pharm 3 set 1

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Author:
kbryant86
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239212
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pharm 3 set 1
Updated:
2013-10-14 14:41:15
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pharm
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pharm 3
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  1. Where is the majority of blood during circulation?
    in the venous side
  2. 3 things that determine cardiac output
    • preload
    • afterload
    • contractility
  3. preload
    • 'the pool'
    • amount of stretch created by the volume
  4. afterload
    • 'the pipes'
    • resistance to outflow
    • blood pressure
  5. contractility
    • 'the pump'
    • HR and rhythm
  6. starlings law
    force of contraction is determined by stretch
  7. Autonomic Control:
    Reflex activation of __________
    Vasomotor Center
    Baroreceptors
    • reflex= SNS and PNS
    • V.C= Medulla Oblongata => heart rate; last resort attempt to sustain life
    • B= Aortic Arch
    •  = Carotid Artieries
    •  = Vena Cava
    •    => these 3 use vessel size to control BP
  8. humoral control list
    1-4
    • Catecholamines:
    • -NE
    • -Epi
    • Aldosterone
    • Renin-Angiotensin-Aldosterone
  9. aldosterone saves h2o and Na+

    but kicks out K+
    aldosterone saves h2o and Na+

    but kicks out K+
  10. Angiotensin II is a strong vasoconstrictor and signals release of Aldosterone
    Angiotensin II is a strong vasoconstrictor and signals release of Aldosterone
  11. Problems with the pump:

    valve problems
    wall problems
    V= stenotic or regurgitant

    • W= structural (congenital or acquired)
    •  = Post MI (akinetic)
  12. dysrhythmias
    • Bad electricity
    • Bad pumping
    • Bad perfusion
  13. acute coronary syndrome
    • chest pain - 1st from blockage
    • SOB
    • Diaphoresis
    • N/V
    • ECG- Elevated ST segment is classic sign of ischemia
  14. blood pressure regulation
    • baroreceptors
    • RAAS
    • Renal regulation
    • Natriuretic peptides
  15. Natriutretic peptides
    • A-atrial
    • B-brain
    •  =Both reduce blood volume, decreasing preload
    •  =Vasodilate
    • C-vascular endothelium
    •  =vasodilation
  16. BP:
    normal
    pre-HTN
    HTN stage 1
    HTN stage 2
    • nl= 120/80
    • pre= 120-139 or 80-89
    • HTN 1= 140-159 or 90-99
    • HTN 2= >160 or >100
  17. Renin-Angiotensin-Aldosterone

    Renin produced by_________in response to_____&______
    Renin coverts Angiotensinogen to ________
    A1 + ACE =A2
    A2 causes______ and releases____
    • Renin produced by Kidneys in response to decreased BPflow
    • Renin coverts Angiotensinogen to Angiotensin I
    • A1 + ACE =A2
    • A2 causes vasoconstriction and releases aldosterone
  18. ACE Inhibitors
    • -PRILS
    • given orally (except Vasotec IV)
    • can be given with food (except Captopril)
    • Pro-drugs= not activated until metab in Liver (except Lisinopril)
    • Excreted by the Kidney
  19. Captopril / Capoten
    • 1st ever ACE inhibitor
    • MANY Problems
    • given orally, BUT not with food
  20. Lisinopril / Prinivil
    • 2nd generation ACE Inhibitor
    • given orally with food
    • NOT A Pro-Drug
  21. actions of ACE inhibitor
    • Prevent Angiotensin II
    • Vasodilation= Dec. BP
    • Loss of Na+ and h2o and INCREASE K+= dec. bld volume
    • Prevent and reverse cardiac remodeling
    • A2 and Aldosterone
  22. 4 therapeutic uses of ACE Inhibitors
    • HTN
    • HF- from acute MI and Left Vent. dysfunction
    • Diabetic and non-D nephropathy= Delay onset / slow progression of renal failure b/c of decrease in Kidney remodeling
    • Prevent MI, stroke, death in pt's at high risk for CV events
  23. Renal Artery Stenosis
    • #1 problem w/ ACE Inhibitors
    • low bld flow in kidney
    • high production of Agio II
    •  - support renal blood flow by:
    •   = elevated renal pressures
    •   = constriction of Efferent (out) arterioles
    • ACE Inhibitor dilates efferent arteriole:
    •   = Angio II mechanisms to overcome the stenotic process fails

    Severe renal failure occurs
  24. Bradykinin causes...
    • arteriolar vasodilation (pulmonary)
    • capillary permeability
  25. ACE / Kinase II
    Kinase is ACE II when it interacts with bradykinin

    Quickly breaks down Bradykinin
  26. If we inhibit ACE/Kinase II...
    promote the metabolic effects of Bradykinin (vasodilation and inc. permeability):

    • angiodema
    • constant cough
  27. adverse effects of ACE inhibs
    • 1st dose HypoTN
    • angiodema
    • cough
    • hyperkalemia
    • renal failure
    • fetal injury
  28. "-sartan"s
    • Angio II Receptor blockers (ARB's)
    • improvement on ACE inhibs
  29. ARB's

    uses:
    • block receptors for Angio II
    • Action blocks all angio II
    •  - ACE/Kinase II not involved
    •  - cough not a problem
    •  - Angiodema still there 

    Uses: MI, HF, HTN, DM nephropathy
  30. adverse effects of ARB's
    • angiodema
    • renal failure (stenosis), Fetal harm
  31. Losartan / Cozaarr
    Angio II Receptor Blocker
  32. Vaksartan / Diovan
    Angio II Receptor Blocker
  33. Direct Renin Inhibitor
    • Aliskiren / Tektura
    • Binds w/ renin and stops creation of Angio I from Angiotensinogen --> no Angio II or Aldosterone
    • ONLY for HTN
    • rare SE's
  34. Aldosterone Antagonists:

    Aldosterone ______
    • Aldosterone - save Na+, decrease K+
    •  - very effective in lowering BP
    •  - Hyperkalemia ONLY adverse effect
    •  - steroid (sex hormones) suppressed
  35. Spironolactone / Aldactone
    • Aldosterone Antagonist
    • NON-SELECTIVE
  36. Eplarenone / Inspra
    • Aldosterone Antagonist
    • SELECTIVE aldosterone receptor blocker
    • - getting rid of fluid w/o SE and w/o hormone problems

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