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Kaplan Section 8 - Review

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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.  
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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.  
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What is the reference range for PT?   12 to 15 seconds  
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What factor is the extrinsic pathway most dependent upon?   Factor 7 (short half life, requires VitK for synthesis)  
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What happens to PT if patient is deficient in VitK?   lengthened PT time  
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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)  
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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  
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What is the reference range for INR?   0.8-1.2  
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What does PTT measure?   Intrinsic Pathway. Partial Thromboplastin Time. Measures time to clot in the intrinsic and common coag pathways. Monitors heparin therapy.  
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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.  
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What is the reference range for PTT?   25 to 39 seconds  
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What factors lengthen a PTT?   Heparin, deficiency in coag factors (hemophilia), antiphospholipid antibody (lupus anticoag --> more tendency toward thrombus)  
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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  
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What do selective COX2 inhibitors do to prothrombin time?   increase PT time when used with warfarin. Inhibit EC fxn --> less coag.  
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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)  
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What happens to warfarin if used in conjunction with barbiturates/carbamazepine/cholestyramine/rifampin/thiazides/vitamin K?   warfarin's actions decreased!  
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T or F: alpha1 blockers improve sx's of BPH and urinary flow rate   TRUE; e.g. doxazosin; relaxes sphincters  
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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.  
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What is used to increase thyroid gland vascularity peroperatively?   KI + Iodine (Lugol's solution)  
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Thyroxine is….   T4  
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Deferoxamine   antidote to Fe poisoning (chelates Fe)  
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Can you combat oral Fe poisoning with activated charcoal?   no you can't  
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How long does it take to reach the peak effect of heparin?   several hours  
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What is the cause of megaloblastic anemia?   Vit B12 or folate deficiency (give folic acid for treatment)  
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What is protamine?   Antidote to heparin  
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Someone on chemotherapy complains of bladder irritation with hematuria. What are they on?   Cyclophosphamide - hemorrhagic cystitis (cyclophosphamide --> cyp450 --> acrolein produced --> irritates bladder epith  
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Why do patients on methotrexate also complain of urinary tract problems?   methotrexate has low water solubility --> crystalluria  
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NEUROgenic diabetes insipidus   decreased response of ADH receptors  
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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)  
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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!)  
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Misoprostol   PGE1 analog; abortifacient  
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Dinoprostol   PGE2 analog; abortifacient  
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Flutamide   androgen receptor antag; used in prostate CA  
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Garlic breath   arsenic poisoning  
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wrist drop   lead poisoning  
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red/black feces   lead poisoning  
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rice water stool   arsenic poisoning  
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tinnitus   lead poisoning  
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Skin pigmentation   arsenic poisoning  
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stocking glove neuropathy   arsenic poisoning  
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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  
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abciximab   bind glycoprotein receptors 2a/3b on platelets--> prevent fibrinogen cross-linking --> antiplatelet action  
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IFN alpha   bind mu opioid receptors --> analgesic and release PGE2 --> fever  
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aldesleukin   IL2 --> stimulate T cell growth  
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filgrastim   G-CSF --> stimulate proliferation and differentiation of granulocytes --> increase neutrophils (used to treat neutropenia)  
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trastuzumab (Herceptin)   monoclonal antibody that binds the HER2/neu receptor --> arrests cells in G1 --> decrease proliferation. Inhibits angiogenesis --> regression in breast cancer.  
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What to give to protect against the toxicity of methotrexate?   Leucovorin rescue (folinic acid) -- provides active form of folate to non-neoplastic cells  
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What to give to protect against the toxicity of cyclophosphamide?   Mercaptoethanesulfonate (mesna) -- inactivates acrolein --> protect against hemmorrhagic cystitis  
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What to give to protect against the toxicity of doxorubicin?   Dexrazoxane (free radical trapping agent) -- reduces the cardiotoxicity of doxorubicin  
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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.  
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Stress situations increase or decrease insulin requirement?   increase  
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Furosemide increase or decrease insulin requirement in diabetic patient?   increase (K+ wasting because loop diuretic -- acts in TAL)  
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Hydrochlorothiazide increase or decrease insulin requirement in diabetic patient?   increase (K+ wasting because thiazide diuretic -- acts in DCT)  
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Prednisone increase or decrease insulin requirement in diabetic patient?   glucocorticoids increase insulin requirement (like stress)  
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Bleomycin   Acts in G2; anti-cancer cytotoxic; causes blisters on hands and feet (palms and soles); BLeo - BListers!  
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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  
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