Anemia, Thromboses, Blood Cancers
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| Hgb <12 Hct <35% | Anemic woman
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| Hgb <14 Hct <40% | Anemic man
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| Hgb: Hct ratio | 1:3
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| Volume of packed rbcs | Hematocrit
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| Molecule which binds/transports O2 | Hemoglobin
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| RBC lifespan | 120days
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| Old rbcs removed by this organ | Spleen
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| Hb: 14-18 Hct: 40-50% | Normal male blood values
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| Hb: 12-16 Hct: 35-45% | Normal female blood values
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| Most immature rbc which will become pronucleates then nucleus will disintegrate forming a reticulocyte | Pronormoblasts
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| What eventually mature into rbcs after 1-2 days | Reticulocytes
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| Retic count shows what "Lots of blue=new" | RBC production
_Normal: .5-2.5%
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| Reticulocytosis | >2.5% retic count
aka Polychromasia
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| Normal MCV values | 80-100
MCV: Hct/rbc count
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| Gives "cytic" values | MCV: Hct/rbc count
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| Gives "chromic" values | MCH: Hgb/rbc count
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| Normal MCH values | 26-34
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| MCHC | Hgb/Hct
Normal: 32-36
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| Normal MCHC values | 32-36
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| Indicator of degree of variation in size of rbcs. Normal=11-15% | Red Cell Distribution Width (RDW)
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| Normal RDW | 11-15%
>15% Anisocytosis
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| Anisocytosis classified as | >15% RDW
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| When do you typically notice anemic symptoms in a sudden onset patient | Hgb <10
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| When do you typically notice anemic symptoms in a gradual onset patient | Hgb <7-8
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| Fatigue, weakness, syncope, DOE, palpitations, headache, Pica | Sx of anemia
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| Pallor, INC pulse, DEC BP, Systolic cardiac murmur, hyperdynamic cardiac impulse, Heme in stool if anemic for blood loss | Physical exam signs of anemia
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| Glossitis, Cheilitis, Koilonychia are all late signs of this | Anemia
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| MOST common cause of hypochromic, microcytic anemia | Iron Deficiency Anemia
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| This disease is usually normochromic, normocytic, but can be microcytic, hypochromic | Anemia of Chronic Disease
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| 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
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| Pt has celiac disease, at risk for? | Iron Deficiency Anemia
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| Pt is post-gastrectomy, at risk for? | Iron Deficiency Anemia
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| Pt has GI blood loss at risk for? | Iron Deficiency Anemia
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| Initially normal MCV, becomes hypochromic(<26), microcytic(MCV<80) RBCs with INC RDW | Iron Deficiency Anemia
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| 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
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| This is NOT a first line test for Iron Deficient anemia | BMM biopsy; do serum ferritin & TIBC+Serum Fe first
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| What commonly presents w/anemia | Colon or upper GI malignancy
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| Anemic patient would you recommend endoscopy or radiograph? | Yes to determine underlying cause of deficiency
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| 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
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| 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
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| Congenitally DEC production of alpha or beta globulin chains of Hb. Occurs in mediterranean, african, arabs, indian, asian descent. | Thalassemias
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| Mild microcytosis seen due to decreased function of this many alpha genes in alpha-thalassemia | Defect of one alpha gene
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| Mild hypochromic, microcytic anemia seen due to decreased function of this many alpha genes in alpha-thalassemia | Defect of two alpha genes
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| Hemolytic anemia, splenomegaly seen due to decreased function of this many alpha genes in alpha-thalassemia | Defect of three alpha genes
_Hgb H disease
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| Hydrops fetalis (still birth) seen due to decreased function of this many alpha genes in alpha-thalassemia | Defect of four alpha genes
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| Reduced or absent beta-globulin chains | Beta Thalassemia
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| Dysfunction of one b-globulin chain. Asymptomatic: hypochromic (<26), microcytic(<80) anemia | Thalassemia Minor
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| Severe dysfunction of both b-globulin chains. Most pt's die by thirty | Cooley's Anemia: Thalassemia Major
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| Microcytic(<80), hypochromic(<26) w/poikilocytosis, target cells, nucleated RBCs. NORMAL RDW | Thalassemia
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| Pt has Thalassemia what would you expect of their MDW | Normal MDW
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| Pt has Iron Deficiency Anemia what would you expect of their MDW | Anisocytosis (>15% MDW)
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| 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
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| What should you check first in microcytic anemia | Serum Ferritin: Low(Iron deficient), Normal then check serum Fe & TIBC
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| Common in longstanding inflamm dz, malignancy, autoimmune disorders, chronic infection. | Anemia of chronic dz
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| Normocytic, normochromic w/microcytes present. Ferritin is normal. NO dx lab test but pt is anemic | Anemia of chronic dz
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| Treatment of anemia of chronic dz: normochromic, normocytic | Treat underlying cause
Epo may help
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| 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
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| Abnormal RBC iron metabolism hereditary or acquired by drugs, lead toxicity, malignancy, chronic inflammation or infection | Sideroblastic Anemia
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| Marked anisocytosis/poikilocytosis with RINGED sideroblasts. Serum ferritin normal as is BMM. See IRON DEPOSITS. | Sideroblastic Anemia
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| Tx of Sideroblastic Anemia | Treat underlying cause
Supportive Therapy
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| Fe very low, TIBC INC. FE/TIBC<16% | Iron Deficiency Anemia
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| Fe and TIBC are normal | NOT Iron deficiency
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| Fe and TIBC are both low | Anemia of chronic disease
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| Fe is high, TIBC is normal | Thalassemia
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| Normochromic, normocytic anemia with INC retic count | Prior/recent hemorrhage or recent hemolysis
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| Normochromic, normocytic anemia with normal retic count. BMM is normal. | Anemia of chronic dz
Hypothyroidism
Liver Disease
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| Normochromic, normocytic anemia with normal retic count. BMM is ABnormal. | Myelofibrosis
Leukemia
Myeloma
Metastases
Renal Failure
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| Large # of reticulocytes (INC RBC) and RBC clumping can mimick large RBCs giving false values for this | MCV. Not really macrocytic
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| Defective DNA synth-->disordered rbc maturation-->cytoplasmic RNA-->INC rbc. | Megaloblastic anemia: folate or B12 deficient
_Smear/BMM will be identical
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| What should you always replace in macrocytic anemias to prevent subacute degeneration of the spinal cord. | B12(Cobalamin)
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| Only available from diet, need 1-2ug. Bound to IF in gastric parietal cells & is release in ileum where it's absorbed | B12(Cobalamin)
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| Intrinsic factor deficiency causing B12 malabsorption & megaloblastic anemia | Pernicious Anemia (B12 Def)
_Megaloblastic
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| Autoantibodies against gastric parietal cells impairing IF secretion & gastric acid secretion. | Pernicious Anemia (B12 Def)(Autoimmune disorder)
_Megaloblastic
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| Partial or complete gastrecetomy can prevent IF secretion causing this | Pernicious Anemia(B12 Def)
_Megaloblastic
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| Ileal disease or resection, bacterial growth or intestinal parasites which prevent B12 absorption cause this | Pernicious Anemia(B12 Def)
_Megaloblastic
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| 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
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| 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
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| Positive Schilling test or Ab's to IF | Pernicious Anemia (B12 defic)
_Megaloblastic
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| INC serum methylmalonic acid AND homocysteine | Pernicious Anemia (B12 defic)
_Megaloblastic
*B12 has BOTH levels INC*
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| Tx of B12 deficiency (Pernicious Anemia) | Parenteral B12. Do NOT treat w/folic acid alone
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| Average daily need of Folic Acid | 200ug/day. INC to 400-800 if pregnant or trying to conceive.
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| How long does it take for folic acid def to cause macrocytic anemia? | 4-5months
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| Alcholism Anti-Convulsants Twd End of Pregnancy Malabsorption syndromes Hemolytic anemias (including sickle cell) | Folic acid deficiency
_Macrocytic
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| Anemic w/low serum folate, INC homocysteine, normal methylmalonic acid | Folic acid deficiency
_Macrocytic
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| When would you use homocysteine & methylmalonic acid testing? | When B12 and Folate levels are equivocal and want to differentiate deficiency
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| How would you treat folic acid defic(macrocytic) | Treat underlying cause
First make sure not B12 deficiency
Replace folate:1 mg or 5mg malabsorption
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| RBC survival btwn 20-100days can or cannot be compensated by BMM production | Can be compensated. <20days survival cannot.
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| Anemic, shortness of breath, jaundice, bilirubin gallstones, increase risk of infection w/salmonella & pneumo | Hemolytic Anemia
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| Destruction of rbcs within bloodstream | Intravascular hemolysis
_Macro & Microangiopathic syndrome(fragment), G6PD Defic, Paroxysmal Nocturnal Hemoglobinuria
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| Destruction of rbcs within spleen(reticuloendothelial system) | Extravascular hemolysis
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| INC retic count (polychromasia), w/immature rbcs, nucleated rbcs, schistocytes(fragmented rbcs). | Hemolysis
_INC unconj bilirubin, serum LDH, plasma Hgb, Hemoglobinuria.
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| 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
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| INC unconj bilirubin, serum LDH, plasma Hgb, Hemoglobinuria. Serum Haptoglobin is normal | Extravascular Hemolysis
_INC retic count(polychromasia), schistocytes
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| Mucoprotein made in liver, binds Hgb, released from lysed rbcs. Will be low in INTRAvascular hemolysis | Serum Haptoglobin
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| Traumatic (MACROangiopathic) from prosthetic heart valve | Intravascular Hemolysis
_Fragment Syndrome (Schistocyte)
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| MICROangiopathic hemolysis caused by rbc destruction from fibrin strands in vessels | Intravascular Hemolysis
_Fragment Syndrome (Schistocyte)
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| G6PD Deficiency-->Heinz bodies(oxid damage & Hgb precipitates) | Intravascular Hemolysis
_RBC Enzyme Defect
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| Paroxysmal Nocturnal Hemolgobinuria | Intravascular Hemolysis
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| Hereditary Spherocytosis. Positive Osmotic Fragility Test | Extravascular Hemolysis
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| Positive Osmotic Fragility Test | Hereditary Spherocytosis
_Extravascular Hemolysis
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| Sickle Cell Anemia | Extravascular Hemolysis
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| Autoimmune hemolytic anemia cuased by IgG. Positive Coombs test (DAT) | Extravascular Hemolysis
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| Positive Coombs test (DAT) | Autoimmune Hemolytic Anemia
_Extravascular Hemolysis
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| Incompatible blood transfusion | Extravascular Hemolysis
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| Drug-induced hemolytic anemia | Extravascular Hemolysis
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| 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
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| 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.
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| 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.
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| 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.
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| 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.
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| Hereditary Hgb structure disorder transmitted through Auto Recessive gene. Hb SS | Homozygous form of Sickle Cell Anemia. Have symptoms.
_Sickle cell DISEASE
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| Hereditary Hgb structure disorder transmitted through Auto Recessive gene. Hb S + HbA | Heterozygous form of Sickle Cell Anemia. Have NO symptoms.
_Sickle cell trait
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| What are the chances for sickle cell anemia? | 1/4
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| RBCs become sickle shaped when deoxygenated, cause painful sx that begin at 4-6months. Pt has delayed growth/devo. INC infections. | Sickle Cell Anemia
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| Sx worse w/dehydration, hypoxia, INC altitude, intense exercise | Sickle Cell Anemia
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| Aplasic crisis(sudden DEC in Hb) & Bilirubin gallstones | Sickle Cell Anemia_Chronic Hemolysis
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| 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
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| Pain crises, Osteonecrosis of femur/humerus heads (bone infarcts), cerebrovascular accident, MI, asplenism, leg ulcers | Vaso-occlusive ischemic tissue injury
_Sickle Cell anemia
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| 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
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| Howell-Jolly bodies | Sickle Cell Anemia
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| Tx of sickle cell anemia | Avoid precip factors
RBC transfusion
Analgesics, fluids, O2
Hydroxyurea to DEC painful crises
BMM transplant
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| Hydroxyurea used when | Sickle Cell anemia to suppress BMM function of all cell lines and DEC painful crises incidences
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| Auto-ab that adhere to rbc causing hemolysis by fixing complement & damage to PM. Phagocytoses the rbcs and spherocytes are formed. | Autoimmune Hemolytic Anemia
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| Polychromasia(INC retic count), spherocytosis, nucleated rbc | Autoimmune Hemolytic Anemia
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| Treatment of Hemolysis | ID & Treat underlying
Corticosteroids
Splenectomy
Folic Acid supplements
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| 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
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| Abnormal BMM stem cells. >50% idiopathic but can be caused by drugs(Benzene,chloramphenicol, chemo), or viruses like Epstein Barr, cytomegalovirus, hepatitis. | Aplastic Anemia
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| What is the hallmark for aplastic anemia? | Pancytopenia
_Anemia, leukopenia, thrombocytopenia
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| Pancytopenia & BMM shows NO normoblasts, granulocytes, megakaryocytes. Weak, infections, bleeding. | Aplastic Anemia
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| Tx of Aplastic anemia(pancytopenia w/no precursors) | ID cause
Differentiate not another disease
Hematology referral for blood component replacement
BMM transplant
Immunosuppressive
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| Preferred treatment for aplastic anemia | BMM transplant
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| Formation of a blood clot in a deep v. | Deep v thrombosis
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| Obstruction of pulmonary a or one of its branches by thrombus, tumor, air or fat. Originates elsewhere in body | Pulmonary embolism
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| Over 90% of cases of acute pulmonary embolism come from where | Lower extremity
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| Hypercoagulability, vessel wall injury, venous stasis | Virchow's Triad of Venous Thromboembolisms
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| Surgery within 3 months(ie hip fracture), immobilization/prolonged bed rest, pregnancy (DEC protein C & S), malignancy(hypercoagulable) | Risk factors for venous thromboembolisms
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| Factor V Leiden mutation & Prothrombin gene mutation 2 most common risk factors for this | Hypercoagulable state
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| Use of oral contraceptices or hormone replacement therapy (DEC Protein C and S) risk peaks in first year | At risk for venous thromboembolisms
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| Lower extremity trauma | At risk for venous thromboembolisms
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| 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
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| Form in deep venous system of extremities where injury, stasis, prothrombotic status coincide | Deep vein thrombosis
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| Subclavian v, vena cava, external iliac v, femoral v, ant/post tibial v | Deep veins
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| Previously called superficial femoral v even though NOT superficial | Femoral v
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| Unilaterall extremity swell, pain, discolored, tender. Superficial venous dilation. Palpable cord | Deep venous thrombosis
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| + Homan's sign (calf tender w/dorsiflexed foot) | Deep venous thrombosis
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| Vein & venous valve damage can lead to abnormal blood pooling in the legs. See chronic leg fatigue, swelling, venous ulceration | Post-thrombophlebitic Syndrome
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| Catheter placement | INC risk for Upper Extremity DVT
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| Brachial v, SVC, radial v, ulnar v | Deep veins
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| Wells test greater than/equal to 3 for DVT | High prob of DVT
_75% predictive
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| Wells test of 2 for DVT | Mod prob of DVT
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| Wells test of 1 for DVT | Low prob of DVT
_96% predictive
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| BMP, CBC, PT/INR ratio, aPPT, D-Dimer | Tests for DVT
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| Measures EXtrinsic coagulation pathway | PT/INR Ratio for DVT
(prothrombin time, internat. normalized ratio)
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| Measures INtrinisc coagulation pathway | aPTT(activated partial thromboplastin time)
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| 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
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| Diagnosis of DVT | Imaging
_Compression ultrasound (veins will NOT collapse if DVT)
_Contrast venography (uncommon)
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| Tx of DVT | Prevent clot movement, PE, recurrent DVT, complications (post-thrombophlebitic syndrome, chronic v insufficiency)
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| Most common cause of pulmonary embolism | DVT travel
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| Fat emboli, Air emboli, amniotic fluid, Talc (IVDU), Parasite eggs(Schistosomiasis) | Cause of pulmonary embolisms
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| Where do blood clots eventually travel causing a PE | Small aa of the lungs
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| 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
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| Don't meet criteria for massive PE | Submassive PE
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| Shortness of breath, dyspnea on exertion is the most common what in PE | Symptom of PE
_Hampton's Hump
_S1Q3T3
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| Tachypnea is the most common what | Sign of PE
_Hampton's Hump
_S1Q3T3
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| Wells criteria >6 for PE | High probability of PE
_78.4% chance
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| Wells criteria 2-6 for PE | Mod probability of PE
_27.8% chance
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| Wells criteria <2 for PE | Low probability of PE
_3.4% chance
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| Patient is stable and evaluating for PE | Proceed w/further dx work-up
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| Patient is UNstable and evaluating for PE | O2, IV, BP support, ICU, thrombolytics
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| BMP, CBC, PT/INR, aPPT, D-Dimer, TROPONIN | Dx of PE
_Hampton's Hump
_S1Q3T3
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| 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
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| Thrombosis <50y/o, hx of PE, thrombosis in vascular beds, warfarin-induced skin necrosis (shows Protein C deficiency) | Risk of Hypercoagulable state
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| Sinus tachycardia & non-specific T wave changes sign of this | Pulmonary embolism
_Hampton's Hump
_S1Q3T3
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| 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
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| 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
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| Pulmonary wedge sign in pt's with pre-existing cardiopulm dz | Pulmonary wedge sign (10% pts)
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| Have a NEG lower extremity ultrasound. Rule out PE? | Cannot rule out PE even if negative LE ultrasound
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| 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
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|
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| 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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