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Cardiovascular > Drugs for Ischaemic Heart Disease > Flashcards

Drugs for Ischaemic Heart Disease Flashcards

1
Q

How many mitochondria are in each cardiomyocyte?

A

5000

Generate ATP- far more than any other organ of the body

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2
Q

What is preload?

A

Volume of blood in the ventricles at the end of diastole

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3
Q

What is preload determined by?

A

Blood volume

Venous tone, capacity of the venous circulation to hold blood (constriction= more return)

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4
Q

What is preload increased by?

A

Sympathetic NS activation
Renal failure
Heart failure

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5
Q

What is afterload?

A

Resistance the heart must overcome to circulate blood

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6
Q

What is afterload determined by?

A

Tone in arterial circulation

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7
Q

What is afterload increased by?

A

SNS activation

Hypertension

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8
Q

What causes narrowing of the coronary arteries?

A

Atheroma
Coronary artery spasm (smooth muscle spontaneously constrict)
leads to ischaemic heart disease

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9
Q

What do stable plaques lead to?

A

Lack of oxygen and chest pain (angina)

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10
Q

What leads to myocardial infarction?

A

Unstable plaque and thrombus

MINOCA= myocardial infarction non obstructed coronary artery

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11
Q

What does vascular endothelium regulate?

A

Blood vessel tone
Permeability
Leukocyte adhesion, platelet aggregation and tendency for thrombus formation

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12
Q

What occurs to lead to lesion formation?

A

Changes in endothelial function

Leukocyte adhesion and migration as endothelial permeability increases

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13
Q

What are the causes of endothelial dysfunction?

A
  • Elevated and modified low density lipoprotein (in familial hypercholesterolaemia)
  • Oxygen free radicals (smoking, hypertension, activated inflammatory cells)
  • Infectious microorganisms (herpes virus, chlamydia pneumoniae, h. pylori)
  • physical damage and gene activation by turbulent flow, high blood pressure
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14
Q

What are the risk factors for endothelial dysfunction?

A

Diabetes, ageing, male (females after menopause)

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15
Q

What are foam cells?

A

Macrophages that take up low density lipoprotein oxidised by interaction with oxygen free radicals

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16
Q

Describe the formation of a fatty streak

A 
Inflammatory cell activation
Smooth muscle migration
Foam cell formation
T cell activation
Adherence and aggregation of platelets
Adherence and entry of leukocytes
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17
Q

Describe the formation of advanced complex lesion

A

Macrophage accumulation
Formation of necrotic core
Fibrous cap formation- stability key to prognosis
Healing response to injury

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18
Q

What is the difference in outcome between unstable and stable angina?

A 
Stable= chest pain
Unstable= cap rupture or erosion= thrombus= heart attack/MI, stroke
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19
Q

Which drug lowers cholesterol and low density lipoprotein?

A

Statins

simvastatin

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20
Q

How is LDL formed?

A

HMG CoA into mevalonate via HMG CoA reductase (rate determining step in liver)
Mevalonate precursor for cholesterol, then LDL
binds to LDL receptors for clearance

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21
Q

What is the mechanism of statin drug action?

A

statins are inhibitors of HMG CoA reductase

Increase expression of LDL receptors (so more clearance)

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22
Q

What are the other effects of statins (pleiotropic)?

A 
Improved endothelial function
Inhibition of inflammation
Plaque stabilisation
Inhibition of thrombus formation
(mevalonate compounds involved in intracellular signal transduction)
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23
Q

What other lipid lowering drugs are used with or as an alternative to statins?

A

Fibrates (bezafibrate, gemfibrozil, fenofibrate)

ezetimibe

24
Q

Describe fibrates

A

Activate intracellular PPARa (peroxisome proliferator receptor a)
Decrease circulating very low density lipoprotein and triglyceride, only very small effect on LDL but also increase protective high density lipoprotein

25
Q

Describe ezetimibe

A

Lowers cholesterol absorption from small intestine vis action in epithelial cells

26
Q

What is angina pectoris?

A

Intermittent chest pain caused by mismatch between demand of oxygen by the heart and supply of oxygen to the heart (stimulates chemoreceptors- chest pain)

27
Q

What is oxygen supply decreased by?

A

Coronary artery disease

Anaemia

28
Q

What is oxygen demand increased by?

A

Exercise
Tachycardia
Hypertension

29
Q

What is the aim of angina treatment?

A

Reduce demand or increase supply

Reduce demand by reduce heart rate/ force of contraction/ preload/ afterload

30
Q

Describe acute angina treatment

A

Rest

Rapid acting organic nitrate (glyceryl trinitrate)

31
Q

Describe prophylactic angina treatment

A

Targets blood vessels- longer lasting nitrate/ K (ATP) channel opener
Targets heart- beta adrenoreceptor antagonist/ calcium antagonist/ funny channel blocker

32
Q

How do nitrates affect the blood vessels?

A

NO in endothelial cells into smooth muscle cell- guanylate cyclase converts GTP into cGMP= relaxation (reduces availability for Ca 2 for contraction)
Veins more than arteries

33
Q

What are the effects of nitrates on venous circulation?

A

Dilate veins, decrease venous return and preload on heart, reduce oxygen demand

34
Q

What are the effects of nitrates on arterioles and coronary arteries?

A

Dilate and reduce afterload on heart therefore reduce oxygen demand
Coronary= improves supply (coronary spasm)

35
Q

What are examples of nitrates?

A
  • Glyceryl trinitrate- acute (sub-lingual or spray), chronic use leads to tolerance (loss of responsiveness) rapid action
  • Isosorbide dinitrate- slow release patch/ oral, can be prophylactic, nitrate free periods required, longer acting
36
Q

What are the effects of nicorandil?

A

Reduces preload and afterload on heart and therefore oxygen demand
Dilates coronary arteries and can increase oxygen supply in coronary spasm

37
Q

What are the mechanisms of nicorandil?

A 
Causes blood vessel dilation by opening ATP sensitive K+ channels in smooth muscle cells
Nitrate moiety (releases NO) in structure therefore additional vasodilator action
38
Q

What are the mechanisms and effects of beta adrenoreceptor antagonists (like atenolol)?

A
  • Blocks cardiac beta 1 adrenoreceptor= reduce heart rate and therefore oxygen demand
  • Blocks renal beta 1 adrenoreceptor= reduce blood volume by reducing renin release and activation of RAAS, reduce preload and therefore oxygen demand
39
Q

What does RAAS stand for?

A

Renin Angiotensin Aldosterone System

40
Q

What are the mechanisms and effect of ivabradine?

A

Blocks ‘funny current’ in sino-atrial node cells= reduces rate of spontaneous depolarisation during action potential generation- reduce heart rate so oxygen demand
(Less side effects than beta blockers)

41
Q

What are the mechanisms and effects of calcium antagonists?

A

nifedipine, diltiazem
Prevent opening of voltage dependent Ca 2 channels= prevents Ca 2 entry into cardiac muscle cells from extracellular space= reduce availability to contractile apparatus= reduce force of contraction and therefore oxygen demand

42
Q

Describe thrombus formation

A

Endothelial cells produce anti-thrombotic mediators, damage= collagen exposure= platelet activation (change shape and stick together)= coagulation cascade= fibrin

43
Q

What are anti-thrombotic drugs?

A

Taken prophylactically to reduce risk of thrombus if atherosclerotic plaque ruptures, in patients at high risk or already had MI

  • Anti-platelet (aspirin, clopidogrel, vorapaxar)
  • Anti-coagulant (warfarin, rivaroxaban)
44
Q

Describe platelet activation

A

Stimulus (collagen)- thrombin activates coagulation cascade- Arachidonic acid via phospholipaseA2- cyclic endoperoxidases via cyclooxygenase (COX)- TxA2 prostaglandin via Tx synthetase- TxA2 receptor= increase in iCa 2+ so activation of platelet

45
Q

What is the mechanism of anti-platelet drugs?

A

Thrombin antagonist

COX inhibitor

46
Q

How do platelets further increase activation?

A

Activated platelets change shape and release contents of granules- adenosine diphosphate (ADP)

47
Q

How do activated platelets stabilise the thrombus?

A

Platelets express glycoprotein 2b/3a receptors for attachment of fibrin, from coagulation cascade

48
Q

What other mechanisms of anti-platelet drugs have directly on the platelet?

A 
P2Y12 receptor antagonists to block ADP so less platelet aggregation
abciximab antibody (IV)- blocks fibrin binding to gp2b/3a
49
Q

What are the overall mechanisms of anti-platelet drugs?

A
  • COX inhibitor- aspirin- irreversible inhibition of COX, prevents formation of TxA2 and platelet activation
  • P2Y12 inhibitor- clopidogrel, ticagrelor- blocks effect of ADP and prevents platelet activation
  • Thrombin-receptor antagonist- vorapaxar- prevent activation of PAR-1 receptors on platelets
50
Q

What are the risks of anti-platelet drugs?

A

Bleeding

Newer drugs shorter acting or reversible

51
Q

What are anti-coagulant drugs and what are the types?

A

Prevent the formation of fibrin to stabilise platelet plug

  • Intravenous= heparin
  • Orally active= warfarin, rivaroxaban
52
Q

What is the action of heparin?

A

Binds to Anti-thrombin 3- released by endothelial cells naturally in response
Promotes action, reduces coagulation cascade

53
Q

What is the action of warfarin?

A

Reduces the action of enzyme reductase so less oxidised Vitamin K is converted into hydroquinone Vitamin K so less Glu converted into Glu-COOH which is involved in active factors 2,7,9,10 (prevents cofactors forming)

54
Q

What are the common indications of warfarin?

A

AF, artificial heart valves, DVT, pulmonary embolism, occasionally after MI

55
Q

What are the cons of warfarin?

A

Narrow optimal range, high risk of bleeding
Broken down in liver, enzymes induced by other drugs, environmental influences
Blood levels must be checked regularly

56
Q

What is the action of rivaroxaban?

A

Inhibits action of Xa in thrombin formation

Cardiovascular (52 decks)

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