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105 Cards in this Set
- Front
- Back
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what is the difference between acute and chronic INFLAMMATION
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Acute:
1. early onset and short duration 2. exudation of fluid and plasma proteins 3. PMN (neutrophils) Chronic: 1. longer duration 2. lymphocytes 3. macrophages 4. proliferation of blood vessels and connective tissue |
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what are the classic signs of acute inflammation
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1. heat
2. redness 3. swelling 4. pain 5. loss of functions |
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what are the most important features of an inflammatory reaction
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neutrophils and monocytes at the site of injury
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what is the sequence of cellular change
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1. margination (when RBC clump together in the center of the vessel and displace the WBC towards the periphery)
2. adhesion and transmigration from venules 3. chemotaxis and leukocyte activation (process by which leukocyte are directed to the site of injury) 4. phagocytosis |
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what are the cells that are involved in inflammation
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1. neutrophils (1st to arrive, predominant cells of acute inflammation, phagocytosis)
2. basophils (type I and IV hypersensitivity) 3. eosinophils (allergy and parasites) 4. mast cells (histamine release) 5. macrophages 6. lymphocytes |
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what are the SIX results of inflammation
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1. complete resolution (return to normal)
2. scarring 3. suppuration (abscess, ulcer, or empyema) 4. chronic inflammation 5. spread (local, lymphatic, blood) 6. death |
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what are the THREE ways chronic inflammation occurs??
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1. healing of acute inflammation is incomplete
2. persistence of the injurious agent 3. abnormal immunological response |
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what are the THREE cells of chronic inflammation
what are granulation tissues? |
MONOCYTES:
1. macrophages 2. lymphocytes 3. plasma cells GRANULATION TISSUE: composed of new blood vessels, proliferating fibroblasts and macrophages |
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what are granulomas
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composed of:
1. epitheloids 2. macrophages 3. lymphocytes 4. giant cells (Langhans) |
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what are granulomas in TUBERCULOSIS called?
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tubercles
central caseous necrosis surrounded by epitheloid cells, Langhans giant cells and lymphocytes |
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what are the FIVE morphological patterns of inflammation
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1. serous
2. catarrhal 3. ulcers 4. fibrinous 5. suppurative or purulent |
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where is SEROUS INFLAMMATION found?
when is it most likely seen? what does it consist of? |
1. found in pleural, pericardial and peritoneal cavities
2. thin, few cells, few proteins 3. seen in early stages of most acute inflammation 4. dominant pattern in mild injuries |
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what is fibrinous inflammation
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1. exudation of large amounts of protein from plasma with deposition of fibrin forming shaggy strands
2. exudates may be absorbed and organized (transformed into vascularized tissue by ingrowth of fibroblasts and capillaries) tuberculous pleuritis rheumatic pericarditis |
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what is suppurative/purulent inflammation
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1. exudation of PUS
2. caused by pyogenic bacteria |
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what is the difference between abscess and empyema
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abscess: pus within the substance of an organ or tissue
empyema: pus within a CLOSED CAVITY (pleural space or gall bladder) |
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what is an ulcer
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local defect/excavation of surface of an organ/tissue
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what is catarrhal inflammation
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exudation of mucoid fluid from MUCOUS MEMBRANE
allergic rhinitis bronchitis |
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what are THREE major systemic manifestation of ACUTE inflammation
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1. endocrine and metabolic
-acute phase proteins secreted by the liver C-reactive protein, complement and coagulation proteins 2. autonomic 3. behavioral -rigors, chills, anorexia, somnolence, malaise |
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what are the ANS manifestations of acute inflammation
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1. blood flow redirected from cutaneous to deep vascular beds
2. increase pulse and blood pressure 3. decrease sweating |
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how does a fever come about
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1. release of cytokines into the circulation
2. IL-1, IL-6, TNF-a 3. IL-1 acts on thermoregulatory centers within hypothalamus |
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what is leukocytosis
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1. increase in WBC in circulation from bone marrow
2. induced by IL-1 and TNF 3. also by proliferation of bone marrow precursors induced by colony stimulating factors 4. can cause a LEUKEMOID REACTION (very high WBC count like in leukemia) |
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where is neutrophilia commonly seen
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1. bacterial infection
2. infarction of tissues |
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what is lymphocytosis?
what is it associated with? |
1. increase in # of circulating lymphocytes
2. viral infection 3. infectious mononucleosis |
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where is eosinophilia commonly seen
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1. parasitic infestation
2. certain allergic reactions |
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what is leukopenia?
what is it associated with? |
1. decrease in # circulating WBC
2. inflammatory condition in patients with chronic debilitating diseases (cancer or systemic infection) |
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what are the TWO processes of wound healing
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1. regeneration (replacement of damaged tissue by parenchymal cells of the same type)
2. replacement by connective tissue (fibrosis) both processes contribute to repair in most cases |
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what determines the regenerative ability of cells
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if they are...
1. labile 2. stable 3. permanent |
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what are labile cells
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continuously dividing cells continuing to multiply throughout life to replace old cells that are lost
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what are stable cells
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quiescent cells (considered being in G0, but after loss can enter G1) normally are not actively multiplying but can under cell division to replace dead cells
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what are permanent cells
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NON-DIVIDING CELLS
DO NOT have the ability to reproduce and once destroyed, CAN NOT be reproduced |
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what are the SIX stages of healing by PRIMARY UNION
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1. exudation and clotting of blood followed by scab
2. acute inflammatory reaction in the margin of wound with PMN (epithelial basal cells begin to proliferate) 3. acute inflammatory subside, PMN replaced by macrophages, granulation appears 4. incision space filled with highly vascularized granulation tissue. collagen appears. epithelial proliferation maximum 5. a lot of fibroblasts and collagen. inflammation and newly formed blood vessels disappears 6. SCAR consisting of connective tissue covered by intact epithelium |
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what is secondary union healing
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1. more extensive loss of cells (ulcer, abscess, large wounds)
2. more time required for healing 3. large amounts of granulation tissue grow in from the margin to fill in defect 4. WOUND CONTRACTION (not seen in primary) |
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what are TWO complications of wound healing
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1. exuberant granulation: protrude about surround skin and blocks reepithelialization
2. keloid: excessive of COLLAGEN in connective tissue resulting in large protruding scar |
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what are the SYSTEMIC factors that influence reparative response
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1. nutrition
2. hematologic derangements 3. diabetes mellitus 4. hormones |
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what are the LOCAL factors that influence reparative response
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1. infection
2. vascularity (blood supply) 3. foreign bodies 4. location of injury |
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what is hematopoeisis and when does it occur
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1. production of blood cells and formed elements in blood
2. fetal period takes place in the LIVER and SPLEEN 3. adult period takes place in BONE MARROW |
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what is the M:E ratio
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myeloid to erythroid ratio: 3:1 in men and women
collected from bone aspiration and smear (bone marrow biopsy) |
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what is the MCV
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mean cell volume (how much cytoplasm is in the RBC)
80-96fL in men and women |
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what is the purpose of the reticuloendothelial system and the spleen in blood
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1. RES and spleen filters out unwanted elements from the blood by phagocytosis
2. assume hemopoietic functions |
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where is the iron found in the body
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1. 80% in hemoglobin, myoglobin and iron containing enzymes
2. 20% in storage pools (ferritin and hemosiderin) |
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what is an indicator of iron storage?
how is iron transported? |
1. FERRITIN is a good indicator of the adequacy of body iron storage
2. TRANSFERRIN |
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what are the FOUR general signs and symptoms of anemia
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1. pallor
2. fatigue 3. tachycardia 4. shortness of breath |
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what are the FIVE key diagnosis of iron deficiency anemia
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1. hypochromia, polychromasia and microcytosis
2. decrease in MCV 3. decrease in serum iron 4. decrease in ferritin and plasma ferritin 5. increase in total iron binding capacity |
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in relation to neurological changes what is the difference between pernicious anemia and folic acid deficiency
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pernicious anemia
-neurological change (balance problems) folic acid deficiency -NO NEUROLOGICAL CHANGE |
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what are the TWO types of antibodies associated with Pernicious Anemia (B12 deficiency)
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1. blocking B12-IF binding, result decrease B12 absorption in ileum
2. parietal cell antibodies (parietal cell loss) |
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what are the diagnostic features of Pernicious Anemia (B12 deficiency)
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1. megaloblastic anemia
2. hypersegmented granulocytes 3. NEUROLOGICAL CHANGE associated with posterolateral columns 4. inability to absorb an oral dose of COBALAMIN |
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what is hemolytic anemia?
what are the two forms of it? |
intravascular hemolysis
extravascular hemolysis DECREASE IN RBC (hemoglobin) 1. premature destruction of RBC 2. accumulation of products of hemoglobin catabolism 3. compensatory increase in erythropoiesis within bone marrow |
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what are the manifestations of intravascular hemolysis
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damage to RBC by mechanical, immune or toxic factors
1. hemoglobinemia 2. hemoglobinuria 3. methealbuminemia 4. jaundice 5. hemosiderinuria 6. decrease in serum haptoglobin |
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what are the manifestations of extravascular hemolysis
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occurs whenever RBC are injured, rendered foreign or become less deformable
are sequestered by the spleen for destruction 1. anemia 2. jaundice 3. decrease in serum haptoglobin |
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what is the pathogenesis of sickle cell anemia
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1. HbS molecules aggregate and polymerize upon deoxygenation leading to the formation of HbS fibers and distortion of RBC
2. repeated episodes of sickling and unsickling leads to irreversibly sickled RBC |
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when do infants display signs of sickle cell anemia?
why? |
1. 5-6 months
2. fetal hemoglobin (HbF) inhibits the polymerization of HbS |
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when you have sickle cell trait, when do you display the signs
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1. heterozygotes RBC sickle under conditions of sever hypoxia
2. vaso-occlusive or painful crisis represents episodes of hypoxic injury and infarction associated with sever pain in affected region |
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how do you diagnose for sickle cell anemia
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1. clinical findings (gallstones, leg ulcers, secondary hemochromatosis, autosplenectomy)
2. peripheral blood smear 3. Hgb electrophoresis 4. Sickling test |
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what is thalassemia
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a lack of or decrease synthesis of either alpha or beta globin chain of HbA
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what are the two categories of beta-thalessemia
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1. B0-thalessmia:
total absence of B-globin chains in the homozygous state 2. B+-thalessmia: reduced but detectable B-globin synthesis in the heterozygous state |
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when would an individual manifest symptoms of B-thalassemia major
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1. 6-9 months when Hgb synthesis switches from HbF to HbA
2. same as all the anemias |
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what are diagnostic features seen in B-thalassemia Major
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1. peripheral blood smears shows anisocytosis and TARGET CELLS
2. RBC are microcytic and hypochromic fragmented and stippled 3. reticulocyte count is elevated but not in proportions with anemia |
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what are two forms of absolute polycythemia
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1. primary: increase in RBC mass results from an intrinsic abnormality of the myeloid stem cells (polycythemia vera)
2. secondary: when the RBC progenitors are normal but proliferate in response to increased levels of erythropoietin (appropriate or physiological: lung diease, cyanotic heart disease, high altitudes) (inappropriate: tumor) |
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what is ACUTE LYMPHOBLASTIC LEUKEMIA/LYMPHOMA
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1. 85% are pre-B Cell Tumors
2. TdT POSITIVE cant tell the difference between ALL/AML NO VISIBLE TUMORS |
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what is the diagnostic criteria of chronic lymphocytic leukemia
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1. lymphocyte count of greater than 4000/mm3 but counts as high as 200000/mm3 can occur
2. SMUDGE CELLS 3. CD19, CD20, and CD5 |
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what are the clinical features of chronic lymphocytic leukemia (CLL)
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1. LYMPHADENOPATHY
2. fatigue 3. weight loss 4. anorexia 5. hepatosplenomegaly |
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what is the diagnostic features of follicular lymphoma
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1. nodular aggregates of lymphoma cells are present throughout lymph node
2. cells are small and cleaved 3. NO CD5 EXPRESSION!!! |
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what are the clinical features of follicular lymphoma
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1. painless generalized lymphadenopathy
2. INCURABLE 3. 7-9 years survival, NOT improved with aggressive therapy |
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what are the tumor markers for diffuse large B-cell lymphoma
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1. CD19, CD20, surface Ig, TdT negative
2. rapidly fatal 3. tumor mass found in LIVER or SPLEEN |
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what are characteristics of multiple myeloma
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1. IL-6 dependent
2. IL-6 also serves as an osteoclastic activating factors 3. FLAME CELLS 4. MOTT CELLS |
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what will you clinically find with multiple myeloma
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1. suppression of humoral immunity (more infections)
2. hyperviscosity syndrome (more Ig) 3. hypercalcemia (from bone resorption) 4. Bence-Jones proteinuria 5. M proteins found in serum POOR PROGNOSIS |
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what are Reed-Sternberg cells
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HODGKIN DISEASE
owl eyes cell |
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what is the most common form of HD
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1. Nodular Sclerosis (65-70%)
2. lacunar cells (variant of RS) 3. RS cells are also seen in lymph node or extralymphatics 4. fibrous bands divide cellular areas into nodules |
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what is mixed cellularity
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1. RS cells and a mononuclear variant of RS cell are seen in lymph node of involved tissue
2. BIPHASIC INCIDENCE 3. present with painless enlargement of lymph nodes 4. orderly spread GOOD PROGNOSIS!!! |
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what is acute myelogenous leukemia?
how do you diagnose for it? |
1. accumulation of immature myeloid cells in the bone marrow
2. diagnostic (+) when there is >30% myeloid blast in bone marrow 3. AUER RODS abundant in M3 type |
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what are the good and bad prognosis of AML
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Acute Myelogenous Leukemia
good: chromosome (8;21) bad: philadelphia chromosome (9;22)t |
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what are FOUR ways to evaluate patients with bleeding disorders
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1. bleeding time
2. platelet count 3. prothrombin time 4. partial thromboplastin time |
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if you have a prolong prothrombin time, whats wrong?
prolong partial thromboplastin time? |
PT: normal 10-13sec, test EXTRINSIC and common coagulation pathways.
factor V, VII, X, prothrombin or fibrinogen PTT: normal 20-34sec, test INTRINSIC and common clotting pathways factor V, VII, IX, X,XI, XII, prothrombin or fibrinogen |
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what is factor VIII-vWF complex?
what does it do? |
von Willebrand factor!!!
1. made up of endothelial cells (vWF) and hepatocytes (factor VIII) 2. function as adhesion of platelets to subendothelial collagen |
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what is von willebrand disease
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1. defective vWF can no longer provide the adhesion between platelets and subendothelial layer and platelet-to-platelet adhesion
2. prolonged bleeding time with NORMAL PLATELET COUNT 3. prolonged PTT |
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what is hemophilia A
how can you tell it apart from hemophilia B |
1. inherited X linked recessive disease
2. occurs in all males and homozygous females 3. massive and/or spontaneous hemorrhages (surgical/dental procedures) 4. prolonged PTT 5. normal PT hemophilia B is a fixed deficiency...indistinguishable from hemophilia A |
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how do you get lung emphysema
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1. long term smoking
2. free radicals from smoke binds to antioxidants in lungs, causing an imbalance. 3. irritant action causes INCREASE mucus secretion and inflammation 4. inflammatory cells (macrophages and neutrophils) release elastase (protease) 5. smoke inactivate ALPHA-1-ANTITRYPSIN 6. imbalance cause alveoli/acini wall and bronchiole destruction |
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what is the pink puffer
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1. predominant emphysema (w/o bronchitis)
2. hyperinflation 3. normal blood gas values S/S: weight loss, BARREL CHEST, breathe through pursed lips, hunched over, prolong expiration |
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how do you diagnose for emphysema
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1. decreased FEV1/FVC
2. decreased diffusion capacity 3. normal blood gas values panacinar (alpha-1-antitrypsin) paraseptal (bullae and spon. pneumothorax) |
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what is definition of emphysema and bronchitis
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1. emphysema:
abnormal enlargement of airspace distal to the terminal bronchioles, with destruction of walls, WITHOUT fibrosis 2. bronchitis: persistant cough with sputum for at least 3months in at least 2 consecutive years |
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how do you get bronchitis
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air pollutants
1 .hyperplasia and hypertrophy of submucosal glands 2. excessive mucus production, result of increased goblet cells of small bronchi and bronchioles 3. proteases released from neutrophils stimulate this mucus hypersecretion |
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how do you diagnose bronchitis
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REID INDEX (assesses mucus gland enlargement)
ratio of thickness of the mucous gland layer to the thickness of the wall between the epithelium and cartikage |
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what is the blue bloater?
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CHRONIC BRONCHITIS
1. recurrent infection 2. hypoxemia and hypercapnia 3. cyanosis |
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what is atelectasis?
what are the FOUR forms? |
incomplete expansion or COLLAPSE of parts of or whole lung
1. resorption (obstruction): tumor, foreign body, secretion 2. compressive (passive): pressure from outside lung 3. contraction (cicatrisation): fibrosis 4. micro-atelectasis (non-obstructive): loss of surfactant |
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chronic diffuse pulmonary disease, what are the two types
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1. obstructive: cant get air out (due to something blocking it)
2. restrictive: cant get air in (due to fibrosis of lung tissue, etc) |
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how do you test for breathing values?
in respects to measurements, what is the difference between obstructive and restrictive |
SPIROMETRY
obstructive: 1. FVC: normal or low 2. FEV1/FVC: LOW 3. TLC: normal or high restrictive: 1. FVC: LOW 2. FEV1/FVC: normal 3. TLC: LOW |
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what is status asthmaticus
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the state of UNREMITTING ATTACKS, in which bronchoconstriction persists for days or weeks
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what is atopic asthma?
how do you go about getting this? |
asthma caused by an allergy
1. allergen travels through bronchioles and gets ingested by macrophage 2. macrophage present it to lymphocyte (TH2) 3. TH2 release IL4 (plasma cells) and IL5 (eosinophils) 4. plasma cells release IgE 5. eosinophils release inflammatory agents IgE is present in acute and chronic stages |
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what is nonatopic asthma?
how do you go about getting this? |
-URTI
-only hypersensitivity to microbial antigens may show on skin test -could be drug induce (aspirin) 1. inflammation leads to upstream obstruction 2. traps air (gas exchange limited) 3. hypoxemia, hypoventilation, hypercapnia 4. lungs hyper inflate because the air is trapped. |
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at a microscopic level what is happening in nonatopic asthma
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1. thickening of the basement membrane
2. overgrowth of submucosal mucus glands 3. edema and infiltration 4. eosinophils |
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what is a disease where the bronchi and bronchioles are PERMANENTLY dilated
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bronchiectasis
destruction of the muscle and elastic tissue, associated with chronic necrosis |
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what are two congenital conditions that can cause bronchiectasis
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1. cystic fibrosis
2. immotile cilia syndrome both are marked with increase accumulation of secretions and pus |
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what type of inflammation will you see in sarcoidosis?
what other microscopy conditions will you see in sarcoidosis? |
1. non-caseating granulomatous inflammation
2. pulmonary interstitial fibrosis 3. epitheloid cells w/ multinucleated giant cells LANGHANS |
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what test will you do with sarcoidosis?
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Kveim Test:
1. skin test using antigen from human sarcoid tissue injected intradermally. 2. BIOPSY (epitheloid granuloma) INCREASED A.C.E. in serum |
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what is pneuconioses
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non-neoplastic lung reaction to inhalation of mineral dust, inorganic particles, chemical fumes or vapors
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what are the FOUR bronchogenic carcinomas
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1. squamous cell
2. adeno 3. small cell 4. large cell |
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what is distinguishable about CML
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1. translocation of BCR on chromosome 9 to ABL of chromosome 22
2. BCR-ABL fusion gene with tyrosine kinase activity leads to abnormal and accelerated cell division 3. peripheral blood smear shows leukocytosis count up exceeding 100000...THIS IS BAD!!! |
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what is the definition of bronchopneumonia
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1. patchy consolidation centered around inflamed bronchi
2. both bronchi and corresponding lobules are involved 3. bronchioles filled with pus |
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what are the outcomes and complications of bronchopneumonia
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1. UNUSUAL resolution
2. pulmonary fibrosis 3. organization of suppurative exudates 4. Lung abscess 5. Empyema, pericarditis 6. bacteremia 7. death |
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what is the definition of lobar pneumonia
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1. acute bacterial infection in which large areas of uniform consolidation affect entire lobe
2. NO BRONCHI INVOLVEMENT |
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what are the four morphological stages of lobar pneumonia
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1. congestion
2. red hepatization 3. gray hepatization 4. resolution |
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what is a lab finding for mycoplasma pneumoniae
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1. cold agglutinins
2. FALSE POSITIVE serologic test for syphilis complications: STEVEN-JOHNSON SYN. |
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morphologically what is the difference between primary and secondary TUBERCULOSIS
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primary:
1. Ghon focus 2. Hilar lymphoadenopathy secondary: 1. simon foci 2. seen as COIN LESION on CXR |
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what are Ghon focus? where are they seen?
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primary tuberculosis:
subpleural lesion in middle zone of lungs |
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where are the tubercle seen in primary tuberculosis
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1. central: caseous necrosis and bacilli
2. pericentral: epitheloid cells, giant cells, lymphocytic infiltrates 3. peripheral: fibroblasts |
