Learning MRCS A - physiology /medicine

  1. Cushing reflex- when - what- indicates
    - When ICP > arterial pressure ⇾ compression of cerebral arterioles ⇾ cerebral ischaemia. 

    • - What:
    •    + initially: ↑ ICP ⇾ stepwise activation of sympathetic NS     
    •          ⇾ peripheral vascular resistance ⇾ HTN, CO↑           
    •                ⇾ detected by aortic arch baroreceptors 
    •    + 2nd stage: ⇾ activation of parasympathetic NS

    - a serious development, indicates imminent coning or other terminal events if not resolved quickly.

    (NS nervous system)
  2. Cushing reflex (another , triad)
    - physiological nervous system response to acute elevations of intracranial pressure (ICP) 

    • - results in Cushing triad
    •    + widened pulse pressure (increasing systolic, decreasing diastolic)
    •    + bradycardia
    •    + irregular respirations.
  3. Renin-angiotensin-aldosterone system
    1. Adrenal cortex (mnemonic)
    (mnemonic GFR - ACD)

    • - Zona glomerulosa (on outside): mineralocorticoids, mainly aldosterone
    • - Zona fasciculata (middle): glucocorticoids, mainly cortisol
    • - Zona reticularis (on inside): androgens, mainly dehydroepiandrosterone (DHEA)
  4. Nephron structure
    Image Upload 1
  5. Renin-angiotensin-aldosterone system - total review
    Image Upload 2
  6. Renin-angiotensin-aldosterone system - total review
    a) renin: release from where, does what, what stimulates release
    • a)Renin
    • - Released by JGA cells in kidney 
    • - Hydrolyses angiotensinogen -> angiotensin I
    • - Factors stimulating renin secretion
    •     + * Low BP
    •     + * Hyponatraemia
    •     + Sympathetic nerve stimulation
    •     + Catecholamines
    •     + Erect posture
    •     + Angiotensin
  7. Renin-angiotensin-aldosterone system - total review
    b) angiotensin: what forms, does what
    • b) ACE 
    • - in lung converts angiotensin I → angiotensin II
    • - effects: main 2: 
    •    * increase BP 
    •       + increase sympathetic activity
    •       + arteriolar vasoconstriction 
    •    * increase circulation volume from water and salt retention
    •       + stimulates aldosterone 
    •       + stimulates ADH release
    •       + stimulates thirst
  8. Renin-angiotensin-aldosterone system - total review
    c) aldosterone: release from where, does what, what stimulates release
    • c) Aldosterone
    • - Released by the zona glomerulosa
    • - in response to raised angiotensin II, potassium, and ACTH levels 

    - Causes retention of Na+ in exchange for K+/H+ in distal tubule
  9. Renin-angiotensin-aldosterone system - total review
    d) (ADH)
    (e) ACTH
    • d) ADH
    • - pituitary gland, posterior lobe - ADH secretion 
    • - acts on collecting duct - water absorption 

    e) ((ACTH regulates cortisol))
  10. Effects of receptor binding - overview
    • - α-1, α-2: vasoconstriction
    • - β-1: increased cardiac contractility and HR
    • - β-2: vasodilatation
    • - D-1: renal and spleen vasodilatation
    • - D-2: inhibits release of noradrenaline 

    (dopamine)
  11. Inotropes and cardiovascular receptors
    • Inotrope & Cardiovascular receptor action
    • - Adrenaline: α-1, α-2, β-1, β-2 (β agonist at lower dose, α at higher dose)
    • - Noradrenaline: α-1,( α-2), (β-1), (β-2)
    • - Dobutamine: β-1, (β 2)
    • - Dopamine: (α-1), (α-2), (β-1), D-1,D-2

    (Minor receptor effects in brackets)
  12. Inotropes - common types
    • - catecholamine type agents: adrenaline, norad, dopamine   
    •    + dobutamine: synthetic cathecholamine
    • - phosphodiesterase inhibitors: milrinone
  13. Inotropes - what, different from
    • - work primarily by increasing cardiac output
    • - distinguised from vasoconstrictor when problem is vasodilatation
  14. Inotropes - catecholamine type agents - general principles, special of dopamine
    • - works by increasing cAMP levels
    •     + by adenylate cyclase stimulation 
    • - then: intra-cellular calcium ion mobilisation 
    •     -> increase force of contraction 

    - dopamine: both HR + BP raised -> less overall myocardial ischaemia
  15. Inotropes - adrenaline
    • beta adrenergic receptor agonist at lower doses
    • an alpha receptor agonist at higher doses

    (lower, bắt đầu là beta, mạnh hơn thành alpha)
  16. Inotropes - dopamine
    • - causes dopamine-receptor mediated renal and mesenteric vascular dilatation and beta 1 receptor agonism at higher doses
    • - both HR + BP raised -> less overall myocardial ischaemia
  17. Inotropes - dobutamine
    • a predominantly beta 1 receptor agonist
    • weak beta 2 and alpha receptor agonist properties
  18. Inotropes - norad
    • an alpha receptor agonist
    • & as a peripheral vasoconstrictor
  19. Inotropes - Phosphodiesterase inhibitors
    • e.g. milrinone 
    • specifically on the cardiac phosphodiesterase
    • -> increase cardiac output.
Author
trincam2008
ID
354153
Card Set
Learning MRCS A - physiology /medicine
Description
Learning MRCS A - physiology /medicine
Updated