pharm final 1

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kbryant86
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252034
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pharm final 1
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2013-12-09 13:56:40
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pharm
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  1. local anasthetics - mechanism of action

    local administration
    • mech= suppress pain by blocking inpulse (Na+ Channels)
    • -Esters= (novacain) metab in bld
    • -Amides- (lidocaine) metab in liver

    • Locally admin= block small unmyelinated neurons BFORE larger myelinated
    • =pain lost first, then temp, tounch, deep pressure
    • = blocks both sensory and motor neurons

    • If used centrally, excites then depresses the CNS and cardiac function
    • **EPI is used to becuase of local vasoconstriction properties and to prolong anes. effects
  2. Epidural
    • Spinal/subarachnoid(CSF circulation)
    • Lumbar region

    • SE= HypoTN-most sig. effect
    • = fecal/urine incontinance or retention
    • = Spinal headache
    •   => Place in supine position and apply a Blood Patch b/c CSF is leaking
  3. Cocaine
    blocks NE reuptake, flooding the body with NE
  4. 4 general anesthesia types
    • balanced
    • gas
    • volatile liquids
    • IV-sedation
  5. Pre-anesthesia- pain, anxiety, amnesia
    Benzodiazapine-midozalam / Versed is DOC plus Opioids & NO2 for pain
  6. Minimal Alveolar COncentration

    Nitrous Oxide
    • MAC
    • [ ] that prodices immobility in 50% exposed to painful stimuilation
    • **LOW MAC indicated HIGH potency (use less)

    NO2= inhalation gas - not good to sedate, but is good for pain
  7. Sublimaze
    Synthetic Morphine

    100X potent
  8. Isoflurane / Forane
    • 2nd generation
    • ***DOC for volatile lquids
    • eliminated in exberation
    • No SE

    When mixed with Succs= Malignant Hyperthermia
  9. Pentobarb, Midazolam / Versed
    • Barbiturates, Benzodiazapines
    • IV general anesth. for sedation
  10. Propofol / Diprivan
    • IV general anesth. for sedation
    • conscious sedation
    • change tubing q12 and glass bottle

    ***HypoTN and high risk for infection b/ of high lipid medium of drug
  11. Opioid analgesics
    • Narcotics
    • Activate Mu Receptors
    • Morphine and synthetic drugs
    • produce euphoria, constipation, urine retention, vasodlation, resp depresion
    • increase intracranial pressure
    • Physical dependence = not seem often w/ therapeutic clinical use
    • = pt will have w/d if abruptly stopped
  12. 3 things that determine cardiac output
    • preload
    • afterload
    • contractility
  13. preload
    • 'the pool'
    • amount of stretch created by the volume
  14. afterload
    • 'the pipes'
    • resistance to outflow
    • blood pressure
  15. contractility
    • 'the pump'
    • HR and rhythm
  16. aldosterone saves h2o and Na+

    but kicks out K+
    aldosterone saves h2o and Na+

    but kicks out K+
  17. Angiotensin II is a strong vasoconstrictor and signals release of Aldosterone
    Angiotensin II is a strong vasoconstrictor and signals release of Aldosterone
  18. 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
  19. 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
  20. 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
  21. 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
  22. Renal Artery Stenosis
    #1 problem w/ ACE Inhibitors

    constricts vessels, causing crappy blood flow
  23. If we inhibit ACE/Kinase II...
    promote the metabolic effects of Bradykinin (vasodilation and inc. permeability):

    • angiodema
    • constant cough
  24. adverse effects of ACE inhibs
    • 1st dose HypoTN
    • angiodema
    • cough
    • hyperkalemia
    • renal failure
    • fetal injury
  25. ACE preload and afterload
    vasodilation witll cause both decrease
  26. Ca channel blockers

    Therapeutic doses affect:
    prevent contraction of smooth muscles

    • T affect:
    • peripheral arterioles and arteries
    • cardiac muscle - decrease force of contract.
    • SA & AV node - dec. impulse speed/conduction
    • Coupling of cardiac Ca channels to Beta 1 receptors - Decrease force, rate, and conduction
  27. activating B1 receptors will cause a 2nd messenger to open Ca++ channels
    activating B1 receptors will cause a 2nd messenger to open Ca++ channels
  28. the "-pines" drugs

    vs

    other blockers
    • Ca++ blockers
    • affects only the arterioles and NOT the HR


    others= affect HR and atrerioles
  29. Ca blocker that do not affect HR have a SE of Reflex Tachycaria
     - can take Beta blocker to compete tachycard

    Ca blocker that affects both HR and arterioles DOES NOT cause Reflex Tachycardia
    • Ca blocker that do not affect HR have a SE of Reflex Tachycaria
    •  - can take beta blocker

    Ca blocker that affects both HR and arterioles DOES NOT cause Reflex Tachycardia
  30. Diltiazem / Cardizem

    uses

    SE
    • Ca++ blocker
    • affects arterioles AND HR

    DOC for A-Fib and SVT to slpw HR enough for the heart to convert to nl rhythm

    • -Peripheral arterioles= vasodilation
    • -Cardiac arteries and arterioles= INc coronary bld flow
    • -SA node= Dec. HR
    • -AV node= slow myocardial conduction
    • -Myocardium= Dec. force of contraction

    • prevent angina
    • HTN
    • Dysrhyth

    Se= same as previous Ca++ blocker
  31. Nimodopine / Nimotop*
    Special Ca++ blocker

    Provides selective blocking of Cerebral blood vessels ONLY

    Only used for rupture of Intracranial Aneurysm and used to prevent future vasospasm and re-bleed
  32. Ca blocker and pre/afterload/force of contraction
    • will decrease force of contraction
    • will dec afterload

    NO significant affect on preload
  33. list of Vasodilators
    1-4
    • ACE inhibitors (prils)
    • Angio II receptor blockers (sartens)
    • Ca+ blockers (pines)
    • Sympatholytics (alpha blockers)
    •   - prevent sympathetic vasocontriction
  34. What vasodilators do...
    • decrease the work load of the heart
    • work on resistance vessels (arterioles)
    • -reduce resistance to LV pumping
    • -decrease afterload
    • work on Capacitance vessels (veins)
    • -reduce amount of blood return to the heart
    • -decrease preload (and therefore BP)
  35. SE of vasodilators
    • Postural hypoTN
    • -venous relaxation
    • -blood pools in venous side

    • Reflex Tachycarida
    • -Central-sympathetic stimulation
    • -Peripheral- baroreceptors

    • Increase blood volume (over time)
    • -decrease renal blood flow (RAA)
    • -Na+ and h2o are reabsorbed
  36. Sodium Nitroprusside / Nipride



    Cyanide/Thiocyanide
    • DOC for HTN Emegencies
    • Arteriole and venous dilation
    • Immediate effects and short 1/2 life
    • Given very slowly IV push
    • Need to protect from light

    • thiocyanide is a metabolic by-product of use and can poison pt.
    • Need to check levels is Nipride in use for >3 days
  37. Beta blockers therp effects
    • dec HR
    • dec force of contraction
    • dec velocity of impulse conduction
    • dec BP but can also affect respers

    uses: HTN, chest pain, HF, MI
  38. 2 types of beta blockers

    after/preload
    selective and non

    • slightly reduce pre/afterload
    • Reduce cardiac output

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