ADRENCORTICAL

HORMONES
Dr Nida Sohail

Aldosterone
Reabsorbing sodium (Na+) ions and water into the blood
Secreting potassium (K+) ions into the urine.
H+ secretion by intercalated cells in the collecting duct
Regulating plasma HCO3

levels and its acid/base

balance.
Increases ECF volume
Increases Blood pressure
Small affect on plasma Na
Affects Na and K transport in sweat, salivary and
intestinal epithelial cells
Adrenal Cortex: Zona Glomerulosa
Plasma protein-
bound cortisol

Adrenals
Free cortisol
in plasma
Tissue
cortisol
Anterior
pituitary
Interrelationships Between Free &
Bound Cortisol

Biological
effects
ACTH
Metabolic Effects of Cortisol
Glycogen

Glucose-P

Glucose
precursors
Glucose
Amino
acids
Protein
+
Free fatty
acids
Glycerol
Stimulate
Inhibit
Muscle
Liver
Adipose
tissue
Glucose
Free fatty acids
Amino acids



Glucose
Plasma
Provision of Energy by Glucocorticoid
Release
EFFECTS OF CORTISOL
Carbohydrates
Stimulate gluconeogenesis ( enzymes, mobilize a.a.)
Decrease glucose utilization ( rate by decreasing NADPH
oxidation) by cells
Adrenal Diabetes (elevates plasma glucose) (impairs insulin
action by fatty acids )
Proteins
Reduction in cellular protein (aa transport, RNA formation)
Increased proteins in liver and plasma
Increased blood amino acids (more to liver less to other tissues)
EFFECTS OF CORTISOL
Fats
Mobilization of Fatty Acids
Obesity caused by cortisol
STRESS
Trauma, infection, extreme temperature, surgery etc.
Allergy
Blocks inflammation in allergy
Infections
Decreases eosinophils and lymphocytes
Atrophy of lymphoid tissue
EFFECTS OF CORTISOL
Inflammation
Stages: chemical release erythema edema
local leucocytosis fibrous tissue growth
CORTISOL blocks start of or stops inflammation
Lysozyme stabilization
Decreases capillary permeability
Decreases WBC migration
Suppresses immunity (lymphocytes)
Decreases IL-1
Resolution of inflammation
ACTIONS OF CORTISOL
Increase lipolysis
Increase glyconeogenesis
Decrease peripheral glucose utilization
Protein catabolic hormone
Modulate fibroblast proliferation and function - mostly inhibition
Inhibit extracellular matrix synthesis - collagen
Decrease osteoblastic function
Aid in maintenance of blood pressure - increase vascular
sensitivity to catacholamines
Inhibition of ADH secretion, or action upon renal tubular cells
Increase GFR
Anti-inflammatory - inhibit synthesis of prostaglandins,
leukotrienes, stablize lysozymes
Suppress lymphocyte proliferation, actions of cytokines
Stablization of microvascular integrity
Hypothalamohypophyseal-
Adrenal Axis
Hypothalamus
Corticotrope
Adrenal Cortex
Glucocorticoids
CRH
ACTH
+
+
_
_
CORTISOL
AXIS
ABNORMALITIES
ALDOSTERONE
CORTISOL
ANDROGENS
Pathophysiology of the
Adrenal Cortex
Cushings syndrome
Cushings disease
Addisons disease
Conns syndrome
Apparent mineralocorticoid excess
Congenital adrenal hyperplasia
21 - Hydroxylase deficiency
11 - Hydroxylase deficiency
Causes of Cushings Syndrome
Adrenal hyperplasia
Adrenal neoplasia
Iatrogenic
Pituitary ACTH
Nonpituitary tumors (ectopic)
Adenoma
Carcinoma
hypothalamic dysfunction
pituitary tumors (Cushings disease)
ACTH
CRH
CORTISOL
AXIS
Thank you
AllahumMa inni lima anzalta
ilayya min khairin faqir