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357 Cards in this Set
- Front
- Back
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how much energy consumption by the RBC is by HMP shunt
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10%
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what is the physiologic chloride shift
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bicarb and chloride exchanged across RBC membrane
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what is poikilocytosis
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varying shapes of RBCs
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what do dense granules in platelet contain
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ADP, calcium
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what do alpha granules in platelet contain
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vWF, fibrinogen
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where are most of the platelets stored in body
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1/3 of platelets are in spleen
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life span of platelet
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8-10 d
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what is the receptor for vWF
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Gp1b
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what is the receptor for fibrinogen
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GpIIb/IIIa
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contents of azurophilic granules
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hydrolytic enzymes, lysozyme, myeloperoxidase, lactoferrin
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are macrophages short or long lived
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long lived
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what leukocyte is best at eating IC
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eosinophil
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what leukocytes produce histaminase and arylsulfatase. Function of these enzymes
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eosinophil, limit rxn after mast cell degranulation
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causes of eosinophilia
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DNAAACP = neoplastic, asthma/asthma, addisons, acute interstitial nephritis, collagen vascular dz, parasite
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is IgE activation always HS1
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no. parasites are destroyed via HS2 w/ IgE
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contents of basophilic granules of basophil
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heparin, histamine, leukotrienes
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what substances are released when mast cells degranulate
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histamine, heparin, eosinophil chemotactic factors, serotonin
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slow reaction of mast cell
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slow reacting substances of anaphylaxis = leukotrienes
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what drug can prevent mast cell degranulation
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cromolyn
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what is the main inducer of 1* antibody response
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dendritic cell
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what is a dendritic cell on skin
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langerhans cell
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do B lymphocytes have memory
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yes
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what are the majority of circulating lymphocytes
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t cells (80%)
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what type of antibody is Rh
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IgG
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2 effects of kallikrein
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1. bradykinin synthesis 2. plasmin synthesis
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how is complement pathway connected to coagulation pathway
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plasmin can activate complement
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where is vWF synthesized
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megakaryocytes, endothelial cells
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what factor carries VIII in blood
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vWF
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what factors does ATIII inhibit
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2,7,9,10,11,12
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review platelet plug formation
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p346
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function of ADP in platelet plug formation
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helps platelets to adhere to endothelium (induces expression of GpIIb/IIIa)
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3 functions of TXA2
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1. vasoconstriction 2. bronchoconstriction 3. platelet aggregation
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why doesn't aspirin stop synthesis of anti-coagulation factors in endotheial cell
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low dose aspirin targets platelet COX
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what drug can block TXA synthase
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dipyramidole
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review thromobosis diagram
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p347
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what is PF3
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platelet phospholipid found on platelet surface, which is needed for clotting
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what is PF4
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heparin neutralizing factor, found on platelets. Is the pathophysiology of HIT
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what is bernard soulier syndrome
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no Gp1b
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what is glanzmann's thrombasthenia
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no Gp2b/3a
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what are acanthocytes associated with
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liver dz, abetalipooroteinemia
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what is basophilic stippling associated with
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thalassemia, ACD, iron deficiency, lead poisoning, sideroblastic anemia
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what causes basophilic stippling
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aggregated ribosomes
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what are bite cells assoc w
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g6pd
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what are ringed sideroblasts assoced with
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sideroblastic anemia
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what are schistocytes assoc w
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DIC, TTP/HUS, traumatic hemolysis
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what are target cells accociated with
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hbc dz, asplenia, liver dz, thalassemia
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what is corrected reticulocyte count
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HCT/45*reticulocyte count. Divide by 2 if you see reticulocytes, >3%=active BM
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cause of heinz bodies
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oxidation of iron leads to denatured hemoglobin. alpha thal, g6pd
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what are howell jolly bodies
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basophilic nuclear remannts in RBCs found in asplenia
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what is RDW
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variation in size of RBCs. Can distinguish between defect in PROCESS of creating rbcs, or defect in starting products
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MCC of iron deficiency in: newborns, women under 50, men under 50, people over 50
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meckel, menorrhagia, PUD, CRC
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cause of iron defiency
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loss (bleeding), poor intake (malabsorption), or increased demand (pregnancy)
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triad of plummer vinson
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esophageal web + glossitis + iron deficiency
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conjunctival pallor + craving for ice + spoon nails
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iron deficiency
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what is Hb barts
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deletion of 4 alpha globin genes -> gamma4
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what is HbH
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deletion of 3 alpha globin genes -> beta 4
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what forms of hemoglobinopathies can HB electrophoresis be used to detect
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beta thalassemia, 3-4 gene deletions of alpha thal
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genetic defect in alpha vs beta thal
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alpha: gene mutations in exons. Beta: gene mutations in splice sites and promotor sequence
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what can cause hydrops fetalis
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Hb barts dz
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what hematologic characteristics contribute to malaria resistance
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beta thal minor, sickle cell trait, g6pd, absence of duffy antigen
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how to diagnose beta thal
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both major and minor will have elevated HbF, minor will also have elevated HbA2
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what can occur if sickle cell trait and b thal minor coexist in person
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mild to moderate sickle cell dz
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mechanism of lead poisoning
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inhibition of ferrochelatase and ALA dehydratase, and of rRNA degradation
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causes of sideroblastic anemia
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1. hereditary XR ALA synthase 2. alcohol 3. lead 4. B6 deficiency
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mechanism of alcohol and sideroblastic anemia
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uncoupling agent in mitochondria, and disrupts heme synthesis in mitochondria
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sx of lead poisoning
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LEAD - lead lines on gingiva (burton's lines) and epiphyses of long bones 2. encephalopathy, erythrocyte basophilic stippling 3. abdominal colic and sideroblastic Anemia 4. wrist and foot Drops
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what is tx of choice for lead poisoning in child
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succimer
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are RBCs the only cells affected in macrocytic anemia
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oft see pancytopenia
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folate vs B12 deficiency megaloblastic anemia
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B12 def: B12 can see neurologic sx cuz of increased methylmalonic acid
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causes of folate defieincy
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1. malnutrition 2. malabsorption 3. impaired metabolism 4. increased requirement
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causes of B12 deficiency
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1. deficient intake 2. malabsorption 3. pernicious anemia 4. D latum
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causes of nonmegaloblastic macrocytic anemia
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1. liver dz 2. alcohol 3. reticulocytosis 4. metabolic disorder 5. drugs
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name some drugs that can cause a nonmegaloblastic macrocytic anemia
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5fu, azt, hydroxyurea
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differences between nonmegaloblastic and megaloblastic macrocytic anemia
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1. macrocytes are round 2. no hypersegmented neutrophils 3. no pancytopenia
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name one metabolic dz that can cause nonmegaloblastic macrocytic anemia
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any congenital deficency in purine or protein synthesis, like orotic aciduria
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4 nonhemolytic causes of normocytic anemia
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1. ACD 2. aplastic anemia 3. kidney dz 4. blood loss
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lab findings in intravascular vs extravascular hemolysis
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both: increased LDH. Intravascular: decreased haptoglobin and hemoglobin in urine Extravascular: increased UCB->jaundice
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what is the schilling test
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test to determine cause of B12 deficiency. Give IM unlabeled B12 and oral labeled B12. If no malabsorption, then will see radioactive urine. If don't see radioactive urine, then give intrinsic factor and see if that fixes it
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pathophys of ACD
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inflammatory state causes increased hepcidin, and decreased release of iron from macrophages
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4 causes of aplastic anemia
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1. radiation and drugs 2. virus 3. fanconi's anemia 4. idiopathic (immune cause, may follow hepatitis)
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what is fanconi anemia
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inherited DNA repair defect, amino aciduria + proteinuria + phosphatauria
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how long does reticulocyte count take to respond
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week
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what is diamond-blackfan
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congenital pure rbc aplasia + congenital anomolies
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causes of pure rbc aplasia
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thymoma, viral (parvovirus), diamond blackfan, others
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what proteins are affected in hereditary spherocytosis
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akyrin, spectrin, band 4.1
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cbc findings of hereditary spherocytosis
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increased mchc and rdw
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intra or extravascular: hereditary spherocytosis, g6pd, pyruvate kinase def, sickle cell, PNH, autoimmune hemolytic anemia, microangiopathic, macroangiopathic
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E, I, E, E, I, warm = E/cold=I, I, E
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what hemolytic anemia is assoc w aplastic crisis after b19 infection
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hereditary spherocytosis, sickle cell
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how to dx hereditary spherocytosis
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osmotic fragility test
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why is there an increased risk of GB stones in heriditary spherocytosis
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increased bilirubin breakdown results in increased unconjugated bilirubin can supersaturate bile and form pigment stone
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back pain with hemoglobinuira a few days later after infection
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g6pd deficiency
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hemolytic anemia in a newborn
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pyruvate kinase deficiency
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what % of af am's have HbS trait
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8
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crew cut skull on xr
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beta thal, sickle
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how much HbS is needed to become symptomatic with sickle cell
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60%
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most common mutation in sickle cell
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G6V on beta chain
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can cause precipitate sickling in sickle cell
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decreased oxygen (or anything which right shifts curve, like acid) or hypovolemia
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mcc of death in adult with sickle cell
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acute chest syndrome: CP + wheezing + dyspnea
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do sickle cell newborns start sickling immediatley
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no, cuz of increased hbf
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sickling is never seen in sickle cell trait
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false, if o2 is low enough can see it
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complications of sickle cell dz
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1. aplastic crisis 2. autosplenectomy 3. salmonella osteomyelitis 4. painful vasoocclusive crisis 5. papillary necrosis in kidney, microhematuria 6. splenic sequestration crisis (rapid splenic enlargement)
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tx of sickle cell
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hydroxyurea, BM transplant
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genetic defect in HbC
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G6L in beta chain
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what is DAF
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CD55/59 that inhibits complement activation on RBC membrane. GPI linked
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why is hemoglobinurea increased at night with PNH
|
relative respiratory acidosis causes increased complement fixation
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what type of antibodies is warm agglutinin
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igg
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what type of antibodies is cold agglutinin
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igm
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what dzz can produce warm agglutinin
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SLE, CLL, drugs (methyldopa, penicillin)
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what is more potent activator of complement: igg or igm
|
igm
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what dzz can produce cold agglutinin
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CLL, mycoplasma pneumoniae, infectious mono, drugs (quinidine)
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mechanism of penicillin hemolysis
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penicillin BPO groups get attached to RBC, may make Ab's -> HSII
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mechanism of methyldopa hemolysis
|
methyldopa chemically alters Rh antigens -> HSII
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mechanism of quinidine hemolysis
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forms immune complex with IgM and deposits onto RBCs
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direct vs indirect coombs
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direct test checks for presence of Ig's on RBC (pt RBCs agglutinate if anti-Ig added). Indirect test checks for presence of Ig's in serum (RBCs agglutinate in pt serum)
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serum iron, TIBC, ferritin, % transferrin saturation in: iron deficiency
|
down, up, down, down
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serum iron, TIBC, ferritin, % transferrin saturation in: chronic disease
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down, down, up, -
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serum iron, TIBC, ferritin, % transferrin saturation in: hemochromatosis
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up, down, up, up
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relationship between transferrin and ferritin
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inverse (usually always)
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serum iron, TIBC, ferritin, % transferrin saturation in: pregnancy/ocp use
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-, up, -, down
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serum iron, TIBC, ferritin, % transferrin saturation in: lead poisoning
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up, down, up/-, up
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serum iron, TIBC, ferritin, % transferrin saturation in: sideroblastic anemia
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up, -, up, up
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what heme intermediate acculates w/ lead poisoning
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ALA or protoporphyrin
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what heme intermediate accumulates w/ AIP
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porphobilinogen
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what heme intermediate accumulates w/ PCT
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uroporphyrin
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what enzyme is affected in AIP
|
porphobilinogen deaminase
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what enzyme is affected in PCT
|
uroporphyrinogen decarboxylase
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5 sx of AIP
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1. painful abdomen 2. photosensitive pink urine 3. polyneuropathy 4. psychosis 5. precipitated by drugs
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tx for AIP
|
glucose and heme (both inhibit ALA synthase)
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what vitamin is needed for heme synthesis
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B6
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sx of PCT
|
blistering cutaneous photosensitivity
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what is PCT assoc w
|
hypertrichosis, HCV
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3 factors that can stimulate ALA synthase, and two factors that can inhibit it
|
Stimulate: 1. Alcohol 2. Hypoxia -> EPO 3. Barbiturate; Inhibit: 1. glucose 2. heme
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sx of coagulation or platelet dz: late rebleeding
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coagulation
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sx of coagulation or platelet dz: epistaxis
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platelet
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sx of coagulation or platelet dz: petechiae and purpura
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platelet
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sx of coagulation or platelet dz: bleeding on tooth extraction
|
coagulation
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sx of coagulation or platelet dz: hemarthrosis
|
coagulation
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sx of coagulation or platelet dz: menorrhagia
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coagulation or mixed
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hemophilia vs vit K deficiency
|
both are coagulation disorder, but vit K will have increased PT whereas hemophilia wont
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what platelet disorder will not have decreased platelet count
|
glanzmann's thrombasthenia
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is idiopathic thrombocytopenic purpura acute or chronic
|
acute = after virus w/o lymphoadenopathy or splenomegaly. Chronic = insidious, see splenomegaly, assoc w SLE/HIV/lymphoproliferative dz
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what is deficient in TTP
|
ADAMTS13 (vWF metalloprotease)
|
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labs in ITP
|
increased megakaryocytes
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5 sx of TTP
|
1. neurologic 2. renal 3. fever 4. thrombocytopenia 5. microangiopathic hemolytic anemia
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3 non-hematologic causes of increased BT
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NSAID, renal failure (toxic products block platelet phospholipid) 3. scurvy
|
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labs in vWF dz: pc, bt, pt, ptt
|
increased BT, potentially increased PTT
|
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inheritance of vWF dz
|
AD
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how to tx vWF dz
|
DDAVP/desmopression, which releases vWF in endothelium
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how to tx vWF dz in women
|
OCP's increase the amount of vWF and vactor VIII
|
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what is vWF dz assoc w
|
MVP, marfan, angiodysplasia
|
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how to dx vWF dz
|
ristocetin cofactor assay
|
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causes of DIC
|
STOP Making New Thrombi - sepsis, trauma, obstetric, pancreatitis, malignancy, nephrotic, transfusion
|
|
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what in amniotic fluid predisposes to DIC
|
thromboplastin
|
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|
most common inherited hypercoagulability
|
factor V leiden
|
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what inherited hypercoagulability is associated with venous clots
|
prothrombin gene mutation
|
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what type of mutation occurs in heritary prothrombin hypercoagulability
|
3' UTR
|
|
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how to dx hereditary AT3 deficiency
|
give heparin, PTT doesn't increase that much
|
|
|
systemic painful adenopathy is always a sign of disseminated infection
|
no, eg SLE can cause systemic painful malignancy
|
|
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OCP effect on coagulation cascasde
|
1. increases V, VIII 2. inhibits AT3 3. increases fibrinogen
|
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|
inheritance of inherited hypercoagulability dz
|
AD
|
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most common cause of decreased PTT after heparin administration
|
OCP
|
|
|
inherited thrombosis w/ risk of thrombotic skin necrosis w/ hemorrhage
|
protein C/S deficiency
|
|
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what is antiphospholipid syndrome seen in
|
SLE, HIV
|
|
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how do babies die in ABO incompatibility
|
HF from severe anemia
|
|
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what blood group is assoc w/ increased duodenal ulcers
|
O
|
|
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what blood group is assoc w increased gastric cancer
|
A
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|
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forward typing vs back typing
|
forward typing = identifying ABO antigens. Back typing = identifying natural antibodies
|
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absence of what blood antigen is protective for P vivax infection
|
duffy
|
|
|
what is major crossmatch
|
pt serum combined with blood of donor to check for rxn.
|
|
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types of transfusion reactions
|
1. allergy (hs1) 2. febrile reaction (hla ab's against donor LEUKOCYTES), no hemolysis 3. hemolytic transfusion rxn - due to ABO incompatibility or memory cell activation
|
|
|
leukemia vs lymphoma.
|
leukemia tends to have large involvement of bone marrow, but may metastasize to lymph nodes. Lymphoma arises from lymph node, but can metastasize to bone marrow
|
|
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leukemoid reaction
|
leukocytosis with left shift (i.e. immature cells). HOWEVER SEE INCREASED leukocyte alkaline phosphatase, which is not true of CML
|
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extranodal involvement in HL vs NHL
|
more common in NHL
|
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type of spread in HL vs NHL
|
HL is contiguous spread
|
|
|
node involvement in HL vs NHL
|
HL affects localized, single group of nodes
|
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|
which is more likely to produce constitutional sx: HL or NHL
|
HL
|
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|
HL or NHL: mediastinal lymphadenopathy
|
HL
|
|
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associations for HL vs NHL
|
mixed cellularity HL more assoc w EBV. NHL more assoc w HIV and immunosuppression
|
|
|
epidemiology for HL vs NHL
|
HL has a bimodal distribution (young/old), affects men more except for nodular sclerosing. NHL = 20-40yo
|
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what can indicate good prognosis in HL
|
low stage, increased lymphocytes w/ fewer RS cells
|
|
|
markers for HL
|
CD15, CD30 RS cells
|
|
|
what are the "eyes" in a RS cell
|
bilobed nuclei
|
|
|
what types of RS variants are seen in nodular sclerosing HL
|
lacunar cells
|
|
|
what is the most common HL
|
nodular sclerosing
|
|
|
what lymphomas can occur in kids
|
burkitts most often occurs in teens. Diffuse large b cell can occur in children. All others are adults
|
|
|
genetics of burkitts
|
cmyc - 8-14
|
|
|
burkitts in africa vs elsewhere
|
africa = jaw. Pelvis or abdomen elsewhere
|
|
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what are the stars and sky in burkitts
|
stars = macrophage, sky = lymphocytes
|
|
|
what is the most common NHL
|
diffuse large b cell lymphoma
|
|
|
what is the most common indolent NHL
|
follicular lymphoma
|
|
|
genetics of mantle cell lymphoma
|
11-14
|
|
|
genetics of follicular lymphoma
|
bcl2 - 14-18
|
|
|
marker for mantle cell
|
CD5+
|
|
|
what populations are most affected by adult t cell lymphoma
|
japan, west africa, caribbean
|
|
|
prognosis of mantle cell
|
poor
|
|
|
prognosis of adult t cell lymphoma
|
aggressive
|
|
|
sx of adult t cell lymphoma
|
cutaneous lesions
|
|
|
sx of mycosis fungoides
|
red exfoliative rash
|
|
|
prognosis of mycosis fungoides
|
indolent CD4+ cells
|
|
|
what causes adult t cell lymphoma
|
HTLV-1
|
|
|
most common 1* tumor arising within bone in elderly
|
MM
|
|
|
what are most common Ig's produced by MM
|
G>A>M
|
|
|
what is a M spike? MM vs waldenstrom
|
M spike is the monoclonal antibody spike seen on electrophoresis. In MM usually GA, in waldenstrom usually M.
|
|
|
sx of waldenstrom vs MM
|
waldenstrom has hyperviscosity and no lytic bone lesions
|
|
|
what is monoclonal gammapathy of undetermined significance
|
monoclonal plasma cell expansion w/o sx of mM
|
|
|
3 sx of leukemia
|
leukemias are functional pancytopenias. :. Anemia, recurrent infections, and bleeding
|
|
|
age group of ALL
|
children
|
|
|
age group of AML
|
15-40yo, MEDIAN ONSET IS 60YO
|
|
|
age group of CML
|
40-60yo
|
|
|
age group of CLL/SLL
|
>60yo
|
|
|
what markers seen in ALL
|
TdT+, CALLA/CD10+, PAS+
|
|
|
common sites of spread for ALL
|
testes, CNS
|
|
|
what translocation has better prognosis for ALL
|
12-21
|
|
|
which blood neoplasm has smudge cells
|
CLL
|
|
|
which blood neoplasm is associated with warm agglutinins
|
CLL. It can also produce cold agglutinins
|
|
|
SLL vs CLL
|
CLL has peripheral blood lymphocytosis
|
|
|
what is the most common leukemia
|
CLL
|
|
|
what is the most common cause of generalized lymphadenopathy in elderly
|
CLL
|
|
|
mature B cell tumor in elderly w/ filamentous, thin projections
|
hairy cell leukemia
|
|
|
what type of AML responds to ATRA
|
M3
|
|
|
markers for AML
|
CD13, CD33, PAS-
|
|
|
leukemia that likes to invade gums
|
AML M5
|
|
|
what is blast crysis
|
CML that rapidly increases production of immature cells to become AML or ALL
|
|
|
the only leukemia that has potential thrombocytosis
|
CML
|
|
|
most common cause of death in CML pt
|
blast crisis
|
|
|
tx for CML
|
imatinib
|
|
|
what is translocation in CML
|
9-22
|
|
|
fever, recurrent bleeding, and constant fatigue in 7yo male
|
ALL
|
|
|
what are auer rods
|
peroxidase-positive inclusions
|
|
|
complication of AML tx
|
release of Auer rods -> DIC
|
|
|
genetics of AML M3
|
15-17
|
|
|
acute promyelocytic leukemia is another name for what
|
AML M3
|
|
|
genetics of ewings sarcoma
|
11-22
|
|
|
markers for langerhans cell histiocytosis
|
S100, CD1a
|
|
|
tennis rackets on EM
|
Birbeck granules of histiocytosis, spores of C tetani
|
|
|
what is Letterer Siwe dz
|
malignant histiocytosis in infants that results in skin and lytic bone lesions
|
|
|
what is hand schuller christian dz
|
malignant histiocytosisi in children that results in DI, exophthalmos, lytic skull lesions
|
|
|
what is eosinophilic granuloma histiocytosis -- in who, what sx
|
benign histiocytosis in teens that can have unifocal lytic bone lesions
|
|
|
which chronic myeloproliferative disorders have JAK2 mutations? Which chromosome
|
chromosome 9. polycythemia vera, essential thromboocytosis, myelofibrosis
|
|
|
describe RBC, WBC, platelet count for: polycythemia vera
|
up, up, up
|
|
|
describe RBC, WBC, platelet count for: essential thrombocytosis
|
-, -, up
|
|
|
describe RBC, WBC, platelet count for: myelofibrosis
|
down, -, -
|
|
|
describe RBC, WBC, platelet count for: CML
|
down, up, up
|
|
|
teardrop cells are often seen in
|
myelofibrosis
|
|
|
what cell is responsible for fibrotic obliteration of bone marrow in myelofibrosis
|
megakaryocytes
|
|
|
pathogenesis of polycythemia vera
|
extra sensitivity to GF's of all BM progenitors
|
|
|
describe plasma volume, rbc mass, o2 sat, EPO levels for: relative polycythemia
|
down, -, -, -
|
|
|
describe plasma volume, rbc mass, o2 sat, EPO levels for: appropriate absolute polycythemia
|
-, up, down, up
|
|
|
describe plasma volume, rbc mass, o2 sat, EPO levels for: inappropriate absolute
|
-, up, -, up
|
|
|
describe plasma volume, rbc mass, o2 sat, EPO levels for: polycythemia vera
|
up, up, -, down
|
|
|
4 sx of polycythemia vera
|
1. increased rbcs -> viscosity -> thrombosis 2. hypervolemia (keeps pace w/ RBC mass) 3. increased HSC descendants -> mast cells -> hyperhistaminemia -> itching esp in hot temp cuz that degranulates, ruddy face 4. increased HSC descendants -> increased turnover -> hyperuricemia
|
|
|
mcc of budd chiari
|
polycythemia vera
|
|
|
ddx of generalized itching
|
bile salt deposition in jaundice, 1* biliary cirrhosis, PV
|
|
|
does heparin cross placenta
|
no
|
|
|
what test is followed to monitor heparin
|
ptt
|
|
|
how to tx heparin tox? How does it work?
|
protamine sulfate, which is positively charged to bind the negatively charged heparin
|
|
|
name a low molecular weight heparin
|
enoxaparin
|
|
|
mechanism of low molecular weight heparin
|
acts more on factor X
|
|
|
advantages of low molecular weight heparin
|
better bioavailability, longer 1/2 life, doesn't need to be monitored
|
|
|
what enzyme does warfarin inhibit
|
epoxide reductase
|
|
|
pathogenesis of heparin induced thrombopenia
|
binding of heparin to PF4, which causes autoimmune rxn
|
|
|
likelihood of forming clots after HIT
|
high, because even though you killed off your platelets, your coagulation factors are active again
|
|
|
mechanism of lepirudien and bivalirudin
|
direct thrombin inhibitor, used in HIT pts
|
|
|
what drug is argatruban
|
direct thrombin inhibitor not derived from hirudin
|
|
|
how is warfarin metabolized
|
CYP - DRUG INTERACTION
|
|
|
what anticoagulant is associated with skin/tissue necrosis
|
warfarin cuz of C,S def
|
|
|
how to rapidly reverse warfarin tox
|
FFP
|
|
|
is warfarin given IV or oral
|
oral
|
|
|
structure of heparin vs warfarin
|
heparin is GAG! - large anionic acidic polymer. Warfarin is small and lipid soluble
|
|
|
when are thrombolytics administered in early ischemic stroke
|
if <3h
|
|
|
what kind of drug is alteplase
|
thrombolytic. It is tPa
|
|
|
what kind of drug is anistreplase
|
thrombolytic. It is streptokinase + plasminogen
|
|
|
about how long does it take for platelets to get reactivated after reversible NSAID
|
48h
|
|
|
5 toxicities of aspirin
|
1. gastric ulcer 2. bleeding 3. acidemia -> hyperventilation 4. Reyes 5. tinnitus
|
|
|
what antiplatelet drug is associated with tinnitus
|
aspirin
|
|
|
mechanism of clopidogrel
|
1. block ADP receptors 2. inhibit gp2b/3a expression
|
|
|
what antiplatelet drug is associated with neutropenia
|
ticlopidine
|
|
|
what drug blocks TXA synthase
|
dipyramidole
|
|
|
what antiplatelet drug is given after coronary stenting
|
clopidogrel/ticlopidine
|
|
|
what is abciximab
|
moncolonal antibody inhiitor of gb2b/3a
|
|
|
what is tirofiban
|
non-peptide inhibitor of gp2b/3a
|
|
|
what is eptifabitide
|
peptide inhibitor of gp2b/3a
|
|
|
what antiplatelet drug is used for percutaneous transluminal coronary angioplasty
|
abciximab
|
|
|
which cancer drugs act at the m phase
|
vinca, taxols, colchicine
|
|
|
where are most of the rapidly dividing stem cells located
|
1. stratum basalis of skin 2. crypts of GI tract 3. bone marrow
|
|
|
which cancer drugs act at the S phase
|
antimetabolites, hydroxyurea, etoposide
|
|
|
which cancer drugs act at the G2 phase
|
bleomycin, etoposide
|
|
|
which cancer drugs alkylate DNA
|
cyclophosphamide, nitrosurea, busulfan, platinum drugs
|
|
|
which cancer drugs create reactive oxygen species
|
anthracycline, bleomycin
|
|
|
what toxicity does leucovorin prevent
|
BM tox by MTX
|
|
|
which cancer drug is associated with steatosis in liver
|
MTX
|
|
|
which cancer drug is associated with mucositis
|
MTX
|
|
|
which cancer drug can cause neural tube defects
|
MTX
|
|
|
which cancer drug is associated with photosensitivity
|
5FU
|
|
|
mechanism of 5FU
|
blocks thymidylate synthase (forms complex w/ folic acid), and decreases dTMP synthesis
|
|
|
mechanism of 6MP
|
purine analog that decreases purine synthesis
|
|
|
what blood neoplasm is 6MP ineffective at treating
|
can treat all leukemias and lymphomas except CLL or HL
|
|
|
what purine analog can be used with allopurinol
|
6 thioguanine
|
|
|
what is the clinical use for 6TG
|
ALL
|
|
|
mechanism of cytarabine
|
pyrimidine analog that blocks DNA polymerase (chain terminator)
|
|
|
what is cladribine
|
purine analog that is used to tx hairy cell. It is resistant to ADA so gets high concentration
|
|
|
what cancer drugs are good for tx of testicular cancer
|
cisplatin, bleomycine, etoposide
|
|
|
what cancer drugs are good for tx of HL
|
MTX, anthracycline, bleomycin, vinca
|
|
|
what cancer drug is good for childhood tumors like wilm's tumor, ewing sarcoma, rhabdomyosarcoma
|
dactinomycin
|
|
|
what cancer drugs are good for tx of NHL
|
MTX, 6MP, cytarabine, cyclophosphamide,
|
|
|
mechanism of cyclophsophamide
|
alkylating agent that works on guanine N7
|
|
|
which alkylating agents must be bioactivated
|
cyclophosphamide, nitrosurea
|
|
|
mechanism of dactinomycin
|
intercalates
|
|
|
mechanism of anthracycline
|
1. ROS 2. intercalates
|
|
|
mechanism of bleomycin
|
ROS
|
|
|
mechanism of etoposide
|
blocks topoisomerase 2
|
|
|
what cancer drug can cause extravasation
|
anthracycline
|
|
|
what is extravasation with respect to drug toxicity
|
skin necrosis at injection site
|
|
|
which cancer drugs can cause pulmonary fibrosis
|
bleomycin, busulfan
|
|
|
which cancer drugs have CNS toxicity
|
nitrosurea
|
|
|
which cancer drugs are associated with hyperpigmentation
|
busulfan, 5FU is photosensitive, maybe bleomycin
|
|
|
which cancer drug is associated with neurotoxicity
|
vincristine (peripheral),nitrosurea (central)
|
|
|
which cancer drug is associated with nephro/ototoxicity
|
cisplatin
|
|
|
what cancer drug is used for ovarian and breast cancers
|
taxols
|
|
|
what cancer drug is used for brain tumors
|
nitrosurea
|
|
|
what cancer drug is used to destroy BM before transplant
|
busulfan
|
|
|
how to tx platinum drug tox
|
amifostine
|
|
|
which cancer drugs prevent MT polymerization? Depolymerization
|
vinca. Taxol.
|
|
|
what drug is used to tx melanoma, CML, and sickle cell
|
hydroxyurea
|
|
|
which cancer can cause a hypersensitivity pneumonitis
|
MTX
|
|
|
what cancer drug can help identify actinic keratosis
|
5FU
|
|
|
tox of prednisone
|
immune suppress, cataract, acne, osteoporosis, HTN, peptic ulcers, hyperglycemia, psychosis and insomnia
|
|
|
complication of tamoxifen vs raloxifene
|
tamoxifen can increase risk of endometrial carcinoma b/c of pt agonist effect in endometrium. Raloxifene doesn't have that problem
|
|
|
mechansim of trastuzumab
|
monoclonal antibody against her2 (erbB2)
|
|
|
toxiciy of trastuzumab
|
cardiotox
|
|
|
what can be used to tx GI stromal tumors
|
imatinib
|
|
|
what is rituximab used to tx
|
NHL (B cell), rheumatoid arthritis
|
|
|
what is rituximab
|
monoclonal against CD20 (found on b cells rmr)
|
|
|
why do children have lower Hg
|
cuz increased phosphate used to build bone means increased 2,3-bPG, which rightshifts curve and decreases EPO
|
|
|
what is HbA
|
alpha2beta2
|
|
|
what is HbF
|
alpha2gamma2
|
|
|
what is HbA2
|
alpha2delta2
|
|
|
what is HbS
|
alpha2beta2 (G6V on beta chain)
|
|
|
what is HbBarts
|
gamma4
|
|
|
what is HbH
|
beta4
|
|
|
what blood group is assoc w pernicious anemia
|
A
|
|
|
what is antibody against in pernicious anemia
|
proton pump or IF
|
|
|
how can cortisol result in an increased WBC
|
cortisol results in neutrophilia
|
|
|
why can Addison's cause eosinophilia
|
cuz cortisol helps to keep them sequestered in lymph nodes
|
|
|
basophilia is seen with what dz
|
chronic myheloproliferative dz
|
|
|
what drug can cause atypical lymphocytosis
|
phenytoin
|
|
|
does adult T cell leukemia have TdT
|
no
|
|
|
how does adult t cell leukemia cause cancer
|
TAX gene blocks p53
|
|
|
sx of splenic infarct
|
LUQ pain + friction rub + left pleural effusion
|
|
|
"sugar coated spleen"
|
perisplenitis from cirrhosis
|
|
|
3 steps for preparing donor blood
|
1. perform ABO, Rh test 2. indirect coombs (generic antibody panel) 3. screen for infectious dz (for newborns need to irradiate)
|
|
|
3 steps for doing a major crossmatch
|
1. direct coombs on pt rbc 2. indirect coombs on pt's blood 3. mix pt and donor blood
|
|
|
correlation of clotting factors and blood types
|
blood type O has less vWF and VIII
|
|
|
how does spleen get damaged in sickle cell dz
|
atrophy
|
|
|
mcc of macrocytosis in sickle cell
|
folate def
|
|
|
causes of splenomegaly
|
1. increased function 2. abnormal blood flow 3. infiltration
|
|
|
what cells secrete PAF? what does it do? intracellular signaling
|
platelets, endothelial, inflammatory. causes vasoconstriction, bronchoconstriction. works through ip3
|
