ILD + DVT, PE Flashcards
Warfarin MOA + EXAMPLES
Anticoagulant
vitamin K antagonist that works by inhibiting the enzyme responsible for activating vitamin K-dependent clotting factors (II, VII, IX, and X). This leads to a reduction in clotting factor production in the liver.
Indications:
Atrial fibrillation (AF), mechanical heart valves, DVT, PE, stroke prevention in certain conditions.
Heparin MOA
Anticoagulant
injectable anticoagulant that works by binding to antithrombin III, enhancing its ability to inhibit thrombin (Factor IIa) and Factor Xa, which are both essential in clot formation.
Indications:
Acute management of DVT, PE, acute coronary syndrome (ACS), unstable angina, periprocedural anticoagulation, and in patients at high risk for thrombosis.
DOACs MOA + examples
DIrect Oral Anticoagulants
INCLUDE: direct thrombin inhibitors (DTIs) + direct Factor Xa inhibitors.
Direct thrombin inhibitors (e.g., dabigatran) **directly inhibit thrombin **(Factor IIa), preventing clot formation.
Direct Factor Xa inhibitors (e.g., rivaroxaban, apixaban) directly inhibit Factor Xa, blocking thrombin generation.
Indications:
Atrial fibrillation (AF), DVT, PE, stroke prevention in AF, and post-surgery anticoagulation.
Dabigatran (direct thrombin inhibitor)
Rivaroxaban, Apixaban, Edoxaban (direct Factor Xa inhibitors)
Heparin adv + disadc
Advantages:
Rapid onset of action (works within minutes).
Reversal agent available (protamine sulfate) for excessive bleeding.
Used in acute settings (hospitalized patients).
Disadvantages:
Need for monitoring: Activated partial thromboplastin time (aPTT) is required to adjust doses.
Risk of heparin-induced thrombocytopenia (HIT), a serious condition where the patient develops a low platelet count and an increased risk of thrombosis.
Warfarin adv + disadv
Advantages:
Rapid onset of action (works within minutes).
Reversal agent available (protamine sulfate) for excessive bleeding.
Used in acute settings (hospitalized patients).
Disadvantages:
Need for monitoring: Activated partial thromboplastin time (aPTT) is required to adjust doses.
Risk of heparin-induced thrombocytopenia (HIT), a serious condition where the patient develops a low platelet count and an increased risk of thrombosis.
DOACs adv, disadv
Advantages:
No routine monitoring required (e.g., no need to check INR or aPTT).
Oral administration for convenience.
Fewer drug-food interactions compared to warfarin.
Faster onset and offset of action compared to warfarin (hours vs. days).
Reversal agents available for certain DOACs (e.g., andexanet alfa for Xa inhibitors and idarucizumab for dabigatran).
Disadvantages:
Cost: More expensive than warfarin and heparin.
Renal and hepatic dosing adjustments may be necessary.
No readily available monitoring tests to ensure therapeutic levels, though this is less of an issue for most patients.
HIT : Heparin-induced thrombocytopenia: Describe the paradox
a condition that lowers platelet count (such as heparin-induced thrombocytopenia or HIT) can also increase the risk of thrombosis, but it is an important concept in medicine.
Heparin-Induced Thrombocytopenia (HIT)
HIT is a rare but serious complication that can occur when heparin is used as an anticoagulant. Here’s how it happens:
Immune Response:
In HIT, the body develops an immune response against heparin-platelet factor 4 (PF4) complexes. When heparin binds to a protein called platelet factor 4 (PF4), it creates a complex that can trigger the immune system.
The immune system mistakenly targets these complexes, producing antibodies that activate platelets.
Platelet Activation:
These antibodies cause platelets to become activated, even though the platelets are in low numbers.
Normally, platelets help form clots to stop bleeding. However, in HIT, the activation of platelets leads to clot formation within blood vessels, a process called thrombosis.
Platelet Consumption:
The activated platelets aggregate and form clots, which consume platelets from the circulation, leading to a decreased platelet count (thrombocytopenia).
So, despite having low platelet counts, the platelets are abnormally activated, and blood clots (thrombosis) form in various areas, particularly in the veins and lungs.
Why It Increases Thrombosis Risk:
The activated platelets in HIT don’t behave normally. Instead of just helping to stop bleeding at an injury site, they clump together and form unwanted clots within blood vessels.
These clots can lead to serious complications such as deep vein thrombosis (DVT), pulmonary embolism (PE), or even stroke.
So, in HIT, even though there are fewer platelets overall, the platelets that remain are abnormally active, which increases the risk of abnormal clotting (thrombosis).
In Summary:
HIT is paradoxical because it involves low platelet count (thrombocytopenia), but the remaining platelets are highly activated and cause clot formation.
The anticoagulant drug (heparin) triggers this immune response, which can lead to an increased risk of thrombosis despite the presence of a low platelet count.
