Cortico/AntiThrombo Flashcards
(27 cards)
MOA of corticosteriods
inhibit phospholipase A2
- decreases arachidonic acid
- inhibits lipooxygenase which decreases leukotrienes
- inhibits cycloxygenase which decreases prostaglandins
- suppresses IL1,3,4,5
How long before you should start a taper
7-14 days
Short term adverse effects of corticosteriods
hyperglycemia, elevated WBC, GI lbleeding, sodium retenstion, hypokalemia, metabolic acidosis, euphoria
Long term Ads of corticosteriods
Cushingoid features, muscle weakness, myopathy, protein wasting, osteoporosis
Thrombus
blood clot formed inset with in the vascular system and impedes blood flow
embolus
blood clot, air bubble, piece of fatty deposit, or other object that has been carried through the bloodstream to lodge in a vessel and cause an embolism
antiplatelet
breaks down fibrin; inhibit activation or aggreagation of platelets
Used for: prevention of arterial events: MI, stroke
Not: DVT
atithrombotic
inhibits clot formation or propagation by inhibiting vitamin K
Used for: DVT, PE, MI
Not for: strokes
thrombolytic
lyses or breaks up a clot by converting inactive proenzyme plasminogen into the active enzyme plasmin that degrades fibrin
Massive PE, acute MI, acute stroke
NOT when you are concerned of intracranial hemorrhage
Prednisone
pro drug for prednisolone
duration of action: 18-36 hours (short acting)
Cortisone/hydrocortisone
interchangeable
8-12 hours (short acting)
methylprednisolone
can be given orally or IV
historically used for asthma
18-36 hours
dexamethasone
historically used for cerebral edema
36-54 hours
physiologic dose
dose your body produces on a normal day
cortisone: 20-25mg
prednisone: 5mg
methylprednisolone: 4mg
dexamethisone: 0.75mg
HPA axis
Hypothalmus: cortocotropin releasing factor
Pituitary: corticotropin
Adrenals
Adverse effects of corticosteroids (short-term)
Hyperglycemia, elevated WBC, GI bleeding sodium retention hypokalemia euphoria
Warfarin/Coumadin
MOA: Inhibits synthesis of Vitamin K prevents vitamin K recycling Route: Oral Delayed onset, 4-5 days Use: stroke prevention (in absence of A-fib) DVT prevention Side E:
Heparin
MOA: Inhibits formation of fibrin clots
inhibits factors 2 and 10 so fibrin can’t be activated
Route of A: IV
Use: limit expansion of thrombi, DVT, PE, post ops prophylaxis
AE: heparin induced thrombocytopeia
Low-molecular weight heparin/LMWH
MOA: complex with antithrombin 3 and inactivate Factor Xa
Use: same as heparin without intensive monitoring
SE: Bleeding, thrombocytopenia, longer half-life than heparin
Dabigatran/pradaxa
MOA: direct thrombin inhibitor, both clot bound and free thrombin are inhibited
Route: IV/SubQ
Use: stroke prevention, heparin alternative
AE: bleeding but no INR checks
Rivaroxaban/xarelto
MOA: Inhibits Factor Xa
Route: oral
use: DVT, PE, stoke patients with non-valvular A fib
AE: bleeding
aspirin
MOA: blocks Cox1 inhibiting thromboxane A2, blocks platelet aggregation
Use: prophylactic treatment for transient ischemia, reduces incidence of recurrent MI, treats mild pain…
AE: hemorrhagic stroke, GI bleeding
ticlopidine (Ticlid)
MOA: blocks platelet aggregation by rirreversibly inhibiting the binding of ADp on platelet receptors required for platelets to bind fibrinogen
Use: prevention of transient ischemic attacks and strokes, prevents stenosis
AE: neutropenia, agranulocytosis, thrombolytic thrombocyteopenic purpura, aplastic anemia
clopidogrel (Plavix)
MOA: blocks platelet aggregation by inhibiting the binding of ADP on platelet receptors required for platelets to bind fibrinogen
Use: prevention of atherosclerotic events following recent MI, stroke
AE:hemorrhage, epistaxis, GI bleeding, pruritus
