Cardiovascular Flashcards

1
Q

Angiotensin system

A

Liver creates angiotensinogen
Kidney produces renin
Renin breaks angiotensinogen to angiotensin I
Endothelial cells produce angiotensin converting enzyme which converts angiotensin I to angiotensin II

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2
Q

What does angiotensin ii do

A

Binds at angiotensin i and angiotensin ii receptors
Vasoconstriction in blood vessel sites
Sodium reabsorption in kidney sites (more fluid reabsorption)
Releases ADH in pituitary gland sites increasing water reabsorption
Releases aldosterone in adrenal gland sites increasing sodium reabsorption

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3
Q

Action of NO

A

Inhibits angiotensin II
Vasodilation & prevention of vasoconstriction
Inhibits platelet adhesion
Anti-inflammatory

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4
Q

Action potential system

A

Phase 0 - Sodium enters cell causing rapid depolarisation
Phase 1 - Potassium leaves cell causing slight repolarisation
Phase 2 - Calcium enters cell slowing repolarisation
Phase 3 - Calcium channels close so rapid repolarisation
Phase 4 - Resting phase as sodium (and calcium) and potassium switch places ready for next depolarisation

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5
Q

Action of Calcium channel blockers (Amlodipine)

A

Bind to calcium channels on heart and blood vessels
Vasodilation
Reduces rate, force and conduction of heart

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6
Q

Action of Beta blockers (Bisopralol)

A

Bind to beta i and beta ii sites on heart and blood vessels
Decreases heart rate and force prolonging action potential by inhibiting potassium channels
Slight vasoconstriction

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7
Q

Blood clotting system

A

Injury to blood vessel
Thromboxane released
Vasoconstriction
Platelets activate and send signals to bring more platelets to area
Von Willebrand Factor protein binds platelets forming plug
Clotting factor proteins stimulate production of fibrin from fibrinogen which forms fibrin clot

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8
Q

Fibrinolysis

A

Plasmin breaks down fibrin and fibrinogen
Plasminogen is always available in blood to prevent clotting and activated by T-PA into plasmin

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9
Q

Action of aspirin

A

COX inhibitor
Reduces pain and inflammation
Lowers temperature
Increases stomach acidity
Inhibits thromboxane synthesis

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10
Q

Action of clopidogrel

A

Binds to platelets (forever)
Prevents platelet adhesion

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11
Q

Action of Ticagrelor

A

Binds to platelets (not forever)
Prevents platelet adhesion

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12
Q

Action of Warfarin

A

Inhibits enzyme that activates vitamin K
Vitamin K synthesises clotting factors

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13
Q

Action of heparin

A

Counters clotting cascade by binding to thrombin and antithrombin preventing the formation of clotting factors

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14
Q

Action of TXA

A

Competitive antagonist to plasminogen so that TPA does not bind and produce plasmin which breaks fibrin clot

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15
Q

Actions of statins

A

Inhibit enzyme involved in the synthesis of cholesterol
Causes liver to increase LDL receptors which then clears LDL which reduces plaqu buildup

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16
Q

Action of GTN

A

Venodilation (due to mechanism with NO)
Lowers blood pressure meaning less preload to heart

17
Q

Inotropic

A

Force of contraction

18
Q

Chronotropic

A

Rate of contraction

19
Q

Dromotropic

A

Rate of conduction

20
Q

Action of amiadarone

A

Potassium channel blockers
Inhibit sodium/ calcium channels
Slows rate and conduction in the heart

21
Q

Action of atropine

A

Muscirinic antagonist blocking acetylcholine in the heart
Stops action of acetylcholine from slowing heart rate

22
Q

Use of fluids

A

Often crystalloid
Increases caridiac output and tissue perfusion
Fluid in bleeding should not exceed 90mmHg or bleeding will increase