissue damage, the tissue gets inflamed
 Sometimes, the inflammation can be more damaging than the trauma or
disease itself
 Giving people lots of cortisol can block inflammation or reverse its effects once
it’s begun
 5 main stages of inflammation:
 Release of things from the injured tissue to trigger inflammation
 Increase in blood flow int eh inflamed area, called erythema
 Leakage of plasma into the damaged area from increased capillary
permeability, leading to clotting of the tissue fluid, causing a nonpitting
edema
 Infiltration by WBCs
 After days or weeks, ingrowth of fibrous tissue (fibrosis)
 Cortisol’s anti-inflammatory effects:
 It blocks inflammation from starting
 It causes rapid resolution of already started inflammation, and speeds
up healing
 Ways cortisol prevents development of inflammation:
 Cortisol stabilizes the lysosomal membranes
o Makes it harder for the lysosomes to rupture, which decreases
release of inflammatory enzymes
 Cortisol decrease the permeability of the capillaries
o So no plasma into the tissue
 Cortisol decreases migration of WBCs into inflamed areas, and
phagocytosis
o Probably because cortisol decreaes the making of
prostaglandins and leukotrienes, which increase vasodilation,
capillary permeability, and mobility of WBCs
 Cortisol suppresses the immune system by decreasing lymphocyte
making, Especially T cells
 Cortisol reduces fever by decreasing the release of Il-1from WBCs
o Il-1 excites the hypothalamus temperature control system to
trigger fever
 Ways cortisol causes resolution of inflammation:
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The immediate effect is to block most of the factors that promote
inflammation
 The rate of healing is also increased
 Often cortisol is used for rheumatic fever
o Administration of cortisol or other glucocorticoids causes the
inflammation to subside within 24 hours
Cortisol blocks the inflammatory response to allergic rxns
o It doesn’t affect the basic allergic rxn between antigen and antibody, just the
inflammation
o Cortisol prevents shock or death in anaphylaxis
Cortisol decreases the # of eosinophils and lymphocytes in the blood
o Often, decreased eosinophils or lymphocytes is part of diagnosing overmaking of
cortisol from the adrenal gland
o Cortisol causes atrophy of all lymph tissue throughout the body, which decrease
making of T cells and antibodies
o So immunity is decreased, which can lead to infection or even death from diseases that
usually aren’t that bad
o Cortisol can be used to prevent rejection of transplants
Cortisol increases making of RBCs
Cortisol is lipid soluble and diffuses through the cell membrane to bind a receptor in the
cytoplasm
o The hormone-receptor complex then interacts with glucocorticoid response elements in
the DNA effect gene transcription
o Needs transcription factors to work
o So effects of cortisol aren’t immediate
ACTH stimulates cortisol secretion
o Cortisol release is almost entirely controlled by ACTH, unlike aldosterone
o Corticotropin releasing hormone (CRH) is made by the hypothalamus and put into the
hypothalamic-hypophyseal portal to go to the anterior pituitary to cause release of
ACTH
 The cell bodies that make CRH are in the paraventricular nucleus of the
hypothalamus, which gets signals from the limbic system and lower brain stem
ACTH activates adrenalcortical cells to make steroids by increasing cAMP
o ACTH’s main effect is to activate adenylyl cyclase in the cell membrane, causing the
making of cAMP in the cell cytoplasm
o cAMP then activates intracellular enzymes that cause the making of adrenocortical
hormones
 cAMP acts as a second messenger
o The most important step for ACTH to control secretion is activating protein kinase A
 Protein kinase A causes the initial conversion of cholesterol to pregnalone,
which the rate-limiting step for all adrenocortical hormones
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 This is why ACTH is needed for any adrenocortical hormone to be made
o Long-term stimulation from ACTH can cause hypertrophy and proliferation, especially
in the zona fasciculate and zona reticularis
Almost any type of physical or mental stress can cause release of ACTH, and then cortisol
o Pain stimuli from physical stress or tissue damage are transmitted first up thorugh the
brain stem and eventually to the median eminence of the hypothalamus
o Here, CRH is secreted into the hypophysial portal system, leading to ACTH and then
cortisol
o Mental stress is thought to work by increased activity in the limbic system, especially
at the amygdala and hippocampus, which then send signals to the hypothalamus
Cortisol has negative feedback on CRH and ATCH
Circadian rhythm of glucocorticoids
o The secretory rates of CRH, ACTH, and cortisol are high early in the morning, and low
late in the evening
o Can be adjusted along with circadian rhythm and sleeping habits
When ATCH is secreted by the anterior pituitary, several other hormones similar in structure are
also secreted
o The gene that is transcribed to make the mRNA for ACTH initially causes the making of a
bigger protein that’s a preprohormone called proopiomelanocortin (POOMC)
 Proopiomelanocortin is the precursor of ACTH, melanocyte-stimulating
hormone (MSH), β-endorphin, and β-lipotropin
o Under normal conditions, none of those are secreted from the pituitary enough to
have any impact
o When there’s excess ACTH secretion, it can increase the secretion of the others too
 Ex: Addison’s disease
o The POMC gene is transcribed in corticotroph cells of the anterior pituitary, POMC
neurons of the hypothalamus, the dermis, and lymph tissue
o The type of breakdown peptide you get from POMC depends on the enzyme in the
tissue
 Pituitary corticotrophs have prohormone convertase 1 (PC1), making ACTH and
β-lipotropin
 The hypothalamus has PC2, and makes melanocyte-stimulating hormone and βendorphin
 In melanocytes of the skin, melanocyte stimulating hormone causes making of
the black pigment melanin to go into the epidermis
o ACTH has a tiny bit of melanocyte-stimulating effect
 Nowhere near as potent as melanocyte-stimulating hormone, but since there’s
way more ACTH, it may be more responsible for determining how much
melanin is in the skin
Adrenal androgens:
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Adrenal androgens are moderately active male sex hormones continually secreted by the
adrenal cortex
The most important one is dehydroepiandrosterone (DHEA)
Usually, the adrenal androgens only have weak effects
Adrenal androgens help in early development of male sex organs
Adrenal androgens can also cause growth of pubic and axillary hair in females
Outside the adrenals, some of the adrenal androgens are converted to testosterone, the main
male sex hormone
Hypoadrenalism (adrenal insufficiency, Addison’s disease)
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Addison’s disease results from failure of the adrenal cortex to make enough adrenocortical
hormones, which usually is caused by a primary atrophy or injury to the adrenal cortex
Most of the time, the atrophy is caused by autoimmunity against the adrenal cortex
o Other causes can be tuberculosis and cancer
Mineralocorticoid deficiency
o Lack of aldosterone decreases kidney sodium reabsorption, and allows sodium, chloride,
and water to be lost in the urine
o This decreases was fluid volume, and causes hyponatremia, ,hyperkalemia, and acidosis
because potassium and hydrogen aren’t traded out for sodium in
o Leads to decreased cardiac output, shock, and death
Glucocorticoid deficiency
o Loss of cortisol makes it impossible to maintain normal blood glucose between meals
cause they can’t make any glucose from gluconeogenesis
o Lack of cortisol also decreases the movement of proteins and fats from tissues
o Makes the muscles weak
o Also makes them prone to infection
Melanin pigmentation of the mucous membranes and skin is often seen in Addison’s
o Decreased cortisol triggers excess ACTH and excess melanocyte-stimulating hormone
o Probably mostly caused by ACTH
You treat Addison’s by giving them glucocorticoids and mineralocorticoids
Addisonian crisis- when a stress is triggered in a person with Addison’s, and they don’t have any
glucocorticoids to meet the body’s need
Secondary causes of hypoadrenalism can be problems with the pituitary in making ACTH, which would
decrease adrenal making of hormones
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Secondary is more common than Addison’s disease
Hyperadrenalism- Cushing’s syndrome (think C – too much Cortisol)
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Most of the effects of Cushing’s syndrome are from excess cortisol, but excess androgens is
involved too
Hypercortisolism can be caused by:
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o Adenomas of the anterior pituitary causing excess ACTH
o Hypothalamus problem causing excess CRH
o Ectopic secretion of ACTH from a tumor not in the pituitary
o Adenoma of the adrenal cortex
Cushing’s disease- when cushing’s syndrome is secondary to excess ACTH from the anterior
pituitary
o Excess ACTH is the most common cause of Cushing’s syndrome and shows high plasma
ACTH and cortisol
Primary overmaking of cortisol by the adrenals is about ¼ of cases of Cushing’s syndrome, and
shows decreased ACTH due to cortisol negative feedback
Dexamethasone, a synthetic glucocorticoid, can be used to tell the difference between ACTHdependent and ACTH-independent Cushing’s syndrome
o If dexamethasone decreases ACTH, it’s probably primary
Cushing’s syndrome has movement of fat from the lower body to the upper body, giving a
“buffalo torso”
Cushing’s syndrome can also cause an edematous face with acne and hirsutism (hair growth),
called “moon face”
The excess cortisol increases blood glucose, from increased gluconeogenesis and decreased
glucose use by the tissues
Cushing’s syndrome will also break down proteins in muscle and everywhere but the liver in
the body, causing weakness and suppressed immune system and osteoporosis
o Skin tears easy showing purple striae
Treat by removing any tumors and decreasing secretion of ACTH from the pituitary
Primary aldosteronism (Conn’s syndrome)
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Tumor of the zona glomerulosa secretes lots of aldosterone
Causes hypokalemia and metabolic alkalosis, increase in blood volume, hypernatremia, and
hypertension
The hypokalemia can cause paralysis
Primary aldosteronism will show decreased renin in the plasma
o Renin is being negative feedbacked by aldosterone
Androgenital syndrome
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Adrenocortical tumor secretes excessive amounts of androgens that masculinize throughout the
body
So girl gets guy characteristics, and guy develops characteristics early
Can be diagnosed by looking for 17-ketosteroids in the urine