Adrenal cortex -10.pptx ( Adrenal cortical hormones- Aldosterone and cortisol)

Adrenal cortex
Dr. Sai Sailesh Kumar G
Professor
Department of Physiology
NRI Institute of Medical Sciences
Email: dr.goothy@gmail.com

Anatomy of adrenal glands
Two adrenal glands
Each weight 4 grams
Lie at the superior poles of two kidneys
Each gland is composed of two parts- adrenal medulla,
adrenal cortex

 Blood supply:
 Superior adrenal arteries
 Middle adrenal arteries
 Inferior adrenal arteries
 Left adrenal vein joins with inferior phrenic vein and enters left
renal vein.
 Right adrenal vein joins directly into IVC

 Histology: three distinct zones
Zona glomerulosa – outermost zone
Zona fasciculata – middle zone
Zona reticularis – innermost zone

Hormones of adrenal cortex
 Two major types of hormones
Mineralocorticoids
Glucocorticoids
Small amounts of sex hormones especially androgens
(testosterone)

Mineralocorticoids
 They especially affect the electrolytes (minerals) of ECF
Especially sodium and potassium
Essential hormone
Aldosterone is principal mineralocorticoid

Mineralocorticoids
 Aldosterone- very potent (90% of all mineralocorticoid activity)
 Deoxycorticosterone – 1/30 as potent as aldosterone
 Corticosterone- slight mineralocorticoid activity
 9 alpha fluoro cortisol- synthetic and slightly more potent than
aldosterone
 Cortisol – very slight mineralocorticoid activity
 Cortisone – slight mineralocorticoid activity

Glucocorticoids
 They exhibit important effects that increase blood
glucose concentration
Cortisol is the principal glucocorticoid

Glucocorticoids
 Cortisol – very potent. 95% of all glucocorticoid activity
 Corticosterone – much less potent than cortisol
 Cortisone – almost as same potent as cortisol
 Prednisone – four times as potent as cortisol ( synthetic)
 Methyl prednisone – five times as potent as cortisol (Synthetic)
 Dexamethasone – 30 times as potent as cortisol (Synthetic) (Zero
mineralocorticoid activity)

Synthesis and secretion of adrenocortical hormones
 Zona glomerulosa
 Thin layer of cells
 Constitutes about 15 % of the cortex
 Contain enzyme aldosterone synthase
 Synthesis of aldosterone
 Angiotensin II and potassium levels in ECF stimulate the secretion

 Zona fasciculata
Middle and widest zone
constitutes about 75 % of the cortex
Secretes the glucocorticoids – cortisol and corticosterone
Also small amounts of androgens and estrogen
Controlled by HPA axis

 Zona reticularis
Inner zone of the cortex
Secretes androstenedione, small amounts of estrogen,
and some glucocorticoids.
ACTH regulates secretion

Biosynthesis
 Cholesterol is the source of all adrenal cortical steroids
Synthesis mainly occurs in mitochondria and ER
Source of cholesterol is provided by the LDL’s in the
circulating plasma

Plasma binding and excretion
 Cortisol – binds with cortisol binding globulin or transcortin
(less extent to albumin)
Degraded mainly in liver
Conjugated especially to glucuronic acid and lesser extent
to sulfates
25% of these conjugates excrete in bile and feces and rest in
urine

Mechanism of action
Adrenocortical steroid hormones binds with a receptor
specific for it
within the cytoplasm of the hormone’s target cells
Mineralocorticoids bind to the mineralocorticoid receptor (MR),
glucocorticoids to the glucocorticoid receptor (GR),
dehydroepiandrosterone to the androgen receptor (AR).

Mechanism of action
 hormone receptor complex moves to the nucleus
 binds with a complementary hormone-response element in DNA
 namely the mineralocorticoid response element, glucocorticoid
response element, and androgen response element.
 This binding initiates specific gene transcription
 leading to the synthesis of new proteins
 that carry out the effects of the hormone

Functions of mineralocorticoids
 The principal site of aldosterone action is on the distal and collecting
tubules of the kidney
 It promotes sodium retention and enhances potassium elimination during
the formation of urine
 The promotion of sodium retention by aldosterone secondarily induces
osmotic retention of H2O,
 expanding the ECF volume (including the plasma volume),
 which is important in the long-term regulation of blood pressure

 Aldosterone increases the reabsorption of sodium and
simultaneously increases the secretion of potassium by
the renal tubular epithelial cells
especially in the principal cells of the collecting tubules
to a lesser extent, in the distal tubules and collecting
ducts.

 A high concentration of aldosterone in the plasma
transiently decreases the sodium loss into the urine to as
little as a few milliequivalents a day.
At the same time, potassium loss into the urine transiently
increases severalfold.

 Total loss of adrenocortical secretion may cause death
within 3 days to 2 weeks
Unless the person receives extensive salt therapy or
injection of mineralocorticoids.

 Without mineralocorticoids
 potassium ion concentration of the extracellular fluid rises markedly
 sodium and chloride are rapidly lost from the body
 ECF volume decreases
 Blood volume becomes greatly reduced
 Diminished cardiac output
 progresses to a shock-like state
 death

 This entire sequence can be prevented
 by the administration of aldosterone
or some other mineralocorticoid.
Therefore, the mineralocorticoids are said to be the acute
“lifesaving” portion of the adrenocortical hormones.

 Mineralocorticoids are essential for life.
Without aldosterone
a person rapidly dies from circulatory shock
With most other hormonal deficiencies, death is not
immediate

Think……
 Although aldosterone has a potent effect on decreasing
the rate of sodium excretion by the kidneys, the
concentration of sodium in the extracellular fluid often
rises only a few milliequivalents.

 Aldosterone increases sodium reabsorption
Along with sodium water also reabsorbed
When sodium levels are high
It stimulates the thirst center (drinks water)
Stimulates ADH
Increased water reabsorption

 The extracellular fluid volume increases almost as much
as the retained sodium, but without much change in
sodium concentration

 Even though aldosterone is one of the body’s most
powerful sodium-retaining hormones, only transient
sodium retention occurs when excess amounts are
secreted.

 Aldosterone increases sodium reabsorption
Along with sodium water also reabsorbed
Extracellular fluid volume increases 5 to 15 percent above
normal
Arterial pressure also increases 15 to 25 mm Hg
Increased BP

 increases kidney excretion of both sodium and water
pressure natriuresis and pressure diuresis
This return to normal sodium and water excretion by the
kidneys as a result of pressure natriuresis and diuresis is
called aldosterone escape

Excess aldosterone causes hypokalemia
 Excess aldosterone causes loss of potassium ions from
the extracellular fluid into the urine
Stimulates the transport of potassium from the
extracellular fluid into most cells of the body.
Plasma potassium concentration decreases from the
normal value of 4.5 mEq/L to as low as 2 mEq/L.

Excess aldosterone causes hypokalemia
 Hypokalemia
 When the potassium ion concentration falls below about one-half normal
 Alteration of the excitability of the nerve and muscle fiber membranes
 Prevents transmission of normal action potentials
 Severe muscle weakness

Excess aldosterone causes alkalosis
 Excess aldosterone
Secretion of hydrogen ions in the intercalated cells of the
cortical collecting tubules
Metabolic alkalosis

Deficiency of aldosterone
 When aldosterone is deficient
 The extracellular fluid potassium ion concentration can rise
 When it rises to 60 to 100 percent above normal
 Serious cardiac toxicity
 weakness of heart contraction
 Development of arrhythmia, heart failure

Aldosterone actions on sweat glands, salivary glands
and intestinal epithelial cells
 Large amounts of sodium chloride in the primary
secretion of sweat and salivary glands
Much of the sodium chloride, upon passing through the
excretory ducts, is reabsorbed
Potassium and bicarbonate ions are secreted

and intestinal epithelial cells
 Aldosterone greatly increases the reabsorption of sodium
chloride and the secretion of potassium by the ducts.

 The effect on the sweat glands is important to conserve
body salt in hot environments
The effect on the salivary glands is necessary to conserve
salt when excessive quantities of saliva are lost.

Aldosterone actions on intestinal epithelial cells
 Aldosterone also greatly enhances sodium absorption by
the intestines, especially in the colon
Prevents loss of sodium in the stools

Cellular mechanism of action
 Aldosterone is lipid-soluble
Diffuses readily to the interior of the tubular epithelial cells
In the cytoplasm of the tubular cells, aldosterone combines
with a highly specific cytoplasmic mineralocorticoid
receptor (MR)

Mineralocorticoid receptor
 has a stereomolecular configuration
that allows only aldosterone or similar compounds to
combine with it

 The aldosterone-receptor complex diffuses into the nucleus
Undergo further alteration
Induces DNA to form one or more types of messenger RNA
(mRNA)
mRNA diffuses back into the cytoplasm
Formation of proteins

 The proteins formed are a mixture of
(1) one or more enzymes (Na+-K+ ATP ase)
(2) membrane transport proteins
For sodium, potassium, and hydrogen transport through
the cell membrane

Cellular mechanism of action (Genomic action)
 Aldosterone does not have an immediate effect on sodium
transport
this effect must await the sequence of events
leads to the formation of the specific intracellular substances
required for sodium transport
45-60 minutes

Cellular mechanism of action (Non-genomic action)
 Binding of steroids to cell membrane receptors
 that are coupled to second messenger systems
Like an increase in cyclic adenosine monophosphate (cAMP)
Rapid actions
 precise structure of receptors responsible for the rapid effects
of aldosterone has not been determined

Regulation of mineralocorticoids
 Increased potassium ion concentration in the extracellular
fluid greatly increases aldosterone secretion
Increased angiotensin II concentration in the extracellular
fluid also greatly increases aldosterone secretion
Increased sodium ion concentration in the extracellular fluid
very slightly decreases aldosterone secretion.

Regulation of mineralocorticoids
 ACTH from the anterior pituitary gland is necessary for
aldosterone secretion
Potassium ion concentration and the renin-angiotensin
system are by far the most potent in regulating aldosterone
secretion

Aldosterone hypersecretion
 Excess aldosterone secretion may be caused by
 (1) a hypersecreting adrenal tumor made up of aldosterone-
secreting cells (primary hyperaldosteronism, or Conn’s
syndrome)

 Excessive Na+ retention (hypernatremia)
K+ depletion (hypokalemia)
mild metabolic alkalosis
a slight increase in extracellular fluid volume and blood
volume
High blood pressure (hypertension) is generally present

Persons with primary aldosteronism are occasional periods
of muscle paralysis caused by hypokalemia
How???

Diagnosis of aldosterone hypersecretion
 Decreased plasma renin concentration
Feedback suppression of renin secretion
by the excess aldosterone or
by the excess extracellular fluid volume and arterial
pressure

Treatment of aldosterone hypersecretion
 Surgical removal of the tumor or of most of the adrenal
tissue when hyperplasia is the cause.
Another option for treatment is pharmacological
antagonism of the mineralocorticoid receptor with
spironolactone.

Mineralocorticoid Deficiency
 greatly decreases renal tubular sodium reabsorption
 sodium ions, chloride ions, and water to be lost into the urine
 greatly decreased extracellular fluid volume
 plasma volume falls
 red blood cell concentration rises markedly
 cardiac output and blood pressure decrease
 patient dies in shock

Mineralocorticoid Deficiency
 Hyponatremia
Hyperkalemia
Mild acidosis develops

Functions of Glucocorticoids
 Cortisol, the primary glucocorticoid
plays an important role in
carbohydrate, protein, and fat metabolism
 executes significant permissive actions for other hormonal
activities
and helps people to resist the stress

Metabolic effects
 The overall effect of cortisol metabolic actions is to
increase the concentration of blood glucose at the expense
of protein and fat stores.
Hyperglycemic hormone

Effects on carbohydrate metabolism
 It stimulates hepatic (liver) gluconeogenesis

 Cortisol increases the enzymes required to convert amino acids into
glucose in liver cells.
 Cortisol causes mobilization of amino acids from the extrahepatic
tissues, mainly from muscle.
 As a result, more amino acids become available in the plasma to enter
into the gluconeogenesis process
 Cortisol antagonizes insulin’s effects to inhibit gluconeogenesis in the
liver.

 Decreased Glucose Utilization by Cells

Moderate decrease in glucose utilization by most cells in
the body.
Although the precise cause of this decrease is unclear
Decrease translocation of the glucose transporters GLUT 4
to the cell membrane, especially in skeletal muscle cells,
leading to insulin resistance.

Increased rate of gluconeogenesis
Moderate reduction in the rate of glucose utilization by the cells
Blood glucose concentrations to rise
Rise in blood glucose stimulates the secretion of insulin
Insulin resistance
Adrenal diabetes

Metabolic effects
 Cortisol inhibits glucose uptake and use by many tissues,
but not the brain
 Thus sparing glucose for use by the brain, which requires it
as a metabolic fuel

Effect on protein metabolism
 Reduction in Cellular Protein
 Decreased protein synthesis
Increased catabolism of protein in the cells

 In the presence of great excesses of cortisol
The muscles can become so weak that the person cannot
rise from the squatting position.
In addition, the immunity functions of the lymphoid tissue
can be decreased.

 Liver proteins are increased
plasma proteins (which are produced by the liver and then
released into the blood) are also increased.
These increases are exceptions to the protein depletion that
occurs elsewhere in the body

 Cortisol enhances amino acid transport into liver cells
but not into most other cells
Enhances the liver enzymes required for protein synthesis

Effects on fat metabolism
 Cortisol facilitates lipolysis
Releasing free fatty acids into the blood
The mobilized fatty acids are available as an alternative
metabolic fuel for tissues
Can use this energy source in lieu of glucose
Conserving glucose for the brain

Effects on fat metabolism
 The mechanism by which cortisol promotes fatty acid
mobilization is not completely understood

Excess cortisol causes obesity
 A peculiar type of obesity develops in many people with
excess cortisol secretion
Excess deposition of fat in the chest and head regions
giving a buffalo-like torso
rounded “moon face.”
The cause is unclear

Excess cortisol causes obesity
This obesity results from excess stimulation of food intake
 with fat being generated in some tissues of the body more
rapidly than it is mobilized and oxidized

Permissive actions
 Cortisol is extremely important for its permissiveness
For example, cortisol must be present in adequate amounts to
permit the catecholamines to induce vasoconstriction (blood
vessel narrowing).
A person lacking cortisol, if untreated, may go into circulatory
shock in a stressful situation that demands immediate
widespread vasoconstriction.

Role in adaptation to stress
 Cortisol plays a key role in adaptation to stress.
 Stress of any kind is the major stimulus for increased
cortisol secretion.
Cortisol’s precise role in adapting to stress is not known

 Almost any type of stress, whether physical or neurogenic
 causes an immediate and marked increase in ACTH
secretion
greatly increased adrenocortical secretion of cortisol

 Stress that increases cortisol release:
 1. Trauma
 2. Infection
 3. Intense heat or cold
 4. Injection of norepinephrine and other sympathomimetic drugs
 5. Surgery
 6. Injection of necrotizing substances beneath the skin
 7. Restraining an animal so it cannot move

 A primitive human or an animal wounded or faced with a
life-threatening situation must forgo eating
A cortisol-induced increased availability of blood glucose
would help protect the brain from malnutrition during the
imposed fasting period.

The amino acids liberated by protein degradation would
provide a supply of building blocks for tissue repair if the
physical injury occurred.
Thus, cortisol increases the pool of glucose, amino acids,
and fatty acids for use as needed.

Stress
Stress is the generalized, nonspecific response of the body
to any factor that overwhelms, or threatens to overwhelm,
the body’s compensatory abilities to maintain homeostasis

stress
Different stressors may produce some specific responses
characteristic of that stressor
for example, the body’s specific response for cold exposure
is shivering

Stress
all stressors produce a similar nonspecific, generalized
response
This set of responses common to all noxious stimuli is
called the general adaptation syndrome

Anti-inflammatory and immunosuppressive effects
 When stress is accompanied by tissue injury
 inflammatory and immune responses accompany the stress
response.
Cortisol exerts anti-inflammatory and immunosuppressive
effects
An exaggerated inflammatory response has the potential of
causing harm

 Five main stages of inflammation

 Release from the damaged tissue cells of chemicals such as
histamine, bradykinin, proteolytic enzymes, prostaglandins, and
leukotrienes that activate the inflammation process

 An increase in blood flow in the inflamed area caused by some
of the released products from the tissues, an effect called
erythema

 leakage of large quantities of almost pure plasma out of the
capillaries into the damaged areas because of increased
capillary permeability, followed by clotting of the tissue fluid,
thus causing a nonpitting type of edema

 infiltration of the area by leukocytes

 after days or weeks, ingrowth of fibrous tissue that often
helps in the healing process

 When large amounts of cortisol are secreted or injected
into a person??

 (1) it can block the early stages of the inflammation process
before noticeable inflammation even begins
or
(2) if inflammation has already begun, it causes rapid resolution
of the inflammation and increased rapidity of healing

 Cortisol stabilizes lysosomal membranes
 Cortisol decreases permeability of the capillaries
 Cortisol decreases both migration of white blood cells into the inflamed area
and phagocytosis of the damaged cells
 Cortisol suppresses the immune system, causing lymphocyte reproduction
to decrease markedly
 Cortisol attenuates fever mainly because it reduces release of interleukin-1
from white blood cells

Synthetic glucocorticoids (drugs) have been developed that
maximize the anti-inflammatory and immunosuppressive
effects of these steroids while minimizing the metabolic
effects

Cortisol decreases the number of eosinophils and
lymphocytes in the blood
 this effect begins within a few minutes after the injection of
cortisol and becomes marked within a few hours.
lymphocytopenia or eosinopenia is an important diagnostic
criterion for overproduction of cortisol by the adrenal gland

Administration of large doses of cortisol
causes significant atrophy of lymphoid tissue throughout
the body
the output of T cells and antibodies from the lymphoid
tissue decreases
Immunity decreases

Cortisol increases the production of red blood cells
mechanisms unclear
When excess cortisol is secreted by the adrenal glands,
polycythemia often results

 When these drugs are administered therapeutically
at pharmacologic levels (that is, at higher than-physiologic
concentrations)
 they are effective in treating conditions in which the
inflammatory response itself has become destructive
such as rheumatoid arthritis

 When cortisol or other glucocorticoids are administered to
patients with these diseases
the inflammation begins to subside within 24 hours
 Even though the cortisol does not correct the basic disease
preventing the damaging effects of the inflammatory
response can often be a lifesaving measure

 These agents have proved useful in managing various
allergic disorders and in preventing organ transplant
rejections
However, these steroids should be used only when
warranted

Anti-allergic effects
 Reaction between antigen and antibody is not affected by
cortisol
inflammatory response is responsible for many of the
serious and sometimes lethal effects of allergic reactions
cortisol effectively prevents shock or death as a result of
anaphylaxis

 First, because these drugs suppress the normal
inflammatory and immune responses that form the
backbone of the body’s defense system, a glucocorticoid-
treated person has limited ability to resist infections

 Second, troublesome side effects may occur with
prolonged exposure to higher-than-normal concentrations
of glucocorticoids
 These effects include the development of gastric ulcers,
high blood pressure, atherosclerosis, menstrual
irregularities, and bone thinning.

 Third, high levels of exogenous glucocorticoids act in negative-
feedback fashion to suppress the hypothalamus–pituitary–
adrenal axis
Prolonged suppression of this axis can lead to irreversible
atrophy (shrinkage) of the cortisol-secreting cells of the adrenal
gland
permanent inability of the body to produce its own cortisol

 That is why nonsteroidal anti-inflammatory drugs (NSAIDs),
such as aspirin and ibuprofen, are used as alternative anti-
inflammatory therapy

Cellular mechanism
 Cortisol diffuses the membrane (lipid soluble)
 binds with receptors in the cytoplasm
 Hormone-receptor complex
 Enters DNA
 Activates glucocorticoid response element
 Stimulates protein synthesis
 Proteins exert physiological effects

Adrenal androgens and estrogen
 In both sexes, the adrenal cortex produces both androgens,
or “male” sex hormones, and estrogens, or “female” sex
hormones.
Under normal circumstances, the adrenal androgens and
estrogens are not sufficiently abundant or powerful to
induce masculinizing or feminizing effects, respectively.

Circadian rhythm of cortisol secretion
 The secretory rates of CRF, ACTH, and cortisol are high in
the early morning but low in the late evening
Measurements of blood cortisol levels are meaningful only
when expressed in terms of the time in the cycle at which
the measurements are made.

Cortisol hypersecretion
 Hyperadrenalism
Hypersecretion by the adrenal cortex causes a complex
cascade of hormone effects called Cushing’s syndrome.

 Excessive cortisol secretion (Cushing’s syndrome) can be
caused by
(1) overstimulation of the adrenal cortex by excessive amounts
of CRH, ACTH, or both
(2) Adrenal tumors that uncontrollably secrete cortisol
independent of ACTH,
 (3) ACTH-secreting tumors

 Excessive gluconeogenesis
When too many amino acids are converted into glucose, the
body suffers from combined glucose excess (high blood
glucose) and protein shortage
hyperglycemia and glucosuria (glucose in the urine) mimic
diabetes mellitus - adrenal diabetes.

 some of the extra glucose is deposited as body fat in the
abdomen, above the shoulder blades, and in the face
The abnormal fat distributions in the latter two locations are
descriptively called a “buffalo hump” and a “moon face,”
respectively

 The appendages are thin because of muscle breakdown
Loss of muscle protein leads to muscle weakness and fatigue
skin of the abdomen becomes overstretched by the excessive
underlying fat deposits, forming irregular, reddish-purple linear
straie
Wounds heal poorly ( decreased collagen)

 loss of the collagen framework of bone weakens the
skeleton, so fractures may result from little or no apparent
injury

Treatment of Cushing’s Syndrome
 Remove an adrenal tumor if this is the cause or decreasing
the secretion of ACTH
Hypertrophied pituitary glands or even small tumors in the
pituitary that oversecrete ACTH can sometimes be
surgically removed or destroyed by radiation

 Drugs that block steroidogenesis, such as metyrapone,
ketoconazole, and aminoglutethimide
or
that inhibit ACTH secretion, such as serotonin antagonists
and GABA transaminase inhibitors
can also be used when surgery is not feasible.

 If ACTH secretion cannot easily be decreased, the only
satisfactory treatment is usually bilateral partial (or even
total) adrenalectomy
followed by administration of adrenal steroids to make up
for any insufficiency that develops

Hypoadrenalism (Adrenal Insufficiency)—
Addison’s Disease
 Adrenal cortex is unable to secrete adequate amounts of adrenal cortical
hormones
 In about 80 percent of the cases, the atrophy is caused by autoimmunity
against the cortices
 Adrenal gland hypofunction may also be caused by tuberculous destruction
of the adrenal glands or invasion of the adrenal cortices by cancer
 Primary adrenal insufficiency

Addison’s Disease
Secondary adrenal insufficiency
Impaired function of pituitary gland
Secrete too less ACTH
cortisol and aldosterone production decrease
eventually the adrenal glands may atrophy
because of a lack of ACTH stimulation

Addison’s Disease
 Mineralocorticoid Deficiency
 Excess of sodium ions, chloride ions, and water to be lost into urine
 greatly decreased extracellular fluid volume
 Plasma volume decreased
 Decreased blood pressure
 Circulatory shock

Addison’s Disease
Mineralocorticoid Deficiency
Hyponatremia
hyperkalemia
mild acidosis

Addison’s Disease
Glucocorticoid Deficiency
impossible to maintain normal blood glucose concentration
between meals
because he or she cannot synthesize significant quantities
of glucose by gluconeogenesis

Addison’s Disease
Decreased mobilization of both proteins and fats from the
tissues
 thereby depressing many other metabolic functions of the
body

Addison’s Disease
highly susceptible to the deteriorating effects of different
types of stress
even a mild respiratory infection can cause death

Addison’s Disease
melanin pigmentation of the mucous membranes and skin
mucous membranes of the lips and the thin skin of the
nipples

Addison’s Disease
Less cortisol
No negative feedback to hypothalamus and anterior pituitary
Excess ACTH and MSH secreted
Stimulate formation of melanin

Addison’s Disease
An untreated person with total adrenal destruction dies
within a few days to a few weeks because of weakness and,
usually, circulatory shock.

Addison’s Disease
Treatment
person can live for years if small quantities of
mineralocorticoids and glucocorticoids are administered
daily.

Addison’s Disease
Addisonian Crisis
 In a person with Addison’s disease, the output of
glucocorticoids does not increase during stress.

Addison’s Disease
 Addisonian Crisis
 during different types of trauma, disease, or other stresses, such as
surgical operations
 a person is likely to have an acute need for excessive amounts of
glucocorticoids
 and often must be given 10 or more times the normal quantities of
glucocorticoids to prevent death

Addison’s Disease
Addisonian Crisis
 This critical need for extra glucocorticoids and the
associated severe debility in times of stress is called an
addisonian crisis

Adrenal androgen hypersecretion
 Excess adrenal androgen secretion
A masculinizing condition, is more common than the extremely
rare feminizing condition of excess adrenal estrogen secretion
 Either condition is referred to as adrenogenital syndrome
The symptoms depend on the sex of the individual and the age
at which the hyperactivity first begins

In adult females
 Develops a male pattern of body hair, a condition referred
to as hirsutism.
Deepening of the voice
More muscular arms and legs
Breasts become smaller
Menstruation may cease

In new born females
 Manifest male-type external genitalia
 pseudo-hermaphroditism
female gonads (ovaries) are present
but the external genitalia resemble those of a male

In pre-pubertal males
 Prematurely develop male secondary sexual characteristics
for example, deep voice, beard, enlarged penis, and sex
drive
This condition is referred to as precocious pseudopuberty
 not accompanied by sperm production or any other
gonadal activity

In adult males
 no apparent effect because any masculinizing effect
induced by the weak DHEA, even when in excess, is
unnoticeable

Adrenal cortex -10.pptx ( Adrenal cortical hormones- Aldosterone and cortisol)

Adrenal cortex -10.pptx ( Adrenal cortical hormones- Aldosterone and cortisol)

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Adrenal cortex -10.pptx ( Adrenal cortical hormones- Aldosterone and cortisol)