ACTH & ACTH & CORTICOSTEROIDSCORTICOSTEROIDS

DR. BALVIR SINGHDR. BALVIR SINGH

IntroductionIntroduction

ACTH is a peptide hormone .ACTH is a peptide hormone .

Produced by Ant. Pituitary.Produced by Ant. Pituitary.

Stimulate synthesis and release of Cortisol.Stimulate synthesis and release of Cortisol.

Synthesized from pro-opiomelanocortin (POMC).Synthesized from pro-opiomelanocortin (POMC).

ACTH release under control of CRH. ACTH release under control of CRH.

Human ACTH – G-protein coupled receptor family.Human ACTH – G-protein coupled receptor family.

Stimulate Adrenal cortex to produce Glucocorticoids. Stimulate Adrenal cortex to produce Glucocorticoids.

Mineralocortecoids Androgen. Mineralocortecoids Androgen.

Regulation of ACTHRegulation of ACTH

Hypothalamic – Pituitary – Hypothalamic – Pituitary – Adrenal axis (Adrenal axis (HPA axisHPA axis))

3 levels of regulation:3 levels of regulation:

1. Diurnal rhythm in basal1. Diurnal rhythm in basal

steroidogenesissteroidogenesis

2. Negative feedback2. Negative feedback

regulationregulation

3. Marked increases in3. Marked increases in

steroidogenesis in steroidogenesis in

response to stressresponse to stress

Diagnostic Appliction of ACTHDiagnostic Appliction of ACTH

Testing the Integrity of the HPA AxisTesting the Integrity of the HPA Axis CosyntropinCosyntropin :- is a synthetic peptide that corresponds to :- is a synthetic peptide that corresponds to

residues 1-24 of human ACTH.residues 1-24 of human ACTH. Cosyntropin testCosyntropin test:-:-

250µg of cosyntropin (im or iv)250µg of cosyntropin (im or iv)

measurment of cortisol measurment of cortisol (just before administration (baseline) and 30-60 (just before administration (baseline) and 30-60

minutes after cosyntropin administration)minutes after cosyntropin administration). .

circulating cortisol level circulating cortisol level

(greater than 18-20µg/dL indicates a normal response(greater than 18-20µg/dL indicates a normal response But low dose test(1µg) more sensitive than standard testBut low dose test(1µg) more sensitive than standard test

Adrenal CortexAdrenal Cortex

CYP11B2CYP11B2:-Aldosterone synthase:-Aldosterone synthase CYP11B1CYP11B1:-11 B Hydroxylase:-11 B Hydroxylase CYP17CYP17:-17:-17αα Hydroxylase Hydroxylase

ClassificationClassification::

A. MineralocorticoidsA. Mineralocorticoids

B. GlucocorticoidsB. Glucocorticoids

C. Adrenal AndrogensC. Adrenal Androgens

Biosynthesis of cortecosteroidsBiosynthesis of cortecosteroidsCholesterol

Pregnenolone

Progesterone

Deoxycorticosterone

Corticosterone

Aldosterone

17αHydroxypregnenolone

17αHydroxyrogesterone

11Deoxycortisol

Cortisol

CYP17Dehydroepiandrosterone

CYP21

CYP11A1

3β-HSD

CYP11B2

CYP11B2

CYP173B-HSD

CYP21

CYP11B1

CYP17

CYP11A1:-DesmolaseCYP11B2:-Aldosterone synthaseCYP11B1:-11 B HydroxylaseCYP17:-17α HydroxylaseCYP21:-21 Hydroxylase3βHSD:-3βHydroxsteroid dehydrogenage

Androstenedione

3B-HSD

DihydrotestosteroneOestradiolOestrone

CYP17

Glucocorticoids - MOAGlucocorticoids - MOA

S:- Glucocorticoid

Action of MineralocorticoidAction of Mineralocorticoid

Electrolyte and water balanceElectrolyte and water balance::• Act on the distal tubules and collecting ducts Act on the distal tubules and collecting ducts • Enhance reabsorption of NaEnhance reabsorption of Na++ and water and water • Increase the urinary excretion of KIncrease the urinary excretion of K++ and H and H++. .

Hyperaldosteronism •Positive Na+ balance, •Expansion of ECF, •Hypokalemia, •Metabolic alkalosis, •Progressive rise in BP.

Hypoaldosteronism •Dilutional hyponatraemia•hyperkalamia, •Metabolic acidosis,•decreased EFC volume.

Action of GlucocorticoidAction of Glucocorticoid

Carbohydrate metabolismCarbohydrate metabolism::• Gluconeogenesis, Gluconeogenesis, • Glycogen synthesis (Activate Glycogen synthetase)Glycogen synthesis (Activate Glycogen synthetase)• ↑↑ lipolysislipolysis• Periphery: Periphery: ↓glucose utilization ↓glucose utilization

Protein metabolismProtein metabolism::• ↑↑protein breakdown (amino acids)protein breakdown (amino acids)• Catabolic effectsCatabolic effects:: decrease muscle mass, atrophy of decrease muscle mass, atrophy of

lymphoid tissue, negative nitrogen balance, thinning lymphoid tissue, negative nitrogen balance, thinning of the skin of the skin

Contd…Contd… Lipid metabolismLipid metabolism::

• Redistribution of body fat (buffalo hump, moon Redistribution of body fat (buffalo hump, moon facies,supraclavicular area with loss of fat in the facies,supraclavicular area with loss of fat in the extremities)extremities)

• Induce lipolysis in adipocytes (Periphery) Induce lipolysis in adipocytes (Periphery) • Lipogenesis (Central)Lipogenesis (Central)

Cardiovascular systemCardiovascular system: : • Mineralocorticoid-induced HT.Mineralocorticoid-induced HT.• Permissive role on pressure effect with Permissive role on pressure effect with

Catecolamines and angiotensin II.Catecolamines and angiotensin II.• Adrenal insufficiency leads to low cardiac output and Adrenal insufficiency leads to low cardiac output and

arteriolar dilatation and poor response to adrenaline.arteriolar dilatation and poor response to adrenaline.

Contd..Contd.. Skeletal muscleSkeletal muscle::

• Steroid myopathy (weakness and fatigue) Steroid myopathy (weakness and fatigue) • Muscular weakness occurs in both Hypocorticism Muscular weakness occurs in both Hypocorticism

(due to hypodynamic circulation) and hypercorticism (due to hypodynamic circulation) and hypercorticism – due to hypokalaemia– due to hypokalaemia

CNSCNS: : • Euphoria – in pharmacological dosesEuphoria – in pharmacological doses• Addison's disease – apathy, depression and Addison's disease – apathy, depression and

psychosispsychosis• High doses – induce seizureHigh doses – induce seizure

Contd..Contd.. BloodBlood::

• Minor effects on HB and RBC productionMinor effects on HB and RBC production

• Glucocorticoids leads to↓Glucocorticoids leads to↓ no. no. of circulating of circulating

lymphocytes, eosinophils, monocytes, and basophils.lymphocytes, eosinophils, monocytes, and basophils.

Anti-inflammatory actionAnti-inflammatory action

Corticosteroids

LipocortinPhospholipase A2

Phospholipids

Arachidonic acids

lipoxygenase Cyclooxygenase

LeucotrinesProtaglandins ThromboxaneA2Protacyclins

PAF by lipocortin

Contd..Contd.. Anti-inflammatory and Immunosuppressive actionAnti-inflammatory and Immunosuppressive action

• Alter immune response of lymphocytes , monocytes Alter immune response of lymphocytes , monocytes

and basophils and basophils

• ↓↓Release of vasoactive and chemoattractive factorsRelease of vasoactive and chemoattractive factors

• ↓ ↓ Extravasation of leukocytes to area of injury Extravasation of leukocytes to area of injury

• ↓ ↓ Secretion of lipolytic and proteolytic enzymesSecretion of lipolytic and proteolytic enzymes

• Reduce exprssion of pro inflammatory cytokine Reduce exprssion of pro inflammatory cytokine

• ↓↓fibrosisfibrosis

Classification of DrugsClassification of Drugs

Mineralocorticoids•Aldosterone•Fludrocortisone•Desoxycorticosterone

Glucocortecoids•Hydrocortisone•Cortisone

•Pednisone•Pednisolone•Methylprednisolone•Triamcinolone

•Paramethasone•Betamethasone•Dexamethasone

Important agentsImportant agents InjectableInjectable::

Betamethasone Dexamethasone Betamethasone Dexamethasone Prednisolone Methylprednisolone Prednisolone Methylprednisolone Hydrocortisone TriamcinoloneHydrocortisone Triamcinolone

OralOral::Betamethasone FludrocortisoneBetamethasone FludrocortisonePrednisolone PrednisonePrednisolone PrednisoneMethylprednisoloneMethylprednisolone

TopicalTopical::Betamethasone ClobetasolBetamethasone ClobetasolFlucinolone MometasoneFlucinolone Mometasone

InhalationInhalation::Beclomethasone BudesonideBeclomethasone BudesonideFlunisolide FluticasoneFlunisolide Fluticasone

Therapeutic uses Therapeutic uses

EndrocrineEndrocrine

1-1-Replacement TherapyReplacement Therapy

A. Acute adrenal insufficiency (acute adrenal crisisA. Acute adrenal insufficiency (acute adrenal crisis))

Cause:Cause: • Destructive lesions secondary to surgery, Destructive lesions secondary to surgery, • TB of the adrenals, TB of the adrenals, • Bilateral adrenal hemorrhage. Bilateral adrenal hemorrhage. • Abrupt withdrawal of glucocorticoids at high doses or Abrupt withdrawal of glucocorticoids at high doses or

prolonged use prolonged use

S/S :S/S :GI symptoms, dehydration, hyponatremia, hyperkalemia, GI symptoms, dehydration, hyponatremia, hyperkalemia, weakness, lethargy, and hypotensionweakness, lethargy, and hypotension..

M/M:-M/M:-

• IV : D5 ,0.3%NaCl solutionIV : D5 ,0.3%NaCl solution

• Monitor for fluid overloadMonitor for fluid overload

• Hydrocortisone (cortisol) 100mg bolus,followed by Hydrocortisone (cortisol) 100mg bolus,followed by

100mg every 8hrs. , once stable, may give 25mg IM 100mg every 8hrs. , once stable, may give 25mg IM

hydrocortisone every 6-8hrs.; thereafter, same M/M hydrocortisone every 6-8hrs.; thereafter, same M/M

with chronic adrenal insufficiencywith chronic adrenal insufficiency

Therapeutic usesTherapeutic usesB. Chronic Adrenal Insufficiency (Addison’s disease)B. Chronic Adrenal Insufficiency (Addison’s disease)S/SS/S: : Hyper pigmentation, wt. loss, inability to maintain fasting Hyper pigmentation, wt. loss, inability to maintain fasting blood sugar, weakness, fatigue, hypotensionblood sugar, weakness, fatigue, hypotension

M/MM/M::Hydrocortisone 20-30mg/day BID + Hydrocortisone 20-30mg/day BID + Fludrocortisone acetate 0.05 – 0.2mg/dayFludrocortisone acetate 0.05 – 0.2mg/day

Valuable indicator of adequate replacementValuable indicator of adequate replacement::• Disappearance of hyperpigmentation and resolution Disappearance of hyperpigmentation and resolution of electrolyte abnormalitiesof electrolyte abnormalities• Monitor plasma ACTH levels or measure urinary free Monitor plasma ACTH levels or measure urinary free

cortisol.cortisol.

Therapeutic usesTherapeutic uses2 a. Congenital Adrenal Hyperplasia2 a. Congenital Adrenal HyperplasiaS/SS/S::

• After puberty with infertility,After puberty with infertility,• Hirsutism,Hirsutism,• Amenorrhea and acne;Amenorrhea and acne;• Female pseudohermaphroditism;Female pseudohermaphroditism;• Accelerated linear growth but height at maturity is Accelerated linear growth but height at maturity is

reduced. reduced. • Salt wasters – CV collapse (volume depletion)Salt wasters – CV collapse (volume depletion)

CauseCause:: 21 21 ββ hydroxylase hydroxylase

M/MM/M::• 11stst seen as acute adrenal crisis seen as acute adrenal crisis• Oral hydrocortisone 0.6mg/kg/day BID or TID Oral hydrocortisone 0.6mg/kg/day BID or TID • Fludrocortisone acetate 0.05-0.2mg/dayFludrocortisone acetate 0.05-0.2mg/day

T/T in-uteroT/T in-utero:: • mothers at risk – glucocorticoid therapy is initiated mothers at risk – glucocorticoid therapy is initiated

before 10 weeks gestation followed by genotyping before 10 weeks gestation followed by genotyping and sex determinationand sex determination

• Stimulation of fetal lung maturation Stimulation of fetal lung maturation –– betamethasone 12mg followed by 12mg betamethasone 12mg followed by 12mg after24 hrs. after24 hrs.

Therapeutic usesTherapeutic usesb. Cushing’s syndromeb. Cushing’s syndrome CauseCause:: pituitary adenoma, tumors of the adrenal glandpituitary adenoma, tumors of the adrenal gland

S/SS/S:: Moon face, truncal obesity, hypertension,Moon face, truncal obesity, hypertension, muscle wasting, purple striae and easy bruising of the muscle wasting, purple striae and easy bruising of the

skin, poor wound healing, osteoporosisskin, poor wound healing, osteoporosis

M/MM/M::• Surgery ,Hydrocortisone 300 mg IV on the day of the Surgery ,Hydrocortisone 300 mg IV on the day of the

surgery, then maintenance oral dosesurgery, then maintenance oral dose . .

Diagnostic Application – Dexamethasone: Diagnostic Application – Dexamethasone: Suppress Test Suppress Test

Hypercortisolism

1mg Dexamethasone orally 11pm

PC at 8am <1.8µg PC at 8am >1.8µg

0.5mg D 6 hr for 48 hrs

PC Obesity, stress

PC

2mg D 6hrs for 48hrs

PCPituitary dependent CS

PCEctopic ACTH production

PC:-Plasma Cortisol, CS:-Cushing Syndrome

Therapeutic usesTherapeutic uses

Non-Endocrine DiseasesNon-Endocrine Diseases

1.1.Rheumatic disorders:-Rheumatic disorders:- • Suppress the disease and minimize resultant tissue Suppress the disease and minimize resultant tissue

damage. damage.

M/M:M/M:• Prednisone oral 10 mg/kg/day (taper there after by Prednisone oral 10 mg/kg/day (taper there after by

decreasing 1mg/kg/day every 2-3 wks)decreasing 1mg/kg/day every 2-3 wks)• Intraarticular injection: triamcinolone acetonideIntraarticular injection: triamcinolone acetonide: :

minimize complications.minimize complications.

Therapeutic usesTherapeutic uses

2. 2. Renal DisordersRenal Disorders – – Nephrotic syndromeNephrotic syndrome

M/M:M/M:• PrednisonePrednisone:: 1-2 mg/kg x 6 wks, followed by gradual 1-2 mg/kg x 6 wks, followed by gradual

tapering over 6-8 wks or alternate-day therapy tapering over 6-8 wks or alternate-day therapy (diminished proteinuria in 85% pts in 2-3 wks and (diminished proteinuria in 85% pts in 2-3 wks and 95% pts will have remission in 3 month.95% pts will have remission in 3 month.

Membranous glomerulonephritis Membranous glomerulonephritis

M/M:M/M: • Alternate-day prednisone 8-10 wks followed by 1-2 Alternate-day prednisone 8-10 wks followed by 1-2

month period of taperingmonth period of tapering

Therapeutic usesTherapeutic uses

3. 3. Allergic DiseaseAllergic Disease: : onset of action of glucocorticoid is onset of action of glucocorticoid is delayed (6-12hrs.)delayed (6-12hrs.)

AnaphylaxisAnaphylaxis::• Epinephrine 0.5ml of a 1:1000 solution IM or SC, Epinephrine 0.5ml of a 1:1000 solution IM or SC,

repeated every 15 mins up to 3 doses is neededrepeated every 15 mins up to 3 doses is needed• Methypednisolone 125mg 6hr.Methypednisolone 125mg 6hr.• Less sever disease Antihistamines is DOCLess sever disease Antihistamines is DOC

Therapeutic usesTherapeutic uses44. Bronchial Asthma. Bronchial Asthma – role of inflammation in the – role of inflammation in the

immunopathogenesis of this disorder.immunopathogenesis of this disorder.

M/M:M/M: IV methylprednisoloneIV methylprednisolone 60-120mg every 6hr initially 60-120mg every 6hr initially followed by oral prednisone 40-60mg daily as acute followed by oral prednisone 40-60mg daily as acute attack resolvesattack resolves

Inhaled steroidsInhaled steroids – reduces bronchial hyperreactivity with – reduces bronchial hyperreactivity with less suppression of adrenal function (SE: dysphonia or less suppression of adrenal function (SE: dysphonia or oropharyngeal candidiasis) oropharyngeal candidiasis)

ex: beclomethasone dipropionate, budesonide ex: beclomethasone dipropionate, budesonide phosphate, flunisolide, fluticasone, mometasone furoate, phosphate, flunisolide, fluticasone, mometasone furoate, triamcinolone acetonidetriamcinolone acetonide

Therapeutic usesTherapeutic uses

55. . Infectious Disease:-Infectious Disease:-• P. carinii pneumonia P. carinii pneumonia – G +Ab increases – G +Ab increases

oxygenation and decreases the incidence of oxygenation and decreases the incidence of respiratory failure and mortality.respiratory failure and mortality.

• H. influenzae type B meningitis H. influenzae type B meningitis – decrease the – decrease the long-term neurological impairment.long-term neurological impairment.

66. . Ocular disease:-Ocular disease:-• 0.1% dexamethasone0.1% dexamethasone• C/IC/I: herpes simplex keratitis (clouding of the cornea) , : herpes simplex keratitis (clouding of the cornea) ,

glaucoma ,lacerated and abrasion of eyeglaucoma ,lacerated and abrasion of eye..

Therapeutic usesTherapeutic uses7. 7. Skin diseasesSkin diseases – – Inflammatory dermatoses Inflammatory dermatoses (1% (1%

Hydrocortisone oimtment twice Daily)Hydrocortisone oimtment twice Daily) Phemphigus & PhemphigoidPhemphigus & Phemphigoid (Prednisolone 40mg (Prednisolone 40mg

daily)daily)

8. 8. GIT diseasesGIT diseases – – Inflammatory bowel diseaseInflammatory bowel disease Mild UC 100mg Hydrocortisone daily.Mild UC 100mg Hydrocortisone daily. Sever cases Prednisolone 10-30mg dailySever cases Prednisolone 10-30mg daily

9. 9. Hepatic diseasesHepatic diseases – Prednisolone – 80% – Prednisolone – 80% histologic remission in pts. with chronic, activehistologic remission in pts. with chronic, active hepatitishepatitis

10. 10. MalignanciesMalignancies – ALL, lymphomas – ALL, lymphomas

Therapeutic usesTherapeutic uses11. 11. Cerebral edema Cerebral edema – neoplasms and parasitic infections – neoplasms and parasitic infections

but not in CVA or traumabut not in CVA or trauma

12. 12. Miscellaneous disMiscellaneous dis – – SarcoidosisSarcoidosis : :(induce remission),(induce remission), ThrombocytopeniaThrombocytopenia: (decrease bleeding tendency): (decrease bleeding tendency),,

Organ transplantationOrgan transplantation: Pednisolone 50-100mg at the : Pednisolone 50-100mg at the time of surgery (reduce Ag expression from grafted time of surgery (reduce Ag expression from grafted tissues, delayed revascularization, interferes with tissues, delayed revascularization, interferes with cytotoxic T-lymphocytes and generation of primary Ab cytotoxic T-lymphocytes and generation of primary Ab formation) formation)

Spinal cord injurySpinal cord injury: (within 1st 8 hrs large dose of : (within 1st 8 hrs large dose of pednisolone: inhibition of free-radical mediated cellular pednisolone: inhibition of free-radical mediated cellular injury .injury .

Toxicity of corticosteroidsToxicity of corticosteroids

Withdrawal of therapy:Withdrawal of therapy:• Flare-up of the underlying disease Flare-up of the underlying disease • Acute adrenal insufficiency Acute adrenal insufficiency • Suppressed the HPA axisSuppressed the HPA axis

S/SS/S• Fever, Fever, • Myalgias, Myalgias, • Arthralgias, Arthralgias, • Malaise, Malaise, • Pseudomotor cerebri ( ↑ICP with papilledema)Pseudomotor cerebri ( ↑ICP with papilledema)

Contd..Contd..

Continued use at supraphysiologic dosesContinued use at supraphysiologic doses• Fluid and electrolyte abnormalities,Fluid and electrolyte abnormalities,• Metabolic changesMetabolic changes• Increased susceptibility to infection,Increased susceptibility to infection,• Peptic ulcer Peptic ulcer • Myopathy,Myopathy,• Behavioral disturbances, Behavioral disturbances, • Cataracts, Cataracts, • Osteoporosis and OsteonecrosisOsteoporosis and Osteonecrosis• Regulation of growth and developmentRegulation of growth and development

ContraindicationsContraindications

peptic ulcer peptic ulcer heart disease or HT with CHFheart disease or HT with CHF InfectionsInfections Psychoses Psychoses DiabetesDiabetes Osteoporosis Osteoporosis Glaucoma Glaucoma Herpes simplex infectionHerpes simplex infection

Antagonists of Adrenocortical AgentsAntagonists of Adrenocortical Agents

Synthetic inhibitors and glucocorticoid antagonistsSynthetic inhibitors and glucocorticoid antagonists

11. Metyrapone:. Metyrapone:––• Selective inhibitor of CYP11B1 (11Selective inhibitor of CYP11B1 (11ββ-hydroxylase), which -hydroxylase), which

converts 11 deoxycortisol to cortisol.converts 11 deoxycortisol to cortisol.• Used in diagnosis of HPA functionUsed in diagnosis of HPA function• Hypercorticism: 4 g/dayHypercorticism: 4 g/day• S/E: Hirsutism,Nausea,Heahache,Sedation,Rashes.S/E: Hirsutism,Nausea,Heahache,Sedation,Rashes.

2. 2. AminoglutethimidAminoglutethimide:e:– – • Blocks the conversion of cholesterol to pregnanenolone and Blocks the conversion of cholesterol to pregnanenolone and

causes a reduction in the synthesis of all hormonally active causes a reduction in the synthesis of all hormonally active steroidssteroids

• Used in hypercotisolism and advance cancer Breast & Used in hypercotisolism and advance cancer Breast & prostate.prostate.

• Enhances metabolism of dexamethasoneEnhances metabolism of dexamethasone

•

Glucocorticoid antagonistsGlucocorticoid antagonists 3.3. Ketoconazole: Ketoconazole:– –

• An antifungal imidazole derivative; potent, non-An antifungal imidazole derivative; potent, non-selective inhibitor of adrenal and gonadal steroid selective inhibitor of adrenal and gonadal steroid synthesis (CYP11,CYP17)synthesis (CYP11,CYP17)

• HepatotoxicHepatotoxic• Inhibits cholesterol side chain cleavageInhibits cholesterol side chain cleavage• USE:Cushing’s syndrome –inoperable (200-USE:Cushing’s syndrome –inoperable (200-

1000mg/d)1000mg/d)

4. 4. Mifepristone (RU 486):Mifepristone (RU 486):––• 1111ββ-aminophenyl-substituted 19-norsteroid-aminophenyl-substituted 19-norsteroid• Has strong anti-progestin activityHas strong anti-progestin activity• Blocks glucocorticoid receptor.Blocks glucocorticoid receptor.

Glucocorticoid antagonistsGlucocorticoid antagonists5. 5. MitotaneMitotane::––

• Adrenal Ca: 3 g/daily ,results in reduction in tumor Adrenal Ca: 3 g/daily ,results in reduction in tumor massmass

• GI disturbances and Ataxia are its major toxicities.GI disturbances and Ataxia are its major toxicities.

6. 6. TrilostaneTrilostane::--• 33ββ- hydroxy steroid dehydrogenase inhibitor that - hydroxy steroid dehydrogenase inhibitor that

interferes with the synthesis of adrenal and gonadal interferes with the synthesis of adrenal and gonadal hormoneshormones

• Not used in human (veterinary medicineNot used in human (veterinary medicine))

Mineralocorticoid AntagonistsMineralocorticoid Antagonists

11. . SpirinolactoneSpirinolactone::– Aldosterone receptor antagonist– Aldosterone receptor antagonist

S/ES/E: Gynecomastia, Impotence,Hirsutism,Menstrual : Gynecomastia, Impotence,Hirsutism,Menstrual

irregularties, ↓libido, deepening of voiceirregularties, ↓libido, deepening of voice

UsesUses:-Hypertention:-Hypertention

Primary HyperaldosternismPrimary Hyperaldosternism

Hepatic cirrhosisHepatic cirrhosis

2. 2. Eplerenone:Eplerenone: –Safe and effective antihypertensive agent, –Safe and effective antihypertensive agent, less side effectless side effect

3. 3. Drospirenone:-Drospirenone:- New Progestrogen with New Progestrogen with antimineralocorticoid and antiandrogen prapertiesantimineralocorticoid and antiandrogen praperties

SUMMARY OF CORTECOSTEROIDS

THANK YOUTHANK YOU

Next seminar:-Antithyroid DrugsSpeaker:- Dr. Sudhir Ku. JainDate;- 10/11/2014

Diurnal variation of CortisolDiurnal variation of Cortisol

Glucocorticoids – Anti-inflammatory Glucocorticoids – Anti-inflammatory and Immunosuppressive effectsand Immunosuppressive effects