Mar 15 - Fisiologi Hormon Adrenal

The Endocrine System
Adrenal
Department of Physiology Diponegoro University Faculty of Medicine

Adrenal (Suprarenal) Glands
 Adrenal glands – paired, pyramid-shaped organs at top

of kidneys
 Structurally and functionally, they are two glands in
one
 Adrenal medulla – nervous tissue that acts as part
of the Sympathic Nerve System
 Adrenal cortex – glandular tissue derived from
embryonic mesoderm

Adrenal Cortex

Adrenal Cortex
 Synthesizes and releases steroid hormones called

corticosteroids
 Different corticosteroids are produced in each of the
three layers
 Zona glomerulosa – mineralocorticoids
(chiefly aldosterone)
 Zona fasciculata – glucocorticoids
(chiefly cortisol)
 Zona reticularis – gonadocorticoids
(chiefly androgens)

Hormones of Adrenal Cortex

Pathway of steroid biosynthesis (simplified)

Mineralocorticoids
 Regulate the electrolyte concentrations of

extracellular fluids
 Aldosterone – most important mineralocorticoid
 Maintains Na+ balance by reducing excretion of
sodium from the body
 Stimulates reabsorption of Na+ by the kidneys

Mineralocorticoids
 Aldosterone secretion is stimulated by:

 Rising blood levels of K+
 Low blood Na+
 Decreasing blood volume or pressure

Mechanisms of Aldosterone Secretion
 Renin-angiotensin mechanism – kidneys release renin,

which is converted into angiotensin II that in turn
stimulates aldosterone release
 Plasma concentration of sodium and potassium –
directly influences the zona glomerulosa cells
 ACTH – causes small increases of aldosterone during
stress
 Atrial natriuretic peptide (ANP) – inhibits activity of the
zona glomerulosa

Regulation of Aldosterone Release
• Direct stimulators of release

- Increased extracellular K+
- Decreased osmolarity
• Indirect stimulators of release: through RAAS

- Decreased blood pressure
- Decreased macula densa blood flow



Glucocorticoids (Cortisol)
 Help the body resist stress by:

 Keeping blood sugar levels relatively constant
 Maintaining blood volume and preventing water
shift into tissue
 Cortisol provokes:
 Gluconeogenesis (formation of glucose from
noncarbohydrates)
 Rises in blood glucose, fatty acids, and amino acids
Cortisol is might possibly be "needed" for:
the normal transcription / translation of the
genes which code for:
• Vasopressin (ADH) receptors
• Angiotensin II receptors
• An adrenergic receptors

Adrenal Cortex Dysfunctions–Hyperadrenalism
Hyperadrenalism – Cushing’s Syndrome
• Caused by exogenous glucocorticoids and by

tumours (adrenal or pituitary)
• Zg tumour increases aldosterone

- increased sodium, blood pressure
• Zr tumour increases cortisol
- excess protein catabolism, redistribution
of fat

Excessive Levels of Glucocorticoids
 Excessive levels of glucocorticoids:

 Depress cartilage and bone formation
 Inhibit inflammation
 Depress the immune system
 Promote changes in cardiovascular, neural, and
gastrointestinal function

Cushing’s Syndrome
Clinical symptoms of Cushing’s Syndrome

• Central obesity
• "Moon face"
• Plethora of the face
• Acne
• Red-purple stretch marks of the skin of the
abdomen

• Depression, lethargy,
Decreased ability to
concentrate
• Muscle atrophy &
weakness
• Osteoporosis
• Immunosuppression
• High blood pressure
• Intermittent diabetes
mellitus

“moon face” Buffalo hump
Striae

Dexamethasone Suppression Test
 Overnight Low dose = Baseline reading, Dexamethasone 1

mg given at 11 pm, measure cortisol at 8am
 If cortisol low (<50 nmol/L) = normal
 If cortisol high (>50 nmol/L) = investigate further –
Cushings syndrome
 Localising the lesion:
 Plasma ACTH
 if undetectable = adrenal cause (as adrenal cause
independent of ACTH)
 If detected – proceed to high dose dex suppression test
 High dose
 if > 90% suppression – pituitary
 if less/no suppression – ectopic source
Adrenal Cortex Dysfunctions–Hypoadrenalism
Hypoadrenalism – Addison’s Disease
• Caused by tuberculosis, drugs, other
• Adrenal cortex produces inadequate amounts of

hormones
• Plasma sodium decreases and may lead to

circulatory collapse

Adrenocortical Insufficiency=Addison’s disease
Clinical Manifestations:
 Skin color changes occur:
hyperpigmentation due to
uninhibited ACTH release
from the anterior pituitary.
 Muscle weakness& fatigue
 Hypotension
 Nausea, vomiting, weight Addison’s disease
loss, diarrhea develops when the
 Loss of hair level of adrenal cortex
 Hypoglycemia hormone is low due to
hyposecretion (lack of
secretion).
3/4/10
Adrenal Crises
Are precipitated in patients with Addison's disease by:

• Surgery / anesthetia
• (serious) injuries
• diarrhea
• serious infections.
They are characterised by:
• sudden, life-threatening drop in blood pressure 
shock
• (sometimes) hypoglycaemia

Gonadocorticoids (Sex Hormones)
 Most gonadocorticoids secreted are androgens (male sex

hormones), and the most important one is testosterone
 Androgens contribute to:
 The onset of puberty
 The appearance of secondary sex characteristics
 Sex drive in females
 Androgens can be converted into estrogens after
menopause

Adrenal Medulla
 Made up of chromaffin cells that secrete epinephrine
and norepinephrine
 Secretion of these hormones causes:
 Blood glucose levels to rise
 Blood vessels to constrict
 The heart to beat faster
 Blood to be diverted to the brain, heart, and skeletal
muscle

Adrenal Medulla
 Epinephrine is the more potent stimulator of the

heart and metabolic activities
 Norepinephrine is more influential on peripheral
vasoconstriction and blood pressure

Function of the Adrenal Medulla
• An extension of the sympathetic nervous system
• Acts as a peripheral amplifier
• Activated by same stimuli as the sympathetic

nervous system
(examples – exercise, cold, stress,
hemorrhage, etc.)

Hormones of the Adrenal Medulla
• Adrenaline, epinephrine
• Noradrenaline, norepinephrine
80% of released catecholamines are epinephrine
• Dopamine


 Adrenaline (epinephrine)
 Noradrenaline (norepinephrine)
 80% of released catecholamines are
epinephrine.
 Hormones are secreted and stored in the
adrenal medulla and released in response to
appropriate stimuli.

Catecholamine Synthesis
tyrosine
tyrosine hydroxylase
dihydroxyphenylalanine
L-aromatic amino acid decarboxylase
dopamine
dopamine-B-hydroxylase
norepinephrine
phenylethanolamine-N-methyltransferase
epinephrine
Elimination of Catecholamines
dopamine homovanillic acid
norepinephrine
vanillylmandelic acid
epinephrine
catechol-O-methyltransferase (COMT)
monoamine oxidase (MAO)

Mechanism of Action
 Receptor mediated – adrenergic receptors

 Peripheral effects are dependent upon the type and
ratio of receptors in target tissues
Receptor  
Norepinephrine +++++ ++
Epinephrine ++++ ++++

Adrenergic Receptors
 Alpha-Adrenergic Receptors
 1: vasoconstriction, intestinal relaxation, uterine
contraction, pupillary dilation
 2:  presynaptic NE, platelet
aggregation, vasoconstriction,  insulin
secretion
 Beta-Adrenergic Receptors
 1:  HR/contractility,  lipolysis,  renin
secretion
 2: vasodilation, bronchodilation,  glycogenolysis
 3:  lipolysis,  brown fat thermogenesis

Mechanism of Action
1 and 2 epi > norepi
1 epi = norepi
2 epi >>> norepi

Differences between E and NE
 Epinephrine >> norepinephrine – in terms of cardiac

stimulation leading to greater cardiac output (
stimulation).
 Epinephrine < norepinephrine – in terms of

constriction of blood vessels – leading to increased
peripheral resistance – increased arterial pressure.
 Epinephrine >> norepinephrine – in terms of

increasing metabolism Epi = 5-10 x Norepinephrine

Effects of Epinephrine
• Metabolism
 Glycogenolysis in liver and skeletal muscle

 lead to hyperglycemia
 Mobilization of free fatty acids
 Increased metabolic rate

 O2 consumption increases

Effects of Epinephrine
• Cardiovascular
-  Heart rate & cardiac contractility
-  BP
Respiration:
 Oxygen consumption & respiratory rate

Pheochromocytoma
• A catecholamine-secreting tumour of chromaffin

cells of the adrenal medulla
 adrenal pheochromocytoma (90%)
• Paraganglioma – a catecholamine secreting tumour
of the sympathetic paraganglia
 extra-adrenal pheochromocytoma

Signs and Symptoms of Pheochromocytoma
• Treatment resistant hypertension (95%)
• Headache
• Sweating Classic triad
• Palpitations
• Chest pain
• Anxiety
• Glucose intolerance
• Increased metabolic rate

Stress and Its Effects
• Two types of stress:

 Physical stress
 Psychological stress
• Survival depends on maintaining homeostasis
• Factors that change the internal environment
are potentially life-threatening
• Sensing such dangers directs nerve impulses to
the hypothalamus
• This can trigger a loss of homeostasis

Responses to Stress
Hormonal signals Stress results from changes

in the external environment
Neural signals
Signals from
sensory receptors
Sympathetic impulses CRH released
Hypothalamus
Norepinephrine
Adrenal medulla Anterior pituitary
released
Epinephrine and ACTH released
norepinephrine
released
Adrenal cortex
Short-term ―fight or flight‖ or alarm stage. Cortisol released
• Blood glucose increases.

• Blood glycerol and fatty acids increase. Long-term adjustment or resistance stage
• Heart rate increases.
• Blood pressure rises. • Increase in blood concentration of amino acids.
• Breathing rate increases. • Increased release of fatty acids.
Air passages dilate. • Increased glucose formed from
• Pupils dilate. noncarbohydrates—amino acids (from
• Blood flow redistributes. proteins) and glycerol (from fats).

Stress and the Adrenal Gland


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The Endocrine System

Department of Physiology Diponegoro University Faculty of Medicine

 Adrenal glands – paired, pyramid-shaped organs at top

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

 Synthesizes and releases steroid hormones called

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

 Regulate the electrolyte concentrations of

Department of Physiology Diponegoro University Faculty of Medicine

 Aldosterone secretion is stimulated by:

Department of Physiology Diponegoro University Faculty of Medicine

 Renin-angiotensin mechanism – kidneys release renin,

Department of Physiology Diponegoro University Faculty of Medicine

• Direct stimulators of release

• Indirect stimulators of release: through RAAS

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

 Help the body resist stress by:

Department of Physiology Diponegoro University Faculty of Medicine

Hyperadrenalism – Cushing’s Syndrome

• Caused by exogenous glucocorticoids and by

• Zg tumour increases aldosterone

Department of Physiology Diponegoro University Faculty of Medicine

 Excessive levels of glucocorticoids:

Department of Physiology Diponegoro University Faculty of Medicine

Clinical symptoms of Cushing’s Syndrome

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

 Overnight Low dose = Baseline reading, Dexamethasone 1

Hypoadrenalism – Addison’s Disease

• Caused by tuberculosis, drugs, other

• Adrenal cortex produces inadequate amounts of

• Plasma sodium decreases and may lead to

Department of Physiology Diponegoro University Faculty of Medicine

Are precipitated in patients with Addison's disease by:

Department of Physiology Diponegoro University Faculty of Medicine

 Most gonadocorticoids secreted are androgens (male sex

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

 Epinephrine is the more potent stimulator of the

Department of Physiology Diponegoro University Faculty of Medicine

• An extension of the sympathetic nervous system

• Acts as a peripheral amplifier

• Activated by same stimuli as the sympathetic

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

dopamine homovanillic acid

Department of Physiology Diponegoro University Faculty of Medicine

 Receptor mediated – adrenergic receptors

Epinephrine ++++ ++++

Department of Physiology Diponegoro University Faculty of Medicine

Department of Physiology Diponegoro University Faculty of Medicine

1 and 2 epi > norepi

2 epi >>> norepi

Department of Physiology Diponegoro University Faculty of Medicine

 Epinephrine >> norepinephrine – in terms of cardiac

 Epinephrine < norepinephrine – in terms of

 Epinephrine >> norepinephrine – in terms of