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USMLE - Pharm
Kaplan Section 8 - Review
| Question | Answer |
|---|---|
| What does PT measure? | Prothrombin Time. Extrinsic coag pathway. Measures clotting tendency of blood, using levels of warfarin dosage, liver damage, and VitK status. |
| How is PT conducted? | blood + citrate in the tube (binds Ca2+) --> prevent coag. Separate blood cells from plasma. Ca2+ + plasma + tissue factor --> clotting. PT is time of plasma to clot after addition of tissue factor. |
| What is the reference range for PT? | 12 to 15 seconds |
| What factor is the extrinsic pathway most dependent upon? | Factor 7 (short half life, requires VitK for synthesis) |
| What happens to PT if patient is deficient in VitK? | lengthened PT time |
| How can a pt become VitK deficient? | warfarin, malabsorption or lack of intestinal colonization by bacteria (such as in newborns), liver dz (poor synthesis of factor 7), increased consumption of Factor 7 (DIC) |
| What is INR? | international normalized ratio: ratio of patient's PT to a normal control sample, raised to the power of the ISI sample, which is the tissue factor sensitivity index, used in the PT assay |
| What is the reference range for INR? | 0.8-1.2 |
| What does PTT measure? | Intrinsic Pathway. Partial Thromboplastin Time. Measures time to clot in the intrinsic and common coag pathways. Monitors heparin therapy. |
| How is PTT conducted? | blood + citrate in the tube (binds Ca2+) --> prevent coag. Separate blood cells from plasma. Ca2+ + plasma + phospholipid --> clotting. PPT is time of plasma to clot after addition of Ca nd phospholipid. |
| What is the reference range for PTT? | 25 to 39 seconds |
| What factors lengthen a PTT? | Heparin, deficiency in coag factors (hemophilia), antiphospholipid antibody (lupus anticoag --> more tendency toward thrombus) |
| Patient is on warfarin. Will Cimetidine increase or decrease that patient's PT? | Cimetidine inhibits CYP450. Warfarin is metabolized by CYP450. Cimetidine ----| CYP450 --> dec warfarin metabolism --> more warfarin in blood --> PT time increases |
| What do selective COX2 inhibitors do to prothrombin time? | increase PT time when used with warfarin. Inhibit EC fxn --> less coag. |
| What happens to warfarin if used in conjunction with ASA/cimetidine/metronidazole/phenytoin/sulfonamides? | warfarin's actions increased (they bind to plasma proteins with greater affinity, so they displace the bound warfarin --> more unbound, active warfarin) |
| What happens to warfarin if used in conjunction with barbiturates/carbamazepine/cholestyramine/rifampin/thiazides/vitamin K? | warfarin's actions decreased! |
| T or F: alpha1 blockers improve sx's of BPH and urinary flow rate | TRUE; e.g. doxazosin; relaxes sphincters |
| What is aminocaproic acid? | anti-fibrinolytic! binds to plasminogen --> prevent its activation to plasmin --> can't break up fibrin clots. Used to treat bleeding disorders. |
| What is used to increase thyroid gland vascularity peroperatively? | KI + Iodine (Lugol's solution) |
| Thyroxine is…. | T4 |
| Deferoxamine | antidote to Fe poisoning (chelates Fe) |
| Can you combat oral Fe poisoning with activated charcoal? | no you can't |
| How long does it take to reach the peak effect of heparin? | several hours |
| What is the cause of megaloblastic anemia? | Vit B12 or folate deficiency (give folic acid for treatment) |
| What is protamine? | Antidote to heparin |
| Someone on chemotherapy complains of bladder irritation with hematuria. What are they on? | Cyclophosphamide - hemorrhagic cystitis (cyclophosphamide --> cyp450 --> acrolein produced --> irritates bladder epith |
| Why do patients on methotrexate also complain of urinary tract problems? | methotrexate has low water solubility --> crystalluria |
| NEUROgenic diabetes insipidus | decreased response of ADH receptors |
| What is used to treat NEUROgenic diabetes insipidus? | desmopressin - replaces ADH, but selective V2 activator in the kidney (V1 activation in smooth muscle leads to vasoconstriction, which we don't want) |
| What is used to treat NEPHROgenic diabetes insipidus? What is the exception? | thiazides except when induced by Lithium (in that case, prefer amiloride because thiazides increase blood levels of lithium!) |
| Misoprostol | PGE1 analog; abortifacient |
| Dinoprostol | PGE2 analog; abortifacient |
| Flutamide | androgen receptor antag; used in prostate CA |
| Garlic breath | arsenic poisoning |
| wrist drop | lead poisoning |
| red/black feces | lead poisoning |
| rice water stool | arsenic poisoning |
| tinnitus | lead poisoning |
| Skin pigmentation | arsenic poisoning |
| stocking glove neuropathy | arsenic poisoning |
| In Type 2 diabetes patient, which is most likely to cause hypoglycemic rxns? Acarbose, glucagon, glyburide, metformin, and rosiglitazone | Acarbose - prevent post prandial hyperglycemia; glucagon - hyPERglycemia; metformin & rosiglitazone - euglycemic - bring blood sugar to normal; sulfonylureas stimulate insulin release & therefore more likely to cause hyPOglycemia |
| abciximab | bind glycoprotein receptors 2a/3b on platelets--> prevent fibrinogen cross-linking --> antiplatelet action |
| IFN alpha | bind mu opioid receptors --> analgesic and release PGE2 --> fever |
| aldesleukin | IL2 --> stimulate T cell growth |
| filgrastim | G-CSF --> stimulate proliferation and differentiation of granulocytes --> increase neutrophils (used to treat neutropenia) |
| trastuzumab (Herceptin) | monoclonal antibody that binds the HER2/neu receptor --> arrests cells in G1 --> decrease proliferation. Inhibits angiogenesis --> regression in breast cancer. |
| What to give to protect against the toxicity of methotrexate? | Leucovorin rescue (folinic acid) -- provides active form of folate to non-neoplastic cells |
| What to give to protect against the toxicity of cyclophosphamide? | Mercaptoethanesulfonate (mesna) -- inactivates acrolein --> protect against hemmorrhagic cystitis |
| What to give to protect against the toxicity of doxorubicin? | Dexrazoxane (free radical trapping agent) -- reduces the cardiotoxicity of doxorubicin |
| How does the level of extracellular K+ affect insulin requirement? | inc extracellular K+ (e.g. spironolactone --> hyperK+) --> doesn't interfere w insulin release from pancreatic B cells. Dec extracellular K+ --> drive K+ out of cells --> maintain hyperpolarization --> prevent insulin release --> inc insulin requirement. |
| Stress situations increase or decrease insulin requirement? | increase |
| Furosemide increase or decrease insulin requirement in diabetic patient? | increase (K+ wasting because loop diuretic -- acts in TAL) |
| Hydrochlorothiazide increase or decrease insulin requirement in diabetic patient? | increase (K+ wasting because thiazide diuretic -- acts in DCT) |
| Prednisone increase or decrease insulin requirement in diabetic patient? | glucocorticoids increase insulin requirement (like stress) |
| Bleomycin | Acts in G2; anti-cancer cytotoxic; causes blisters on hands and feet (palms and soles); BLeo - BListers! |
| HGPRT | hypoxanthine guanine phosphorybosyl transferase --> activates purine synthesis as well as 6-mercaptopurine (drug that blocks purine synthesis); resistance to this drug = decrease in HGPRT activity |
Created by:
christinapham
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