Topic Overview

CORTICOSTEROIDS

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Definition

• Corticosteroids are steroid hormones produced by the adrenal cortex or their synthetic analogues that regulate metabolism, inflammation, immune response, and electrolyte balance.

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Classification

Glucocorticoids

• Predominantly affect metabolism and inflammation

• Examples: Hydrocortisone, Prednisolone, Dexamethasone

Mineralocorticoids

• Regulate water and electrolyte balance

• Example: Fludrocortisone

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Natural vs Synthetic Corticosteroids

• Natural → Cortisol (hydrocortisone), Aldosterone

• Synthetic → Prednisolone, Dexamethasone, Betamethasone

• Synthetic drugs have:

  • ↑ anti-inflammatory action

  • ↓ mineralocorticoid activity

  • ↑ duration of action

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Sources (Adrenal Cortex Zones)

• Zona glomerulosa → Mineralocorticoids

• Zona fasciculata → Glucocorticoids

• Zona reticularis → Androgens

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Structure–Activity Relationship (VERY HIGH-YIELD)

• Steroid nucleus essential

• Double bond at C1–C2 → ↑ glucocorticoid activity

• Fluorination (C9) → ↑ potency

• Methyl group at C16 → ↓ mineralocorticoid activity

• OH at C11 → required for activity

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PHYSIOLOGY

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HPA Axis Regulation

• Hypothalamus → CRH

• Pituitary → ACTH

• Adrenal cortex → Cortisol

• Cortisol exerts negative feedback on hypothalamus and pituitary

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Circadian Rhythm

• Peak cortisol → early morning (6–8 AM)

• Lowest → midnight

• Morning dosing mimics physiology

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Stress Response

• Stress → ↑ CRH → ↑ ACTH → ↑ cortisol

• Effects:

  • ↑ glucose availability

  • Maintains BP

  • Anti-inflammatory protection

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Glucocorticoid vs Mineralocorticoid Functions

Feature	Glucocorticoids	Mineralocorticoids
Hormone	Cortisol	Aldosterone
Function	Metabolism, anti-inflammatory	Na⁺ retention, K⁺ loss
BP effect	Indirect ↑	Direct ↑
Immune effect	Suppression	Minimal

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Plasma Transport

• Cortisol bound to:

  • CBG (Transcortin)

  • Albumin

• Only free cortisol is active

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MECHANISM OF ACTION (VERY HIGH-YIELD)

• Steroid enters cell → binds cytosolic receptor

• Complex enters nucleus → binds GRE

Core Mechanisms

• Transactivation → ↑ lipocortin

• Transrepression → ↓ NF-κB, ↓ AP-1

• Lipocortin → ↓ PLA2 → ↓ prostaglandins & leukotrienes

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PHARMACOLOGICAL ACTIONS

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Metabolic

• ↑ gluconeogenesis → hyperglycemia

• Protein catabolism → muscle wasting

• Fat redistribution → truncal obesity

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Anti-inflammatory

• ↓ capillary permeability

• ↓ leukocyte migration

• ↓ cytokines

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Immunosuppressive

• ↓ T-cell proliferation

• ↓ antibody production

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Hematological

• ↑ neutrophils

• ↓ lymphocytes, eosinophils

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CVS

• Maintains vascular tone

• ↑ catecholamine response

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Renal

• Na⁺ retention

• K⁺ loss

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CNS

• Mood changes

• Euphoria / depression

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Bone

• Osteoporosis

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Skin

• Thinning, striae

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PHARMACOKINETICS

• Good oral absorption

• Protein binding (CBG)

• Hepatic metabolism (CYP3A4)

• Renal excretion

Half-life

• Plasma vs biological (important exam point)

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ROUTE-SPECIFIC PHARMACOLOGY

Inhaled

• Budesonide, Fluticasone

• High first-pass metabolism

Topical

• Absorption ↑ with:

  • Thin skin

  • Occlusion

  • Inflammation

Intranasal

• Allergic rhinitis

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PREPARATIONS

Drug	Duration
Hydrocortisone	Short
Prednisolone	Intermediate
Dexamethasone	Long

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THERAPEUTIC USES

• Addison disease

• Congenital adrenal hyperplasia

• Asthma, COPD

• Rheumatoid arthritis

• SLE

• Dermatological disorders

• Transplantation

• Cerebral edema

• Leukemia, lymphoma

• Fetal lung maturation

• Septic shock (adjunct)

• ARDS / COVID

• Nephrotic syndrome

• Myasthenia gravis

• Giant cell arteritis

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ADVERSE EFFECTS

• Cushingoid features

• Hyperglycemia

• Osteoporosis

• Avascular necrosis

• Steroid myopathy

• Peptic ulcer

• Infection risk

• Growth retardation

• Cataract, glaucoma

• Electrolyte imbalance

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CONTRAINDICATIONS

• Diabetes

• Hypertension

• Peptic ulcer

• Infections

• Osteoporosis

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DRUG INTERACTIONS

• Rifampicin → ↓ steroid effect

• Ketoconazole → ↓ synthesis

• NSAIDs → ↑ ulcer risk

• Diuretics → hypokalemia

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SPECIAL CLINICAL CONCEPTS

• Alternate-day therapy

• Pulse therapy

• Steroid resistance

• Steroid dependence

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WITHDRAWAL & TAPERING

• Abrupt stop → adrenal crisis

• Gradual taper required

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DIAGNOSTIC TESTS

• Dexamethasone suppression test

• ACTH stimulation test

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TABLES (HIGH-YIELD)

Relative Potency

Drug	Anti-inflammatory	Mineralocorticoid
Hydrocortisone	1	1
Prednisolone	4	0.8
Dexamethasone	25	0

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DIAGRAMS / FLOWCHARTS

Anti-inflammatory Pathway

• Steroid → Lipocortin → ↓ PLA2 → ↓ AA → ↓ PG + LT

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Steroid Tapering

• Long-term therapy → gradual dose reduction → prevents adrenal crisis

 

 

MINERALOCORTICOID SYSTEM (FULL)

Aldosterone Mechanism

• Acts on distal convoluted tubule & collecting duct

• Binds intracellular mineralocorticoid receptor → gene transcription

• ↑ ENaC (epithelial Na⁺ channels) → ↑ Na⁺ reabsorption

• ↑ Na⁺/K⁺-ATPase activity → Na⁺ retention, K⁺ excretion

• Water follows Na⁺ → ↑ ECF volume

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RAAS Regulation

• ↓ BP / ↓ renal perfusion → ↑ renin (JG cells)

• Renin → Angiotensin I → (ACE) → Angiotensin II

• Angiotensin II:

  • ↑ aldosterone secretion

  • Vasoconstriction

• Final effect → ↑ BP, ↑ volume

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Volume and BP Regulation

• Aldosterone → Na⁺ + water retention → ↑ blood volume

• Maintains circulatory homeostasis

• Excess → hypertension

• Deficiency → hypotension

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Fludrocortisone Role

• Potent mineralocorticoid analogue

• Used in:

  • Addison disease

  • Orthostatic hypotension

• Strong Na⁺ retaining action

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Pseudohyperaldosteronism

• Clinical features of aldosterone excess without ↑ aldosterone

• Causes:

  • Licorice (glycyrrhizin → inhibits 11β-HSD2)

  • Apparent mineralocorticoid excess

• Mechanism → cortisol acts on mineralocorticoid receptor

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MECHANISM OF ACTION (VERY HIGH-YIELD CORE)

Genomic Mechanism

• Steroid diffuses into cell → binds cytosolic glucocorticoid receptor (GR)

• Complex translocates to nucleus → binds GRE (glucocorticoid response element)

• Alters gene transcription

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Transactivation

• ↑ synthesis of anti-inflammatory proteins

  • Lipocortin (Annexin-1)

• ↑ anti-inflammatory mediators

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Transrepression (VERY IMPORTANT)

• ↓ transcription factors:

  • NF-κB inhibition → ↓ cytokines (IL-1, TNF-α)

  • AP-1 suppression → ↓ inflammatory gene expression

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Arachidonic Acid Pathway Inhibition

• Lipocortin → inhibits PLA2

• ↓ arachidonic acid

• ↓ prostaglandins + leukotrienes

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Non-genomic Effects

• Rapid actions (seconds–minutes)

• Membrane stabilization

• Ion channel modulation

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PHARMACOLOGICAL ACTIONS

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Metabolic Effects

• ↑ gluconeogenesis → hyperglycemia

• ↓ glucose uptake in tissues

• Protein catabolism → muscle wasting

• Fat redistribution → truncal obesity, moon face

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Anti-inflammatory Effects

• ↓ capillary permeability

• ↓ leukocyte migration

• ↓ inflammatory mediators

• Stabilizes lysosomal membranes

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Immunosuppressive Effects

• ↓ T-cell proliferation

• ↓ cytokine production

• ↓ antibody formation

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Hematological Effects

• ↑ neutrophils (demargination)

• ↓ lymphocytes

• ↓ eosinophils

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Cardiovascular System

• Maintains vascular tone

• ↑ sensitivity to catecholamines

• Prevents shock

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Renal & Electrolyte Effects

• Na⁺ retention

• K⁺ excretion

• Water retention → edema

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Central Nervous System

• Mood elevation (euphoria)

• Depression, psychosis (high dose)

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Bone

• ↓ osteoblast activity

• ↑ bone resorption

• → osteoporosis

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Skin

• ↓ collagen synthesis

• → skin atrophy, striae

 

PHARMACOKINETICS (DETAILED)

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Absorption

• Well absorbed by multiple routes:

  • Oral → good bioavailability

  • IV → rapid action (emergency use)

  • Topical → variable (depends on skin condition)

  • Inhalational → local lung delivery with minimal systemic exposure

  • Intra-articular → localized effect in joints

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Distribution

• Highly protein bound:

  • CBG (Transcortin) → major binding protein

  • Albumin → secondary

• Only free (unbound) fraction is pharmacologically active

• Wide tissue distribution including CNS

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Metabolism

• Primarily hepatic metabolism (CYP3A4)

• Converted into inactive metabolites

• Drugs like prednisolone may require hepatic activation (prednisone → prednisolone)

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Excretion

• Metabolites excreted via kidneys (urine)

• Minor biliary excretion

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Plasma Half-life vs Biological Half-life (VERY HIGH-YIELD)

Parameter	Plasma Half-life	Biological Half-life
Definition	Time in blood circulation	Duration of pharmacological action
Duration	Short (minutes–hours)	Long (hours–days)
Importance	Pharmacokinetics	Clinical dosing
Example	Hydrocortisone short	Dexamethasone long action

• Biological half-life determines dosing frequency (EXAM FAVORITE)

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ROUTE-SPECIFIC PHARMACOLOGY

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Inhaled Corticosteroids (ICS)

• Examples: Budesonide, Fluticasone

• Delivered directly to lungs → ↓ systemic effects

• High first-pass hepatic metabolism → minimal systemic toxicity

• Used in:

  • Asthma

  • COPD

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Topical Steroids

Absorption Factors (VERY HIGH-YIELD)

• Skin thickness

  • Thin skin (face, eyelids) → ↑ absorption

  • Thick skin (palms, soles) → ↓ absorption

• Occlusion

  • ↑ hydration → ↑ drug penetration

• Inflammation

  • Damaged skin → ↑ absorption

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Intranasal Steroids

• Used in allergic rhinitis

• Minimal systemic absorption

• Examples: Fluticasone, Mometasone

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Intra-articular Steroids

• Local injection in joints

• Used in:

  • Rheumatoid arthritis

  • Osteoarthritis

• Provides local anti-inflammatory effect

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PREPARATIONS (VERY HIGH-YIELD)

Drug	Type	Duration
Hydrocortisone	Natural	Short
Prednisolone	Synthetic	Intermediate
Methylprednisolone	Synthetic	Intermediate
Dexamethasone	Synthetic	Long
Betamethasone	Synthetic	Long
Fludrocortisone	Mineralocorticoid	Long

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Key Exam Points

• Dexamethasone → highest anti-inflammatory potency, no mineralocorticoid activity

• Hydrocortisone → both glucocorticoid + mineralocorticoid

• Fludrocortisone → strong mineralocorticoid

• Prednisolone → most commonly used systemic steroid

 

THERAPEUTIC USES (VERY HIGH-YIELD — FULL)

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Replacement Therapy

• Addison disease

  • Hydrocortisone ± fludrocortisone

• Congenital adrenal hyperplasia

  • Suppresses ACTH → ↓ adrenal androgen excess

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Anti-inflammatory Uses

• Respiratory

  • Bronchial asthma (ICS + systemic in severe cases)

  • COPD exacerbations

• Rheumatologic

  • Rheumatoid arthritis

  • Ankylosing spondylitis

• Gastrointestinal

  • Inflammatory bowel disease (UC, Crohn’s)

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Immunosuppressive Uses

• Organ transplantation

  • Prevention of graft rejection

• Autoimmune diseases

  • SLE

  • Vasculitis

  • Dermatomyositis

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Dermatological Uses (VERY IMPORTANT)

• Eczema

• Psoriasis

• Lichen planus

• Pemphigus vulgaris

• Contact dermatitis

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Allergic Disorders

• Anaphylaxis (adjunct to adrenaline)

• Allergic rhinitis (intranasal steroids)

• Urticaria

• Drug reactions

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Central Nervous System

• Cerebral edema

  • Brain tumors

  • Neuroinflammation

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Oncology

• Leukemia

• Lymphoma

• Reduce tumor-associated inflammation

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Antenatal Use

• Betamethasone / dexamethasone

• Fetal lung maturation → ↑ surfactant

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Shock

• Septic shock (adjunct)

  • When refractory to fluids & vasopressors

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ARDS / COVID

• Dexamethasone

• Reduces cytokine storm and mortality

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Antiemetic Use

• Chemotherapy-induced vomiting

• Often combined with 5-HT₃ antagonists

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Myasthenia Gravis

• Immunosuppression → ↓ antibody production

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Nephrotic Syndrome

• Especially minimal change disease

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Giant Cell Arteritis / Temporal Arteritis

• Prevents vision loss (emergency indication)

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ADVERSE EFFECTS (VERY HIGH-YIELD COMPLETE)

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Endocrine & Metabolic

• Iatrogenic Cushing syndrome

  • Moon face, buffalo hump

• Hyperglycemia → steroid-induced diabetes

• Truncal obesity

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Musculoskeletal

• Osteoporosis (↓ osteoblast activity)

• Avascular necrosis of femoral head (VERY HIGH-YIELD)

• Steroid myopathy

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Gastrointestinal

• Peptic ulcer

• Gastritis

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Infections

• Immunosuppression

• Reactivation of:

  • TB

  • Fungal infections

• Masking of infection signs (clinical trap)

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Growth

• Growth retardation in children

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Neuropsychiatric

• Mood swings

• Euphoria

• Depression

• Psychosis (high doses)

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Ophthalmic

• Cataract

• Glaucoma

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Electrolyte Disturbances

• Na⁺ retention → edema

• K⁺ loss → hypokalemia

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CONTRAINDICATIONS & PRECAUTIONS

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Relative Contraindications

• Diabetes mellitus

• Hypertension

• Peptic ulcer disease

• Osteoporosis

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Infections

• Tuberculosis

• Fungal infections

• Avoid or use cautiously (unless life-saving)

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General Precautions

• Use lowest effective dose

• Prefer local therapy (topical/inhaled) when possible

• Monitor:

  • Blood glucose

  • BP

  • Bone density

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Important Clinical Pearl

• Long-term therapy → never stop abruptly

• Always taper → prevents adrenal crisis

 

DRUG INTERACTIONS

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CYP3A4 Inducers → ↓ Steroid Effect

• Examples: Rifampicin, Phenytoin, Carbamazepine

• Mechanism:

  • ↑ hepatic metabolism → ↓ plasma steroid levels

• Clinical implication:

  • Loss of therapeutic effect

  • May precipitate adrenal insufficiency in dependent patients

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CYP3A4 Inhibitors → ↑ Steroid Effect

• Examples: Ketoconazole, Erythromycin

• Mechanism:

  • ↓ metabolism → ↑ steroid levels

• Clinical implication:

  • ↑ risk of toxicity (Cushingoid features)

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NSAIDs

• Combined use → ↑ risk of peptic ulcer & GI bleeding

• Mechanism:

  • Both inhibit prostaglandins → mucosal damage

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Diuretics

• Especially loop/thiazide diuretics

• Effect:

  • ↑ K⁺ loss → severe hypokalemia

• Risk:

  • Arrhythmias

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Vaccines

• Live vaccines contraindicated

• Mechanism:

  • Immunosuppression → uncontrolled infection risk

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SPECIAL CLINICAL CONCEPTS (VERY HIGH-YIELD)

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Steroid Resistance

• Reduced responsiveness to corticosteroids

• Causes:

  • Altered glucocorticoid receptor function

  • Increased inflammatory mediators

• Seen in:

  • Severe asthma

  • Some autoimmune disorders

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Steroid Dependence

• Disease relapses on dose reduction

• Requires prolonged therapy

• Common in:

  • Asthma

  • Autoimmune diseases

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Alternate-Day Therapy (VERY IMPORTANT)

Principle:

• Give double dose on alternate days (morning)

Mechanism:

• Allows partial recovery of HPA axis on off days

• Reduces:

  • Adrenal suppression

  • Growth retardation

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Pulse Therapy

• High-dose IV corticosteroids for short duration

• Example:

  • IV methylprednisolone (1 g/day for 3–5 days)

Indications:

• Severe autoimmune diseases

• SLE flare

• Nephrotic syndrome

• Transplant rejection

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WITHDRAWAL & TAPERING

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HPA Axis Suppression Mechanism

• Long-term steroids → ↓ CRH & ACTH

• Adrenal cortex atrophy

• Sudden withdrawal → inadequate cortisol production

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Adrenal Crisis (VERY HIGH-YIELD)

• Life-threatening condition

Features:

• Hypotension

• Hypoglycemia

• Weakness

• Shock

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Tapering Protocols

• Gradual dose reduction required

General Principles:

• Short course (<2 weeks) → abrupt stop possible

• Long-term therapy → slow taper

• Reduce dose stepwise

• Monitor for:

  • Disease relapse

  • Symptoms of adrenal insufficiency

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Important Clinical Pearls

• Always give steroids in morning (mimic circadian rhythm)

• Avoid abrupt withdrawal

• Use lowest effective dose for shortest duration

 

DIAGNOSTIC & MONITORING ASPECTS

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Dexamethasone Suppression Test (VERY HIGH-YIELD)

Principle

• Dexamethasone suppression test evaluates negative feedback of glucocorticoids on the HPA axis

• Dexamethasone → suppresses ACTH → ↓ cortisol in normal individuals

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Types

Low-dose test

• Used for screening Cushing syndrome

• Normal → cortisol suppressed

• Cushing syndrome → no suppression

High-dose test

• Differentiates causes of Cushing syndrome

Condition	Cortisol Response
Pituitary adenoma (Cushing disease)	Partial suppression
Adrenal tumor	No suppression
Ectopic ACTH	No suppression

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ACTH Stimulation Test (Synacthen Test)

Principle

• ACTH stimulation test assesses adrenal gland responsiveness

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Procedure

• Administer synthetic ACTH (cosyntropin)

• Measure cortisol before and after

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Interpretation

Condition	Cortisol Response
Normal	↑ cortisol
Primary adrenal insufficiency (Addison)	No rise
Secondary (pituitary)	Delayed/partial rise

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Monitoring Long-Term Therapy

Clinical Monitoring

• Weight gain

• BP

• Edema

• Features of Cushingoid appearance

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Laboratory Monitoring

• Blood glucose

• Electrolytes (Na⁺, K⁺)

• Bone density (DEXA scan)

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Special Monitoring

• Eye examination → cataract, glaucoma

• Growth monitoring in children

• Infection surveillance

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PATHOLOGICAL CONDITIONS

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Cushing Syndrome

Definition

• Excess glucocorticoid levels (endogenous or exogenous)

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Causes

• Exogenous steroid therapy (most common)

• Pituitary adenoma (Cushing disease)

• Adrenal tumor

• Ectopic ACTH production

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Clinical Features

• Moon face

• Buffalo hump

• Truncal obesity

• Purple striae

• Hypertension

• Hyperglycemia

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Addison Disease

Definition

• Primary adrenal insufficiency due to adrenal cortex failure

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Causes

• Autoimmune destruction (most common)

• Tuberculosis

• Adrenal hemorrhage

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Clinical Features

• Weakness

• Weight loss

• Hypotension

• Hyperpigmentation (↑ ACTH)

• Hyponatremia, hyperkalemia

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Steroid-Induced Complications

Metabolic

• Diabetes

• Obesity

Musculoskeletal

• Osteoporosis

• Avascular necrosis

Infections

• Opportunistic infections

• Reactivation of TB

Dermatological

• Skin thinning

• Striae

• Acne

Endocrine

• HPA axis suppression

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Important Clinical Pearls

• Exogenous steroids → most common cause of Cushing syndrome

• Addison disease → life-threatening if untreated

• Long-term steroids → require regular monitoring to prevent complications

 

📊 TABLES (FINAL COMPLETE)

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Glucocorticoids vs Mineralocorticoids

Feature	Glucocorticoids	Mineralocorticoids
Main hormone	Cortisol	Aldosterone
Primary action	Metabolic + anti-inflammatory	Electrolyte balance
Na⁺ retention	Mild	Marked
K⁺ excretion	Mild	Marked
Immune effect	Immunosuppressive	Minimal
Clinical use	Anti-inflammatory, autoimmune	Replacement therapy

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Short vs Intermediate vs Long-Acting Steroids

Duration	Drugs	Biological Half-life
Short	Hydrocortisone	8–12 hr
Intermediate	Prednisolone, Methylprednisolone	12–36 hr
Long	Dexamethasone, Betamethasone	36–72 hr

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Relative Potency Table (VERY HIGH-YIELD)

Drug	Anti-inflammatory	Mineralocorticoid
Hydrocortisone	1	1
Prednisolone	4	0.8
Methylprednisolone	5	0.5
Dexamethasone	25	0
Betamethasone	25	0

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Steroid Equivalence Doses (VERY HIGH-YIELD)

Drug	Equivalent Dose (mg)
Hydrocortisone	20
Prednisolone	5
Methylprednisolone	4
Dexamethasone	0.75
Betamethasone	0.75

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Anti-inflammatory vs Mineralocorticoid Activity

Drug	Anti-inflammatory	Mineralocorticoid
Hydrocortisone	Low	High
Prednisolone	Moderate	Moderate
Dexamethasone	Very high	None
Fludrocortisone	Low	Very high

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Systemic vs Topical Steroids

Feature	Systemic	Topical
Route	Oral/IV	Skin application
Effect	Whole body	Local
Adverse effects	High	Minimal (if used properly)
Uses	Autoimmune, severe disease	Dermatological conditions

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Topical Steroid Potency Classification (VERY IMPORTANT)

Potency	Drugs
Super high	Clobetasol propionate
High	Betamethasone dipropionate
Moderate	Mometasone, Triamcinolone
Low	Hydrocortisone

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Uses (System-wise)

System	Uses
Endocrine	Addison disease, CAH
Respiratory	Asthma, COPD
Rheumatology	RA, SLE
Dermatology	Psoriasis, eczema
CNS	Cerebral edema
Oncology	Leukemia, lymphoma
Renal	Nephrotic syndrome

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Adverse Effects (Organ-wise)

System	Effects
Metabolic	Hyperglycemia, obesity
Musculoskeletal	Osteoporosis, myopathy
GI	Peptic ulcer
CNS	Mood changes, psychosis
Eye	Cataract, glaucoma
Skin	Atrophy, striae
Immune	Infection risk

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Drug Interaction Summary

Drug/Class	Effect
Rifampicin, Phenytoin	↓ steroid levels
Ketoconazole	↑ steroid levels
NSAIDs	↑ ulcer risk
Diuretics	Hypokalemia
Live vaccines	Contraindicated

 

 

🧠 DIAGRAMS / FLOWCHARTS (FINAL CORE)

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HPA Axis Regulation

• Hypothalamus → CRH

• Pituitary → ACTH

• Adrenal cortex → Cortisol

• Cortisol → Negative feedback on hypothalamus & pituitary

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Cortisol Synthesis Pathway

• Cholesterol
  → Pregnenolone
  → Progesterone
  → 17-hydroxyprogesterone
  → 11-deoxycortisol
  → Cortisol

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Mechanism of Action (Genomic + Transrepression)

• Steroid enters cell
  → binds glucocorticoid receptor
  → complex enters nucleus
  → binds GRE

Two pathways:

• Transactivation → ↑ anti-inflammatory proteins (lipocortin)

• Transrepression → ↓ NF-κB, ↓ AP-1 → ↓ cytokines

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Anti-inflammatory Pathway (PLA2 Inhibition)

• Steroid
  → ↑ Lipocortin (Annexin-1)
  → ↓ PLA2
  → ↓ Arachidonic acid
  → ↓ Prostaglandins + Leukotrienes
  → ↓ Inflammation

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RAAS–Aldosterone Pathway

• ↓ BP / ↓ renal perfusion
  → ↑ Renin
  → Angiotensin I
  → (ACE) → Angiotensin II
  → ↑ Aldosterone
  → Na⁺ + water retention
  → ↑ BP

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Stress Response Pathway

• Stress
  → ↑ CRH
  → ↑ ACTH
  → ↑ Cortisol

Effects:

• ↑ Glucose

• Maintains BP

• Anti-inflammatory

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Steroid Tapering Algorithm

• Short-term use (<2 weeks)
  → Stop directly

• Long-term use
  → Gradual dose reduction
  → Monitor symptoms

• If adrenal insufficiency signs
  → Slow taper further

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Cushing Syndrome Pathogenesis

• Excess glucocorticoids
  → ↑ gluconeogenesis → hyperglycemia
  → Protein breakdown → muscle wasting
  → Fat redistribution → truncal obesity
  → ↑ Na⁺ retention → hypertension
  → ↓ immunity → infections

 

🔬 SLIDES (EXAM FAVORITE)

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Adrenal Cortex Histology

• Three zones:

  • Zona glomerulosa → mineralocorticoids

  • Zona fasciculata → glucocorticoids

  • Zona reticularis → androgens

• Fasciculata shows lipid-rich vacuolated cells (spongiocytes)

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Cushingoid Features (Moon Face, Buffalo Hump)

• Moon face → facial fat deposition

• Buffalo hump → dorsocervical fat pad

• Truncal obesity with thin limbs

• Due to fat redistribution by glucocorticoids

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Striae

• Purple (violaceous) wide stretch marks

• Common sites: abdomen, thighs

• Due to collagen breakdown & skin thinning

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Osteoporosis (Vertebral Collapse)

• ↓ osteoblast activity + ↑ bone resorption

• Leads to:

  • Fragility fractures

  • Vertebral compression collapse

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Steroid-Induced Acne

• Monomorphic papules and pustules

• No comedones (unlike acne vulgaris)

• Common on face, chest, back

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Skin Atrophy

• Thinning of skin

• Visible vessels (telangiectasia)

• Easy bruising

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Fungal Infection (Immunosuppression)

• Steroids suppress immunity → opportunistic infections

• Example: tinea incognito (atypical fungal infection)

• Lesions become less inflammatory but more widespread

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