• Metabolic; increased protein catabolism, increased hepatic glycogenesis and gluconeogenesis (raised plasma glucose). Raise peripheral tissue insulin resistance
• Permissive effects on other reactions
• Are required for catecholamines to produce calorigenic and lipolytic effects,pressor responses (vascular reactivity) and vasodilatation
• Inhibit ACTH secretion (feedback)
• Impair water excretion (mechanism unclear)
• Reduce circulating basophils and eosinophils and increase other elements
• Required for stress response
• Affect EEG waveforms (mild personality changes in insufficiency)

• Basal secretion and stress response both dependent on ACTH
• (Other substances may stimulate adrenal directly but no evidence of role in physiologic regulation)
• Free glucocorticoids produce negative feedback on ACTH secretion at both hypothalamic and pituitary levels. Effect mediated by action on DNA
• Stress response ACTH secretion mediated almost exclusively via hypothalamic release of  corticotrophin releasing hormone
• Circadian rhythm. ACTH released in irregular bursts throughout day but much more common in early morning. 75% of cortisol secreted at this time

• Adipose: glucose in, fatty acid + glycerol synthesis, TG deposition, K in
• Muscle: glucose in, glycogen synthesis, Aas in, protein synthesis, ketones in, K in
• Liver: glycogen, protein + lipid synthesis,
• General: cell growth

• Rapid: glucose, AAs, K into sensitive cells
• Intermediate: protein synthesis, glycolysis and synthesis, inhibition gluconeogenesis
• Delayed: lipogenesis

• Heart: chronotropic, inotropic (increased beta receptors, enhanced response to catecholamines)
• Adipose tissue: catabolic (lipolysis)
• Musculoskeletal: catabolic (increased protein breakdown), developmental (promote growth and development)
• Most (except adult brain, uterus, testes, spleen): calorigenic (increased O2 consumption of metabolically active tissues)
• CNS: developmental (promotes brain development)
• GIT: metabolic (increased carbohydrate absorption)
• Lipoprotein: metabolic (increased LDL receptors)

Pass criteria:

• Need 2 of first 4 to pass PLUS 2 others

• BP: norad; ad
• HR: norad; ad
• CO: norad; ad
• TPR: norad; ad

• Low concentrations – some beta effects, high concentrations alpha predominates

• Na/ Cl mild increased, fluid retention (follows Na),
• decreased K, alkalosis (alkalaemia only if K+ depletes)
• Urine K+/ H increased

• Mineralocorticoid- Via Principal cells- collecting ducts

2 effects:

• Genomic- Intracellular to nuc signalling > mRNA
  • a) Inc ENAC insertion/ activity (quick)
  • b) > production (slow)
• Membrane bind IP3 mediated Na/K exchange >

All = > Na reabsorb K/H loss to urine

• PTH increased plasma Ca⁺⁺ by:
  • increased Ca⁺⁺ mobilization increased bone reabsorption,
  • increased Ca⁺⁺ reabsorption in distal tubule and (3) Ca reabsorption

Pass Criteria:

• Ca ++ increased  PO4 decreased + some idea of how these achieved OR additional other mechs

1. decreased plasma phosphate: decreased PO₄ reabsorption in proximal tubules
2. increased 1,25 dihydrocholecalciferol: renal  ( > Ca absorption)
3. Over a longer time: increased osteoblastic and osteoclastic stimulation- prob anabolic

Pass Criteria:

• Parathyroid related hormone- (prob fetal/ cartilage growth + teeth/ breast- skin) ?
• PO4 < +1 other in either section

• CNS
  • Development CNS -cerebral cortex, basal ganglia cochlea
  • increased activity, mentation speed/ agitation (catechol / dop+ direct brain effects)
  • increased refexes
• CVS
  • 1)vasodil (2ary heat)
  • > circ vol/ HR/ CO
  • Ht- > myosin heavy chain (+ isoforms)/ faster twitch genes (+ Ca ++, Na K ATPase etc?) + down reg others, > contraction/ HR/ speed of contraction
  • > sens to Catechols (synergistic effects + up regulated ß receptors and effector systems) HR, contract more

Pass Criteria:

• 3-4 overall at least 1 in each

• Lipolysis – adipose tissue
• Formation of LDL receptors on lipoprotein
• Protein breakdown in muscle
• Skeletal development promoted
• Increased carbohydrate absorption from the gut
• Stimulates O₂ consumption by metabolically active tissues
• Increased BSL/ insulin resistance

Pass Criteria:

• At least 2

• Retention of water (antidiuretic hormone) (V2 receptors)
• Vasoconstrictor effect (V1A receptors)
• Central effect brain (area postrema) to decrease CO
• Glycogenolysis in liver (V1A receptors)
• Mediate increased ACTH secretion (V1B receptors)
• Neurotransmitter in brain and spinal cord

• Increases permeability of CD, acting on V2 receptors
• Insertion of protein water channels (aquaporin 2) in uminal membranes.
• Water enters hypertonic interstitium
• Urine becomes concentrated and volume decreases
• Retention of water in excess of solute

• Factors increasing vasopressin secretion
  • increased effective osmotic pressure of plasma
  • decreased ECF volume
  • Pain, emotion, “stress”, exercise, standing
  • Nausea and vomiting
  • Clofibrate, carbamezepine, angiotensin 2
• Factors decreasing vasopressin secretion
  • decreased effective osmotic pressure of plasma
  • increased ECF volume

• Insulin receptor: tetramer – 2 alpha and 2 beta glycosolated subunits
  alpha subunits extracellular + bind insulin; beta subunits span membrane, intracellular parts have tyrosine kinase activity
• Insulin binding triggers tyrosine kinase activity of beta subunits -> autophosphorylation of  beta subunits on tyrosine residues
• -> phosphorylation and  de-phosphorylation of  proteins
• -> Effectors and secondary mediators – Insulin receptor substrate (IRS-1);phosphoinositol 3-kinase (PI3K)
• Once bound, insulin receptors aggregate in patches and are  endocytosed -> enter lysosomes -> broken down or recycled
• Peak effect 30 minutes IV / 1 hour oral

• Net effect: storage of CHO, protein and fat
  • Rapid (seconds): ­ increased transport of glucose, amino acids and K into insulin-sensitive cells
  • Intermediate (minutes): stimulation of protein synthesis and inhibition of protein degradation; activation of glycolytic enzymes and glycogen synthase;inhibition of phosphorylase and gluconeogenic enzymes
  • Delayed (hours): ­ mRNAs for lipogenic\other enzymes

• Increase reabsorption of Na⁺ from urine
  • Acts on principal cells (P cells) of collecting ducts, leading to increased amounts of Na⁺ exchanged for K⁺ and H⁺ in renal tubules, producing a K⁺diuresis and fall in urine pH
• Increase reabsorption of Na⁺ from sweat, saliva and colon

Pass Criteria:

• Aldosterone cause retention of Na⁺ in ECF leading to ECF volume expansion

• ACTH from pituitary
• Renin from kidney via angiotensin II
• Direct stimulatory effect of rise in plasma K⁺ concentration on adrenal cortex
• Clinical causes:
  • Surgery
  • Anxiety
  • Physical trauma
  • Haemorrhage
  • High K intake and Low Na intake
  • Standing
  • Constriction of IVC in thorax
  • 2⁰ hyperaldosteronism  (eg CCF, cirrhosis, nephrosis)

Pass Criteria:

• Bolded PLUS 2 others

• Fall in ECF / blood volume -> reflex increase in renal nerve discharge &decrease in renal artery pressure
• -> increase in renin secretion -> increase in angiotensin II -> increase in aldosterone secretion
•  -> Na⁺ & water retention  -> expanded ECF volume  -> decrease in stimulus that initiated renin secretion

Pass Criteria:

• Bolded