6.2 Antiplatelets Flashcards
pathophysiology of venous thrombosis
stasis of blood, +/- damage to veins
pathophysiology of arterial thrombosis
forms at site of atherosclerosis following plaque rupture
compare the cell content of venous and arterial thrombi
venous- high RBC, high fibrin, low platelet
arterial- low fibrin, higher platelet
describe the process of platelet activation and aggregation
-endothelial damage so platelets come and adhere
-release chemical mediators (thromboxane A2, ADP, serotonin, PAF)
-more platelets recruited by signalling cascade, into platelet plug
-chemical mediators cause increased calcium
-activates GP11b/111a receptors and fibrinogen
which type of drugs are used for
1. arterial thrombi
2. venous thrombi
- antiplatelts and fibrinolytics
- anticoagulants
MOA aspirin
inhibits COX-1 so less thromboxane A2 produced so less platelet aggregation
IRREVERSIBLE
why doesn’t aspirin completely inhibit platelet aggregation?
-other chemical mediators apart from thromboxane A2 cause aggregation
-can inhibit COX-1 on every platelet
2 doses of aspirin
75mg- non analgesia, children
300mg- loading dose, ACS
adverse effects of aspirin
GI irruption, dyspepsia, bleeding, haemorrhage
reye’s syndrome
hepatic failure and cognitive disruption typically post viral, can be fatal
so avoid aspirin
when to avoid aspirin
reyes syndrome
third trimester (premature closure of ductus arterioles)
hypersensitivity
drugs to be careful with when on aspirin
other antiplatelets or anticoagulants (synergistic effect)
why does anti-lately effect last the lifespan of platelets (7-10 days)?
no nuclei so cant produce more COX, irreversibly inhibited
indications for aspirin
AF post stroke
stroke/TIA secondary
ACS secondary
post PCI/stent
NSTEMI/STEMI 300mg
what to presicbe when on aspirin long term
PPI for gastric protection
name 3 ADP receptor antagonists
clopidogrel
prasugrel
ticagrelor
adverse effects of ADP receptor antagonists
bleeding dyspepsia
thrombocytopenia
contraindications for ADP receptor antagonists
high bleed risk with renal/hepatic impairment
important DDIs for ADP receptor antagonists
CYP inhibitors
other gnutplatelts/anticoagulants
NSAIDs
indications for ADP receptor antagonists
ischameic stroke/ TIA
aspirin contraindicated
phosphodiesterase inhibitors
-adverse effects
-contraindicstions
-indications
-V+D, dizziness
-antiplatelets, anticoagulants, adenosine
-ishcaemic stroke/ TIA secondary
why are GP11b/111a inhibitors effective?
target final common pathway of platelet aggregation
tranexamic acid indications
iachasmeic stroke
heavy periods
epistaxis
big bleeds
why can streptokinase only be used once?
antibodies develop
reperfusion injury from PCI
calcium and ROS flood into tissue
typical drug regime for secondary ACS prevention when haemodynamically stable
ACEi (or ARB)
B blcoker
75mg aspirin + ADP receptor antagonist
statin
GLP-1
-how can we target it?
-is promoting its action good?
-DPP4 inhibitors, and GLP-1 agonists
-yes, insulin secretion and senses increased glucose levels
