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PBL SEM 2 > PBL 5 - PHARMACOLOGY - acute coronary syndromes > Flashcards

PBL 5 - PHARMACOLOGY - acute coronary syndromes Flashcards

1
Q

stable angina is just caused by what?

A

atherosclerosis

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2
Q

what is the fundamental difference between stable angina and ACS?

A

in ACS, blood vessels are nit just partially blocked by an atherosclerotic plaque, there is also an involvement of a blood clot (thrombus)

+ not relieved by rest

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3
Q

what are the 3 main categories of ACS?

A
  • unstable angina
  • NSTEMI
  • STEMI
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4
Q

what is the most acute form of ACS?

A

STEMI

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5
Q

how do you diagnose which ACS a patient is suffering from?

A
  • ECG — ST elevation = STEMI
  • NSTEMI or unstable angina — blood tests — in NSTEMI there is tissue damage to cardiac muscle — releases cardiac specific proteins into the blood
  • no blood markers = unstable angina
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6
Q

what can be used to relieve pain in ACS?

A

opioids

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7
Q

what can be used to reduce cardiac workload/improve blood supply?

A
  • beta blockers - same as in stable angina —> decrease HR and reduce force of contraction, and improve blood supply by lengthening diastole
  • GTN (also reduces pain) — causes peripheral blood vessel dilation to reduce cardiac workload, and dilates collateral vessels
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8
Q

how do beta blockers reduce risk of dysthymias?

A

by reducing sympathetic stimulation

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9
Q

name 2 anti-platelet drugs

A
  • aspirin

- ticagrelor/clopidogrel

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10
Q

name 4 drugs to prevent further thrombosis

A
  • aspirin
  • ticagrelor/clopidogrel
  • heparins
  • atorvastatin
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11
Q

platelets are fragments of cells derived from what?

A

bone marrow cells called megakaryocytes

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12
Q

what do platelets lack?

A

a nucleus — they are fragments of cytoplasm

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13
Q

what does damage to endothelium expose?

A

collagen and glycoproteins

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14
Q

what is the 1st step in platelet aggregation and activation?

A

adherance to collagen and other glycoproteins through their receptors

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15
Q

the activation of collagen and glycoprotein receptors does what?

A

activates platelets — enables platelets to change shape (dramatically - more star shaped)

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16
Q

what do activated platelets release into the blood to activate other platelets?

A

TXA2 and ADP

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17
Q

name 3 stimuli for platelet aggregation/activation

A
  • thrombin
  • ADP
  • TxA2
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18
Q

what is TxA2 synthesised from?

A

arachidonic acid by cyclooxygenase (COX)

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19
Q

explain platelet aggregation/activation

A
  • platelets synthesise TxA2 when activated and release it — enhances expression of glycoprotein 2B and 3A receptors on the platelet membrane
  • these receptors can bind fibrinogen (precursor of fibrin)
  • receptors on the membranes of adjacent platelets can actually bind the same fibrinogen molecule — allows platelets to link together — become aggravated
  • clump of platelets form — continue to release ADP and TXA2 — activate other platelets — cross link to those additional platelets
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20
Q

what is released to stop this chain reaction from turning the blood jelly-like?

A

prostacyclin is released from the intact endothelium

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21
Q

what does prostacyclin do?

A

has the opposite effect of TXA2 — it inhibits platelet activation

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22
Q

how does TXA2 increase platelet aggregation?

A

by decreasing amount of cAMP in the platelet

23
Q

how does prostacyclin decrease platelet aggregation?

A

by increases cAMP in platelet

24
Q

why does the TXA2 receptor not directly decrease cAMP levels in the platelet?

A

it is coupled to Gq

25
Q

what is COX1?

A
  • “housekeeping gene”
  • expressed in most cells
  • involved in synthesis of TXA2 and prostacyclin
26
Q

what is COX2?

A
  • expressed mainly in inflamed tissues
  • it is the target of non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen (and aspirin where it is used as an analgesic and anti-inflammatory)
27
Q

what is COX3?

A

has a frameshift mutation and so doesn’t produce an active enzyme

28
Q

NSAIDs produce their anti-inflammatory effects by acting on COX2 and what?

A

COX2 but also COX1 — this is what produces most of the side effects (eg. worsening GI tract ulcers)

29
Q

what are coxibs?

A
  • a group of COX2 selective NSAIDs that are analgesic and anti-inflammatory and avoid the GI tract problems of non-selective drugs
  • however now not on the market as they can increase rate of serious CVD problems
30
Q

describe aspirin

A

= inhibitor of cyclooxygenases

  • irreversibly blocks platelet COX enzyme, reducing TxA2 synthesis
  • low doses of aspirin used to avoid reducing enzyme in endothelium (source of prostacyclin)
  • aspirin alters balance between platelet TXA2 and endothelial prostacyclin (PGI2)
31
Q

what happens if we irreversible inhibit COX in platelets and why?

A

not able to make any more enzyme as they have no nucleus

32
Q

what are some unwanted effects of aspirin?

A
  • extended bleeding time
  • indigestion
  • allergy (rare)
  • may provoke asthma attacks
  • Reye’s syndrome (under 16s) — liver and brain damage, aspirin use during viral illness
33
Q

what is a signalling molecule produced by vascular endothelium that inhibits platelet activation?

A

prostacyclin

34
Q

what 2 drugs act via modulating expression of glycoproteins IIb/IIIa receptors?

A

clopidogrel and ticagrelor

35
Q

what does clopidogrel do?

A

it is a prodrug that inhibits glycoprotein IIb/IIIa receptor expression on platelets by blocking the ADP receptor irreversibly

36
Q

what does ticagrelor do?

A

allosterically inhibits the ADP receptor

37
Q

clopidogrel is a prodrug that needs to be metabolised by what to become active?

A

CYP2C19

38
Q

why do around 30% of the population not respond well to clopidogrel?

A

around 30% of the population have a low functioning allele for CYP2C19

39
Q

what are some unwanted effects of clopidogrel and ticagrelor?

A
  • extended bleeding time
  • GI tract problems (nausea, indigestion etc)
  • headaches, dizziness
  • gout (ticagrelor)
  • breathlessness (ticagrelor)
40
Q

what are 2 unwanted effects of ticagrelor but not clopidogrel?

A

gout and breathlessness

41
Q

what does dipyridamole do?

A
  • phosphodiesterase (PDE3) inhibitor
  • prevents the breakdown of cAMP in platelets
  • raises cAMP levels — prevent aggregation of platelets
42
Q

what are some unwanted effects of dipyridamole?

A
  • GI tract problems (nausea, indigestion etc)
  • headaches, dizziness
  • muscle pain
  • flushing/feeling hot (vasodilator)
  • can precipitate/worsen angina
43
Q

what is currently only drug approved in the UK for prevention of atherothrombotic events in patients with ACS or who have had a MI?

A

ticagrelor

44
Q

describe coronary steal after dipyridamole

A
  • healthy vessels dilated but no dilation of the collateral vessel
  • blood vessel with atherosclerotic plaque has a higher resistance than healthy vessels so therefore the dilation of healthy vessels dilates blood away from partially occluded vessel
  • reduces blood flow to ischaemic tissue even further = coroanry steal
45
Q

what is plasmin?

A

proteolytic enzyme that breaks down fibrin to fibrin degradation products

46
Q

what is the inactive precursor of plasmin in circulation?

A

plasminogen

47
Q

plasminogen has to be cleaved by what to be activated?

A

tissue plasminogen activator

48
Q

what 3 drugs used in thrombolysis act by supplementing the tissue plasminogen activator?

A

reteplase, alteplase, streptokinase

49
Q

reteplase vs alteplase vs streptokinase

A
  • reteplase is slightly mutated to have better stability in circulation
  • alteplase is a recombinant version
  • reteplase and alteplase are very similar to tissue plasminogen activator
  • streptokinase is a bacterial enzyme — used less than other 2
  • all work if give quickly —useful for dissolving clots
  • 4 1/2 hour window to initiate thrombolysis before the clot sits, matures and changes its structure so it is resistant to the thrombolytics
50
Q

is PCI or thrombolysis used more in the initial stages of HA treatment?

A

PCI

51
Q

what is a risk of thrombolyis?

A

haemorrhage

52
Q
A
  1. alteplase
  2. plasmin
  3. aspirin
  4. COX1
  5. thromboxane A2
53
Q

dipyridamole is an anti platelet drug that primarily acts as what?

A

an inhibitor of phosphodiesterase

54
Q

what does the block of platelet ADP receptors by clopidogrel inhibit?

A

glycoprotein receptor mediated aggregation

PBL SEM 2 (44 decks)

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