.
Warfarin
Heparin
Xarelto
Eliquis
Diagnosis of MI is confirmed with detection of rise and/or fall of cardiac biomarkers, mainly Troponin T or I.
Checking patient symptoms, PMH and ECG.
STE, ST-segment depression and T-wave inversion.
All of the answers
Beta blockers
Statins
ACE inhibitors
All of the answers
Abciximab
Clopidogrel
Xarelto
Warfarin
DVT
Pulmonary embolism
Acute MI
All of the answers
Protamine for unfractionated heparin
Vitamin K
Plasma
Prothrombin complex concentrates
Abciximab
Tirofiban
Eptifibatide
Clopidogrel
Aspirin
Clopidogrel
Plavix
Ticlopidine
Acute renal failure
Development of antiplatelet antibodies
Encephalitis secondary to liver dysfunction
Hemorrhagic stroke
Neutropenia
Heparin-induced Thrombocytopenia
Antithrombin III
Glycoprotein IIb/IIIa
LMW heparins
Clotting cascade
LMW heparins
Heparin-induced Thrombocytopenia
Glycoprotein IIb/IIIa
Activates antithrombin III
Impairs post-translational modification factors II, VII, IX and X
Both
None of the answers
Activated Partial Thromboplastin time (aPTT) test
Antithrombin III
Prothrombin time (PT) test
Glycoprotein IIb/IIIa
Glycoprotein IIb/IIIa
Clotting cascade
Prothrombin time (PT) test
LMW heparins
Clotting cascade
Heparin-induced Thrombocytopenia
LMW heparins
Prothrombin time (PT) test
Small Intestines
Skin
Blood
Liver
XIa
VIIIa
X
Va
Aminocaproic acid
Heparin
Lepirudin
Reteplase
Warfarin
Clopidogrel, prasugrel and the older drug Ticlopidine are converted in the liver to active metabolites that irreversibly inhibit the platelet ADP receptor and thereby prevent ADP-mediated platelet aggregation.
Clopidogrel, prasugrel and the older drug Ticlopidine are converted in the liver to inactive metabolites that irreversibly inhibit the platelet ADP receptor and thereby prevent ADP-mediated platelet aggregation.
Clopidogrel, prasugrel and the older drug Ticlopidine are converted in the blood to inactive metabolites that irreversibly inhibit the platelet ADP receptor and thereby prevent ADP-mediated platelet aggregation.
Clopidogrel, prasugrel and the older drug Ticlopidine are converted in the liver to active metabolites that reversibly inhibit the platelet ADP receptor and thereby prevent ADP-mediated platelet aggregation.
Prothrombin time (PT) test
Glycoprotein IIb/IIIa
Heparin-induced Thrombocytopenia
LMW heparins
Cilostazol
Clopidogrel
Aspirin
None of the answers
Activation of antithrombin III
Blockade of post-translational modification of clotting factors
Inhibition of thromboxane production
Irreversible inhibition of platelet ADP receptors
Reversible inhibition of glycoprotein IIb/IIIa receptors
Heparin-induced Thrombocytopenia
Antithrombin III
Clotting cascade
LMW heparins
LMW heparins
Heparin-induced Thrombocytopenia
Glycoprotein IIb/IIIa
Clotting cascade
Clotting cascade
Glycoprotein IIb/IIIa
Antithrombin III
Heparin-induced Thrombocytopenia
Clotting cascade
Activated Partial Thromboplastin time (aPTT) test
Prothrombin time (PT) test
FTIR
Cerebral hemorrhage must be positively ruled out before each use.
It is not indicated for sever pulmonary embolism.
Under ideal conditions such as treatment within 24hrs, these agents can promptly recanalize the occluded coronary vessel.
Very prompt use of tPA, such as within 6hrs of the 1st symptoms of ischemic stroke, is associated with a significantly better clinical outcome.
Dipyridamole and Cilostazol can prolong the platelet-inhibiting action of intracellular cAMP by inhibiting the phosphodiesterase enzymes that degrade cyclic nucleotides and they also inhibit the uptake of Adenosine – it acts through platelet adenosine A2 receptors to increase cAMP and inhibit aggregation.
Dipyridamole and Cilostazol can prolong the platelet-inhibiting action of intracellular cAMP by inducing the phosphodiesterase enzymes that degrade cyclic nucleotides and they also inhibit the uptake of Adenosine – it acts through platelet adenosine A2 receptors to increase cAMP and inhibit aggregation.
Dipyridamole and Cilostazol can prolong the platelet-inhibiting action of intracellular cAMP by inducing the phosphodiesterase enzymes that degrade cyclic nucleotides and they also induce the uptake of Adenosine – it acts through platelet adenosine A2 receptors to increase cAMP and inhibit aggregation.
Dipyridamole and Cilostazol can prolong the platelet-inhibiting action of intracellular cAMP by inhibiting the phosphodiesterase enzymes that degrade cyclic nucleotides and they also inhibit the uptake of Adenosine – it acts through platelet adenosine A3 receptors to increase cAMP and inhibit aggregation.
Vancomycin
Clofazimine
Clindamycin
Metronidazole
Moxifloxacin
Small Intestines
Blood
Skin
Liver
Heparin is the drug of choice when an anticoagulant must be used in pregnancy.
Heparin does not cross the placental barrier.
The action of Heparin is monitored by PT.
Option 4
Platelet dissolution
Platelet lysis
Platelet aggregation
All of the answers
Alpha receptors
5HT receptors
Glycoprotein IIb/IIIa receptor
All of the answers
Glycoprotein IIb/IIIa
Antithrombin III
LMW heparins
Glycoprotein IIb/IVa
Atenolol
Atorvastatin
Amlodipine
Captopril
Aminocaproic acid
Aspirin
Lepirudin
Warfarin
IX
XIa
II
X
Abciximab
Alteplase
Factor VIII
Streptokinase
Vitamin K
Has a narrow therapeutic window
Antidote is Protamine
Can inhibit Xa Factors
The effect of warfarin is monitored by aPTT test
Hold tobramycin and restart at a lower dose/ frequency.
Increase tobramycin frequency but keep dose the same.
Continue tobramycin at the same dose and frequency.
Discontinue tobramycin and start amikacin.
Discontinue tobramycin and start ciprofloxacin
Early restoration of blood flow to infarct-related artery to prevent infarct expansion.
Prevention of death and other complications
Prevention of coronary artery reocclusion
Relief of ischemic chest discomfort
Resolution of ST-segment and T-wave changes on ECG
Control of Cardiovascular risk factors
Prevention of additional CV events and Improvement in quality of life.
Aspirin
NSAIDs
Abciximab
Warfarin
Cefuroxime
Sulfamethoxazole
Ceftaroline
Doxycycline
Doripenem
Thrombocytopenia
Serotonin syndrome
Torsades de pointe
Hypertensive crisis
jaundice
Cefepime
Azithromycin
Piperacillin/tazobactam
Linezolid
They are oral Xa Inhibitors
Have a rapid onset of action and shorter half-lives than warfarin
They require monitoring
They undergo cytochrome P450-dependent and cytochrome P450-independent elimination.
Their MOA is to directly bind to and inhibit both free factor Xa and factor Xa bound in the clotting complex
Hospital admission – oxygen if saturation is low, frequent measurement of vital signs, bed rest for 12 hours in hemodynamically stable patients and pain relief.
Assess kidney function – serum creatinine and creatinine clearance – to identify patient who may need dosing adjustments and those at high risk of morbidity and mortality.
CBC
APTT and INR
CT Scan and MRI
It either comes in the form of tPA or a protein synthesized by streptococci.
All are given in IV
TPA is an enzyme that directly converts plasmin to plasminogen
Alteplase is normal human plasminogen activator while Reteplase is a mutated form of human tPA with similar effects but a slightly slower onset of action and longer duration of action.
The major application of Thrombolytic agents is an alternative to percutaneous coronary angioplasty in the emergency treatment of coronary artery thrombosis.
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