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ClinMed2_Test1
Anemia, Thromboses, Blood Cancers
| Question | Answer |
|---|---|
| Hgb <12 Hct <35% | Anemic woman |
| Hgb <14 Hct <40% | Anemic man |
| Hgb: Hct ratio | 1:3 |
| Volume of packed rbcs | Hematocrit |
| Molecule which binds/transports O2 | Hemoglobin |
| RBC lifespan | 120days |
| Old rbcs removed by this organ | Spleen |
| Hb: 14-18 Hct: 40-50% | Normal male blood values |
| Hb: 12-16 Hct: 35-45% | Normal female blood values |
| Most immature rbc which will become pronucleates then nucleus will disintegrate forming a reticulocyte | Pronormoblasts |
| What eventually mature into rbcs after 1-2 days | Reticulocytes |
| Retic count shows what "Lots of blue=new" | RBC production _Normal: .5-2.5% |
| Reticulocytosis | >2.5% retic count aka Polychromasia |
| Normal MCV values | 80-100 MCV: Hct/rbc count |
| Gives "cytic" values | MCV: Hct/rbc count |
| Gives "chromic" values | MCH: Hgb/rbc count |
| Normal MCH values | 26-34 |
| MCHC | Hgb/Hct Normal: 32-36 |
| Normal MCHC values | 32-36 |
| Indicator of degree of variation in size of rbcs. Normal=11-15% | Red Cell Distribution Width (RDW) |
| Normal RDW | 11-15% >15% Anisocytosis |
| Anisocytosis classified as | >15% RDW |
| When do you typically notice anemic symptoms in a sudden onset patient | Hgb <10 |
| When do you typically notice anemic symptoms in a gradual onset patient | Hgb <7-8 |
| Fatigue, weakness, syncope, DOE, palpitations, headache, Pica | Sx of anemia |
| Pallor, INC pulse, DEC BP, Systolic cardiac murmur, hyperdynamic cardiac impulse, Heme in stool if anemic for blood loss | Physical exam signs of anemia |
| Glossitis, Cheilitis, Koilonychia are all late signs of this | Anemia |
| MOST common cause of hypochromic, microcytic anemia | Iron Deficiency Anemia |
| This disease is usually normochromic, normocytic, but can be microcytic, hypochromic | Anemia of Chronic Disease |
| Menstrual blood loss, INC iron requirements, GI blood loss, DEC iron absorption (celiac disease/post gastrectomy), and lactation/pregnancy can all cause this | Iron Deficiency Anemia |
| Pt has celiac disease, at risk for? | Iron Deficiency Anemia |
| Pt is post-gastrectomy, at risk for? | Iron Deficiency Anemia |
| Pt has GI blood loss at risk for? | Iron Deficiency Anemia |
| Initially normal MCV, becomes hypochromic(<26), microcytic(MCV<80) RBCs with INC RDW | Iron Deficiency Anemia |
| Special tests for Iron Deficiency Anemia: _Initially normal MCV, becomes hypochromic(<26), microcytic(MCV<80) RBCs with INC RDW | Serum Ferritin: first to fall in Fe deficiency Serum Fe <50 TIBC >450 BMM Biopsy shows absent iron stores |
| This is NOT a first line test for Iron Deficient anemia | BMM biopsy; do serum ferritin & TIBC+Serum Fe first |
| What commonly presents w/anemia | Colon or upper GI malignancy |
| Anemic patient would you recommend endoscopy or radiograph? | Yes to determine underlying cause of deficiency |
| How would you treat Iron Deficient Anemia _Initially normal MCV, becomes hypochromic(<26), microcytic(MCV<80) RBCs with INC RDW | Treat underlying cause Replace Iron Stores: orally w/ferrous sulfate or IM for pts intolerant of oral iron or can't absorb |
| When would you use a blood transfusion to treat Iron Deficient Anemia? _Initially normal MCV, becomes hypochromic(<26), microcytic(MCV<80) RBCs with INC RDW | If cerebrovascular or cardiopulmonary compromised _Not recommended |
| Congenitally DEC production of alpha or beta globulin chains of Hb. Occurs in mediterranean, african, arabs, indian, asian descent. | Thalassemias |
| Mild microcytosis seen due to decreased function of this many alpha genes in alpha-thalassemia | Defect of one alpha gene |
| Mild hypochromic, microcytic anemia seen due to decreased function of this many alpha genes in alpha-thalassemia | Defect of two alpha genes |
| Hemolytic anemia, splenomegaly seen due to decreased function of this many alpha genes in alpha-thalassemia | Defect of three alpha genes _Hgb H disease |
| Hydrops fetalis (still birth) seen due to decreased function of this many alpha genes in alpha-thalassemia | Defect of four alpha genes |
| Reduced or absent beta-globulin chains | Beta Thalassemia |
| Dysfunction of one b-globulin chain. Asymptomatic: hypochromic (<26), microcytic(<80) anemia | Thalassemia Minor |
| Severe dysfunction of both b-globulin chains. Most pt's die by thirty | Cooley's Anemia: Thalassemia Major |
| Microcytic(<80), hypochromic(<26) w/poikilocytosis, target cells, nucleated RBCs. NORMAL RDW | Thalassemia |
| Pt has Thalassemia what would you expect of their MDW | Normal MDW |
| Pt has Iron Deficiency Anemia what would you expect of their MDW | Anisocytosis (>15% MDW) |
| Treatment for Thalassemia: Microcytic(<80), hypochromic(<26) w/poikilocytosis, target cells, nucleated RBCs. NORMAL RDW | Transfusions _Keep Hgb>9 to prevent skeletal deformities/fractures _Possible splenectomy by removing site of extravascular hemolysis _Iron Chelation therapy for long-duration transfusions |
| What should you check first in microcytic anemia | Serum Ferritin: Low(Iron deficient), Normal then check serum Fe & TIBC |
| Common in longstanding inflamm dz, malignancy, autoimmune disorders, chronic infection. | Anemia of chronic dz |
| Normocytic, normochromic w/microcytes present. Ferritin is normal. NO dx lab test but pt is anemic | Anemia of chronic dz |
| Treatment of anemia of chronic dz: normochromic, normocytic | Treat underlying cause Epo may help |
| Acquired disorder of hematopoietic stem cells leading to refractory anemia. Idiopathic or secondary to radiation, chemo, toxin. Can progress to BMM failure or leukemia. | Myelodysplastic Syndrome |
| Abnormal RBC iron metabolism hereditary or acquired by drugs, lead toxicity, malignancy, chronic inflammation or infection | Sideroblastic Anemia |
| Marked anisocytosis/poikilocytosis with RINGED sideroblasts. Serum ferritin normal as is BMM. See IRON DEPOSITS. | Sideroblastic Anemia |
| Tx of Sideroblastic Anemia | Treat underlying cause Supportive Therapy |
| Fe very low, TIBC INC. FE/TIBC<16% | Iron Deficiency Anemia |
| Fe and TIBC are normal | NOT Iron deficiency |
| Fe and TIBC are both low | Anemia of chronic disease |
| Fe is high, TIBC is normal | Thalassemia |
| Normochromic, normocytic anemia with INC retic count | Prior/recent hemorrhage or recent hemolysis |
| Normochromic, normocytic anemia with normal retic count. BMM is normal. | Anemia of chronic dz Hypothyroidism Liver Disease |
| Normochromic, normocytic anemia with normal retic count. BMM is ABnormal. | Myelofibrosis Leukemia Myeloma Metastases Renal Failure |
| Large # of reticulocytes (INC RBC) and RBC clumping can mimick large RBCs giving false values for this | MCV. Not really macrocytic |
| Defective DNA synth-->disordered rbc maturation-->cytoplasmic RNA-->INC rbc. | Megaloblastic anemia: folate or B12 deficient _Smear/BMM will be identical |
| What should you always replace in macrocytic anemias to prevent subacute degeneration of the spinal cord. | B12(Cobalamin) |
| Only available from diet, need 1-2ug. Bound to IF in gastric parietal cells & is release in ileum where it's absorbed | B12(Cobalamin) |
| Intrinsic factor deficiency causing B12 malabsorption & megaloblastic anemia | Pernicious Anemia (B12 Def) _Megaloblastic |
| Autoantibodies against gastric parietal cells impairing IF secretion & gastric acid secretion. | Pernicious Anemia (B12 Def)(Autoimmune disorder) _Megaloblastic |
| Partial or complete gastrecetomy can prevent IF secretion causing this | Pernicious Anemia(B12 Def) _Megaloblastic |
| Ileal disease or resection, bacterial growth or intestinal parasites which prevent B12 absorption cause this | Pernicious Anemia(B12 Def) _Megaloblastic |
| Pt presents w/glossitis, jaundice, splenomegaly & typical anemia sx. See decreased vibratory & position sense, ataxia, parasthesias, confusion & dementia | Pernicious Anemia(B12 Def) _Megaloblastic -Low serum B12 level _Pos Schilling Test or Ab's to IF _INC methylmalonic acid AND homocysteine |
| Hypersegmented PMN, macro-ovalocytes, anisocytosis, poikilocytosis. | Pernicious Anemia (B12 Def) -Low serum B12 level _Pos Schilling Test or Ab's to IF _INC methylmalonic acid AND homocysteine |
| Positive Schilling test or Ab's to IF | Pernicious Anemia (B12 defic) _Megaloblastic |
| INC serum methylmalonic acid AND homocysteine | Pernicious Anemia (B12 defic) _Megaloblastic *B12 has BOTH levels INC* |
| Tx of B12 deficiency (Pernicious Anemia) | Parenteral B12. Do NOT treat w/folic acid alone |
| Average daily need of Folic Acid | 200ug/day. INC to 400-800 if pregnant or trying to conceive. |
| How long does it take for folic acid def to cause macrocytic anemia? | 4-5months |
| Alcholism Anti-Convulsants Twd End of Pregnancy Malabsorption syndromes Hemolytic anemias (including sickle cell) | Folic acid deficiency _Macrocytic |
| Anemic w/low serum folate, INC homocysteine, normal methylmalonic acid | Folic acid deficiency _Macrocytic |
| When would you use homocysteine & methylmalonic acid testing? | When B12 and Folate levels are equivocal and want to differentiate deficiency |
| How would you treat folic acid defic(macrocytic) | Treat underlying cause First make sure not B12 deficiency Replace folate:1 mg or 5mg malabsorption |
| RBC survival btwn 20-100days can or cannot be compensated by BMM production | Can be compensated. <20days survival cannot. |
| Anemic, shortness of breath, jaundice, bilirubin gallstones, increase risk of infection w/salmonella & pneumo | Hemolytic Anemia |
| Destruction of rbcs within bloodstream | Intravascular hemolysis _Macro & Microangiopathic syndrome(fragment), G6PD Defic, Paroxysmal Nocturnal Hemoglobinuria |
| Destruction of rbcs within spleen(reticuloendothelial system) | Extravascular hemolysis |
| INC retic count (polychromasia), w/immature rbcs, nucleated rbcs, schistocytes(fragmented rbcs). | Hemolysis _INC unconj bilirubin, serum LDH, plasma Hgb, Hemoglobinuria. |
| INC unconj bilirubin, serum LDH, plasma Hgb, Hemoglobinuria. Serum Haptoglobin is low | Intravascular Hemolysis _Macro & Microangiopathic syndrome(fragment), G6PD Defic, Paroxysmal Nocturnal Hemoglobinuria _INC retic count(polychromasia), schistocytes |
| INC unconj bilirubin, serum LDH, plasma Hgb, Hemoglobinuria. Serum Haptoglobin is normal | Extravascular Hemolysis _INC retic count(polychromasia), schistocytes |
| Mucoprotein made in liver, binds Hgb, released from lysed rbcs. Will be low in INTRAvascular hemolysis | Serum Haptoglobin |
| Traumatic (MACROangiopathic) from prosthetic heart valve | Intravascular Hemolysis _Fragment Syndrome (Schistocyte) |
| MICROangiopathic hemolysis caused by rbc destruction from fibrin strands in vessels | Intravascular Hemolysis _Fragment Syndrome (Schistocyte) |
| G6PD Deficiency-->Heinz bodies(oxid damage & Hgb precipitates) | Intravascular Hemolysis _RBC Enzyme Defect |
| Paroxysmal Nocturnal Hemolgobinuria | Intravascular Hemolysis |
| Hereditary Spherocytosis. Positive Osmotic Fragility Test | Extravascular Hemolysis |
| Positive Osmotic Fragility Test | Hereditary Spherocytosis _Extravascular Hemolysis |
| Sickle Cell Anemia | Extravascular Hemolysis |
| Autoimmune hemolytic anemia cuased by IgG. Positive Coombs test (DAT) | Extravascular Hemolysis |
| Positive Coombs test (DAT) | Autoimmune Hemolytic Anemia _Extravascular Hemolysis |
| Incompatible blood transfusion | Extravascular Hemolysis |
| Drug-induced hemolytic anemia | Extravascular Hemolysis |
| Auto Dominant disorder w/mild hemolytic anmeia. Normal MCV but DEC surface A. RBCs DENSE, GLOBULAR, lack central pallor. Not deformable & get caught in spleen. | Hereditary Spherocytosis |
| RBC life span is reduced in pts w/a spleen and normal in splenectomized pts | Hereditary Spherocytosis Auto Dominant disorder w/mild hemolytic anmeia. Normal MCV but DEC surface A. RBCs Hereditary Spherocytosis _DENSE, GLOBULAR, lack central pallor. Not deformable & get caught in spleen. |
| Chronic hemolysis creates need for INC folate. If intake not adequate a megaloblastic anemia can develop. Positive osmotic fragility test. | Hereditary Spherocytosis _Auto Dominant disorder w/mild hemolytic anmeia. Normal MCV but DEC surface A. RBCs Hereditary Spherocytosis _DENSE, GLOBULAR, lack central pallor. Not deformable & get caught in spleen. |
| Positive Osmotic Fragility Test | Hereditary Spherocytosis Auto Dominant disorder w/mild hemolytic anmeia. Normal MCV but DEC surface A. RBCs Hereditary Spherocytosis _DENSE, GLOBULAR, lack central pallor. Not deformable & get caught in spleen. |
| Treatment of choice for hereditary spherocytosis: (pos osmotic fragility) | Splenectomy which restores rbc lifespan to normal & removes risk of future bilirubin gallstones. Give w/pneumococcal vaccine since increased risk. Delay splenectomy till adulthood. |
| Hereditary Hgb structure disorder transmitted through Auto Recessive gene. Hb SS | Homozygous form of Sickle Cell Anemia. Have symptoms. _Sickle cell DISEASE |
| Hereditary Hgb structure disorder transmitted through Auto Recessive gene. Hb S + HbA | Heterozygous form of Sickle Cell Anemia. Have NO symptoms. _Sickle cell trait |
| What are the chances for sickle cell anemia? | 1/4 |
| RBCs become sickle shaped when deoxygenated, cause painful sx that begin at 4-6months. Pt has delayed growth/devo. INC infections. | Sickle Cell Anemia |
| Sx worse w/dehydration, hypoxia, INC altitude, intense exercise | Sickle Cell Anemia |
| Aplasic crisis(sudden DEC in Hb) & Bilirubin gallstones | Sickle Cell Anemia_Chronic Hemolysis |
| MOST common feature of sickle cell | Pain crises in back, ribs, limbs lasting 5-7 days. Tx is analgesics & fluids _Vaso-occlusive ischemic tissue injury |
| Pain crises, Osteonecrosis of femur/humerus heads (bone infarcts), cerebrovascular accident, MI, asplenism, leg ulcers | Vaso-occlusive ischemic tissue injury _Sickle Cell anemia |
| Hgb 5-11, normochromic/normocytic. INC retic count (10-20%). Hgb electrophoresis shows Hb S. Sickled/nucleated RBCs. Target cells. Howell-Jolly bodies. Thrombocytosis | Sickle Cell Anemia |
| Howell-Jolly bodies | Sickle Cell Anemia |
| Tx of sickle cell anemia | Avoid precip factors RBC transfusion Analgesics, fluids, O2 Hydroxyurea to DEC painful crises BMM transplant |
| Hydroxyurea used when | Sickle Cell anemia to suppress BMM function of all cell lines and DEC painful crises incidences |
| Auto-ab that adhere to rbc causing hemolysis by fixing complement & damage to PM. Phagocytoses the rbcs and spherocytes are formed. | Autoimmune Hemolytic Anemia |
| Polychromasia(INC retic count), spherocytosis, nucleated rbc | Autoimmune Hemolytic Anemia |
| Treatment of Hemolysis | ID & Treat underlying Corticosteroids Splenectomy Folic Acid supplements |
| ABO/Rh blood group antigens against rbcs caused by blood transfusion or hemolytic disease of the newborn(erythroblastosis fetalis). Positive Coombs test | Incompatible Blood Transfusion _Causes hemolysis |
| Abnormal BMM stem cells. >50% idiopathic but can be caused by drugs(Benzene,chloramphenicol, chemo), or viruses like Epstein Barr, cytomegalovirus, hepatitis. | Aplastic Anemia |
| What is the hallmark for aplastic anemia? | Pancytopenia _Anemia, leukopenia, thrombocytopenia |
| Pancytopenia & BMM shows NO normoblasts, granulocytes, megakaryocytes. Weak, infections, bleeding. | Aplastic Anemia |
| Tx of Aplastic anemia(pancytopenia w/no precursors) | ID cause Differentiate not another disease Hematology referral for blood component replacement BMM transplant Immunosuppressive |
| Preferred treatment for aplastic anemia | BMM transplant |
| Formation of a blood clot in a deep v. | Deep v thrombosis |
| Obstruction of pulmonary a or one of its branches by thrombus, tumor, air or fat. Originates elsewhere in body | Pulmonary embolism |
| Over 90% of cases of acute pulmonary embolism come from where | Lower extremity |
| Hypercoagulability, vessel wall injury, venous stasis | Virchow's Triad of Venous Thromboembolisms |
| Surgery within 3 months(ie hip fracture), immobilization/prolonged bed rest, pregnancy (DEC protein C & S), malignancy(hypercoagulable) | Risk factors for venous thromboembolisms |
| Factor V Leiden mutation & Prothrombin gene mutation 2 most common risk factors for this | Hypercoagulable state |
| Use of oral contraceptices or hormone replacement therapy (DEC Protein C and S) risk peaks in first year | At risk for venous thromboembolisms |
| Lower extremity trauma | At risk for venous thromboembolisms |
| Catheters, CHF, COPD, Drug-Induced lupus anti-coagulants, estrogen, factor V mut, fractures, immobile, malignancy, OC, prior PE/DVT, post-op, post-pg, preg, Protein C/S defic, trauma, venous stasis, Warfarin | At risk for venous thromboembolisms |
| Form in deep venous system of extremities where injury, stasis, prothrombotic status coincide | Deep vein thrombosis |
| Subclavian v, vena cava, external iliac v, femoral v, ant/post tibial v | Deep veins |
| Previously called superficial femoral v even though NOT superficial | Femoral v |
| Unilaterall extremity swell, pain, discolored, tender. Superficial venous dilation. Palpable cord | Deep venous thrombosis |
| + Homan's sign (calf tender w/dorsiflexed foot) | Deep venous thrombosis |
| Vein & venous valve damage can lead to abnormal blood pooling in the legs. See chronic leg fatigue, swelling, venous ulceration | Post-thrombophlebitic Syndrome |
| Catheter placement | INC risk for Upper Extremity DVT |
| Brachial v, SVC, radial v, ulnar v | Deep veins |
| Wells test greater than/equal to 3 for DVT | High prob of DVT _75% predictive |
| Wells test of 2 for DVT | Mod prob of DVT |
| Wells test of 1 for DVT | Low prob of DVT _96% predictive |
| BMP, CBC, PT/INR ratio, aPPT, D-Dimer | Tests for DVT |
| Measures EXtrinsic coagulation pathway | PT/INR Ratio for DVT (prothrombin time, internat. normalized ratio) |
| Measures INtrinisc coagulation pathway | aPTT(activated partial thromboplastin time) |
| Endog fibrinolysis almost always causes this release from fibrin clot in presence of DVT/PE. Not specific but highly sensitive | D-dimer _INC w/post-op, DVT, Malignancy, Pregnancy |
| Diagnosis of DVT | Imaging _Compression ultrasound (veins will NOT collapse if DVT) _Contrast venography (uncommon) |
| Tx of DVT | Prevent clot movement, PE, recurrent DVT, complications (post-thrombophlebitic syndrome, chronic v insufficiency) |
| Most common cause of pulmonary embolism | DVT travel |
| Fat emboli, Air emboli, amniotic fluid, Talc (IVDU), Parasite eggs(Schistosomiasis) | Cause of pulmonary embolisms |
| Where do blood clots eventually travel causing a PE | Small aa of the lungs |
| PE w/SBP <90 or drop in SBP >40 from baseline longer than 15mins. NOT explained by other dz. Leads to acute R ventricle failure & death | Massive PE |
| Don't meet criteria for massive PE | Submassive PE |
| Shortness of breath, dyspnea on exertion is the most common what in PE | Symptom of PE _Hampton's Hump _S1Q3T3 |
| Tachypnea is the most common what | Sign of PE _Hampton's Hump _S1Q3T3 |
| Wells criteria >6 for PE | High probability of PE _78.4% chance |
| Wells criteria 2-6 for PE | Mod probability of PE _27.8% chance |
| Wells criteria <2 for PE | Low probability of PE _3.4% chance |
| Patient is stable and evaluating for PE | Proceed w/further dx work-up |
| Patient is UNstable and evaluating for PE | O2, IV, BP support, ICU, thrombolytics |
| BMP, CBC, PT/INR, aPPT, D-Dimer, TROPONIN | Dx of PE _Hampton's Hump _S1Q3T3 |
| Reflects acutre RV microinfarction due to INC P, impaired coronary blood flow, hypoxia from PE. Adverse prognostic factor in pts w/acute PE. Shows RV dysfunction | INC troponin for dx of pulmonary embolisms |
| Thrombosis <50y/o, hx of PE, thrombosis in vascular beds, warfarin-induced skin necrosis (shows Protein C deficiency) | Risk of Hypercoagulable state |
| Sinus tachycardia & non-specific T wave changes sign of this | Pulmonary embolism _Hampton's Hump _S1Q3T3 |
| S1Q3T3 _S wave in lead 1, Q wave in lead 3, inverted T wave in lead 3 | The "Classic" ECG for PE _Only seen in <10% pts |
| Pleura based shallow wedge shaped consolidation in pleura indicating pulmonary infarction due to PE-induced atelectasias. Pathognomic for PE but very rare finding | Hampton's Hump in PE seen on chest X-Ray |
| Pulmonary wedge sign in pt's with pre-existing cardiopulm dz | Pulmonary wedge sign (10% pts) |
| Have a NEG lower extremity ultrasound. Rule out PE? | Cannot rule out PE even if negative LE ultrasound |
| Ventilation/Perfusion scan where radioactive gas is inhaled & imaged of pulm tree, then perfuse lungs w/radioactive albumin & see areas of DEC perfusion | V/Q Scan to dx PE _Positive if 1 or more mismatch |
| Diagnostic for PE when intraluminal pulmonary arterial filling defect is surrounded by contrast. | CT Scan _May miss small peripheral emboli(subsegmental emboli) |
| What is the GOLD standard for dx of PE | Angiogram _Though not frequently used bc of CTs _Reserve for pts who have had anticoagulants |
| Most widely used to ID right heart hemodynamic changes that indirectly suggest PE. RV dilation, hypokinesis, INC RV Pressure, marked tricuspid regurg | Echo for PE dx |
| Anticoagulants, Thrombolytics, IVC filter, Prophylactic measures | Tx for Venous Thromboembolisms |
| Initial Venous Thromboembolism tx that inhibits the clotting cascade by inactivating thrombin. Bolus 80 units then IV infuse at 18/hr. Ck CBC daily, aPTT often. Want aPTT 1.5-2x normal. | IV Unfractioned Heparin -S.E: Bleeding, thrombocytopenia -Antidote: Protamine _Use w/Coumadin until INR therapeutic |
| IV unfractioned Heparin antidote | Protamine |
| IV unfractioned Heparin used simult w/this till INR therapeutic | Coumadin(Warfarin) |
| Use for Out-pt tx of DVT and stable PE | Low molecular weight heparin _SC inject QDay or BID _SE: bleeding, thrombocytopenia |
| Cannot be used in pt's w/Creatine clearance <30, elderly, obese to tx PE | Low molecular weight Heparin |
| Long-term tx of VTW. Acts on liver to block Vitamin K dependent coagulant proteins. Monitor PT/INR (INR@2-3 want). | Warfarin (Coumadin) _SE: Bleeding _Antidote: Vitamin K, Fresh frozen plasma _Pregnancy Category X |
| Antidote to Coumadin (Warfarin) | Vitamin K Fresh frozen plasma |
| What should you use till PT/INR is therapeutic in DVT or PE patients | Heparin or Lovenox + Coumadin _Stay on Heparin AT LEAST 5 days or two days after INR btwn 2-3 (whichever longer) |
| Why do you need to administer Heparin during the first few days of coumadin therapy? | Because pt's are prothrombotic while must clear pre-existing clotting factors |
| Pt w/first episode of DVT, how long Coumadin? | Min of 3 months |
| Pt w/first episode of PE, how long Coumadin? | Min of 6 months |
| Pt w/recurrent VTE how long Coumadin? | Lifelong? |
| Pt w/inherited coagulopathy, how long Coumadin? | Lifelong |
| Activates plasminogen to form plasmin leading to quicker lysis of thrombi. Used for unstable pt's w/PE | Thrombolytics _Streptokinase _Urokinase _Recombinant tissue plasminogen activator (re-PA, alteplase) |
| Massive PE & cardiogenic shock, severe hypoxemia, substantial perfusion deficit, RV dysfunction, Extensive DVT | Unstable pt's w/PE _Use Thrombolytics |
| Placed as filter in IVC prevents DVT from going to lungs(IVC filter). Use when? | Recurrent PE despite ok anti-coagulation Anti-coagulation complication(severe bleeding) Hemodynamic or respiratory compromise that's life threatening |
| Sequential compression devices and thromboembolic deterrants can be used for what? | DVT prophylaxis |
| Low dose SQ Heparin & Lovenox can be used for hospitalized pts. Why | Prevent DVT |
| What is a suitable replacement for Heparin for a stable pt w/a DVT or PE (outpatient) | Lovenox |
| Who's responsible for monitoring pt's anti-coagulation | PCP, Cardiologist or Anticoagulation Clinic _MUST have a plan before starting tx |
| Asymptomatic, intermittent claudication, critical leg ischemia | Arterial (Peripheral arterial disease) |
| Venous thrombosis, varicose vv, chronic venous insufficiency | Venous (Peripheral vascular disease) |
| Chronic arterial insufficiency of LE. Most common in elderly & caused by atherosclerosis. | Arterial insuffiency |
| MOST common form of peripheral vascular disease | Arterial insuffiency |
| Shows Peripheral arterial disease | Subtraction angiogram |
| MOST common site of arterial insufficiency | Superficial femoral & popliteal aa |
| 40-50% of patients have arterial insufficiency in this location | Tibial a & peroneal a |
| Where do atherosclerotic plaques occur? | Bifurcations (Femoral) |
| Ischemic pain in lower legs when walking. Crampy, tight sensation in calf when walking or pain in thigh/butt w/aortoiliac dz. Pain resolves @rest or standing still. | Claudication _MAIN Sx of Arterial insuffiency |
| MAIN Sx of Arterial insufficency | Claudication |
| Can only walk one block before claudication | Moderate claudication |
| Can walk >2 blocks before claudication | Mild claudication |
| Can walk <1 block before claudication | Severe claudication |
| Where is claudication more common? | Calves (not usually butt/thighs) |
| Butt, hip, thigh discomfort. Erectile Dysfunction secondary to vascular insufficiency | Leriche Syndrome: aortoiliac disease (arterial insufficiency) |
| Claudication improves when leg in dependent position, worse when leg raised. Numbness/cold as dz progresses. "Rest pain" devo if severe | Arterial insufficiency |
| Leg/foot pain which improves when leg is raised, worse when in dependent position | Venous Insufficiency |
| Sx remain stable or improve w/time due to devo of collateral vessels. Very few actually need surgery/angioplasty. Low risk of losing a limb | Claudication with arterial insufficiency |
| Pt's w/DM are at risk of this when experiencing claudication/arterial insufficiency | Losing a limb (20%) |
| Who has WORST prognosis in arterial insufficiency | Smokers & diabetics |
| Pallor w/raised extremity, dependent rubor(redness), hair loss on legs/feet, artophic skin, ulcers, necrosis/gangrene | Arterial insufficiency _Claudication sx |
| Hear bruits in abdominal aorta, femoral, popliteal aa. Palpable pulse in legs/feet. Cool skin temp. Delayed capillary refill | Arterial insufficiency _Claudication sx |
| Ankle Systolic Pressure/Brachial Systolic Pressure | Ankle-Brachial Index: For Peripheral Vascular Disease (PAD) _Normal: >1 _Mild: .7-.99 _Mod:.5-.69 _Severe: <.5 |
| Treadmill test for ABI to simultaneously test for CAD. Duplex Ultrasound. Doppler wave-form analysis. MR Angiography | Non-Invasive Testing for arterial insufficiency |
| Shows occlusion of proximal superficial femoral profunda femoris | MR Angiography _Non-Invasive Testing for arterial insufficiency |
| Tx for claudication (arterial insufficiency), not drugs. | regular walks as fast/far as possible. Use near max pain as sign to stop. Resume walking when pain gone. Can walk 120-180% further with training (Stop-Start Walking regimen) |
| Risk factor modification for claudication (arterial insufficiency) | Stop Smoking Aggressive lipid lowering therapy Anti-HTN tx |
| Tx for claudication (arterial insufficiency) that's pharma approved | Trental, Pletal, Anti-Platelet agents like aspirin, Ticlid, Plavix |
| Tx for claudication (arterial insufficiency) that's surgical | Endarterectomy Percutaneous transluminal angioplasty Stents Revascularization |
| Removal of atherosclerotic plaque to treat for claudication (arterial insufficiency) | Endarterectomy |
| For localized dz with short segments of obstructing plaque for claudication (arterial insufficiency) | Percutaneous Transluminal Angioplasty(PTA) |
| Alternative to simple angioplasty to treat for claudication (arterial insufficiency) | Stents |
| Aortofemoral bypass graft, femoral-popliteal revascularization, axillary-femoral revascularization | Revascularization Surgery for claudication (arterial insufficiency) |
| Bypass grafts are used for this | Aortoiliac & Femoral-popliteal disease |
| What is the most common graft? | Knitted Dacron grafts |
| Sudden stop of blood flow to extremity caused by embolism(from heart) or thrombus in situ | Acute Arterial Obstruction _ER!! |
| Hypercoagulable state, or external compression of an aa can cause this | Acute Arterial Obstruction _ER!! _Sudden stop of blood flow to extremity |
| Thoracic outlet syndrome | Subclavian a compression-->acute arterial obstruction |
| 5 P's of Acute Obstruction | Pain, Pallor, Parasthesia, Paralysis, Pulselessness |
| Tx of Acute Obstruction | ER Consult Remove thrombus/emboli(thrombectomy/embolectomy) Dissolve embolus/thrombus(thrombolytic infusion) Anticoagulation-heparin Surgical bypass of obstruction |
| Marker for systemic atherosclerosis therefore should undergo a thorough med eval for cardio risk(walking, risk factor mod, pharm trial) | Claudication |
| Initial tx for aortoiliac or iliac disease | Angioplasty or stenting |
| Tx for aortoiliac or iliac disease if longer than 5cm, or concomitant aneurysms & occlusion in common femoral artery | Surgery |
| Femoropopliteal disease initial tx | Prolonged course of medical therapy |
| Caused by arterial vasospasm followed by arterial & capillary dilation. Cold or emotional stress. Goes white(pallor), blue(cyanosis), red(rubor) | Raynaud's Phenomenon |
| Secondary causes for vasoconstriction have been excluded | Raynaud's "Disease" (idiopathic or primary) |
| Collagen vascular diseases: scleroderma, SLE, RA | Collagen Vascular Disease(Secondary Raynaud's Phenom) |
| Buerger's disease, ASCVD | Arterial occlusive disease(Secondary Raynaud's Phenom) |
| Polio, tumors, carpal tunnel | Neuro disorders(Secondary Raynaud's Phenom) |
| Cryoglobulinemia, cold agglutinins | Blood dyscrasia(Secondary Raynaud's Phenom) |
| Vibration injury, repetitive stress | Trauma(Secondary Raynaud's Phenom) |
| Ergotism, methysergide, vinblastine | Drugs(Secondary Raynaud's Phenom) |
| Tx Raynaud's Phenom | Reassure, avoid tobacco use, treat underlying condition _Ca2+ Channel Blockers _Reserpine _Prazosin _Surgical sympathectomy |
| Nifedipine, Diltiazem | Calcium Channel Blocker used for Raynaud's |
| Reserpine | Adrenergic Blocker for Raynaud's |
| Prazosin | Alpha-1 adrenergic blocker for Raynaud's |
| Surgical Sympathectomy | Last resort for Raynaud's tx |
| Pathological dilation of aortic lumen >1.5x normal. Symmetrical dilation involving full circumference | Fusiform aortic aneurysm |
| Pathological dilation of aortic lumen >1.5x normal. More localized, appears as outpouching of a portion of the aortic wall | Saccular aortic aneurysm |
| Most common cause of aortic aneurysm | Atherosclerosis |
| Marfan's Syndrome(thoracic aneurysm) | Connective tissue disease causing aortic aneurysm |
| Mycotic Aneurysms | Infection |
| Pseudoaneurysms | Trauma |
| Cystic Medial degeneration | Disease causing aortic aneurysm |
| Tear in the intima causes blood to enter media which splits longitudinally can involve thoracic and/or abdominal aorta. Can be assoc w/HTN & trauma. | Dissections |
| Acute onset of "tearing" pain in either chest or abdomen, potentially lethal | Dissections |
| Most common site of abdominal aortic aneurysm | Infrarenal abdominal aorta |
| Rupture or dissection, thromboembolism, compromised renal blood flow can be caused by this | Progression of abdominal aortic aneurysm |
| Usually asymptomatic, most common complaint is back pain. If ruptures have abdominal pain, pulsatile abdominal mass, tender, HYPOtension | Abdominal aortic aneurysm |
| Best to screen for abdominal aortic aneurysm | Ultrasound |
| Most accurate for abdominal aortic aneurysm | CT scan. Used to follow size of established abdominal aortic aneurysm (every 6mos) _Ultrasound still preferred |
| Standard study for pre-op eval of collateral vessels | Aortography _Ultrasound still preferred |
| Define size/extent of abdominal aortic aneurysm | MRA (Magnetic Resonance Angiogram) _Ultrasound still preferred |
| Surgical repair w/Dacron graft & percutaneous stent grafts now used. Criteria to repair >5cm. >6cm if high risk patient | Surgical repair of abdominal aortic aneurysm |
| Varicose veins, chronic venous insufficiency, venous thrombosis | Venous Insufficiency |
| Risk of DVT when venous disease where | Deep veins |
| Venous disease in superficial vv | varicosities |
| Dilated, tortuous superficial cc due to defective structure/fcn of valves, weakness of vein walls and/or INC venous pressure | varicose veins |
| Aching or burning sensation in area of varicosities. Tired, Heavy feeling. Worse with standing...relieved by elevation. | Varicose veins |
| Prominent surface veins, superficial thrombosis may devo. Occasional rupture w/bleeding. Stasis dermatitis(dark pigemnt), ulcerations at ankle, edema | Varicose veins |
| Valvular incompetence as a result of deep v thrombosis w/residual damage to v. Recanalization occurs after DVT. Post-phlebitic syndrome develops. | Venous Insufficiency |
| High P devo in distal vv, distending the walls-->further valve incompetence | Venous Insufficiency |
| Tx for Venous Insufficiency(varicose) | Limb elevation: 30mins 3-4x/day Compression Tx with hose(to INC deep venous flow) Intermittent pneumatic compression hose if morbidly obese |
| Wound care for Venous Insufficiency (varicose) | Promote healing, decrease pain Wet dressing, occlusive hydrocolloidal, Zinc paste impregnated bandage(Unna Boot) |
| Medications for Venous Insufficiency | Diuretics to DEC edema. Abx if secondary infection |
| Surgery for Venous Insufficiency | Vein stripping if significant Sclerotherapy for small surface veins Skin grafting for some ulcers |
| Innate immune system | Natural, Non-specific |
| Adaptive immune system | Specific, humoral/cell-mediated |
| Shared in both innate & adaptive immune system | T cells and NKT cells |
| Specific to adaptive immunity | B Cell, CD4 & CD8 T Cells |
| Innate immunity | Macs, granulocytes, NKT, complement, physical barriers |
| Immediate, non-specific response. NO memory. Response does NOT increase w/repeat exposure | Innate Immunity |
| Protects against invasion, acidic pH of sweat, FAs and enzymes from pores/follicles | Skin barrier, part of INNATE immunity |
| Microbial antagonist both external/internal. Compete w/potential pathogens. Upset by abx use | Normal bacteria flora |
| Granulocytes | PMN, Eosinophil |
| Tears, saliva, mucus, gastric secretions(acidic pH) | Mucus Membranes _All contain lysozyme which protects against G+ bacteria |
| Basophils/mast cells share progenitor. Which matures in the marrow? | Basophil |
| Basophils/mast cells share progenitor. Which matures in the tissues? | Mast cells |
| Damaged tissue-->histamine-->vasodilation & leaky capillaries-->cell-mediated heparin release-->decreased clotting | Inflammation process _RESULT: Inc blood flow to area, immun factors leak out of capillaries into interstitial space |
| Least common granulocyte. Circulates in bloodstream. Responds to allergens & helminths. Release histamine & heparin | Basophils |
| Releases histamine & heparin to reduce clotting & inc blood flow resulting from vasodilation | Basophils: least common granulocyte _Responds to allergic & helminth |
| Derived from BMM(1-6% of circulating wbcs) they circulate in bloodstream & present w/organs esp GI & respiratory tract | Eosinophils: granulocyte |
| Release H2O2 & other ROS to kill microbes/viruses/parasites(helminths). Active in allergic rxns, asthma by releasing leukotrienes | Eosinophils: granulocyte |
| Lipid signaling molec that causes airway smooth m contraction | Leukotrienes: released by eosinophils |
| Active in allergic rxns, asthma. Stimulate T-lymphocytes & act as antigen presenting cell. Weak phagocytosis | Eosinophils _stimulate via leukotrienes |
| First responder to bacteria infection & in response release cytokines to amplify immune response | PMN(drawn by cytokines IL & IFN) _Strongly phagocytic |
| Neutrophil extracellular traps (NETs) | PMN "throw out" extracellular fibers that bind bacteria |
| Release histamine & heparin. Mature in tissues & present in those that are boundaries (ie MUCOSA). | Mast cells |
| When will mast cells degranulate & release histamines? | Injured, exposed to complement, activated by ab's binding to antigen |
| Massive release of histamine by mast cells results in this | Anaphylaxis _Body wide vasodilation-->edema, DEC BP etc |
| Gives rise to dendritic cells & macrophages | Monocytes |
| Where do monocytes develop & migrate? | Develop in marrow, migrate to spleen _Devo if stimulated by pathogen |
| Antigen presenting cell | Dendritic cells |
| Capture antigens & migrate to nearest lymph node & present antigen to T & B cells. | Dendritic Cells |
| Specialized DCs in skin | Langerhans Cells |
| Large phagocytes which act as APCs. Have 3 staged of readiness(resting, primed, hyper-activated) | Macrophages |
| Cleaning up of cellular debris is this stage of macrophage | Resting stage |
| More active engulfment of bacteria, display fragments of bacteria for T cells (acting as APCs) is this stage of macrophage | Primed |
| Inflammatory cytokines causes macs to INC & start phag'ing & digesting pathogens/cancerous cells. This stage of macrophage | Hyper-activated |
| Specialized mac's in the liver that destroy bacteria/old rbcs. Chronic activation leads to overproduction of inflamm cytokines & chronic inflammation causing liver damage, CA | Kupffer Cells |
| Toxin, EtOH over-exposure to Kupffer cells results in this | Overproduction of cytokines & chronic inflamm causing liver damage/CA |
| Cytotoxic lymphocytes that don't need to "recognize"/remember a pathogen to kill it. Killing activity INC by cytokines(from mac) | NKT cells |
| Kill their target by releasing perforins & proteases that cause cell membrane lysis/triggering apoptosis in target cell. | NKT Cells _Cytotoxic lymphocytes |
| "on call" cells which operate on a "kill" or "no kill" system. Will kill cells w/unusual surface receptors. Have granules which contain destructive enzymes. Can kill even during rest, but better when activated | NKT Cells _Cytotoxic lymphocytes |
| Activated by antigens to signal to others that defensive immune state needed | Complement _Made by liver |
| Most abundant complement protein in humans | C3 |
| Enhance phag of antigens by marking them for destruction | Opsonization |
| Attract/activate macs, pmn inducing mast/basophils to degranulate | Chemotaxis |
| Rupturing pathogen cell membranes by forming the MAC (Membrane Attack Complex) | Lysis _Disrupts osmotic balance so microbe swells/bursts |
| Responds to bacteria | PMN |
| Eosinophilia/Basophilia want to make sure to ask about this if not allergic related | GI Symptoms (Helminths) |
| See eosinophilia/basophilia. What would you think | Allergens Helminths |
| Anaphylactic shock | Mast cells & Eosinophils & Basophils |
| Allergic rxn | No Mast cells(not anaphylactic) Eosinophils & Basophils |
| Weapons of adaptive immunite | B Cell, T cell, Ab's (from B-cells), APCs, Complement |
| What arises from the B cells? | Antibodies |
| Mediated by lymphocytes to eliminate microbes. (type of Adaptive Immunity) | Humoral Adaptive Immunity |
| Uses DCs in antigenb presentation & activation of other immune cells & cytokines (type of Adaptive Immunity) | Cell-mediated Immunity |
| What secretes antibodies? | Plasma cells |
| How many B cells are made each day? | A billion |
| How many types of ab's can a B cell make? | Only one type of ab _BUT can recognize numerous foreign substances |
| B cell receptor binds to the surface of the foreign antigen | B Cell activation |
| Many B cell receptors binding to an antigen to activate a B cell | Cross linking |
| Main function of ab's | Tag foreign antigens |
| Activated B cells give rise to this | Plasma cells & memory cells |
| Four classes of ab's in blood (GAME on) | IgG, IgA, IgM, IgE |
| Antibodies composed of this | Light & heavy chains |
| How many ab's does a human have | 100 million |
| Ab's DONT kill, but tag antigens for destruction. What does the Fc region do? | Binds to macrophages or other immune cells |
| Ab binds to virus OUTSIDE of cell preventing it entering | Neutralizing ab's |
| Activated Ab's produce these ab's in this order (MAGE) | IgM first, then IgA, IgG, IgE |
| Activated ab's produce this ab first, which is a good complement activator. | IgM _~1day half-life |
| Help "complement" bind to surface bacteria to destroy it | Innate & Adaptive Immunity working together |
| Fc arm of IgM can bind many C1 "complement" triggering this | MORE "complement" |
| This ab is an ok complement fixer, good OPSONIZER. Good at NEUTRALIZING VIRUSES. | IgG ~3 wk halflife |
| This ab can easily pass from mom to fetus via placenta | IgG ~3 wk halflife |
| Has receptors for "Natural Killer" cells to bring them closer to their destruction targets | IgG3 |
| IgG ab pooled from human donors exposed to a virus. Injected to neutralize a virus like HepA | Gamma Globulin Injection |
| MOST abundant Ab class in the body. Guards mucosa surfaces. | IgA |
| "Clipped" tail structure of this ab allows it to traverse the lining of the digestive tract. Good at collecting pathogens & eliminating them thru feces or mucus. POOR complement fixer. | IgA _MOST abundant Ab class in the body. Guards mucosa surfaces. |
| Made on FIRST ALLERGEN exposure | IgE |
| Mast cells have receptors on Fc region for this ab; when this ab(on Mast cell surface) binds to an allergen, signals the mast cell to degranulate & INC immune activity | IgE _Made on FIRST ALLERGEN exposure |
| This ab immune response can cause anaphylactic shock. | IgE _Made on FIRST ALLERGEN exposure |
| Defender against "parasites" | IgE _Made on FIRST ALLERGEN exposure |
| Recognition proteins on T cells extend outside their cell. Will cluster around antigen doing what to T cell | Activating T cell |
| Born in BMM, mature in thymus | T cells _takes a wk to proliferate |
| When can ab's attack viruses? | Only before virus is inside a cell. If inside cell, cannot touch it. |
| Contacts infected cells & induce suicide via killer cells | T cells |
| Work w/ MHC Class II to release cytokins to attack infected cell | Helper T cells |
| Killer T cells that ID/kill infected body cells. Can kill a virus hiding in a cell by assisted suicide. (CD8) | Cytotoxic T Cells _Killer T cells |
| Assist activation of killer T cells. Signals B cells to make ab's. Direct actions of proteins & cytokines like IL2 & INF. (CD4) | Helper T Cells |
| May keep T cells under control | Regulatory T cells |
| These cells signal B cells to make ab's, activates B cells/cytokines. The cytokines will activate macs | Helper T cells |
| Central Function of the Adaptive Immune response? | Antigen Presentation |
| What's the job of APCs? | Activate "killer T cells" & helper T cells |
| What helps present to the T cells? | MHC Class 1 & 2 proteins on the APC |
| Present antigen to T cells. Must properly be presented by this. | MHC(Major Histocompatibility Complex) |
| Bind & form a complex w/proteins from foreign antigens that contain a protein component for T cells to recognize/destroy | MHC(Major Histocompatibility Complex) |
| HLA-A, HLA-B, HLA-C | 3 genes for Class I MHC proteins on Chromosome 6 |
| This MHC class binds/presents proteins functioning as "billboards" that display something foreign has entered the cell | MHC Class I |
| When a virus enters the cell it's broken down in endoplasmic reticulum where some will bind to C1-MHC. What does this do? | Presents the viral protein on the MHC complex as a signal for killer T cells so it can be checked out/killed |
| MHC that is designed to alert helper T cells that an immune battle is occuring | Class II MHC |
| Alerts natural killer T cells | Class I MHC |
| Both MHC are assembled in the endoplasmic reticulum, but for this class the antigen protein fragments are next transported to endosome & mixed w/other antigens/microbes in the cell | Class II MHC |
| For Class II MHC what type of APCs can you have | B cell, DC, Mac |
| 2 most common allergies | Hay Fever & Asthma _IgE ab's for allergies |
| This ab(for allergies) binds to "ANTIGEN cells" causing mast cells to degranulate releasing histamine etc | IgE Ab |
| What do NONallergic people respond to allergens with | IgG Ab (NOT IgE) |
| What do Allergic people respond to allergens with | IgE Ab |
| MHC molecules present peptides derived from "self". B & T cells may have receptors for "self" antigens. | Causes of autoimmune diseases _Frequently occurs after bacterial/viral infections |
| Immune system attacking beta cells of pancreas that occurs mos/yrs before sx occur. Cytotoxic T cells may mount the attack on B cells | Insulin-Dependent DM |
| "Self" reactive ab's bind to receptor for ACh. ACh can no longer bind causing this | Myasthenia Gravis -m weakness/paralysis |
| One of this virus' proteins is similar to ACh receptor proteins. Can activate lymphocytes to attack ACh receptor giving sx of myasthenia gravis. | Poliovirus |
| T cells against "self" w/chronic inflammation destroying myelin sheaths. Macs recruited by T cells also play large role in inflamm. | Multiple Sclerosis _Strong genetic component |
| T cells isolated from MS patients are noted to recognize these 2 viruses | EBV & Herpes |
| Autoimmune dz resulting in inflamed joints. T cells attack cartilage protein. | Rheumatoid Arthritis |
| Joints of rheumatoid arthritis pt's have these complexes which activate macrophages, causing inflammation | IgM-IgG Complexes |
| Macrophages stimulate this in Rheumatoid arthritis which invades the joint space and causes inflammation | TNF |
| Would rather have acute or chronic leukemia? | Chronic leukemia |
| Auer rods in blast cells | AML |
| Aggressive leukemia w/a malignant transformation | Acute leukemia _Grave dx |
| Immature blast cells proliferate abnormally. Accumulate in BMM & spill into peripheral blood circulation | Acute leukemia _Grave dx |
| Many acute leukemia pts are this, making them harder to treat & with poor prognosis | Elderly |
| Most common childhood leukemia, though 20% of adult leukemia | ALL (Acute Lymphocytic Leukemia) _Need >30% peripheral blast cells in marrow to dx |
| 80% of acute leukemias are this | ALL (Acute Lymphocytic Leukemia) _Need >30% peripheral blast cells in marrow to dx |
| Usually this cancer occurs at 4-5 y/o, but can also appear at age 50 | ALL (Acute Lymphocytic Leukemia) _Need >30% peripheral blast cells in marrow to dx |
| Higher in twins, trisomy 21, Klinefelter's, Fanconi's anemia, EBV, Varicella | ALL (Acute Lymphocytic Leukemia) _Need >30% peripheral blast cells in marrow to dx |
| EBV & Varicella associated with this | ALL (Acute Lymphocytic Leukemia) _Need >30% peripheral blast cells in marrow to dx |
| FATIGUE, bruising, bleeding, dyspnea, dizziness, INFECTION, fever, night sweats, weight loss. | ALL (Acute Lymphocytic Leukemia) _Need >30% peripheral blast cells in marrow to dx |
| FATIGUE, bruising, bleeding, dyspnea, dizziness, INFECTION, fever, night sweats, weight loss. Children: Extremity, joint pain may be only sx. | ALL (Acute Lymphocytic Leukemia) _Need >30% peripheral blast cells in marrow to dx |
| Abdominal mass at presentation with this leukemia | B-Cell ALL _Need >30% peripheral blast cells in marrow to dx |
| >30% peripheral blast cells in marrow (normal: <5%) found in immunophenotyping & cytogenic abnormalities | ALL (Acute Lymphocytic Leukemia) |
| Normal amt of peripheral blasts in marrow | <5% |
| Potential targets for cancer tx | T cell surface receptors |
| What makes for a worse prognosis in ALL? | 1)High WBC at dx 2)Advanced age at dx 3)Have B-cell phenotype |
| Tx for ALL | Complex: 1)Induction therapy w/combo chemo 2)Consolidation therapy w/combo chemo 3)Responder Maintenance 4)Anti-CD20, Anti-CD52, Anti-CD33 ab TARGET THERAPY |
| 5 year survival rate in younger patients | 54% _BEST response rate since younger |
| Transplant of cells from donor | Allogeneic transplant _BEST results in first remission |
| Common in ALL | Fatal infections |
| Most common leukemia in adults | AML _More common in men _Pancytopenia(low rbc, wbc, platelets) _Tumor lysis syndrome _Sternal tenderness, organomegaly |
| Avg age of AML patients | 64yrs _AML: Most common leukemia in adults/men |
| Radiation exposure, chemo(melphalan, cyclophosphamide), chloramphenicol, benzene can make you high risk for this | AML _Pancytopenia(low rbc, wbc, platelets) _Tumor lysis syndrome _Sternal tenderness, organomegaly |
| This cancer can occur SECONDARY to MDS(Myelodysplastic syndrome) | AML _Pancytopenia(low rbc, wbc, platelets) _Tumor lysis syndrome _Sternal tenderness, organomegaly |
| FATIGUE, bruising, bleeding, fever, infection, PANCYTOPENIA, TUMOR LYSIS syndrome(spontaneous cell destruction), STERNAL tender | AML _More common in adults/men |
| Difference btwn AML & ALL | AML has Auer rods in blasts (ALL does not) If 3% blasts stain+Sudan Black B dye or MPO in AML |
| Increased blast cells in BMM (>20%), Auer rods in blasts(crystalized granules). 3% blasts stain+ for Sudan Black B dye or MPO+ | AML _Pancytopenia(low rbc, wbc, platelets) _Tumor lysis syndrome _Sternal tenderness, organomegaly |
| When doing MPO+ staining for AML what should you remember | Do NOT do MPO on mature cells |
| Tx of AML | Tx high WBC(>75,000) soon to prevent pulmonary distress or death: med ER Intensive combo chemo |
| Goal of AML tx | Achieve a CR(Complete response)= <5% blasts in marrow, normal platelets, normal WBC |
| Prognosis for trisomy 21 pt with AML | Favorable prognosis |
| Prognosis for younger pt with AML | Respond better to therapy |
| Prognosis for older pt with AML | 32% of pt's >60y/o will die within first 10wks of tx Only 6% will be alive in 36mos after tx |
| If first tx response lasted >12-18mos in AML pt, prognosis | Better long term survival |
| Lymphocytosis | Increase in lymphocytes |
| Beta-2 microglobulin elevated in which cancer? | CLL(Chronic Lymphocytic Leukemia) _Swollen cervical/axillary/inguinal nodes |
| 95% of these pt's are CD20 therefore use target therapy of CD20 for them | CLL(Chronic Lymphocytic Leukemia) _Swollen cervical/axillary/inguinal nodes _INC b2-microglobulin & CD20 |
| Overall what is the majority prognosis for AML | NOT alive in 5yrs |
| Change in LYMPHOCYTE which overtime will replace normal lymphos. High # of these cells in marrow crowd normal. The mutated cells are NOT able to fight infection. | CLL(Chronic Lymphocytic Leukemia) _Swollen cervical/axillary/inguinal nodes _INC b2-microglobulin & CD20 |
| See a clonal expansion of CD5 T and B cells in this cancer | CLL(Chronic Lymphocytic Leukemia) _Swollen cervical/axillary/inguinal nodes _INC b2-microglobulin & CD20 |
| 95% of this cancer is a B cell line malignancy | CLL(Chronic Lymphocytic Leukemia) _Swollen cervical/axillary/inguinal nodes _INC b2-microglobulin & CD20 |
| More people are living with this cancer than any other cancer | CLL(Chronic Lymphocytic Leukemia) _Swollen cervical/axillary/inguinal nodes _INC b2-microglobulin & CD20 |
| Most people with this cancer are 50 y/o or older (~90%) | CLL(Chronic Lymphocytic Leukemia) _Swollen cervical/axillary/inguinal nodes _INC b2-microglobulin & CD20 |
| Mutated tumor suppressor genes; can see chromosome deletions. Exposure to herbicides/pesticides/Agent Orange can be cause | CLL(Chronic Lymphocytic Leukemia) _Swollen cervical/axillary/inguinal nodes _INC b2-microglobulin & CD20 |
| FATIGUE, Infection may be presenting feature. Some pt's have a hemolytic anemia. SWOLLEN cervical & axillary nodes(possible inguinal nodes also) | CLL(Chronic Lymphocytic Leukemia) _Swollen cervical/axillary/inguinal nodes _INC b2-microglobulin & CD20 |
| Lymphocytosis, INC Beta-2 microglobulin | CLL(Chronic Lymphocytic Leukemia) _Swollen cervical/axillary/inguinal nodes _INC b2-microglobulin & CD20 |
| Stem Cell transplant | Tx of choice for CML(Philadelphia Chromosome) |
| Prognosis for CLL(Chronic Lymphocytic Leukemia) pt with lymphocytosis ONLY | Low risk _Live >10yrs |
| Prognosis for CLL(Chronic Lymphocytic Leukemia) pt with lymphocytosis, enlarged nodes, & increased spleen/liver | Intermediate risk _Live 5-7yrs |
| Prognosis for CLL(Chronic Lymphocytic Leukemia) pt with lymphocytosis, anemia, thrombocytopenia | High risk _Live 2-3yrs |
| Tx for CLL(Chronic Lymphocytic Leukemia) | Fludarabine+cyclophosphamide(35% CR) Fludarabine+Anti-CD20 monoclonal ab(63% CR) |
| Do any of the tx for CLL(Chronic Lymphocytic Leukemia) significantly prolong pt survival? | None significantly prolong _Stem Cell transplant=87% CR rate(53% alive in CR at 36mos) |
| Bence Jones protein & INC b2 microglobulin | Multiple Myeloma |
| 90% women effected in this dz which causes rash, lung inflammation, kidney damage, hair loss, paralysis. See IgG ab attacking "self" antigens. Complexes then clog the filtering organs(liver/kidney) | Lupus Erythematosus |
| Ab's in Lupus | IgG |
| Virus enters cell to take over cell to replicate self. Our body will then make specific B, helper T cells, cyto T cells to combat. Virus hides in cell's DNA making it impossible for detection by cyto T cells. Can then constantly mutate/hide from immune | HIV-1-->AIDs |
| Non-tender lymphadenopathy | Hodgkin's Lymphoma |
| Reed-sternberg cells | Hodgkin's Lymphoma |
| Tender lymphadenopathy | Infection |
| What makes up cell proliferation systems in a cell | Proteins |
| How does body protect against cancer cells | 1)Systems to prevent mutation 2)Systems that deal w/mutations once they occur |
| Guards against uncontrolled cell growth. Mutated in many cancers | P53 Tumor suppressor gene |
| Virus that leads to cancer development | HPV causing cervical cancer thru infection |
| Why don't cytotoxic T cells kill cancer cells? | They don't LEAVE the blood but just cannot SEE the tumor(actually protective so we don't attack self). Cancer is always one step ahead of cytotoxic T cell surveillance. |
| Surveillance of the immune system | Cytotoxic T cells |
| Clonal proliferation of early progenitor cells causing EXCESS myeloid, erythroid, megakaryotes. LACK of apoptosis in these cells. | Chronic Myelogenous Leukemia (CML) _Philadelphia Chromosome |
| In this cancer 85-95% have RECIPROCAL translocation of chromosomes 9 and 22 | Chronic Myelogenous Leukemia (CML) _Philadelphia Chromosome _Excess myeloid, erythroid, megakaryotes caused by lack of apoptosis |
| Myeloid stem cell disorder that affects daughter cells | Chronic Myelogenous Leukemia (CML) _Philadelphia Chromosome _Excess myeloid, erythroid, megakaryotes caused by lack of apoptosis |
| Rare in children, median age=65. Incidence will increase with age. 15% of leukemias | Chronic Myelogenous Leukemia (CML) _Philadelphia Chromosome _Excess myeloid, erythroid, megakaryotes caused by lack of apoptosis |
| NO associated chemical exposure, infection. ONLY increased risk with RADIATION | Chronic Myelogenous Leukemia (CML) _Philadelphia Chromosome _Excess myeloid, erythroid, megakaryotes caused by lack of apoptosis |
| Fatigue, EARLY SATIETY, left sided pain(splenomegaly), SOB, fever, drenching night sweats, weight loss. | Chronic Myelogenous Leukemia (CML) _Philadelphia Chromosome _Excess myeloid, erythroid, megakaryotes caused by lack of apoptosis |
| Dx Chronic Myelogenous Leukemia (CML) | Routine CBC _on exam see: splenomegaly, minor lymphadenopathy, hepatomegaly _Philadelphia Chromosome |
| In accelerated or blast phase of this cancer will see: fever, wt loss, WORSEN ANEMIA, THROMBOCYTOPENIA, increase wbcs, IMMATURE MYELOID cells in peripheral blood circulation | Chronic Myelogenous Leukemia (CML) _Philadelphia Chromosome _Excess myeloid, erythroid, megakaryotes caused by lack of apoptosis |
| Establishes the dx of Chronic Myelogenous Leukemia (CML) | Philadelphia Chromosome |
| Tests for Lupus | ANA |
| Three Dz phases of CML | Chronic, Accelerated, Blast _Order of least to most blast cells present in BM |
| How long does a chronic CML Patient typically live? | 5-6yrs <5% blast cells in BM or blood |
| How long does a accelerated CML Patient typically live? | 6-12mos >5% blasts, >20%basophils in blood, fever, splenomegaly, bone pain |
| How long does a blast phase CML Patient typically live? | 3-6 month >30% blasts in blood and BM |
| Best tx for CML | Stem Cell Transplant _If done w/in first 2 yrs of dx, offers potential cure. _Risk: GVHD |
| Other Tx for CML besides stem cell transplant | Interferon Therapy (41% complete remission) Imatinib(63% complete remission): potent inhibitor of Bcr-Abl; works in all dz phases |
| Imatinib | Used for CML tx by inhibiting Bcr-Abl it reverses the fusion of these genes on the chromosomes |
| Malignancy of B-lymphocytes(or plasma cells) that secrete immunoglobulins. What is the disease | Multiple Myeloma _60% of time IgG is malignant |
| Most common immunoglobulin in multiple myeloma when there's monoclonal expansion of plasma cells. | IgG |
| Incidence of Multiple Myeloma | More men than women More common in blacks ~1% of all malignancies |
| Leather tanner, Benzene, Hair Dyes, Formaldehyde, Asbestos, Atomic bomb exposure, rubber/paper-mill/radiology workers. INC risk of? | Multiple myeloma _Bone pain, lesions. Compression fractures _Hypecalcemia-->Renal Failure |
| Bone pain in back/ribs caused by INC osteoclast activity(bone lesions). See compression fracture. Recurrent infection & HYPERcalcemia. 80% have anemia. 25%renal failure caused by HYPERcalcemia | Multiple Myeloma _Bone pain, lesions. Compression fractures _Hypecalcemia-->Renal Failure |
| >10% plamsa cells in BMM >3g/dL of M protein in urine Bence Jones proteinuria INC b2M(beta2 microglobulin) | Multiple Myeloma _Bone pain, lesions. Compression fractures _Hypecalcemia-->Renal Failure |
| Bence Jones proteinuria | Incomplete immunoglobulins containing only LIGHT chain of ab. Found in MULTIPLE MYELOMA pts. _Would also see INC M protein(>3) & b2M |
| Single BEST prognostic(how well you'll do) factor for Multiple Myeloma | beta2microglobulin level _If <3.5 have a better prognosis |
| Multiple Myeloma pt with HIGH LDL(lactic dehydrogenase) | shorter survival |
| Multiple Myeloma pt with LOW plasma RNA levels | shorter survival |
| Multiple Myeloma pt with <3.5g b2M protein | longer survival |
| Multiple Myeloma pt with >3.5g b2M protein | shorter survival |
| Tx for Multiple Myeloma | NO Curative Tx. Just manage & observe as it progresses. _Thalidomide+dexamethasone for untreated pt's |
| Thalidomide+dexamethasone for untreated pt's of this disease gives 70% CR+PR | Multiple Myeloma _Bone pain, lesions. Compression fractures _Hypecalcemia-->Renal Failure |
| Stem cell transplant can increase survival rate in these patients | Multiple Myeloma _Bone pain, lesions. Compression fractures _Hypecalcemia-->Renal Failure |
| Hematopoietic neoplasm arises from B lymphocyte cell lines. Localized in cervical/axillary lymph nodes. Reed-Sternberg cells | Hodgkin's Lymphoma |
| Tumor localized in cervical/axillary lymph nodes | Hodgkin's Lymphoma _B Cell line |
| Reed-Sternberg cells (large cells w/pale cytoplasm & 2 oval nuclei) ESSENTIAL to this dx | Hodgkin's Lymphoma _B cell line _Cervical/axillary lymph nodes _Reed-Sternberg |
| Has a bimodal age distribution: age mid 20's & again in mid 60's | Hodgkin's Lymphoma _B cell line _Cervical/axillary lymph nodes _Reed-Sternberg |
| May be a relationship to this Epstein-Barr virus. Also has smoking link. | Hodgkin's Lymphoma _B cell line _Cervical/axillary lymph nodes _Reed-Sternberg |
| 80% pt's have enlarged CERVICAL NODES, 50% have MEDIASTINAL NODES large too. | Hodgkin's Lymphoma _B cell line _Cervical/axillary lymph nodes _Reed-Sternberg |
| Unexplained fever, drenching night sweats (B Cell Sx). Unexplained wt loss. Will see a pleural effusion if mediastinal mass present. | Hodgkin's Lymphoma _B cell line _Cervical/axillary lymph nodes _Reed-Sternberg |
| Hodgkin's Lymphoma dx | Leukocytosis, slight INC platelets, mild normo anemia. 80% have enlarged cervical nodes. _LFT may be slightly abnormal _INC serum COPPER |
| Dx for Hodgkin's Lymphoma by biopsy | Biopsy LARGEST, most CENTRAL node _Look for REED-STERNBERG _CD15/30 POS _CD20/45 NEG May be seen EBV |
| Nodes on both sides of diaphragm in Hodgkins lymphoma. Prognosis? | Poor prognosis |
| Organ involvement in Hodgkins lymphoma. Prognosis? | Poor prognosis |
| >10cm mediastinal mass in Hodgkins lymphoma. Prognosis? | Poor prognosis |
| Night sweats, fever, weight loss in Hodgkins lymphoma. Prognosis? | Poor prognosis |
| ESR>30(Erythtocyte Sedimentation Rate) in Hodgkins lymphoma. Prognosis? | Poor prognosis |
| Tx of Stage 1/2 Hodgkins lymphoma | Local disease _Radiation |
| Tx of Stage 3 Hodgkins lymphoma | Nodal involvement above/below diaphragm _Radiation +/- Chemo |
| Tx of Stage 4 Hodgkins lymphoma | Extra-Nodal Disease _Combo Chemo |
| Lymphomas are malignant tumors coming from lymph may spread to ANY site in body. Grp of HETEROGENOUS tumors(more than just made up of lymph=other tissues) | Non-Hodgkin Lymphoma |
| Most non-hodgkin lymphoma are made of this cell line | B-Cell origin |
| Most common form of non-hodgkin lymphoma | Follicular Lymphoma |
| This cancer has steadily increased at rate of 4% per year over past 20 yrs with mortality rate rising | Non-hodgkin lymphoma _Unexplained/persistent lymphadenopathy or waxing/waning lymphadenopathy |
| HIV/Drug use leading to a weak immune system increases risk of this | Non-hodgkin lymphoma _Unexplained/persistent lymphadenopathy or waxing/waning lymphadenopathy |
| Infections w/EBV, H Pylori Bacteria, HCV increase this risk | Non-hodgkin lymphoma _Unexplained/persistent lymphadenopathy or waxing/waning lymphadenopathy |
| Most Non-hodgkin lymphoma are this age | >60 y/o |
| Non-hodgkin lymphoma associated w/this | Obesity & Herbicides |
| Unexplained, persistent lymphadenopathy. Waxing & Waning lymphadenopathy | Non-hodgkin lymphoma |
| Dx of Non-hodgkin lymphoma | Cytogenetic studies to see chromosomal abnormality, NHL type |
| Indolent B cell lymphoma _Non-hodgkin lymphoma | Older people |
| Aggressive B Cell lymphoma _Non-hodgkin lymphoma | Older people, 70s |
| Highly aggressive B cell lymphoma _Non-hodgkin lymphoma | Mostly children |
| Highly aggressive T cell lymphoma _Non-hodgkin lymphoma | Young adults |
| Non-hodgkin lymphoma which can remain stable for long period of time | Indolent Lymphoma _Good Prognosis. Survival ~10yrs. Not curable in late stages |
| Non-hodgkin lymphoma which is aggressive | Aggressive Lymphoma _Good potential for curing (30-60%). 50-60% are alive @5yrs. Relapse common at 2yrs |
| Tx of Non-hodgkin lymphoma | Chemo Radiation (w/or w/o chemo) CD20/22/54 Target therapy Vaccines Transplant |
| In children extremity or joint pain may be the only sx of this cancer which is MOST common in kids | ALL _Need >30% peripheral blast cells in marrow to dx _If B Cell: See abdominal mass |
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glittershined
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