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Flashcards

L14 - Treating Hypertension

Jack Rowe CPP Year 1 English 56 cards

Cards in this deck (56)

  1. 1give the primary central causes of hypertensionthere are no identifiable single cause, can be combinations of the following
    - combination of genetics and environmental factors
    - diabetes/ obesity
    -stress
  2. 2what is secondary hypertensionelevation of blood pressure due to a specific underlying cause
  3. 3give some example of secondary causes of hypertension- renal disease
    - hormonal imbalance (e.g in steroidogenisis pathway)
  4. 4what % of hypertension is primary and what % is secondary90-95% primary
    5-10% secondary
  5. 5what MAP values would suggest hypertension140/90 mmHg and above
  6. 6give the equation for ABPCO x TPR
  7. 7how can the MAP equation be altered by the body to cause hypertension?- CO can be increased by HR and SV
    - TPR can be increased by sym activity at the arterioles
  8. 8give some pathological changes which can increase the TPR- Atherosclerosis
    - vascular smooth muscle contraction
    - vascular smooth muscle remodelling
  9. 9how can ventricular hypertrophy alter ABP- initially causes increased CO which will increase ABP
    - later when heart becomes baggy itll decrease the CO
  10. 10how can diabetes the risk of Hypertensioincreased osmolality of the blood increases water movement into the blood vessles from the tissue
  11. 11how can obesity lead to hypertensionincreased plasma lipid conc increases viscosity and can cause Atherosclerosis which increases TPR
  12. 12what can diabetes do to production of NO and howreduced amount of NO produced due to oxidative stress
  13. 13what does reduced NO mean for hypertension and whydecreases vasodilative effects so greater constriction leading to higher TPR
  14. 14how can renal failure cause hypertension (HINT: think salt and hormones)- kidney dysfunction can increase sodium and therefore water retention leading to hypervolumiea
    - increased angiotensin 2 production will have a greater vasoconstrictive effect
  15. 15how can altered steroidogenisis cause hypertensionincreased production of aldosterone causes increased salt and water retention leading to hypertension
  16. 16give some different potential drug targets in Hypertension treatmentvascular smooth muscle
    SAN
    RAAS
    kidney
  17. 17what is the first option to reduce hypertension just after diagnosisgive patient chance to make lifestyle choices to reduce their BP without drugs
  18. 18what are the NICE guidlines used for in hypertension treatmentsuggests which treatment options should be used for different people with different causes
  19. 19what is the first anti-hypertensive often used?drugs which target the RAAS system such as through ACE inhibitors
  20. 20what is the preferred treatment method used for people over 55 or from African American descentchannel blockers or diuretics
    (options which target the kidneys )
  21. 21what are ARB's in terms of anti-hypertensive treatmentsangiotensin receptor blockers
  22. 22can you use anti-hypertensive drugs in combination with one and otheryes most can be
  23. 23which type of anti-hypertenstive drugs shouldnt be used in pregnant womenACE inhibitors
  24. 24how do ACE inhibitors aid in hypertension treatmentprevents conversion of ANG1 to ANG2 which decreases the vasoconstrictive effects to decrease the TPR
  25. 25other than decreasing vasoconstriction how do ACE inhibitors target hypertensionthey decrease production of Aldosterone to decrease water reabsorption in the kidney
  26. 26what is the common side effect of ACE and whya dry cough caused by increased production of bradykinin
  27. 27why can ACE cause oedemadecreased metabolism of and therefore increased levels of bradykinin causes oedema
  28. 28why could ANG2 blockers be a better treatment than ACE inhibitors?they cause the same vasodilation without effecting bradykinin so dont cause dry cough
  29. 29what side effects ARE associated with aNG2 blockersheadache and fatigue
  30. 30what type of receptor do ARBs bind toAT1 receptors on blood vessel's preventing ANG2 binding
  31. 31why can ARBs cause headachebecause they work on receptors in the brain too which can cause vasodilation there
  32. 32what channels are blocked by Ca++ channel blockersL - Type Ca++ channels
  33. 33what is the state of the vascular smooth muscle channels at restinactive and close
  34. 34explain the initial Calcium dependant calcium release when smooth muscle cells are stimulated- stimulation of alpha 1 adreno receptors causes influx of Ca++ through L type channels
    - calcium influx causes CDCR which causes release of Ca++ from the SR through the activation of IP3
  35. 35how does increased Ca++ in SMC cause constrictionCa++ binds to myosin filaments causing constriction
  36. 36how do Ca++ reduce vasoconstrictiondecreases Ca++ through L type channels so decreases Ca++ release from the SR leading to dilation
  37. 37give some side effects of Ca++ channel blockersheadaches, ankle oedema, hot flushes
  38. 38genrally how do diuretics treat hypertensionreduce circulating blood volume to decrease BP
  39. 39specifically how does a decreased circulating volume reduce BPdecreases venous return and therefore CO leading to lower ABP
  40. 40in what 2 ways do diuretics which target sodium decrease blood pressure- decreases circulating volume
    - decreases sodium retention and therefore decreased activation of L type channels to cause decreased Ca++
  41. 41give some side effects of thiazideshyperkalemia, diabetes, goute and impotence
  42. 42how do beta blockers address hypertensio- prevent binding of NAD and adrenaline to decrease contractility, HR and conduction velocity
    - decreases CO to decrease the ABP
  43. 43what beta receptors are found on blood vessel's and what innervates them to cause hypertension- B2 receptors innervated by circulating adrenaline
  44. 44what beta receptors are found on the heartbeta 1 and 2 receptors
  45. 45how do beta receptors act on the kidneythey reduce renin release which reduces BP by decreasing ANG2 and aldosterone
  46. 46in what 2 ways do alpha adrenoreceptor antagonists work?- block NAD binding to alpha receptors on smooth muscle cells
    - inhibit A2 receptors on nerve terminal which inhibits NAD release
  47. 47which blood vessles are targeted by alpha blockersboth arteries and veins bc both have Sym innervation
  48. 48what do Alpha blockers do to veinsalso decrease venous constriction
  49. 49give the side effects of alpha blockerslethargy, headache, dizziness, postural hypotension
  50. 50what is postural hypotensionhypotension when in specific positions e.g stood up
  51. 51how do centrally acting anti-pypertensive therapies work?prevents central ANS control
  52. 52how do centrally acting A2 receptro agonists treat hypertensionA2 receptor agonists decrease SYM outflow to periphery to reduce TPR
  53. 53where specifically do centrally acting drugs work?the NTS of the brain
    (the vasomotor centre)
  54. 54what other anti-hypertensive medication is often used with centrally acting A2 agonosistdiuretics
  55. 55what types of drugs are used in acute hypertensive crisisIV infused vasodilators such as NO modulators
  56. 56—

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Year 1 CPP Flashcards on L14 - Treating Hypertension, created by Jack Rowe on 25/12/2022.
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