Adrenal Gland PARA v2

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PHYSIOLOGY OF THE

ADRENAL GLAND

By
Dr.M.Anthony David MD
Professor of Physiology

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ADRENAL GLANDS
• ALSO CALLED AS
SUPRARENAL GLANDS.
• EACH IS A TWO-IN-ONE GLAND.
• ADRENAL CORTEX & ADRENAL
MEDULLA.
• THEY DIFFER IN:
– EMBRYOLOGY
– HISTOLOGY
– PHYSIOLOGY
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ADRENAL MEDULLA
• FORMS 28% OF THE
GLAND.
• IS CENTRALLY PLACED.
• HORMONES HELP IN
DEALING WITH
EMERGENCIES.

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ADRENAL CORTEX
• ENVELOPES THE MEDULLA.
• FORMS 72% OF THE GLAND & LIES
PERIPHERALLY
• IS ESSENTIAL FOR LIFE.
• SECRETES:
– MINERALLOCORTICOIDS
– GLUCOCORTICOIDS
– SEX STEROIDS

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ADRENAL GLAND : CYTO-
ARCHITECTURE

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FUNCTIONS OF ZONES
• ZONA GLOMERULOSA SECRETES
ALDOSTERONE.
• BOTH Z.FASCICULATA & RETICULARIS
FUNCTION TOGETHER:
– They are stimulated by ACTH
– They secrete:
Cortisol, Corticosterone, Androgenic
Steroids & Estrogens.
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GLUCOCORTICOIDS
• Enhance Glucose formation
• So are Diabetogenic
• Examples:
– Cortisol
– Corticosterone

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MINERALLOCORTICOIDS
• They promote Renal:
– Sodium Retention
– Potassium Excretion
• Example:
– Aldosterone

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GONADOCORTICOIDS
• Also called Sex steroids or Androgens
• They have a weak masculinizing effect.
• Examples:
– Dehydro Epi Androsterone (DHEA)
– Androstenedione

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CIRCADIAN RHYTHM OF PLASMA
CORTISOL LEVELS

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CORTISOL : FUNCTIONS 1
• CARBOHYDRATE METABOLISM:
– Diabetogenic
– Excess causes: Hyperglycemia, Glycosuria,
Resistance to Insulin & More of Hepatic
gluconeogenesis.
– Deficiency can cause Hypoglycemia
• PROTEIN METABOLISM:
– Causes protein catabolism

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CORTISOL : FUNCTIONS 2
• LIPID METABOLISM:
– Excess causes truncal obesity

• ELECTROLYTES & WATER:


– Aldosteronic effect:
– Sodium retention
– Potassium excretion

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CORTISOL : FUNCTIONS 3
• MUSCLES : Deficiency
causes weakness • CNS:
• BLOOD: Deficiency – Deficiency -
causes Eosinophilia, restlessness,
Lymphocytosis, insomnia & slow EEG
Neutropenia & Anemia. waves.
• CVS: – Excess causes
– Deficiency causes excitability & euphoria
Hypotension & Excess
causes Hypertension
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CORTISOL : FUNCTIONS 4
• GASTRO-INTESTINAL SYSTEM:
– Excess causes acidity & Acid peptic disease.
• BONES:
– Is a Calcitriol (D3) antagonist so causes
Osteoporosis.
• INFECTION/INFLAMMATION:
– Excess causes increased susceptibility

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CORTISOL: THERAPEUTICS
• Is used as treatment for Anaphylactic
shock.
• Also in severe cases of Bronchial
asthma.
• Is given as replacement in cases of
deficiency.

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ANAPHYLACTIC SHOCK

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BRONCHIAL ASTHMA

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ALDOSTERONE
• Is the chief minerallo-corticoid hormone.
• Maintains the electrolyte balance.
• Causes:
– Sodium retention & Potassium
excretion
• Acts on the DCT of the Nephrons
promoting Sodium absorption in exchange
for Potassium or Hydrogen ions.

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ADRENOCORTICAL SEX
HORMONES
• Are high in Fetal life due to Fetal Adrenal.
• They again peak at around pubertal age.
(Adrenarche)
• They increase the muscle mass, pubic
hair, seborrhea
• They also increase the libido or the sex
drive in females.

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REGULATION OF CORTISOL EMOTION
TRAUMA via
Via Limbic Cortex
NOCICEPTIVE
PATHWAYS DRIVE FOR
Hypothalamus CIRCADIAN
RHYTHM

N
E CORTICOTROPIN
RELEASING
G HORMONE CRH

F
E
E Ant. Pituitary
D
B ACTH
A
C
K
Adrenal
CORTISOL Cortex

SYSTEMIC EFFECTS
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REGULATION OF ADH : RENIN- ANGIOTENSIN
MECHANISM

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APPLIED ASPECTS:
EXCESS
• Primary Hyper aldosteronism: Conn’s
Disease
• Secondary: to
– CCF (Congestive Cardiac Failure)
– Nephrosis
– Pregnancy Induced Hypertension(PIH)
– Cirrhosis

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APPLIED ASPECTS:
EXCESS
• ADRENOGENITAL SYNDROME:
– VIRILISM
– FEMINISM
• CUSHING’S SYNDROME:
– ACTH DEPENDENT: CUSHING’S DISEASE
• ACTH
• ECTOPIC ACTH
• IATROGENIC
– ACTH INDEPENDENT:
• ADENOMA/CARCINOMA OF ADRENAL CORTEX
• IATROGENIC

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ADRENOGENITAL SYNDROME :
Virilism

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APPLIED ASPECTS: DEFICIENCY
• DESTRUCTION OF TISSUE: ‘ECTOMY’
• DECREASED SECRETION OF ACTH
• CONGENITAL DEFICIENCY OF
ENZYMES
• ACUTE
• CHRONIC: ADDISON’S DISEASE
– Weakness
– Hyperpigmentation
– Hypotension

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CUSHING’S SYNDROME
“A clinical disorder resulting from the
exposure of body tissues to sustained
supraphysiological blood levels of
corticosteroids either endogenous in
origin or iatrogenically produced.”
In one word: HYPERCORTISOLISM

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CUSHING’S SYNDROME:
CLINICAL FEATURES
• FAT PADS IN THE • MOON FACIES
NECK • RED CHEEKS
• THIN SKIN • POOR MUSCULAR
• PURPLE STRIAE DEVELOPMENT
• EASY BRUISABILITY • TRUNCAL OBESITY
• ECCHYMOSES • THIN SPINDLY
• POOR WOUND LIMBS
HEALING • INCREASED BODY &
FACIAL HAIR
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CUSHING’S SYNDROME

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CUSHINGS SYNDROME:
Truncal Obesity, Purple Striae

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ADRENAL MEDULLA
• CONTRIBUTES TO FIGHT OR FLIGHT
REACTIONS
• HORMONES: CATECHOLAMINES:
– EPINEPHRINE
– NOREPINEPHRINE
– DOPAMINE

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NE/EPINEPHRINE EFFECTS 1
• Similar to those of nervous discharge(Nor
epinephrine neurotransmitter)
• Stimulate the Nervous system
• Metabolic effects:
– Glycogenolysis
– FFA Mobilisation
–  Plasma Lactate
–  Metabolic Rate

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NE/EPINEPHRINE EFFECTS 2
• Receptors:
– Alpha 1
– Alpha 2
– Beta 1
– Beta 2
• Beta 1 receptor mediated effects:
– Positive Inotropic & Chronotropic effect
– Positive Bathymo tropism causing
Extrasystoles & Arrhythmias

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NE/EPINEPHRINE EFFECTS 3
• Alpha 1 receptor mediated:
– NE : Generalized vasoconstriction
• Beta 2 receptor mediated:
– E : Vasodilatation in skeletal muscles & Liver
• Slow infusion of NE causes:
– Increased Blood pressure, Reflex Bradycardia
and Decreased Cardiac Output.

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NE/EPINEPHRINE EFFECTS 4
• Increased Alertness
• Anxiety & Fear (E)
• Glycogenolysis
• Increased secretion
of Insulin & Glucagon.
• Increase in Metabolic
rate.

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PHEOCHROMOCYTOM
A
• An Adrenal medullary tumor usually benign
• Cause for < 1% of Hypertension
• Cured by surgery
• Clinical Features:
– Paroxysmal Sustained Hypertension
– Hyper thermia
– Hyperglycemia
–  BMR
–  Sweating

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PHEOCHROMOCYTOMA

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o for
e t’s g ak!
L e
a br

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