Drugs of CVS Flashcards

1
Q

ace inhibitors

A
  • perindopril
  • inhibits action of angiotensin converting enzyme ACE so cant make get affects of A2 so no vasoconstriction/reabsorption from the kidney -side effect; dry cough b of bradykinin builds dup
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2
Q

what is ACE used for

A
  • heart failure ( CO cant match the body’s requirement) because they decrease water absorption so deal with the peripheral oedema of Rsided heart failure, by doing that (v the VR to the heart, the heart doesnt need to contract as hard due toStarlings law, so you decrease CO= v after-load), also because you v blood pressure you decrease preload of the heart
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3
Q

ARBc ? who is used on ? and mechanism of action?

A

angiotensin 2 receptor blocks

  • used for patients who cant tolerate ACE d the bradykinin build up, examples LOSARTAN
  • used in treatment of heart failure and hypertension
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4
Q

diuretics

A
  • used in heart failure and hypertension
  • espceaily in cases of pulomonary and peripheral oedema

–act on kidneys and increase loss of sodium and water through the kidney

  • breathless d oedema
  • furosemide works on loop of Henley and works to decrease peripheral oedema
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5
Q

calcium channel blockers types?

examples?

mechanism

A

-THERE ARE 2 TYPES; some act on heart , some act on smooth muscle ;

if they act on smooth muscle they are ; DIHYDROPYRIDINE Ca2+ channel blockers

  • examples are Amolpidine , Nicardipine
  • act in vascular smooth muscle to decrease force of contraction and how much contraction occurs since ca2+ is needed for the troponin fibres, however they aren’t effective with arrythmias
  • L type channel blocker
  • reduce contraption and v peripheral resistance so v bp,,useful for angina, coronary artery spasm and hypertension

the other heart type are NON-DIHYROPYRIDINE ca2+ blockers , reduce workload of heart by reducing the contraction, examples include verapamil, and diltiazem

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6
Q

positive inotropes

A
  • increase heart work load
  • increase contraction
  • cardiac glycosides e.g. digoxin
  • beta adrenogic agonsists e.g dobutamine (c^ ATP to be converted to cAMP by AC thereofre more PK to phosphrylate more ca2+ dependent ion channels so more ca2+ can enter into the cell and be used in contraction or stored in SERCA and used for contraction)
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7
Q

cardiac glycosides

A
  • improve symptoms- but not good long term
  • ca2+ is normally removed from the cell by NCX exchanged wc is driven by NA+ moving out the cell due to the K/NA+ATPase pump thats also in the membrane,
  • calcium glycosides block NA/K atpase so theres a rise in Na+ inside the cell,this causes the function of NCX to decrease becuae no more conc gradient ,so the NCX reverses to remove that Na+ so pumps Ca2+ in, so more CA2+ stored in SR so more released during contraction so me forceful contraction
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8
Q

other action of cardaic glycoside

A

another action is to act on medullary centres to increase vagal output to heart slowing down HR and AV

  • so can be used for arrythmias
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9
Q

dobutamine

A
  • s b1 ; stomulates the b1 receptors present at SAN and AVN nodes and work to ^atp into camp, ^PK the ca2+ channels so more Ca2+ enter cell and can be used for contraction
  • used in cardiogenic shock
  • acute but reversible heart failure following cardiac surgery
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10
Q

treat heart failure

A
  • use ACEin, or ARBS and duirtics
  • beta blockers to reuce workload
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11
Q

nitrates

A
  • contains nitrates (organic nitrates) with thiol -SH groups wc when they react with veins c NO2- to be realeased
  • promote veinodilation of the veins (VASODILATION OF VEINS NOT ARTERIES)
  • andis usually as GTN spray under the tongue for angina
  • GTN is short acting but quick
  • Isosorbide dinitrate (longer acting)
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12
Q

why do organic nitrates work on veins, how do you administer GTN?

A

– act on veins and not arteries b less endogenousNO in veins and so has very little effect on arteries

-given GTN undertone tongue spray (short acting)

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13
Q

mechanism of nitric oxide

A
  • Nitric oxide acts on guanylate cyclase increases GTP convertio to cGMP which activates PKG (cGMP dependent protein kinase) wc lowers intracellular ca2+ c less contraction and effecively vasodilation
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14
Q

how does nitric oxide alleivate symptoms in primary and secondary action?

A
  • primary = c venodilation by decreasing preload and reducing work load to heart,heart fills less and so contracts less, wc lowers 02 demand
  • secondary; act on collateral arteries improving 02 delivery to ischameic mycocardium (not arterioles just collateral aarteries)
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15
Q

how to treat angina

A
  • imporve work load of heart; betarecpetorblcokers, ca2+ channels antagonist, organic nitrates
  • improve the blood supply to heart; ca2+ channe; amtagonsit, minor effect on NO
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16
Q

conditions which increase risk of thrombosis and anti-thrombotic drugs

A
  • AF, acute myocardial infarction, mechanical prosthetic heart valve
  • anticoagulants, prevent venous thromboembolism ;

herparin (inhibits thrombin, used for short term action), then fractionated heparin (subcutaneous injection), then warfarin (given orally), inhibits vit K which is needed to make the cofactors, also theres directly acting thrombin inhibitors such as dabigtran

  • antiplatelet drugs; aspirin, clopidogrel (used for acute MI or high risk MI)