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Anemia, Thromboses, Blood Cancers

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
Created by: glittershined