Lipid lowering drugs Flashcards

1
Q

What are statins?

A
  • They –|HMG - CoA reductase
  • Competitive and reversible
  • More effective at reducing cholesetrol than other drugs.
  • Not great for moderate to high TG
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2
Q

What is the MOA of statins?

A

Decreases cholesterol synthesis upregulates LDL recptor synthesis, leading to LDL-C clearance from plasma to liver. Reduces plasma LDL-C, decreases plasma TG & increases HDL-C

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3
Q

What other protective effect does statins have?

A
  • Plaque stability
  • Increases neovascularisation of ischemic tissue
  • Anti-thrombotic
  • Anti-oxidant
  • Anti-inflammatory
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4
Q

What are fibrates?

A

Derivative of fibric acid - structually related to thiozolidones (Bezafibrate, Ciprofibrate, Fenofibrate, Genfibrozil)

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5
Q

What is the MOA of Fibrates?

A
  • Agonsit of PPAR-α
  • Increases LDL-C uptake, form LDL with higher affinity to LDL
  • Increases fatty acids uptake & conversion to acyl-coA by the liver, therefore fatty acids arent available for TG synthesis.
  • Decrease in VLDL from liver & hence TG lvls reduced.
  • Anti-inflammatory effects.
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6
Q

What is ezetimibe?

A

–| of cholesterol absorption, used where statin is C/I or in addition to statins.

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7
Q

What is the MOA of ezetimibe?

A
  • Specifically block absorption of cholesterol without affecting absorption of fat-soluble vitamins, TG or bile acids.
  • Conjugated in the intestine to ezetimibe glucuronide & excreted in stools.
  • Lowers LCL-C 17%
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8
Q

What is the MOA of Nicotinic Acid?

A
  • Mobilisation of FFA
  • Decrease TG synthesis
  • Decreases APoB and decreases VLDL
  • Decreased serum VLDL results in lipolysis to LDL
  • Decreased LDL
  • Increased HDL
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8
Q

What are Nicotinic Acid Derivatives?

A

Lowes both LDL-C & TG by –|of synthesis
Increases HDL-C
–| Hepatic TG production & VLDL secretion

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8
Q

What is Inclisiran ?

A

Small interfering RNA treatment that –| the translation of PCSK9 mRNA.

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9
Q

What are PCSK9?

A

Bind to hepatic LDL receptors & promote their lysosomal degradation.
Prevents recycling of LDLR back onto cell surface of hepatocytes -> limits LDL uptake into the liver

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9
Q

What is the MOA of PCSK9?

A

–| PCSK9 -> Increases receptor number & LDL uptake.

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10
Q

What is the MOA of Inclisiran?

A
  • Interacts with RICS complex which degrades mRNA of PCSK9
  • Less PCSK9 therefore less likely to interfere with LDL receptor expression.
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11
Q

What is the mechanism of platelet adhesion, activation & secretion?

A
  • Exposed to dmg & becomes activated. Exposure of the basement membrane to the ECM - they combine & cab cause platelet adhesion.
  • Soluble factors, TXA2, ADP binding of the ligands can cause platelet activation
  • Platelet aggregation -> platelet activation. Receptors will bind to fibrin & fibrin will form links between platelets & cause aggregation & further stimulation.
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11
Q

How can you influence platelet aggregation?

A
  • –| either TXA2, or ADP
  • By stimulating g prostacyclin / nitric acid.
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12
Q

What molecules activate platelets?

A
  • Serotonin
  • Epi
  • PAF
  • Thrombin
  • ADP
  • TXA2
  • Collagen
13
Q

What do antiplatelet drugs do?

A

Decrease platelet aggregation & –| thrombus formulation in arterial circulation.

14
Q

Name some antiplatelet drugs?

A

Aspirin
Thienopyridines (Clopidogrel)
Ticagrelor
Glycoprotein 11b/11a –|(Eptifibatide, Tirofiban, Abciximab)

15
Q

How does aspirin work as an antiplatelet?

A

Irreversibly inactivates COX-1 in platelets.
* Decreases TXA2 formation
* Reduces platelet aggregation
Irreversibly inactivates COX-2 in Endothelium
* Decreases prostacyclin formation
* Increases platelet aggregation.
Endothelial cells can synthesise new COX-2
Lower doses just –| platelet
Higher doses –| both

16
Q

How does clopidogrel work?

A
  • Pro-drug additive effects to aspirin, but work on different pathways
  • –| ADP induced aggregation
  • Antagonises the platelet P2Y12 receptor.
17
Q

How does ticagrelor work?

A
  • Nucleoside analogue like adenosine.
  • Blocks p2y12 ADP receptors on platelets.
  • Diff binding site than ADP so allosteric –| & Blockage is reversible _. acts faster for a short period of time.
18
Q

What are the side effects of Ticagrelor?

A

More non-lethal bleeding, effects more quickly.

19
Q

How do glycoprotein 11b/11a work?

A

–| all pathway of platelet activation be it binds to glycoprotein 11b/11a receptors, blocking fibrinogen binding -> –| aggregation.

20
Q
A