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Clutch City 2-14 War
Medicine - AntiCoag
| Question | Answer |
|---|---|
| Polio (ORAL) | Polio Oral Vaccine OPV in India is IgA For example, most intramuscular vaccinations lead to IgG production while the rotavirus vaccine, which is given orally, leads to IgA production. |
| IgA | Prevents attachment of bacteria and viruses to mucous membranes; does not fix complement. Uses transcytosis. Produced in GI tract (eg, by Peyer patches) and protects against gut infections (eg, Giardia) |
| NSAIDS on Renal Arteries Affect | NSAIDs, by inhibition of prostaglandins and bradykinin, produce vasoconstriction of the afferent renal arteriole and reduce the ability of the kidney to regulate (increase) glomerular blood flow |
| NSAIDs and Acute Kidney Injury NSAIDs can cause two different forms of acute kidney injury1. | Haemodynamically mediated (eg, pre-renal injury and/or acute tubular necrosis). Immune mediated (eg, acute interstitial nephritis). Acute kidney injury is characterised by a rapid fall in glomerular filtration rate (GFR) over hours to days. |
| Heparin Tox Rx | Activates Antithrombin III activity by 1000 folds given acutely~ toxicity treated with protamine sulfate |
| Warfarin | Warfarin inhibits vit k epoxide reductase Toxicité rx fresh frozen plaza and vit K Most of these factors are produced by liver cells, and it turns out that producing coagulation factors II, VII, IX, and X requires an enzyme that uses vitamin K. |
| Heparin MOA | works by indirectly inhibiting two clotting factors called thrombin and factor X by binding to and enhancing the activity of an anticoagulant protein called antithrombin III. |
| LMWH low molecular weight heparin | Compared to unfractionated heparin, LMWH like Enoxaparin and Dalteparin have better bioavailability and have a two to four times longer half-life.Fondaparinux |
| Warfarin Route of Admin | Warfarin, can be taken peroral so it’s the drug of choice for chronic management since the person can take the medication home. |
| Heparin Uses | acute deep vein thrombosis, preventing postoperative deep vein thrombosis and pulmonary embolism, maintaining extracorporeal circulation during open heart surgery and renal hemodialysis. |
| Heparin Efficacy measured via | primarily operates on factors in the common and intrinsic pathway, a laboratory value called the aPTT or activated partial thromboplastin time is used to measure its efficacy. |
| aPTT MOA | measures the speed at which blood clots via the intrinsic and common coagulation pathways. |
| Heparin Tox | Heparin’s main toxicity profile includes its increased risk of bleeding, HIT, and osteoporosis. |
| Difference b/w Unfract and LMWH | Unfractionated heparin inhibits both factor X and thrombin while low molecular weight heparin only inhibits factor X. |
| HIT | heparin induced thrombocytopenia--thrombocyte referring to platelets and penia meaning small or little, so thrombocytopenia means low platelets. |
| If HIT occurs | he heparin should be stopped and the person switched to a different anticoagulant--like direct thrombin inhibitors, which includes medications like argatroban, bivalirudin, and dabigatran. |
| Thrombin | activated factor II, is a very important clotting factor, because it has multiple pro-coagulative functions. Think of thrombin as the accelerator on a car--the pedal that takes secondary hemostasis from 20 miles per hour to 100 miles per hour! |
| Thrombin MOA | binds to receptors on platelets causing them to activate. activates two cofactors; factor V used in the common pathway, and factor VIII used in the intrinsic pathway. |
| Heparin has been known to have decreased anticoagulation effect with | medications like digitalis, tetracyclines, antihistamines and nicotine. |
| anticoagulant warfarin MOA | is an anticoagulant that works by inhibiting vitamin k epoxide reductase for factors II, VII, IX, X, protein C and protein S.In total, there are twelve coagulation factors numbered factors I-XIII, there’s no factor VI. |
| Warfarin is taken per-oral and it affects | the extrinsic pathway first since factor VII has the shortest half life and it’s the first coagulation factor to run out. Next, levels of factor II, IX, and X also drop, causing inhibition of the intrinsic and common pathways. |
| warfarin’s efficacy is monitored using a blood test called | prothrombin time, or PT, which is a measure of how well the extrinsic and common pathways are functioning. |
| normal INR is | international normalized ratio s 1.1 or less |
| The main use for warfarin is | the prevention of disorders caused by blood clots. DVTs can cause pulmonary embolism when they travel to the lungs and block off arteries. atrial fibrillation, the blood could pool in the heart, leading to blood clot formation. |
| Warfarin Tox | uncontrollable bleeding, most commonly in the GI tract. risk increases when INR is higher than 3. warfarin is broken down in the liver by an enzyme called CYP2C9 |
| cause warfarin to accumulate | Certain common medications like cimetidine, omeprazole, metronidazole, trimethoprim/sulfamethoxazole, and amiodarone can inhibit this enzyme, CYP2C9 which belongs to a class of enzymes called CYP450 oxidase. |
| drugs that speeds up the metabolism of warfarin and we get an subtherapeutic INR that’s under 2. | some medications like griseofulvin, barbiturates, phenytoin and carbamazepine can enhance the activity of CYP450 |
| CYP Inducers | Most Chronic Alcoholics steal phen-phen and never refuse greasy carbs. Modafinil, Chronic Alcohol Use , st.jhons wart, phenytoin, phenobarbital, nevirapine, rifampin, griseofulvin, Carbamazepine |
| CYP Inhibitors | SICKFACES.COM (when i AM drinking GRAPEFRUIT juice) sodium valproate, isoniazid, cimetidine, ketoconazole,fluconazole, acute alcohol use, chloramphenicol, erthro/calrithromycin, sulfonamides, ciprofloxacin, omeprazole, metronidazole |
| warfarin is contraindicated in pregnancy due to its teratogenic effects such as | increases the risk of fetal hemorrhage, spontaneous abortion, bone deformities and ophthalmologic abnormalities, such as optic neuritis. |
| who has increased risk of warfarin induced skin necrosis. | congenital protein C deficiency use “heparin bridge”. |
| At what INR warfarin must be stopped | INR higher than 10, warfarin should be stopped and vitamin K. patient should be given fresh frozen plasma, , since it contains all prothrombin complex concentrate which contains the coagulation factors II, VII, IX and X along with proteins C and S. |
| Thrombolytic, also called | fibrinolytics, are medications that break up blood clots formed during hemostasis, where hemo means blood, and stasis means to halt or stop. |
| fibrinolysis is | Approximately two days after an injury occurs to a blood vessel and the blood clot forms, it's time to for the body to dissolve the blood clot through a process called fibrinolysis, which is the gradual degradation of the fibrin mesh. |
| circulating protein produced by the liver called | plasminogen, gets converted by an enzyme called tissue plasminogen activator, or tPA, into its active form called plasmin. |
| a few other proteins activate plasmin as well | including coagulation factors IXa, XIIa, kallikrein, and protein C. |
| thrombolytics derived from tPA include | alteplase, reteplase, and tenecteplase. Streptokinase is derived from beta hemolytic bacteria proteins with a similar mechanism of action. |
| which has highest affinity for fibrin. | tenecteplase |
| adverse effect of thrombolytic medications | primary adverse effect is bleeding, for which aminocaproic acid or tranexamic acid can be given |
| Which fibronylitic therapy often used | The thrombolytics derived forms of tPA are used more frequently than streptokinase because they are clot specific--meaning they will not cause fibrinolysis and unnecessary bleeding outside of the area of the clot unlike streptokinase. |
| Thrombolytics are used for | the short-term emergency management of pathological thrombosis.They are used to break up clots during myocardial infarctions, deep vein thrombosis, pulmonary embolisms, and ischemic strokes. |
| Why do we first rule out hemorrhagic strokes with a CT before fibronylitic therapy | These strokes are caused by bleeding from damaged arteries, and thrombolytics will make them worse. |
| Why are these medications used in early administration. | If pt has MI due to a blood clot in a cardiac vessel, give tPA within 12 hours.If a person suffers a stroke, give medication within 3 hours. cuz tissue supplied by the blood vessel dies from the lack of O2, reperfusion cant help necrotic tissue. |
| when are tPAs never given | when a person has active internal bleeding, before major surgeries, after recent trauma, or in people with any history of intracranial bleeding, bleeding disorders, or severe hypertension. |
| Direct thrombin(II) inhibitors like | bivalirudin, lepirudin, and argatroban, which are given intravenously, desirudin, which is given subcutaneously, and dabigatran, which is given peroral. |
| Direct thrombin(II) inhibitors derived from | this class of medications was initially isolated from the saliva of leeches due to its anticoagulant effect. |
| Direct thrombin(II) inhibitors are 2nd line medication after Heparin | in people with a history of deep vein thrombosis to prevent pulmonary embolism, or atrial fibrillation to prevent strokes. Use in heparin induced thrombocytopenia pts |
| heparin-platelet factor 4 leads | leads to platelet activation and aggregation, hence thrombosis. |
| People who experience uncontrolled bleeding from dabigatran | reversal agent called idarucizumab, an antibody, which binds to and inactivates dabigatran can be administered to people who experience uncontrolled bleeding from this medication. |
| direct factor Xa inhibitors | like apixaban, edoxaban and rivaroxaban are all peroral medications. |
| Factor Xa inhibitors are becoming more commonly used for the treatment and prevention of | DVTs, pulmonary embolism, and stroke prevention in patients with atrial fibrillation. e they do not require laboratory monitoring unlike warfarin, have fewer drug interactions, and have a rapid onset of action. |
| direct factor Xa inhibitors Tox and its Reversal | The main toxicity of these medications is also uncontrollable bleeding; the FDA just approved andexanet alfa as a reversal agent for Factor Xa inhibitors. Andexanet alfa binds to factor Xa inhibitors inhibiting them from binding to factor Xa. |
| Factor Xa inhibitors are metabolized by an enzyme called | cytochrome P450, so any medications that inhibit this enzyme like cimetidine, metronidazole, trimethoprim/sulfamethoxazole, and amiodarone, can cause the accumulation of these medications in the body, leading to bleeding. |
| Neural Crest Derivatives MOTEL PASSES | Melanocytes, Odontoblasts, Tracheal lining, Enterochromaffin cells, Leptomeninges (arachnoid, pia), PNS ganglia, ( Adrenal medulla, Schwann cells, Spiral membrane (aorticopulmonary septum), Endocardial cushions, Skull bones. |
| Enterochromaffin (EC) cells | also known as Kulchitsky cells) a neuroendocrine cell. They reside alongside the epithelium lining the lumen of the digestive tract and play a crucial role in gastrointestinal regulation, particularly intestinal motility and secretion. |
Created by:
DrInsitu
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