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180 Cards in this Set
- Front
- Back
What ar ethe compensatory mechanisms in anemia?
|
increased cardiac output: palpitaitons, dizziness, syncope
redistribution of blood: pallor Right shift in Hb-O2 curve due to increased 2,3-BPG |
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What are the causes of micrcytic anemia?
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iron deficiency, ACD, thalassemia, sideroblastic anemia, hemoglobin E
|
|
What anemia have a dificiency in heme synthesis?
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iron deficiency, ACD, sideroblastic anemia
|
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What anemias have a deficiency in globin synthesis?
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thalassemia and HB E
|
|
What are the pts at risk for iron deficiency?
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Infants (breast milk), women of reproductive age (menses), disease w/ chronic blood loss (GI CA)
|
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What is the presentation of Fe deficiency?
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Plummer Vinson syndrome: esophageal web, koilonychias, glossitis,
pica |
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What are the 2 products released in ACD?
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hepcidin: prevents lease of iron from macrophages
lactoferin: sequesters iron from bacteria |
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What pts get ACD?
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chronic inflammatory disease: RA, TB
alcoholics, cancer |
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What makes up HbA2, HbF?
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alpha w/ either delta, gamma
|
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What is does beta thalassemia major looks like?
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no HbA, increased HbF & HbA2
sever anemia, splenomegaly, expanded marrow (distorted bones) requires frequent RBC transfusions overtransfusion --> hemosiderosis |
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Which thalassemia has normal Hb electrophoresis?
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alpha thalassemia trait
|
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What thalassemia results in hydrops fetalis? What virus?
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Hb Bart
Parvovirus B19 |
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What 2 enzymes are damaged by Pb in anemia?
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ferrochelatase: addes Fe to protoporphyrin
ribonuclease: degrades RNA of ribosomes --> basophilic stippling |
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What causes basophilic stippling in Pb poisoning?
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Pb denatures ribonuclease whihc normally degrades RNa of ribosomes
|
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What is the presentation of Pb poisoning?
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GiL colic w/ diarrhea, Franconi's proximal RTA, loss of GAP in urine (glucose, amino acids, phosphate)
CNS: encephalopathy, PNS (wrist and foot drop) sideroblastic anemia w/ basophilic stippling |
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How does Pyridoxine cause anemia? Presentation? Causes?
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B6 is a cofeacter for delta-aminolevulinic acid synthase
seizures, irritability, cheilitis, anemia diet, INH |
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What chemical is found in both folic acid and B12 deficiency? What chemical is only found in B12 and leads to demyelination?
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homocysteine
methylmalonyl CoA |
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What are causes of B12 deficiency?
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malnutrition, gastric bypass, pernicious anemi, chronic pancreatitits, ileal diseases, bacterial overgrowth or diphyllobothrium latum
|
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What are causes of folate defiicency?
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malnutrition, pregnancy, drug induced (5-Fu, methotrexate, trimethoprim-sulfa
|
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What is the clinical precentation of megaloblastic anemia?
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macrocytic anemia, jaundice secondary to RBC lysis, pancytopenia, HYPERSEGMENTED PMNS, prothrombotic effect form elevated homocysteine
Neurological effect (B12 only)- subacute combined degeneration of posterior columns and lateral STT --> decrease in vibratory and proprioception and umn lesions w/ hyperrreflexia |
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What are other cuase of megaloblastic anemia?
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liver disease, myelodysplasia,
|
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What are causes of reticulocytosis?
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hemolysis, hemorrhage, hematinic
polychromasia |
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What are causes of normocytic anemia with low retic count?
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aplastic anemia, chronic renal failure, acute blood loss, early ACD
|
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What worsens HbS sickling?
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low O2 tension: acidosis, volume depletion, hypoxemia
|
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What is the presentation of sickle cell anemia?
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hemolytic crisis
aplastic crisis, thrombosis, sequestration |
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How do you diagnose sickle cell?
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sickle cell solubility screen, electrophoresis (HbAS), peripheral blood smear has target cells, sickled cells, Howell-Jolly bodies
|
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What is the defect in hereditary spherocytosis? How do you diagnose?
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autosomal dominant defect in ankyrin and spectrin
Blood smear (spherocytes-round w/o central pallor) and osmotic fragility test |
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What is the mutation in hereditary elliptoctosis?
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spectrin or band 4.1
oval shaped |
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What is the pathogenesis of paroxysmal nocturnal hemoglobinuria? Presentation? dx?
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Loss of anchoring protein for decay accelerating factor and CD59 --> susceptilibty to destruction by complement
episodic hemoglobinuria (night time acidosis -->complement binding due) risk for AML, increased thrombosis, especially hepatic vein (Budd-Chiari syndrome) Dx: Sugar water test, Ham test |
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What is the pathogenesis, causes, and dx of G6PD deficiency?
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X linked deficiency
cannot maintain glutathione which protects RBCs form oxidative damage oxidized Hb precipitates as Heinz bodies and which are removed by splenic macrophages to form bite cells Causes: infection, oxidizing drugs, malaria drugs ingestion of fava beans Heinz bodies, bite cells |
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PK deficiency pathogenesis? Dx?
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Autosomal recessive defect in PK, normally converts PEP to pyruvate with gain of ATP
low ATP causes hemolytic anemia Dx: Echinocytes, RBC enzymes |
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What are the alloimmune hemolytic anemias?
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hemolytic transfusion reactions, hemolytic disease of the newborn
|
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what are the 2 types of autoimmune hemolytic anemias?
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Warm AIHA- IgG at body temp. Viral, SLE, CLL, drug, penicillin, alpha-methyldopa
Cld- IgM. infection, drug induced. Complement |
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What are the causes of microangiopathic hemolytic anemias? what is seen on blood smear?
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DIC, TTP (ADAM TS13), HUS
schistocytes and helmet cells |
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What is a left shift?
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increase i number of bands (immature PMNs)
|
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What are reactive changes in PMNs associated w/ infection?
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toxic granulation, vacuolization, Dohle bodies
|
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What are the age groups form leukemia?
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ALL 0-14, AML 15-60, CML 40- 60, CLL 60+
|
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What is myelodysplasia? Peripheral blood/bone marrow presentation?
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Ineffective hematopoeiesis and dyspoiesis of other cell lines.
Cells stuck in marrow --> thick marrow and thin blood pancytopenia with macrocytic anemia non-responsive to B12/folate circulating blasts or nucleated RBCs abnormal blood cell morphology (dyspoiesis): erythrocytes: megaloblastic, oval, weird nuclei, ring sideroblasts leukocytes: hypogranular, abnormal segmentation (Pelger-huet), basophilia, megakaryocytes w/ unusual lobulation and hypogranular platelets Hypercellular bone marrow and less than 20% of marrow are blasts |
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What is ALL?
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MC leukemia in 0-14, association w/ Down's syndrome
Sx of bone marrow suppression (pancytopenia), FUO, bone pain. Mets to various organs- MC CNS, mediastinum, testicles, renal, bone/joint. Prognosis: Hyperdiploidy has better prognosis. Age 1-10 is better. t(12;21) is better. WBC > 100k has poorer prognosis. T-cell and Burkitt's have poorer prognosis. |
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What is AML?
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adults>children 15-60
M2/M3 have Auer rods Staining: myeloperoxidase and sudan black (M3), alpha naphthyl esterase (M4/5) Bone marrpow suppression |
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What are the significant AMLs?
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M3- promyelocytic: multiple Auer rods, DIC, translocation t(15;17), all-trans retinoic acid (vit A) tx
M5 (monocytic): gingival hyperplasia |
|
What is CML?
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hypercellular bone marrow and increased peripheral cells --> thick blood, thick marrow
Splenic enlargement as spleen tries to clear malignant cells Progressive marrow fibrosis transform into AML aka blast crisis translocation t(9;22) w/ bcr-abl fusion gene on Philadelphia chromosome 22. Gleevec or Imatinib is a tyrosine kinase inhibitor used to treat. Decreased LAP score |
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What is associated with Pelger-Huet segmentation?
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myelodysplasia
|
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What is CLL?
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old patients,
dusfunctional B cells results in hypgammaglobulinemia Smudge cells on peripheral blood smear. CD5 B cells are present |
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What is hairy cell leukemia?
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hair cells are cells with porjection of cytoplasms. Peripherla blood: pancytopenia. Splenomegaly.
Resistance to TRAP stain. |
|
Polycythemia Vera?
|
proliferation of erythroid cell line --> increased Hb and Hct, increased plasma volume, decreased EPO
Presentation: hyperviscosity --> thrombotic events (Budd-Chiari) and HF hyperuricemia --> gout (breakdown of cells --> purine release Histamine release --> flushing, red/congested skin Tx: phlebotomy differential: hypoxic states have elevated EPO and decrease SaO2 Ectopic EPO has increased EPO Polycythemia vera has decreased EPO |
|
Myelofibrosis with myeloid metaplasia?
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fibrotic bone marrow form inappropriate growth factors form neoplastic megakaryocytes
splenomegaly as cells move to spleen and cause extramedullary hematopoiesis teardrops RBCs due to fibrosis of bone marrow immarture RBCs and myeloid cell in periphery variable platelet count WBCs eleavted, but immature |
|
Essential thrombocytopenia?
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proliferaiton of megakaryocytes --> overproduction of useless platelets --> high count, but bleeding
|
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What is the presentation of multiple myeloma?
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hypercalcemia, renal failure, anemia (Rouleaux formation), bone lesion
|
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Lymphoma?
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painless LAD
fever, wt loss, night sweats |
|
What characterizes Hodgkin's versus Non-Hodgkin's?
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Hodgkin's: axial, contiguous, polyclonal lymphoid cells
Non-Hodgkin's: Peripheral, non-contigous, common mesenteric and extranodal sites |
|
What are low-grade Non-Hodgkin's lymphomas?
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Small lymphocytic lymphoma- oslid counterpart to CLL. CD5 on B cells
Follicular lymphoma- BCL-2 oncogene expression, t(14;18) translocation |
|
What are high-grade B-cell lymphonmas?
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Diffuse large B cells
Burkitt's lymphoma- starry sky macrophagges. C-myc onocogene w/ t(8;14) translocation |
|
What are the T-cell lymphomas?
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Mycosis fungoides- psoriatic rash unresponsive to steroids
Sezary syndrome- T cells enter blood and circulate- Buttock cells |
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Hodgkin's lympa?
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Ree-Sternberg Cells
contigous spread, rearely extranodal nodular sclerosing MC type with bands of fibrosis transecting the node with lacunar cells |
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Why do platelets release serotonin?
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vasoconstriction
|
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What are the reactions of platelets?
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adhesion-interaction between specific platelet surface glycoprotein receptors and subendothelial collagen
activation of coagulation cascade- contributes platelet phospholipids- makes activation of thrombin possible arachadonic acid metabolism- leads to formation of thromboxane A2- vasoconstrictor and platelet aggregant platelet aggregation stabilization of platelet plug- by fibrin |
|
What makes factor XIII and factor VIII?
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platelets
endothelial cells |
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What are the Vitamin K dependant factors?
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II, VII, IX, X require gamma-carboxylation in the LIVER
protein C, S |
|
What is the common pathway?
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X--> Xa
Xa complexes with factor Va, Ca2+ and phospholipids Xa-Va-Ca2+-PL complex (prothimbinase) converts prothrombin to thrombin |
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What is the extrinsic pathway?
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Tissue factor (thromboplastin) is released upon tissue injury and activates factor VII.
TF-VII complex and active IX, X Measured by PT which measures II, V, VII, X, and fibrinogen |
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What is the intrinsic pathjway?
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High molecular weight kininogen and kallikrein activate factor XII
Factor XIIa activate factor XI which activate factor IX. Factor IXa + factor VIIIa and vWF activate factor X Measured by PTT Measures everything except 7 and 13. 2, 5, 8-12, fibrinogen |
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What is the process of fibrinolysis?
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tPA converts plasminogen to plasmin. Plasmin splits fibrin --> fibrin degradation productions (FDPs) and d-dimer
d-dimer eleated in PE, DVT, DIC |
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What are inhibitors of the coagulation factors?
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Antithrombin III- Proteinase inhibitor- enhanced by heparin
Protein c cleaves factor Va into its inactive form, inactivates VIIIa and requires Protein S as cofactor and thrombomodulin on endothelium. Tissue factor pathway inhbittor binds TF-VIIa-Xa comple to inactivate extrinisc pathway |
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What are Virchow's triad?
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hypercoaguability
statsis endothelial injury |
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What are Pts w/ antithrombin III deficiency resistant to?
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heparin
|
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What is Factoir V Leiden
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Factor V mutation prevents activated protein C from binding and inactivating factor Va.
|
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What is the 20210A transition in Prothrombin?
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eleavted prothrombin levels and increase in venous thrombosis
|
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What is MTHFR C677T mutation adn tx?
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increased homocystein --> thrombosis
Tx: folic acid, B12, and B6 to counteract methionine loading |
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What are examples of antiphospholipid antidbodies? What do they do?
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Lupus anticoagulant, anti-cardiolipin Abs
they prevent clotting cascade --> recurrent thromboembolism, fetal loss, thrombocytopenia |
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What nerves are used for nerve biopsy?
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sural nerve (sensory), peroneal nerve (motor)
|
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What are used for muscle biopsy?
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vastus lateralis, deltoid, biceps brachii, tibialis anterior
|
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What are the nerve layers from in to out?
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endoneurium, perineurium, epineurium
|
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What are the muscle fiber types?
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Type I- slow twitch. Many mitochondira, lipid rich. Red appearance. Light on ATYPase pH 9.4 stain.
Type II "fast twitch" few mitochondria, glycogen rich. White appearance. Dark on ATPase 9.4 stain. |
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What is a motor unit?
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1 lower motor neuron and the muscle fibers it innervates
|
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What is segmental demyelination?
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Dmage to Schwann cells w/o dmage to axon
Axon sends out message for differentiation of neraby regenerative cells into new Schwann cells Schwann cells cells phagocytose dead myelin and undergo mitois New myelin sheath is thinner and has increased Nodes of Ranvier --> slow conduction time Onion bulbs Teased nerve fibers w/ lipid stain --> thining due to lack of myelin |
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What are onion bulbs in the context of neuronal injury?
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Seen w/ repeititive cycles of demyleination.remyleination
concentric layers of Schwann cell projections surrounding the axon |
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What is axonal degeneration? When is regeneration possible?
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Primary destruction of the axon w/ secondary degeneraiton of the myelin sheath
nerve body is intact |
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What is Wallerian degeneration?
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distal degeneration after axonal damage
swelling and vacuolization of nerve fibers enlarged nerve cells, lots o dark cytoplasm w/ abundant lipid |
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What is a traumatic neuroma?
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nodular mass of nerve fibers and Schwann cells
occurs when scarring obstructs new growth cone fro it endpoint |
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What is muscle denervation?
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loss of LMN results in muscle fiber atrophy
Muscle can survive until reinnervationed, but willl be angulated and shrunken may be reinnervated by a nearby neuron, can result in a switch of fiber type or grouping |
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What are 4 muscle pathological reactions?
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fiber necrosis: segmental, macrophage infiltration and dead myofibrils on H&E
Fiber regeneraiton: can occur if endomysial tube remains intact [basophilic cytoplasm and regenerative nuclei] internal nuclei: very non-specific change Ringed fibers: fibers run perpendicular to normal orientation |
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What are the Sx of UMN and LMN lesions?
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UMN- hyper-reflexia, spasticity, + Babinski
LMN- muscular atrophy, weakness, fasiculations |
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What is spinal muscular atrophy?
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autosomal recessive disase with progressive loss of LMNs
SMN1- responsible for disease SMN2- extra copy --> less severe disease As Type's increase in number, severity decreases Macroscopic: Anterior roots are grey and atrophic Microscopic: nerve biopsy --> overall loss of neurons, w/ few swollen residual neurons muscle biopsy --> atrophic cell sheets with some hypoertorphic cells |
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What is poliomyelitis?
|
polio virus invades the nervous system and damages motor neurons
Respiratory and GI Sx LMN --> flaccid paralysis respiratory failure atrophic muscle replaced w/ fat Post-Polio syndrome- progressive weakness associated w/ decreased muscle bulk and pain |
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What is the presentation of diabetic neuropathy?
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symmetrical, decreased sensation andparesthesia in distal extremities
autonomic: gastroparesis, impotence, neurogenic bladder, orthostasis thinkly myelinated fibers and vascular thickening |
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What characterizes sarcoidosis neuropathy?
|
granulomas in perineurium w/ atrophic nerve fibers
mononeuropathy |
|
What characterizes amyloidosis neuropathy?
|
Sensory or sensorimotor neuropathy
pink, hyaline material in nerve cells |
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What is the pathology of ischemic neuropathy?
|
widespread axonal loss w/ fascicles on EM
|
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What is Charcot-Marie-Tooth
|
mutations in neural proteins affecting the myelin sheath and axon. Autosomal dominant
presents in childhood w/ atrophy of lower leg muscles peroneal nerve atrophy legs have inverted bottle appearance onion bulb changes |
|
What is GBS?
|
autoimmune inflammation w/ demyleinatoin of peripheral motor fibers
ascending muscle weakness, starting with LE --> neurological deficits T cells infilitration and attacking myelin sheaths autoimmune response to infection or vaccines |
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What is myasthenia gravis?
|
autoantibodies against ACH receptors
ptosis, double vision, worsens w/ use muscle weakness. thymic hyperplasia > thymoma prolong survival w/ tx |
|
What is Lambert-Eaton syndrome?
|
auto-antibody against pre-synaptic Ca channel
similar to M, proximal muscle weakness praneoplastic syndrome associated with small cell CA |
|
What helps with dx of polymyositis and dermatomyosistis?
|
anti-Jo-1 Abs, 50% ANA
lymphoid inflammation and atrophy/necrosis of muscle |
|
What is inclusion boy myositis?
|
distal muscle weakness
rimmed vacuoles on trichome stain EM of vacuoles just shows membraneous debris in cytoplasm |
|
What are mitochondrial myopathies?
|
mutaitons in mitochondrial DNA or DNA coding leads to deficient ATP production
presents in young adulthood with proximal and ocular muscle weakness neurological Sx, lactic acidosis, cardiomyopathy ragged red fibers characteristic on trichome (aggregates of abnormal mitochondria) parking lot inclusion on EM (abnormally stacked cristae) |
|
What is nemaline rod myopathy?
|
non-progressive, proximal muscle weakness
nemaline rods within fibers on trichome staine Z-band like material in clumps on EM |
|
What causes toxic necrotizing myopathies? Vacuolar myopathy?
|
alcohol, stains, snake venoms
colchicine, chloroquine |
|
Wha tis the inheritance of Becker's muscular dystrophy?
|
X-linked recessive
|
|
What is myotonic dystrophy?
|
CTG repeat tha taffects the mRNA for a muscle protein kinase
grip and percussion myotinia distal muscle and facial weakness (ptosis) frontal cataracts, balding cardiac internal nuceli, variation in fiber size, ringed fibers |
|
hyperkeratosis
|
thickening of stratum corneum --> scaly appearance (psoriasis)
|
|
parakeratosis
|
persistence of nuclei in cornified layer (normal on mucous membranes)
|
|
ancanthosis
|
thickening of basal and spinosum layers (psoriasis)
|
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Spongiosis
|
intercellular edema in the epidermis (eczema)
|
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Exocytosis
|
inflammatory cels entering the epidermis
|
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acantholysis
|
loss of connections between keratinocytes
|
|
dyskeratosis
|
premature keratin in lower layers
|
|
Seborrheic keratosis
|
round/elevated/pigments, raisin-like, stuck on
may resemble melanomas hyperkeratosis and acanthosis w/ pseudohorn cysts (islands of keratin within epidermis) |
|
What is Leser Trelat sign?
|
multiple seborrheic keratoses in a short time due to paraneoplastic syndrome of GI CA
|
|
What is a fibrous dermal core surrounded by normal epidermis?
|
acrochordon
|
|
What is an epidermal cyst (sebaceous cyst)?
|
pea-like nodul under the skin surface
cyst wall w/ keratin debris, surrounded by normal epidermis spontaneous inflammation, rupture |
|
What is a dermatofibroma?
|
firm, tan/brown papules on leg (dermal tumro = under epidermis)
Histology: spindel cell proliferation w/ hyperpasia of overlying layer |
|
What is a freckle? What are liver spots? what causes them?
|
ephelis
lentigenes Sun/increase in melanocytes |
|
What are actinic keratosis (Bowen's disease)?
|
red/raised plaque w/ scale in sun exposed regions; scale returns if scraped
dysplasia of keratinocytes Pre-malignant- basal or squamous cell |
|
What are keratoacanthoma?
|
resemble squamous cell carcinoma
volcano-like crater filled w/ keratin may progress in to SCC regresses due to immune reaction |
|
What are nevocellular nevus?
|
mole
proliferation of nevus cells (modified melanocytes) juncitonal, compound, inttradermal clustersof typical looking melanocytes BENIGN |
|
What is a dysplastic nevus?
|
pre-malignant version of nevocellular nevus, irregularly pigmented/bordered
Histo: atypia of melanocytes, dermal fibrosis, inflammation, melanocytes migrating to surface Risk of melanoma dysplatic nevus syndrom- hundred of nevi |
|
Solar elastosis?
|
actinic damage
severely wrinkled skin secondary to chronic sun exposure UV light activates proteases degernation of dermal collagen |
|
Basal cell carcinoma
|
papule, pearly borders; teleanectasia
sun exposed areas above the mouth MC skin cancer in US blue staining cells, bud off the basal alyer does not metastasize --> local excision is curative |
|
Squamous Cell Carcinoma
|
nolduar/scaly lesion, may be ulcerated/crusted
sun exposed areas below the mouth MC skin cancer associate w/ immunosuppression pink stainig atypical squamous cells w/ keratin perals low risk of metastasis if neglected |
|
Malignant melanoma
|
melanocyte cancer, lower legs & back
majority de novo, some pre-existing nevi MC fatal skin cancer Risk: ligh complexion, freckles, sun exposure, peeling sunburns, dysplastic nevus syndrome or increased number of nevi, Xeroderma pigmentosum Radial and vertical growth phases Superficial spreading: radial growth Lentigo malgina: occurs on face, least metatastic Nodular: aggressive, starts in vertical phase Acral lentiginous: palms, soles, under nails; dark skinned Prognosis: depth of invasion |
|
Verruca vulgaris
|
HPV
|
|
Moluscan contagiosum
|
firm papules w/ central umbilication (dimpling)
molluscum bodies- viral inclusion within epidermal cells poxvirus |
|
Impetigo
|
staph aureus- persistent bullae
honey-colored crust of dried pus - Group A Strep |
|
Folliculitis-
|
painful yellow pustules within surrounding erythema around hair follicleStaph/Strep or pseudomonas
topical corticosteroid use- staph/strep hot tub- pseudomonas |
|
Erysipelas-
|
infection of top half of dermis; edematous/warm/erythematous
associated fevers, rigors, vomitting, fatigue STREP |
|
Cellulitis
|
deeper infection of skin spreading through dermis or subQ
lymphatic streaks signifies a severe case of spread may resulting in necrotizing fasciitis caused by staph/strep or H. flu |
|
What are the stages of eczema?
|
acute eczema- weeping papules, vesicles, bullae
histo: spongiotic edema secondary to congestion, vascular dilation subacture eczema- red/scale/crusting lesion form reactive hyperplasia Histology: hyperkeratosis chronic eczema- dry, red/scaly, fissuring Histo: hyperkeratoris and acanthosis, relongation of rete ridges |
|
What are the subtypes of eczema?
|
atopic eczema- flexural areas, children, asthma
Seborrheic dermatitis (cradle cap)- yellow sclaes on infant scalp discoid eczema- discrete erythematous coin-shaped lesions lichen simplex- respnse to chronic rubbing/scratching Contact dermatitis- irritant vs allergic |
|
Psoriasis
|
symmetrical salmon-pink patchesw/ silvery scale on extensor surfaces
due to increased epithelial turnover, leading to epidermal hyperplasia associated w/ rheumatoid-like psoriatic arhtritis PMN infiltrate, hyperkeratosis/acanthosis, dilated dermal papillae |
|
pityriasis rosea
|
herald patch- initial oval-shaped scaly plaque on trunk --> followed by pink patches w/ ring of scale (target) spreading in a Christmas tree distribution
|
|
Lichen planus
|
pataches of purple, pruritic, polygonal papules; slow epithelial turnover
Koebner phenomenon, also seen in psoriasis lymphocyte infilitrate at basal layer, Civate bodies (destroyed basal cells), sawtooth appearance at dermis-epidermis junction |
|
Acne vulgaris
|
androgen- driven overactivity of sebaceous glands w/ ductal obstruction
bacteria convert sebum to inflammatory fatty acids comedones, papule, pustule, cysts, scars |
|
Rosacea
|
papules/pustules w/ flushing and erythema of cheeks, forehead, nose, chin
Histology: vascular dilation (leads to flushing) and sebaceous hyperplasia |
|
Bullous pemphigoid
|
abs to basement membrane at dermal-epidermal junction (hemidesmosomes)
epidermis separating from dermis in an intact later tense, itchy bullae vesicle that don't pop easily due to intact laters biopsy w/ immunofluorescence, Ab-Ag complex at junction |
|
Pemphigus
|
Abs to intraepidermal junction (desmisomes)
results in epidermal cellsseparating from each other, thus skin easy to break Easily broken bliders, painful erosing, espec mucous membranes immunofluorescence shows IgG, C3 between epidermal cells |
|
Toxic erythema
|
ithcy, red maculopapular
|
|
Erythema multiforme
|
symmetrical target lesion, may have blisters
lymphoid dermail inflammation infeciton, drugs, SLE, vasculitis |
|
Stevens-Johnson is related wot which erythema?
|
erythema multiforme majorum
|
|
What cause urticaria?
|
type 1 hypersensitivity
transient red swelling w/ central pallor |
|
What are diaphysis- metaphysis, and epiphysis?
|
long shaft, middle area, rounded edges
|
|
What are 2 gross bone types?
|
cortical and trabecular
|
|
What are the molecular bone types?
|
lamellar, woven bone
|
|
What are the fractures types?
|
simple vs complex
complete vs incomplete comminuted fracture pathologica fracture stress fracture |
|
What are the steps of fracture healing?
|
osteoblasts/osteoclasts at ends of fracture die due to ischemia
collagen is laid down vascularity increases osteoprogenitor cells stimulated --> callus formation endochondrial bone formation may occur woven bone remodeled to stronger lamellar bone |
|
Factors that poorly affect healing
|
poor alignment
failure to immobilize --> delay healing, pseudoarthrosis- fibrosis rather than bony bridge infection, low blood supply, nutrition, foreign bodies, corticosteroid use |
|
Legg-Calve-Perthes
|
avascular necrosis of the femoral head
artery of ligamentum teres closes before medial circumflex femoral artery can supply blood to the femur |
|
What are causes of osteonecrosis?
|
fracture/trauma, corticosteroid use, vascular insufficiency
|
|
What are the causes of osteomyelitis?
|
hematogenous, post-traumatic w/ direct implantation, overlying ulcers
|
|
What are the patheogens of osteomyelitis?
|
Staph aureus- MC overall
TB- Pott's disease (spine) w/ spread to soft tissue (Psoas abscess) Salmonella- Sickle cell Pseudomonas- puncture through rubber shoes |
|
What are the complications of osteomyelitis?
|
sequestrum-dead bone surrounded by infeciton
involucrum: bone beneath periosteum, surrounding sequestrum bone abscess periosteal inflammation w/ spread to soft tissue septic arthritis pathological fractures |
|
How does estrogen protect bone in premenopausal women?
|
estrogen modulates IL-1 (osteoclast activating factor) activit, inhibiting production of osteoclasts and enhancing osteoblasts
|
|
What are the complications of osteoporosis?
|
vertebral body compression fracture
femoral neck fracture Colles' fracture of dital radiu |
|
What is osteopetrosis?
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increased densirty of bone due to genetic defect of osteoclasts
unable to break down bone and unable to remodel weak woven bone fractures, cranial nerve compression (visual/hearing loss) pancytopenia due to loss of bone marrow space Marble bone- weaken woven bone visualized on polarized microscopy Sclerotic changes on radiograph, ehrlenmeyer flask deformities of long bones, lack of cortical-medullary differentiation |
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What is Paget's disease of bone?
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increased osteoblast and clast activity
targets pelvis, skull, femur may be viral (paramyxovirus) osteolysis --> osteoblastic --> sclerotic enlarged forehead, CNS findings (stenosis of foramen), elevated alk phos chalk stick fractur secondary osteoarthritits, increased osteosarcoma |
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What are secondary causes of osteoarthritis?
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jount deformity, systemic disease (hemochromatosis), alkaptonuria, repetitive trauma)
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What are the pathological findings with OA?
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loss of intra-articular cartilage (Eburnation, sclerosing bone plates)
Osteophytes, subchondral custs, mild lymphoid inflammation in synovium |
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What is the presentation of OA?
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Nodal OA- Heberden-DIP, Bouchard-PIP, Hallux valgus
Axial OA- spinal stenosis and spondylosis Weight bearing joints- hips and knees |
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What is the genetic component of RA?
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HLA-DR4
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What is the pathogenesis of RA?
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RF- IgM aginst Fc receptor of IgG
RF complexes --> complement activation --> destruction of tissue by PMNs Pannus: hyperplastic synovium secondary to chronic inflammation --> joint fusion, fibrosis (ankylosis) Results in joint deformity |
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What is the presentation of RA?
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morning stiffness that improves as day goes on
PIP an dMCP--> ulnar deviation RA nodules arterititis, neuropathy, pericarditits, pleuritis, LAD --> lymphoma risk |
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What are the disease association with RA?
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Felty- splenomegaly + neutropenia
Caplain- pneumoconiosis Sjorgen's RA + Sicca |
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What is juvenile idopathic arthritis
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tends to hit larger joints, less destructive, more liekly to have systemic findings
often RF negative Systemic JIA (Still's disease): fever, rash, polyarthritis |
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What is ankylosing spondylitis?
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HLA B27 spondylarthropathy
destruction of articular cartilage of the spine --> fusion (bamboo spine) Lower back pain and stiffness in males 20-30 associated with UC, uveitis, and restrictive lung disease |
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What is the presentation of gout?
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first MTP (podagra)
chronic --> tophio joint aspirate - yellow, needle shaped, negative birefringence |
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What are the disease associations of gout?
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Lesch-Nyhan
kidney failure leukemia |
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What is pseudogout?
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deposition of Ca pyrophosphate
knee is most common rhomboid, positive birefringence, blue |
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What are the MCC of septic arthritis?
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staph aureus- children
N. gornorrhea- urban esp C5-C9 Lyme diease-BAKE Pasturella multocide- cat bite |
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What is a disk herniation?
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nucleus pulposus through annulus fibrosus
posterior herniation will compress nerve fibers |
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What is osteoid osteoma?
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MC benign bone tumor;late peds and young adult
long bones (femur) night pain from prostaglandins central area (nidus) of woven bone surrounded by sclerotic bone |
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What is osteochondroma?
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outgrowth of bone off the shaft of a long bone, capped by articular cartilage
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What is aneurysmal bone cyst?
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tumor full of multinodular cysts and vascular tissue (hemosiderin staining)
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What is a giant cell tumor of bone?
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histiocyte sand giant cells around KNEE, may become malignant
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What is a osteoma?
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cortical bone mass found on facial bones, projects in sinus of head
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Enchondroma
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lump of cartilage within shaft of long bone, usually phalanges
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What is a osteosarcoma?
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MC primary malignant bone tumor
long bones near knee association w/ Paget's Codman's triangle Sunburst appearance tumor cells making osteoid |
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Ewing sarcoma?
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t(11;22)
onion skin aronud bone small blue cell tumor of undifferentiated cells |
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What is a fibromatosis?
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fibrosis rxn at tendons --> thick tendons become scarred and contract
Palmar- Dupuytren's contracture Penile- Peyronie's disease |
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What is a Morton's neuroma?
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reactive fibrosis of entrapped nerve
women in high heels painful bump between metatarsals |
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What characterizes the myxoid liposarcoma?
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younger pt, chicken wire pattern
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