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100 Cards in this Set
- Front
- Back
- 3rd side (hint)
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Bisphosphoglycerate mutase
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enzyme found in erythrocytes that makes 2,3-bisphosphoglycerate
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dense granules of platelets contain...
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AP, Ca2+
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alpha-granules of platelets contain...
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vWF, fibrinogen
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Life span of platelet
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8-10 days
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Contents of basophil granules
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heparin, histamine, leukotrienes
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Contents of eosinophil granules
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histaminase, arylsulfatase (neutralizes leukotrienes)
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Eosinophilia
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CHINA: connective tissue disease, Helminthic disease, Idiopathic hypereosinophilia, neoplasms, allergy/atopy
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Myeloperoxidase activity of monocytes vs. macrophages
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monocytes have myeloperoxidase activity, but once they differentiate into macrophages, they lose it
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The majority of circulating lymphocytes are...
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T-cells (80%)
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Duffy antigen
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binding point for P. vivax
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Black population has lower incidence of Duffy because of natural selection (due to resistance to malaria)
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In people who have never been transfused for blood, who would be most likely to have a hemolytic reaction to blood?
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Previous prego and spontaneous abortion, because they have a higher chance of being exposed to the fetus' blood
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Delayed hemolytic transfusion reaction
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patient was exposed to antigen long ago and developed memory B cells, who have since then stopped working and the antibody titer is low
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when re-exposed, the memory B-cells ramp up and the patient develops a hemolytic anemia a few days later
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Difference between plasma and serum
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serum is the supranate after blood is allowed to clot, so it doesn't have fibrinogen, prothrombin, factors V and VIII
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Is the intrinsic pathway more potent or the extrinsic pathway?
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Intrinsic pathway, because IXa, VIIIa complex is better at activating X
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Function of XII (hageman's factor)
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Convert prokallikrein into kallikrein. Kallikrein can then convert HMWK into bradykinin and also plasminogen into plasmin
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Function of XIII
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makes fibrin insoluble and also enhances cross-linking of the clot
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Function of thromboxane A2
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potent vasoconstriction, bronchoconstriction, platelet aggregator
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Protein C is activated by and it inactivates what?
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Activated by protein S, thrombomodulin, thrombin into APC
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Cleaves: Va, VIIIa
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Target cell is seen in these diseases
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HbC disease, Asplenia, Liver disease, Thalassemia
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Craving for ice, allopecia
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iron deficiency
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MCC of iron deficiency by age bracket
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Children: Meckel's, Male and female over 50: colon cancer
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Male <50: PUD, Female <50: menorrhagia
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Deletion of 4 alpha-globin genes
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Hb Barts (4 gammas) disease, hydrops fetalis
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Deletion of 3 alpha-globin genes
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HbH (4 betas) disease, severe anemia
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Defect in B-thalassemia
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point mutations in splicing sites and promoter sequences
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Which hemoglobin is increased in both B-thalassemias
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HbF
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Treatment of sideroblastic anemia
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pyridoxine therapy (cofactor for d-ALA synthase)
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What does an increase in d-ALA lead to?
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increased permeability of cerebral blood vessels that leads to encephalopathy
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What does an increased homocysteine do?
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increases chance of thrombosis and MI
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What blocks the absorption of folate in the intestines
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EtOH and OCPs
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Most common non-megaloblastic macrocytic anemia
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Alcoholism
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Phases of anemia of chronic disease
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Early: normocytic anemia
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Late: microcytic, hypochromic
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Fanconi's anemia
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inherited defect in DNA repair that leads to marrow aplasia
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Howell jolly bodies in spherocytosis
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since splenectomy is the cure, patients who have already had their spleen removed show howell jolly bodies
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What kind of hemolysis is G6PD deficiency
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predominantly intravascular
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Hemolytic anemia in a newborn
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pyruvate kinase deficiency
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Splenic sequestration crisis
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sequestration of RBCs in spleen leads to hypovelmic shock
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seen in Sickle cell
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#1 cause of death in paroxysmal nocturnal hemoglobinuria
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thrombosis due to hypercoagulable state
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Penicillin associated hemolytic anemia
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penicillin binds RBCs and a type II hypersensitivity reaction is launched against the "foreign" antigen, leading to hemolysis
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Methyldopa associated hemolytic anemia
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Methyldopa alters the Rh antigen, causing a type II hypersensitivity reaction against the altered Rh antigen
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Quinidine associated hemolytic anemia
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Quinidine leads to a type III hypersensitivity where IgM-ICs form, leading to intravascular hemolysis
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Microcytic anemia w/ calcified aortic stenosis
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The calcified valve leads to microangiopathic hemolytic anemia, but over time, the patient becomes iron deficient and develops a microcytic anemia
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Porphyria cutanea tarda MOA and Sx
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deficiency in uroporphyrinogen decarboxylase, leads to buildup of uroporphyrinogen
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Sx: cutaneous blistering
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Acute intermittent porphyria MOA and Sx
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Deficiency in porphobilinogen deaminase (uroporphyrinogen synthase)
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Sx: abdominal pain, pink urine, exacerbated by drugs (barbiturates), psychological problems, polyneuropathy
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Tx of acute intermittent porphyria
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glucose and heme to inhibit d-ALA synthase
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Most common porphyria
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porphyria cutanea tarda
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1st treatment for lead poisoning in children
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succimer
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Labs in ITP
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increased megakaryocytes
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TTP labs and Sx
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Labs: schistocytes, increased LDH
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Sx: fever, renal, neuro, thrombocytopenia, microangiopathic hemolytic anemia
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PT tests what?
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VII (extrinsic pathway)
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PTT tests what?
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all factors except VII (intrinsic pathway)
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Most common cause of inherited hypercoagulability
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Factor V Leiden, where there is a mutant factor V that cannot be degraded by protein C
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Prothrombin gene mutation
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mutation in 3' untranslated region
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associated w/ venous clots
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Reduced increase in PTT after heparin administration indicates...
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ATIII deficiency
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vWF is stored in what granules in the endothelial cells
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Weibel-Palade bodies
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Hodgkin's disease is more common in men except for which variant
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Nodular-sclerosing
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Hodgkin's disease associated w/ EBV
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mixed cellularity
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Biopsy of nodular sclerosing Hodgkin's
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collagen banding where involved lymph nodes are split, lacunar RS cells
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RS variant in mixed cellularity Hodgkin's
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mononuclear
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RS variant in lymphocyte predominant Hodgkin's
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L and H
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all 3 translocations associated w/ Burkitt's
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t(8;14), t(2;8), t(8;22)
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Most common adult NHL
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Diffuse large B-cell lymphoma
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Cell markers in Mantle cell lymphoma
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CD5+, CD23- (as opposed to CLL, which is CD5+, CD23+)
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t(11;14) with upregulation of cyclin D1
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Pautrier microabscesses
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seen in Mycosis fungoides where there are little microabscesses under the epidermis
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DIfference between M spikes in multiple myeloma and Waldenstrom's macroglobulinemia
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Multiple myeloma: IgG spike
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Waldenstrom: IgM spike
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Clinical presentation of T-ALL
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Child presents w/ signs indicating compression of the great vessels or the trachea due to a mediastinal mass
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Only leukemia without lymphadenopathy
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hairy cell leukemia
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Is hairy cell leukemia a lymphoid neoplasm or a myeloid neoplasm?
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Lymphoid
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AML w/ gum hyperplasia
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Monocytic leukemia (M5)
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Cell markers of Histiocytosis X
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S-100, CD1a
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Letterer-Siwe disease
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child less than 2 years old with erupting seborrheic-like cutaneous lesions, rapidly fatal
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Hand-schuller Christian disease
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bone defects, diabetes insipidus, exophthalmos
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Which test do you use to follow heparin?
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PTT
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Which test do you use to follow warfarin?
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PT/INR
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Difference between enoxaparin and heparin
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acts more on Xa, has better bioavailability, and doesn't need lab monitoring
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S/E of warfarin
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teratogenic, bleeding, skin/tissue necrosis
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Names of thrombolytics and what reverses their effect?
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streptokinase, urokinase, alteplase, anistreplase (APSAC)
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aminocaproic acid
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Why is d-dimer better than FDP
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FDP indicates whether fibrinogen is still being broken down. In the case of cirrhosis, plasmin-inhibiting factor is lost, and FDP is increased. However, D-dimer wouldn't be increased, because it is solely a measure of how much fibrin is being broken down.
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Ticlopidine S/E
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neutropenia (which can cause mouth ulcers), severe bone marrow toxicity
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Chemo drugs that work in S-phase
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methotrexate, 5-FU, 6-MP, 6-TG, cytarabine, Etoposide, Hydroxyurea,
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Chemo drugs that work in the G2 phase
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Bleomycin, etoposide,
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Chemo drugs that work in the M phase
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Vinka alkaloids, paclitaxel
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2 drugs whose toxicities increase w/ allopurinol
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6-MP and azathioprine
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Cancer drug that CAN be given w/ allopurinol
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6-TP
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MTX S/E
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macrovesicular fatty liver, mucositis, teratogenic
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5-FU S/E
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photosensitivity
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Cytarabine MOA and S/E
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MOA: pyrimidine antagonist that inhibits DNA polymerase
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S/E: leukopenia, megaloblastic anemia
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Doxorubicin MOA and S/E
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MOA: generates free radicals, noncovalently intercalates DNA, disrupts fluid and ion transport
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S/E: cardiotoxicity, myelosuppression, alopecia. Can be prevented w/ dexrazoxane
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ABVD Tx for Hodgkins
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Adriamycin, bleomycin, vinblastine, dicarbazine
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Bleomycin MOA and S/E
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MOA: G2-phase specific formation of free radicals leading to DNA strand breaks
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S/E: pulmonary fibrosis, minimal myelosuppresion, skin changes
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Etoposide uses and S/E
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Uses: small cell carcinoma of lung and prostate
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S/E: myelosuppression, GI, alopecia
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Cyclophosphamide MOA and S/E
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MOA: covalently cross-link DNA at guanine N-7. Requires bioactivation by liver
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S/E: myelosuppression, hemorrhagic cystitis (can be prevented w/ mesna)
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Nitrosureas (-mustine, streptozocin) MOA and S/E
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Cross BBB and cross-link DNA strands. Requires bioactivation
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S/E: CNS toxicity
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Busulfan MOA and S/E
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MOA: alkylates DNA
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S/E: pulmonary fibrosis, hyperpigmentation (similar profile to bleomycin)
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Cladribine MOA and use
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MOA: purine analog that is resistant to adenosine deaminase and penetrates CNS
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Use: hairy cell leukemia
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Vincristine S/E
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neurotoxicity (peripheral neuritis, areflexia), and paralytic ileus
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Vinblastine S/E
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bone marrow suppression
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Cisplatin MOA and S/E
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MOA: cross-link DNA
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S/E: nephrotoxicity, acoustic nerve damage (amifostine can be given to prevent nephrotoxicity)
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Prednisone S/E
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aside from Cushing-like symptoms, there are cataracts, acne, PUD, psychosis
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Imatinib S/E
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fluid retention
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Herceptin/Trastuzumab S/E
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Cardiotoxicity
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