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3MED FB Pato Teorico > Parcialito 12 - Hematolinfoide > Flashcards

Parcialito 12 - Hematolinfoide Flashcards

1
Q

Average volume per cell, expressed in femtoliters.

A

Mean cell volume (MCV)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 423

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2
Q

A reduction in the oxygen-transporting capacity of blood.

A

Anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 422

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3
Q

The average content of hemoglobin per red cell, expressed in picograms.

A

Mean cell hemoglobin (MCH)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 423

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4
Q

The average concentration of hemoglobin in a given volume of packed red cells, expressed in g/dL.

A

Mean cell hemoglobin concentration (MCHC)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 423

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5
Q

The coefficient of variation of red cell volume.

A

Red cell distribution width (RDW)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 423

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6
Q

Anemia of acute blood loss is described as ______.

A

Normocytic, normochromic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 423

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7
Q

Life span of a normal red cell.

A

120 days(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424

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8
Q

Anemia characterized by an increased rate of cell destruction, a compensatory increase in erythropoeisis that results in reticulocytosis, and retention of products of cell destruction, including iron.

A

Hemolytic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424

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9
Q

A circulating protein that binds and clears free hemoglobin.

A

Haptoglobin(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424

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10
Q

Hemolysis that can result from mechanical trauma, or biochemical or physical agents that damage the red cell membrane.

A

Intravascular hemolysis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424

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11
Q

Hemolysis which takes place largely within phagocytic cells of the spleen and liver.

A

Extravascular hemolysis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424

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12
Q

This disorder is characterized by an intrinsic defect in the red cell membrane, that renders the cells spheroidal, less defomable and vulnerable to splenic sequestration and destruction.

A

Hereditary spherocytosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424

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13
Q

Small, dark nuclear remnants seen within red cells in PBS of hereditary spherocytosis.

A

Howell-Jolly bodies(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 425

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14
Q

On PBS, red cells are spherical which lack central pallor, and they show increased osmotic fragility when placed in hypotonic salt solutions.

A

Hereditary spherocytosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 425

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15
Q

Structural proteins that are defective in hereditary spherocytosis.

A

Spectrin and ankyrin(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 425

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16
Q

This results from substitution of valine for glutamic acid at the 6th position of the B-globin chain, producing HbS.

A

Sickle cell anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 426

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17
Q

Bizarre, elongated, spindled or boat-shaped cells on PBS.

A

Sickle cell anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 427

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18
Q

Prominent cheekbones and changes in skull resembling a “crew-cut” skull x-ray.

A

Sickle cell anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 427

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19
Q

Patients with sickle cell disease are predisposed to infections caused by these type of bacteria.

A

Encapsulated bacteria(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 428

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20
Q

Treatment for sickle cell disease by increasing levels of HbF.

A

Hydroxyurea(TOPNOTCH)

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21
Q

Treatment for sickle cell disease by increasing levels of HbF.

A

Hydroxyurea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 428

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22
Q

Feared complication of sickle cell disease which can be trigerred by pulmonary infections or fat emboli from necrotic marrow that secondarily involve the lung.

A

Acute chest syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 428

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23
Q

Major complication of sickle cell disease which occurs in the setting of acute chest syndrome, causing ischemic injury to the CNS.

A

CNS stroke(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 428

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24
Q

Represents a sudden but usually temporary cessation of erythropoeisis, usually trigerred by parvovirus B19 infections in patients with sickle cell disease.

A

Aplastic crises(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 428

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25
Q

In beta thalassemia, an individual who inherits one abnormal allele (out of 2) has this asymptomatic to mildly symptomatic condition.

A

B- Thalassemia minor/trait(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 429

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26
Q

Individuals with B-thalassemia who inherit two abnormal alleles, with severe anemia requiring regular blood tranfusions.

A

B- Thalassemia major(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 429

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27
Q

Red cells with a central, dark-red puddle due to collection of hemoglobin.

A

Target cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 430

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28
Q

Target cells are often seen in this condition.

A

B-thalassemia minor(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 430

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29
Q

In the PBS of this condition, nucleated red cells (normoblasts) are seen, which reflect underlying erythropoeisis.

A

B-thalassemia major(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 430

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30
Q

Anemia of beta thalassemia.

A

Microcytic, hypochromic(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 430

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31
Q

Disease caused by deletion of 3 alpha globin genes.

A

Hemoglobin H disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 431

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32
Q

Condition caused by deletion of 1 alpha globin gene.

A

Silent carrier(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 431

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33
Q

Condition caused by deletion of 2 alpha globin genes.

A

Alpha thalassemia trait(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 431

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34
Q

Condition caused by deletion of all four alpha globin genes.

A

Hydrops fetalis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 429

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35
Q

Precipitates of denatured globin seen in RBC’s.

A

Heinz bodies(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 432

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36
Q

Heinz bodies are seen in the blood smear of this condition.

A

G6PD Deficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 432

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37
Q

Bite cells are seen in ________.

A

G6PD Deficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 432

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38
Q

A rare disorder of unknown etiology, causes hemolytic anemia which results from an acquired membrane defect secondary to a mutation that affects myeloid stem cells. Hemolysis occurs during sleep.

A

Paroxysmal nocturnal hemoglobinuria(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 432

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39
Q

Hemolysis caused by IgG or IgA antiodies that are active at 37 degC, which results in opsonization of red cells by the autoantibodies.

A

Warm antibody immunohemolytic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 433

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40
Q

Anemia caused by low-affinity IgM which bind to red cell membranes only at temp

A

Cold antibody immunohemolytic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 433

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41
Q

Anemia observed in a variety of pathologic states, in which small vessels become particularly obstructed.(e.g. DIC, malignant HTN, SLE, etc.)

A

Microangiopathic hemolytic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 433

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42
Q

Schistiocytes, burr cells, helmet cells, triangle cells are seen in this condition.

A

Microangiopathic hemolytic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 433

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43
Q

X-linked disorder in which red cells are unusually susceptible to damage cause by oxidants.

A

G6PD Deficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 432

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44
Q

Red blood cells in iron deficiency anemia.

A

Microcytic, hypochromic(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 436

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45
Q

Diagnostic criteria for iron deficiency anemia:____ Ferritin____Serum iron level____Transferrin saturation____Total Iron Binding Capacity (TIBC)

A

Low ferritin
Low serum iron levels
Low transferrin saturation
Increased TIBC
(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 435

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46
Q

Diagnostic criteria for anemia of chronic disease:____ Ferritin____Serum iron level____Transferrin saturation____Total Iron Binding Capacity (TIBC)

A

Increased ferritin
Low serum iron levels
Low transferrin saturation
Decreased TIBC
Normocytic, normochromic anemia
(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 435

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47
Q

Principal causes of megaloblastic anemia.

A

Folate deficiency
Vitamin B12 deficiency
(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 437

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48
Q

Bone marrow is markedly hypercellular as a result of increased number of megaloblasts, which are large cells that have delicate, finely reticulated nuclear chromatin and abundant basophilic cytoplasm.

A

Megaloblastic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 437

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49
Q

PBS finding in neutrophils and red cells of patients with megaloblastic anemia.

A

Hypersegmented neutrophils, large, egg-shaped macro-ovalocytes(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 437

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50
Q

Difference between megaloblastic and pernicious anemia.

A

Presence of neurologic abnormalities in pernicious anemia.(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 438

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51
Q

Deficiency in folate causes this type of anemia.

A

Megaloblastic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 438

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52
Q

Deficiency in Vitamin B12 absorbtion causes this type of anemia.

A

Pernicious anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 438

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53
Q

Etiology of pernicious anemia.

A

1.Vitamin B12 malabsorption secondary to autoantibodies against parietal cells and intrinsic factor which is needed in its absorption.
2. Gastrectomy or ileal resection
(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 438

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54
Q

Principal neurologic lesion in pernicious anemia.

A

Demyelination of posterior and lateral columns of the spinal cord.
(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 439

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55
Q

Bone marrow is markedly hypocellular, with >90% of the intertrabecular space being occupied by fat.

A

Aplastic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 439

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56
Q

Tear drop cells are also called __________.

A

Dacrocytes(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 440

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57
Q

Dacrocytes are found in peripheral blood of patients with this type of anemia.

A

Myelophthisic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 440

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58
Q

Increase in blood concentration of red cells, with an increase in Hgb concentration.

A

Polycythemia or erythrocytosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 441

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59
Q

Polycythemia secondary to reduced plasma volume.

A

Relative polycythemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 441

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60
Q

Polycythemia secondary to abnormal proliferation of myeloid stem cells and low erythropoeitin levels.

A

Primary polycythemia (Absolute)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 441

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61
Q

Polycythemia secondary to increased erythropoeitin levels due to lung disease, high-altitude living, cyanotic heart disease and EPO secreting tumors.

A

Secondary polycythemia (Absolute)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 441

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62
Q

Total white cell count is reduced to 1000 cells/uL. Affected persons are extremely susceptible to bacterial and fungal infections.

A

Neutropenia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 441

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63
Q

A self-limited disease of adolescents and young adults that is causd by B lymphocytotropic EBV characterized by fever, sore throat and generalized lymphadenitis, an increase of atypical lymphocytes in blood and an antibody and T cell response to EBV.

A

Infectious mononucleosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 442

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64
Q

Cells with abundant cytoplasm 12-16um in diameter that contains azurophilic granules, and an oval, indented or folded nucleus.

A

Atypical lymphocytes (Infectious mononucleosis)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 442

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65
Q

Inflamed nodes are swollen, gray-red and engorged. There are large germinal centers containing numerous mitotic figures. Affected nodes are tender and fluctuant if with extensive abscess formation.

A

Acute nonspecific lymphadenitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 444

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66
Q

This pattern is associated with infections or inflammatory processes that activate B cells which create a follicular or germinal center reaction. Lymph node architecture is preserved, lymphoid nodules vary in shape and size, mixed lymphocytic infiltrates with prominent phagocytic and mitotic activity within germinal centers.

A

Follicular hyperplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 444

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67
Q

Reactive pattern characterized by distention and prominence of the lymphatic sinusoids, due to marked hypertrophy of lining endothelial cells and an infiltrate of histiocytes. Encountered in lymph nodes draining cancers.

A

Sinus histiocytosis(TOPNOTCH)

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68
Q

Characterized by reactive changes within T-cell regions of the lymph node, usually encountered during viral infections, following certain vaccinations, and immune reactions induced by certain drugs.

A

Paracortical hyperplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 444

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69
Q

Formation of sarcoid-like ganulomas that undergo central necrosis associated with neutrophil accumulation. This irregular stellate necrotizing granuloma is seen in patients presenting with a raised inflammatory node, vesicle or eschar at site of injury. History of exposure to cats.

A

Cat scratch disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 444

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70
Q

Causative agent for cat scratch disease(TOPNOTCH)

A

Bartonella henselae(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 444

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71
Q

Lymphoblasts with irregular nuclear contours, condensed chromatin , small nucleoli and scant agranular cytoplasm. Blasts compose >25% of marrow cellularity. Most common childhood leukemia.

A

Acute lymphocytic leukemia (ALL)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 447

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72
Q

Frequent small “cleaved” cells mixed with large cells, growth pattern nodular, centroblasts present. Occurs in older adults, usually involves nodes, marrow, spleen. Associated with t(14;18).

A

Follicular lymphoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 451

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73
Q

Small to intermediate-sized irregular lymphocytes growing in a diffuse pattern, no centroblasts and proliferation centers. Occurs mainly in older males, GI tract commonly affected. Associated with t(11;14).

A

Mantle cell lymphoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 452

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74
Q

Plasma cells in sheets, with prominent nucleoli or inclusion containing Ig. Presents as disseminated bone disease, with destructive lytic lesions.

A

Plasmacytoma / plasma cell myeloma(TOPNOTCH)

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75
Q

Intermediate-sized round lymphoid cells with 2-5 prominent nucleoli. Nuclear remnants phagocytosed by interspersed macrophages with abundant clear cytoplasm, “starry sky pattern”

A

Burkitt lymphoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 453

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76
Q

Sheets of small, round lymphocytes and scattered ill-defined foci of larger, actively dividing cells diffusely efface involved LN. A foci of mitotically active cells called proliferation centers are pathognomonic.

A

Small lymphocytic leukemia (SLL) / Chronic lymphocytic leukemia (CLL)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 450

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77
Q

Fragile neoplastic lymphocytes that are frequently disrupted during smear preparation.

A

Smudge cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 450

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78
Q

Smudge cells are seen in this type of leukemia.

A

CLL(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 450

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79
Q

Tumor cells have large nuclei with open chromatin and prominent nucleoli. Most important type of lymphoma in adults, accounting to ~50% of adult NHL.

A

Diffuse large B-cell lymphoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 452

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80
Q

Multifocal destructive bone lesions seen as punched-out defects in bone radiographs.

A

Multiple myeloma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 455

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81
Q

Excess light or heavy chains along with complete Igs synthesized by neoplastic plasma cells.

A

Bence-Jones proteins(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 454

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82
Q

Cells with two mirror-image nuclei or nuclear lobes, each containing a large acidophilic nucleolus surrounded by a distinctive clear zone, imparting an owl-like appearance.

A

Reed-Sternberg cell(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 456

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83
Q

A distinctive groups of neoplasms that arise almost invariably in a single lymph node or chain of lymph nodes and spread characteristically in a stepwise fashion to anatomically contiguous nodes.

A

Hodgkin Lymphoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 456

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84
Q

Most common form of Hodgkin lymphoma, characterized by a large cell which has a single multilobate nucleus with small nucleoli and an abundant pale-staining cytoplasm called lacunar cells.

A

Nodular sclerosis HL(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 457

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85
Q

Most common form of HL in patients greater than 50 years old, with male predominance, plentiful RS cells and heterogenous cellular infiltrates.

A

Mixed cellularity HL(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 458

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86
Q

Cells found in adult T-cell lymphoma which appear to have multilobulated nuclei.

A

Cloverleaf or flower cell(TOPNOTCH)

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87
Q

Subgroup of HL characterized by a large number of small resting lymphocytes admixed with a variable number of benign histiocytes. Variant RS cells described as multilobed, puffy nucleus Which appears like a “popcorn”. Excellent prognosis.

A

Lymphocyte-predominance HL(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 458

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88
Q

Cells with fiery red cytoplasm, seen in Multiple myeloma

A

Flame cells(TOPNOTCH)

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89
Q

Cells with pink globular cytoplasmic inclusions, seen in Multiple myeloma

A

Russell bodies(TOPNOTCH)

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90
Q

Cells with blue globular nuclear inclusions, seen in Multiple myeloma

A

Dutcher bodies(TOPNOTCH)

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91
Q

Multiple nuclei, prominent nucleoli, and cytoplasmic droplets containing Ig.

A

Bizarre, multinucleated cells(TOPNOTCH)

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92
Q

Bizarre multinucleated cells, flame cells, Russel bodies and Dutcher bodies are all seen in what disease?

A

Multiple myeloma(TOPNOTCH)

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93
Q

Bone marrow aspirate shows hypercellular martow packed with myeloblasts and azurophilic needle-like material called Auer rods.

A

Acute Myelogenous Leukemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 462

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94
Q

Leukemia of children most responsive to chemotherapy.

A

Acute Lymphoblastic Leukemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 461

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95
Q

Hodgkin lymphoma subgroup most commonly associated with EBV infection.

A

Lymphocyte depleted(TOPNOTCH)

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96
Q

Mature B-cell tumor in the elderly, where cells have fine hair-like projections (hairy cells).

A

Hairy cell leukemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 459

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97
Q

t(9;22) is also called ______.

A

Philadelphia chromosome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 465

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98
Q

Hodgkin lymphoma subgroup with highest count of RS cells.

A

Mixed cellularity type(TOPNOTCH)

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99
Q

This correlates with good prognosis in Hodgkin lymphoma.

A

High Lymphocyte : Reed-Sternberg cell ratio(TOPNOTCH)

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100
Q

Hodgin lymphoma subgroup not associated with EBV.

A

Nodular sclerosis and lymphocyte predominant(TOPNOTCH)

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101
Q

Hodgkin lymphoma subgroup with poorest prognosis.

A

Lymphocyte depleted HL(TOPNOTCH)

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102
Q

Tumor of the thymus associated with myastheni gravis and pure red cell aplasia.

A

Thymoma(TOPNOTCH)

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103
Q

Pentalaminar tubules, often with a dilated terminal end (tennis racket-like appearance).

A

Birbeck granules(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 467

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104
Q

Proliferative disorder of the dendritic cells which has birbeck granules.

A

Langerhans Cell Histiocytosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 467

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105
Q

Pathology behind polycythemia vera.

A

Mutation in tyrosine kinase JAK2, which acts in signalling pathways of the erythropoeitin receptors, rendering them hypersensitive to erythropoeitin.(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 466

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106
Q

Treatment for polycythemia vera.

A

Phlebotomy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 466

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107
Q

Collection of aggressive tumors that are comprised of immature myeloblasts which replace the marrow and suppress normal hematopoiesis.

A

Acute Myelogenous Leukemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 467

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108
Q

Myeloid tumor arising from a pluripotent stem cell associated with mutatios of the BCR-ABL gene. If untreated, may progress to a blast crisis.

A

Chronic Myelogenous Leukemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 467

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109
Q

Most common myelodysplastic syndrome. A myeloid tumor in which abnormal megakaryocytes stimulate marrow fibroblasts to release collagen, replacing the marrow space, leading to pancytopenia and extramedullary hematopoeisis.

A

Myeloid metaplasia with Myelofibrosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 467

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110
Q

Other name for acute disseminated Langerhans cell histiocytosis.

A

Letterer-Siwe disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 468

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111
Q

Caused by a systemic activation of coagulation pathways, leading to formation of thrombi throughout the microcirculation.

A

Disseminated intravascular coagulation(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 469

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112
Q

Characterized by spontaneous bleeding, prolonged bleeding time, and normal PT and PTT.

A

Thrombocytopenia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 471

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113
Q

Drug-induced disorder caused by IgG antibodies that bind to platelet factor IV on platelet surfaces, which activates platelets and induce their aggregation.

A

Heparin-Induced Thrombocytopenia (HIT)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 472

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114
Q

Associated with pentad of fever, thrombocytopenia, microangipathic hemolytic anemia, transient neurologic deficits and renal failure.

A

Thrombotic thrombocytic purpura(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 472

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115
Q

Associated with childhood onset microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure. No neurologic symptoms.

A

Hemolytic uremic syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 472

116
Q

Caused by antiplatelet antibodies directed against glycoproteins IIb-IIIa, Ib-IX.

A

Immune thrombocytopenic purpura(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 472

117
Q

Decreased gp Ib leads to defective platelet adhesion, associated with decreased platelet count.

A

Bernard-Soulier Syndrome(TOPNOTCH)

118
Q

Caused by deficiency of ADAMTS13, a vWF metalloprotease.

A

Thrombotic thrombocytopenic purpura(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 472

119
Q

Caused by shiga-like toxin in EHEC (E. coli O157:H7) from improperly cooked burgers.

A

Hemolytic uremic syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 472

120
Q

Decreased gp IIb-IIIa leads to defective platelet aggregation, associated with normal platelet count.

A

Glanzmann thrombasthenia(TOPNOTCH)

121
Q

Most common bleeding disorder.

A

vWF disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 474

122
Q

Most common hereditary disease associated with life threatening bleeding,

A

Hemophilia A(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 474

123
Q

An X-linked recessive disorder caused by reduction in factor VIII activity.

A

Classic Hemophilia/ Hemophilia A(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 474

124
Q

An X-linked disorder caused by deficiency of Factor IX, or Christmas factor. Bleeding time is normal, PTT is prolonged.

A

Hemophilia B/ Christmas Disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 474

125
Q

A state associated with excessive removal of formed elements of blood, resulting in anemia, leukopenia or thrombocytopenia.

A

Hypersplenism(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 476

126
Q

A 17 y/o male presented with a short history of fever, tonsillitis and monolateral enlarged cervical lymph nodes. PE revealed enlargement of righ cervical lymph node, 3 cm in diameter hard , and pharyngeal hyperemia. Biopsy was done and showed a malignant population of round monomorphic B cells interspersed with macrophages forming the start in the “starry sky” pattern. This is a case of:

A

Burkitt lymphoma (TOPNOTCH)

127
Q

An 18 y/o male presents with easy fatigability, fever, and cutaneous bleeding. Bone marrow biopsy showed 40% myeloblasts. What is the most likely diagnosis?

A

AML (TOPNOTCH)

128
Q

The most common cause of agranulocytosis

A

Drug toxicity (TOPNOTCH) Robbins Pathologic Basis of Disease, 9th ed., p. 582

129
Q

What laboratory finding differentiate leukemoid reaction from CML?

A

Elevated leukocyte alkaline phosphatase. (TOPNOTCH)

130
Q

An 8 month old presented with anemia. Red cells were noted to be oval and macrocytic. Nutritional history revealed that the infant was exclusively fed raw goat’s milk. The most likely cause of his anemia is:

A

Folate deficiency (TOPNOTCH)

131
Q

A 2 y/o child arrived at well-child clinic. Mother reported that her child is exclusively breastfed for 6 months and then supplemented mainly by carrots. The patient is most likely prone to developing anemia caused by:

A

Vitamin B12 deficiency (TOPNOTCH)

132
Q

Most common type of cancer in children; highly aggressive tumors manifest with signs and symptoms of bone marrow failure, or as rapidly growing masses

A

Acute lymphoblastic leukemia/Lymphoblastic lymphoma(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 598

133
Q

Most common leukemia of adults which usually presents with bone marrow and lymph node involvement.

A

Small lymphocytic lymphoma/CLL(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 598

134
Q

Most common leukemia of adults which usually presents with bone marrow and lymph node involvement.

A

Follicular lymphoma(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 598

135
Q

Most common lymphoma of adults

A

Diffuse Large B-Cell Lymphoma(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 598

136
Q

Very aggressive tumor of mature B cells that usually arise at extranodal sites; strongly associated with translocations involving MYC proto-oncogene

A

Burkitt Lymphoma(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 598

137
Q

Plasma cell neoplasm commonly associated with lytic bone lesions, pathologic fractures, chronic pain, hypercalcemia, renal failure, and acquired immune abnormalities.

A

Multiple Myeloma(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 599

138
Q

Major pathologic feature of multiple myeloma

A

Bone destruction mediated by neoplastic plasma cells(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 599

139
Q

True or False. Cellular immunity is relatively unaffected in Multiple myeloma

A

True(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 600

140
Q

Single most important factor in the pathogenesis of renal failure in Multiple myeloma

A

Bence-Jones proteinuria(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 600

141
Q

True or False. Age younger 2 years is associated with a worse prognosis in ALL.

A

True(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 592

142
Q

Abrupt stormy onset, symptoms of depressed marrow function, and mass effects by neoplastic infiltration , including bone pain are more common in ALL or AML?

A

ALL (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 592

143
Q

The leading cause of cancer deaths in children

A

ALL (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 592

144
Q

This lymphoma often presents a mass involving the mandible and shows an unusual predilection for involvement of abdominal viscera, particularly the kidneys, ovaries, and adrenal glands.

A

Endemic Burkitt lymphoma(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 597

145
Q

A 40 y/o male presented with unexplained weight loss, fever, and night sweats. Chest radiograph showed a mediastinal mass. Histologic findings showed large cells with multiple nuclei with large inclusion-like nucleolus. What is the most likely diagnosis?

A

Hodgkin Lymphoma (Presence of Reed-Sternberg cells) (TOPNOTCH)

146
Q

A 52 y/o female presents with dragging sensation in the abdomen associated with anemia, weakness, and weight loss. Chromosomal analysis showed presence of BCR-ABL fusion gene. What is the most likely diagnosis?

A

CML (TOPNOTCH)

147
Q

Presence of anemia, hemoglobinemia, hemoglobinuria, hemosiderinuria, and jaundice are manifestations of intravascular or extravascular hemolysis?

A

Intravascular hemolysis(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 631

148
Q

Patient presents with anemia, splenomegaly, and jaundice. Peripheral blood smear shows small, dark-staining red cells lacking the central zone of pallor. Father had prolonged jaundice since childhood. What is the most likely diagnosis?

A

Hereditary spherocytosis(TOPNOTCH)

149
Q

A 5 y/o male presented with malaise and low grade fever for 10 days. He was diagnosed with toxoplasmosis and was given pyrimethamine and sulfadiazine. Three days after, patient presented with jaundice and dark urine. PBS showed Heinz bodies and bite cells. What is the most likely diagnosis?

A

G6PD Deficiency(TOPNOTCH)

150
Q

Hemolysis and vaso-occlusive crisis are common in this form of anemia caused by mutaion of glutamic acid to valine.

A

Sickle-cell anemia(TOPNOTCH)

151
Q

The most common trigger for episodic hemolysis in G6PD Deficiency

A

Infection(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 634

152
Q

A 19 y/o African-American male presented with severe pain in the chest and extremities, splenomegaly, and anemia. PBS showed reticulocytosis, presence of target cells, and sickled cells. Three days prior , patient developed cough and fever. For the past 3 years, patient had suffered from recurrent pains and jaundice. What is the pathophysiologic mechanism responsible for the most serious clinical features of this disease?

A

Microvascular occlusion (in Sickle cell disease) (TOPNOTCH)

153
Q

Leading cause of disease-related death in individuals with PNH

A

Thrombosis(TOPNOTCH) Robbins Basic Pathology, 9th ed. P. 642

154
Q

The immediate cause of megaloblastosis, and a common denominator of folic acid and vitamin B12 deficiency

A

Suppressed synthesis of DNA (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 648

155
Q

Most common nutritional disorder in the world

A

Iron Deficiency Anemia(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 649

156
Q

An 18 y/o female complained of generalized weakness, lethargy, and light headedness. She revealed she was having excessive bleeding during menstruation from the previous 6 months. Upon examining, she was noted to have pallor, tachycardia, and swollen tongue. Most likely morphology of RBC:

A

Microcytic, hypochromic anemia (Case of IDA) (TOPNOTCH)

157
Q

Presents signs and symptoms of anemia, thrombocytopenia, and neutropenia. Splenomegaly is characteristically absent. And the red cell are usually macrocytic and normochromic. (+) Reticulocytopenia. Bone marrow is hypocellular. What is the condition described?

A

Aplastic anemia(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 654

158
Q

Virus implicated in acute red cell aplasia

A

Parvovirus B19 (TOPNOTCH)) Robbins Basic Pathology, 9th ed., p. 655

159
Q

Most feared complication of thrombocytopenia

A

Intracranial bleeding (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 657

160
Q

Most common presenting symptoms of this condition are spontaneous bleeding from mucous membranes, excessive bleeding from wounds, or menorrhagia. Bleeding tendency often goes unnoticed until some hemostatic stress, such as surgery, reveals its presence. Patients may have defects in platelet function despite a normal platelet count, prolonged PTT.

A

von Willebrand disease (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 662

161
Q

Patient with this disease has a tendency toward easy bruising and massive hemorrhage after trauma or operative procedures, and recurrent bleeding into the joints. Petechiae are absent. Patients have a prolonged PTT and normal PT.

A

Hemophilia A and B (Factor VIII and IX Ddeficiency) (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 663

162
Q

Two major mechanisms that trigger DIC

A

Release of tissue factor and widespread endothelial injury(TOPNOTCH) Robbins Basic Pathology, 9th ed. P. 663

163
Q

A 5 year old male is observed by his mother to have tea-colored urine whenever he has infections. One particular episode of pneumonia required hospital admission, where the child developed jaundice also. A peripheral blood smear showed red cells with Heinz bodies, while other red cells had parts of their cytoplasm “plucked out”. The child likely has a deficient enzyme required in the production of reduced glutathione, the gene for which is found on (A) X chromosome (B) Y chromosome (C) chromosome 21 (D) chromosome 22

A

X chromosome (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P 431-432

164
Q

An 8 year old child from the slums has easy fatigability and pallor. A peripheral blood smear shows large, egg-shaped red cell precursors, and hypersegmented neutrophils. Short of measuring serum folate and vitamin B12 levels, what finding will suggest a vitamin B12 deficiency, rather than a folate deficiency? (A) gastrointestinal symptoms (B) neurologic symptoms (C) development of congestive heart failure (D) megaloblasts on bone marrow aspirate smears

A

neurologic symptoms (TOPNOTCH)Robbins Basic Pathology, 8th Ed. Pp 437-439

165
Q

A 33 year old female presents with pallor, easy fatigability, and echymoses. Her spleen is not enlarged. A CBC showed profound anemia and markedly decreased WBC and platelet counts. A bone marrow core biopsy showed marrow that is predominantly replaced by fat, with few lymphocytic and plasma cells. The most common cause of her condition is (A) myelotoxic drugs (B) viral infection (C) bacterial infection (D) idiopathic

A

idiopathic (aplastic anemia) (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P439

166
Q

A 14 year old male develops fever, sore throat, lymphadenitis, and fatigue. His CBC shows leukocytosis, with a lymphocytic predominance. Peripheral blood smear shows some large leukocytes with abundant cytoplasm occasional azurophilic granules, and indented nuclei with fine chromatin. Monospot test and anti-EBV titers are positive. The large leukocytes seen are (A) monocytes (B) megakaryocytes (C) B cells (D) T cells

A

T cells (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P 443

167
Q

Lymph nodes that drain cancers but do not yet harbor metastatic deposits often show (A) follicular hyperplasia (B) paracortical hyperplasia (C) sinus histiocytosis (D) fibrous obliteration

A

sinus histiocytosis (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P 444

168
Q

A 55 year old male presents with pallor and easy fatigability. Physical exam showed massive splenomegaly. CBC showed marked leukocytosis, and a peripheral smear showed numerous neutrophils, metamyelocytes, and myelocytes. Basophils are also seen. A bone marrow aspirate shows a similar picture. This man likely has (A) a BCR-ABL fusion gene (B) a JAK2 mutation (C) an 8:22 translocation (D) an 11:22 translocation

A

a BCR-ABL fusion gene (Chronic myelogenous leukemia) (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P 464

169
Q

In primary myelofibrosis, marrow fibroblasts are stimulated to proliferate by PDGF and TGF-beta released from (A) granulocyte precursors (B) erythroid precursors (C) lymphoid cells (D) neoplastic megakaryocytes

A

neoplastic megakaryocytes (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P 466

170
Q

A 28 year old female is found to have a mediastinal mass on chest xray during a preemployment medical exam. On history, she is found to have muscle fatigue that worsens as the day progresses. She undergoes surgery where her mediastinal mass is resected. Microscopic examination showed sheets of bland spindle cells with sparse inflammatory infiltrates. Her tumor is (A) a metastasis from an undiagnosed endometrial mass (B) a metastasis from an occult breast malignancy (C) a lymphoma(D) a thymoma

A

a thymoma (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P 476

171
Q
A

AML - Acute Myeloid Leukemia
ALL - Acute Lymphoblastic Leukemia
CL - Chronic Leukemia
MPD - MYELOPROLIFERATIVE DISORDERS
- PV - Policitemia Vera
- CML - Chronic Myeloid Leukemia
- ET - Essential Trombocytemia

172
Q
A

Imagen de nodulo linfático y que regiones estarán agrandadas en caso de diferentes enfermedades
Corteza - Linf. B - Artritis Reumatoide y HIV
Paracorteza - Linf. T - Infecciones virales (Epstein Barr)
Medula - drenage de una region del cuero que tenga cancer

173
Q

Cuales son los tejidos linfoides?

A

 Timo
 Ganglio linfático
 Bazo

174
Q

MORFOLOGIA MICRO DE UN GANGLIO
LINFATICO:

A

Tinción H&E o giemsa
* Corterza
* Zona paracortical/ interfolicular
* Zona medular
* Sistema sinusoidal
* Capsula y tejido adyacente

175
Q

INMUNOHISTOQUIMICA
Marcadores utilizados rutinariamente:

A

CD45: celula inmadura
Linfocitos B: CD19, CD20, CD79a, KiB5,
VS38c, cadenas livianas, CD23, CD10, Bcl6,
Ciclina D1.
Linfocitos T: CD3, CD43, CD45RO, CD2,
CD7, CD4/8.
Macrófagos: CD68
Otros: Bcl2, CD15, CD30, ALK-1, MUM-1, MPX, CD34, CD1a, Pax 5, etc.

176
Q
A

Ganglio linfatico normal

177
Q

Importante al resecar un ganglio:

A
  • Evitar biopsias inguinales
  • Elegir cervicales y supraclaviculares
  • En caso de existir un grupo de ganglios
    seleccionar el mayor
  • Resecarlo completo
178
Q

Cuales son los tipos de neoplasias LINFOIDES?

A

o Neoplasias de precursores de Linfocitos B
o Neoplasia de Linfocitos B periféricos
o Neoplasias de precursores de Linfocitos T
o Neoplasias de Linfocitos T y NK periféricos
o Linfoma de Hodgkin

179
Q

NEOPLASIA DE PRECURSORES DE LINFOCITOS B

A

Leucemia/linfoma linfoblástico agudo de linfocitos B (LLA-B)

180
Q

NEOPLASIAS DE LINFOCITOS B PERIFERICOS:

A
  • Leucemia linfocítica crónica/linfoma linfocitico pequeño
  • Leucemia prolinfocítica de linfocitos B
  • Linfoma linfoplasmocítico
  • Linfomas esplénicos y ganglionares de la zona marginal
  • Linfoma de las células del manto
  • Linfoma folicular
  • Linfoma de la zona marginal
  • Tricoleucemia
  • Plasmocitoma mieloma de células plasmáticas
  • Linfoma difuso de linfocitos B grandes
  • Linfoma de Burkitt
181
Q

NEOPLASIA DE PRECURSORES DE LINFOCITOS T:

A

Leucemia/linfoma linfoblástico agudo de
infocitos T

182
Q

NEOPLASIAS DE LINFOCITOS T Y LINFOCITOS CITOLÍTICOS NATURALES PERIFERICOS

A
  • Leucemia prolinfocítica de linfocitos T
  • Leucemia linfocítica de gránulos grandes
  • Micosis fungoide/Sindrome de Sézary
  • Linfoma anaplásico de células grandes
  • Linfoma angioinmunoblástico de linfocitos T
  • Linfoma de linfocitos T asociado a enteropatía
  • Linfoma de linfocitos T similar a paniculitis
  • Linfoma de linfocitos T hepatoesplénico
  • Leucemia/linfoma de linfocitos T del adulto
  • Linfoma de linfocitos citolíticos naturales/T extraganglionar
  • Leucemia de linfocitos citolíticos naturales
183
Q

Linfoma de Hodgkin

Cuales son los subtipos clasicos?

A
  • Esclerosis nodular
  • Celularidad mixta
  • Rico en linfocitos
  • Depleción linfocítica

NO CLASICO: Predominio linfocitico nodular

183
Q

Linfoma de Hodgkin

Cuales son los subtipos clasicos?

A
  • Esclerosis nodular
  • Celularidad mixta
  • Rico en linfocitos
  • Depleción linfocítica

Predominio linfocitico nodular

184
Q

Nacen de la medula osea, se diferencian en el ganglio, termina su maduración y se transforman en células plasmáticas.

A

Linfoma B

185
Q

FACTORES ETIOLÓGICOS Y PATOGÉNICOS

Translocaciones cromosómicas y otras
mutaciones adquiridas:

A
  • MALT1
  • BCI10
  • BCL6
  • C-MYC
186
Q

Factores genéticos hereditarios:

A
  • Síndrome de Bloom, anemia de Fanconi ↑ leucemia en adultos
  • Síndrome de Down y NF1 ↑ leucemia en infancia
187
Q

Que virus están involucrados con diferentes tipos de enfermedades del sist. linfatico?

A
  • HTLV-1 (virus 1 de la leucemia de linfocitos T humana) LEUCEMIA/LINFOMA DE LINFOCITOS T DEL ADULTO
  • VEB LINFOMA DE BURKITT Y Linfoma de Hodgkin
  • KSHV/HHV-8 (herpes virus de sarcoma de Kaposi/herpes humano 8)
188
Q

FACTORES ETIOLÓGICOS Y PATOGÉNICOS

Estimulación inmunitaria crónica:
El H. pylori y HIV están relacionados a que tipos de linfomas?

A
  • H. pylori - LINFOMA B
  • HIV - LINFOMAS B ASOCIADOS A VEB
189
Q

Neoplasias que se presentan con afectación extensa y normalmente de la MO, pero puede presentar en la sangre periférica. No se presenta como masa, pues afecta la MO.

A

Leucemia

190
Q

Proliferaciones que surgen como masas tisulares delimitadas. Mucho mas frecuente en ganglios, con característica predominante de una masa. Existen algunos tipos que pueden leucemizarse al afectar la MO.

A

Linfoma

191
Q

2/3 de los LNH (linfoma no hodgkin) y
prácticamente todos los LH (linfoma hodgkin) se presentan con …….. y ………...

A

2/3 de los LNH (linfoma no hodgkin) y
prácticamente todos los LH (linfoma hodgkin) se presentan con adenopatías y adenomegalia.

192
Q

LEUCEMIA/LINFOMA LINFOBLASTICOS AGUGOS

Son neoplasias compuestas por células ……….. B (pre-B) o T (pre-T) que se consideran linfoblastos.

A

LEUCEMIA/LINFOMA LINFOBLASTICOS AGUGOS

Son neoplasias compuestas por células inmaduras B (pre-B) o T (pre-T) que se consideran linfoblastos.

193
Q

o 85%
o Se manifiestan como “leucemias” agudas
o Infancia (3 años)

A

LLA-B

194
Q

o menos frecuentes
o Se manifiestan como “linfomas” del timo
o Varones adolescentes
*es la neoplasia mas fr en niños (< 15 anos)

A

LLA-T

195
Q

INMUNOMARCACION
- TdT + 95 %
- LLA-B:
- LLA-T:

A
  • LLA-B: CD19, PAX5, CD10
  • LLA-T: CD1, Cd2, CD5, Cd7
196
Q

Dolores en las articulaciones sin infecciones en jóvenes siempre sospechar de:

A

Leucemia

197
Q

Clínica de las leucemias agudas

A

o Inicio brusco “tormentoso” DÍAS O SEMANAS
o Síntomas por depresión de lafunción medular:
 Anemia
 Fiebre por infecciones
 Hemorragias
o Efectos de masa
 Dolor óseo
 Linfadenopatías
 Esplenomegalia
o Manifestaciones en el SN
 Cefalea
 Vómitos

198
Q

Leucemias agudas. Pronóstico

A

o Con QT 95% de los niños remisión completa, 75-85% se cura
o Con QT solo el 35-40% de los adultos se cura

199
Q

Es la leucemia más frecuente en adultos
 Edad media: 60 años, V:M 2:1
 linfocitos > 5000/mm3

A

LEUCEMIA LINFOCÍTICA CRÓNICA (LLC)

200
Q
  • Neoplasias de los linfocitos B periféricos
  • Dos trastornos que difieren solo en el grado de linfocitosis en sangre periférica.
A

LEUCEMIA LINFOCÍTICA CRÓNICA (LLC)
LINFOMA LINFOCITICO PEQUEÑO (LIP)

201
Q

Que son las sombras de Gumprecht?

A

Son núcleos desnudos, como resultado de la destrucción de linfocitos, que por su fragilidad intrínseca adoptan un aspecto amorfo y desestructurado, al realizarse la extensión de sangre.
Las sombras de Gümprecht en los frotis de sangre periférica pueden ser indicadores de la presencia de patologías malignas como la leucemia linfocítica crónica.

202
Q

LEUCEMIA LINFOCITICA CRÓNICA (LLC)

Que encontramos en sangre periferica, MO, bazo e hígado?

A
  • Sangre periférica: linfocitosis
  • MO: infiltrados intersticiales o agregados tumorales
  • Bazo: infiltración en pulpa blanca y roja
  • Higado: infiltración en tractos portales
203
Q

LEUCEMIA LINFOCÍTICA CRÓNICA (LLC)/
LINFOMA LINFOCITICO PEQUEÑO (LLP)
Clínica

A
  • Asintomática
  • Síntomas inespecíficos (cansancio, perdida de peso y anorexia)
  • 50% Linfadenopatías y hepatoesplenomegalia
  • Se asocia a anemia hemolítica autoinmune y trombocitopenia inmune
  • Tendencia a transformarse a Linfoma difuso de grandes células B (Síndrome de Richter).
  • Mal pronóstico.
204
Q

Cuale es el linfoma NO Hodgkin INDOLENTE más frecuente?

A

LINFOMA FOLICULAR

205
Q
  • Ambos sexos
  • Edad mediana
  • Surge de linfocitos B del centro germinal
  • Se asocia a translocaciones cromosómicas que afectan al gen BCL-2
  • BAZO: pulpa blanca
  • HIGADO: triadas portales

Que linfoma es?

A

LINFOMA FOLICULAR
- LNH indolente más frecuente

206
Q

Nódulos prominentes que representan folículos de pulpa blanca

A

LINFOMA FOLICULAR

DD:
- LLP: linfoma de linfocitos pequeños;
- LCM: linfoma células del manto;
- LZM: linfoma de la zona marginal

207
Q
A

LINFOMA FOLICULAR
- Crecimiento nodular o nodular y difuso
- Células pequeñas con núcleos irregulares o hendidos y citoplasmas escasos (células hendidas pequeñas). Son la mayoría
- Células mayores con cromatina nuclear abierta, varios nucléolos, citoplasmas moderados (centroblastos)

208
Q

LINFOMA FOLICULAR
Cual es la traslocación que determina esta enfermedad?

A

t[14;18]
INMUNO: CD19, CD20, CD10, BCL-6, BCL-2 (90%)

209
Q

LINFOMA FOLICULAR
Clínica

A
  • Linfadenopatías indoloras generalizadas
  • Tubo digestivo
  • SNC
  • Testículos
  • Evolución con recaídas y mejorías
  • Supervivencia mediana 7-9 años
210
Q
  • Es la forma mas frecuente de LNH (Linfoma NO de Hodgkin)
  • Mortal sin tratamiento
  • Hombres, 60 años
A

LINFOMA DIFUSO DE LINFOCITOS B GRANDES

211
Q

LINFOMA DIFUSO DE LINFOCITOS B GRANDES
Clínica

A
  • Masa tumoral destructiva, grande ganglionar o extra-ganglionar
  • Puede afectar: Anillo de Waldeyer, amígdalas, adenoides, hígado, bazo, tubo digestivo, piel, hueso, cerebro
  • MO infrecuente, tardía
212
Q

Micro:

A

LINFOMA DIFUSO DE LINFOCITOS B GRANDES

Infiltración difusa por células grandes con núcleos grandes multilobulados, nucléolos múltiples, citoplasma abundante
INMUNO: CD19, CD20, CD10, BLC-6

213
Q
  • 30% LNH en la infancia
  • Niños y adultos jóvenes
  • Muy agresivo
  • 3 subtipos “histológicamente idénticos”:
    AFRICANO O ENDEMICO *relacionado al virus Epstein-barr, afecta la mandibula con grandes masas tumorales
     ESPORADICO
     ASOCIADO A HIV
  • Difieren en la clínica, genotipo y virología. - > localizaciones extraganglionares
A

LINFOMA DE BURKITT

214
Q

LINFOMA DE BURKITT
Que se ve en la micro?

A
  • Macrófagos (“patrón en cielo estrellado”)
  • Infiltrado difuso de células linfoides de tamaño intermedio con núcleos redondeados, cromatina grosera, varios nucléolos y moderado citoplasma
  • Elevado índice mitótico
  • Numerosas células apoptóticas
215
Q

LINFOMA DE BURKITT
Expresa que tipos de “CD”? Que gen es traslocado?

A
  • CD19, CD20, CD10, BCL-6 + (LB centro germinal)
  • NO expresa BCL-2
  • Translocación del gen c-MYC (crom 8)
216
Q

Poco frecuente
< 10% de los LNH
50-60 años, varones
Mal pronóstico

A

LINFOMA DE LAS CELULAS DEL MANTO

217
Q

LINFOMA DE LAS CELULAS DEL MANTO
Micro:

A
  • Las células tumorales se parecen a los LB normales de la ZM que rodean los CG.
  • Linfocitos pequeños con núcleos irregulares, a veces hendidos, citoplasma escaso, nucléolos débil, cromatina condensada.
218
Q
  • Linfadenopatías indoloras generalizadas
  • Afectación del Sistema Pulmonar 20-40% de los casos
  • Afectación esplénica (50%) e intestinal (poliposis colónica)
  • Agresivo, sobrevida 3-4 años dependiendo de diferentes factores
  • Trasplante de MO
A

LINFOMA DE LAS CELULAS DEL MANTO

219
Q

LINFOMA DE LAS CELULAS DEL MANTO
Inmuno:

A

CD19, CD20, CD 5, Ciclina D1+
CD23 -

220
Q

Inicialmente se describió en mucosas - linfomas MALT (tejido linfoide asociado a mucosas).
Surgen de tejidos afectados por trastornos inflamatorios crónicos de etiología autoinmune o infecciosa.
- Glándula salival en la Enf. de Sjögren,
- Tiroides en la tiroiditis de Hashimoto
- Estomago en la gastritis por H. pylori.

A

LINFOMA DE LA ZONA MARGINAL

Se mantienen localizados durante periodos de tiempo prolongados, diseminándose sistémicamente en etapas avanzadas.
Puede haber remisión si se erradica el agente causal.

221
Q

LINFOMA DE LA ZONA MARGINAL
MICRO:

A
  • linfocitos B pequeños (patrón de infiltración)
  • Presencia de folículos
  • Lesiones intraepiteliales
222
Q

LINFOMA DE LA ZONA MARGINAL
LOCALIZACIONES + fr:

A
  • Estomago
  • Cabeza y cuello
  • Ojo
  • Piel
  • pulmón
223
Q
  • Proliferaciones de linfocitos B que producen/liberan Ig monoclonal
  • La más frecuente es el mieloma múltiple (MM)
A

NEOPLASIA DE CÉLULAS PLASMATICAS

224
Q
  • Sintetizan una cantidad excesiva de cadenas ligeras o pesadas junto a las Ig completas, a la cual se denomina Componente M.
  • Las cadenas ligeras libres son pequeñas y se eliminan por orina (proteína de Bence Jones)
A

NEOPLASIA DE CÉLULAS PLASMATICAS

225
Q

NEOPLASIA DE CÉLULAS PLASMATICAS
Entidades clínico patológicas:

A
  • Mieloma Múltiple - plasmocitoma
  • Macroglobulinemia de Waldenström - IgM
  • Enfermedad de cadenas pesadas
  • Amiloidosis primaria
  • Gammapatía monoclonal de significado incierto (GMSI)
226
Q
  • Es la gammapatía monoclonal más importante
  • Proteína M >3g/dl + compromiso MO >10% células plasmáticas
  • 65 años
A

MIELOMA MULTIPLE

227
Q

MIELOMA MULTIPLE

A
  • Masas tumorales de células plasmáticas destructivas dispersas por todo el esqueleto (fracturas patológicas, dolor crónico)
  • Producción excesiva de Ig
  • Supresión de la inmunidad humoral normal (infecciones bacterianas recurrentes)
  • Anemia, lesiones oseas, hipercalcemia, fallo renal
228
Q

MIELOMA MULTIPLE
Huesos mas afectados:

A
  • Columna vertebral,
  • costillas,
  • cráneo,
  • pelvis,
  • fémur,
  • clavícula
  • escapula
229
Q

Rx: Defectos en saca bocados (1.4 cm.)
MO: plasmocitos 30% de la celularidad (10% celularidad + CM)
SP: Eritrocitos en pilas de monedas (característico, no especifico)

A

MIELOMA MULTIPLE

230
Q

MIELOMA MULTIPLE

A
  • Pronóstico variable
  • Frecuente recaídas
  • Tratamiento inmunomodulador, inhibidores proteosoma y Trasplante MO
231
Q

Variante MM quiesciente (smoldering)

A
  • Proteína M >3g/dl, infiltrado MO >10% células plasmáticas pero SIN síntomas
  • Evolucionan a MM
232
Q
  • Variante infrecuente que se presenta como una masa aislada en hueso o partes blandas
A

PLASMOCITOMA (MIELOMA SOLITARIO)

233
Q

El plasmocitoma óseo solitario evoluciona
casi inevitablemente a un …….. ……….

A

Mieloma Multiple

234
Q
  • Lesiones extraóseas: Pulmones,
    orofaringe, senos paranasales
A

PLASMOCITOMA (MIELOMA SOLITARIO)

235
Q
  • Síndrome en donde los niveles altos de IgM causan síntomas por hiperviscosidad sanguínea
  • Adultos mayores
A

MACROGLOBULINEMIA DE WALDENSTROM

236
Q
  • Rara
  • Asociada a linfoma linfoplasmocitario
  • Síntesis y secreción de los fragmentos libres de cadenas pesadas.
A

ENFERMEDAD DE CADENAS PESADAS

237
Q

Ocurre como consecuencia de una proliferación monoclonal de células plasmáticas que segregan cadenas ligeras que se depositan como amiloide

A

Amiloidosis primaria

238
Q
  • Sin síntomas que tienen componentes M en sangre (<3g/dl), ancianos, 1% anual se transforma a MM
  • Asociada a otras entidades autoinmunes y linfoproliferativas
A

Gammapatía monoclonal de significado indeterminado (GMSI)

239
Q
  • Mal pronóstico
  • CLINICA: linfadenopatías generalizadas, eosinofilia, prurito, fiebre, pérdida de peso
    MICRO:
  • Ninguna característica morfológica patognomónica
  • Borramiento difuso del GC por parte de linfocitos T pleomórficos de tamaño variable
  • Eosinófilos y macrófagos (reactivos)
  • Neoangiogenia
    INMUNO: CD2, CD3, CD5 +, CD19 -, CD 25 -
A

LINFOMA DE LINFOCITOS T PERIFÉRICOS

240
Q
  • Poco frecuente
  • Se define por la presencia de reordenamientos del gen ALK en el crom 2p23 (actividad tirosina quinasa que activa vía JAK-STAT)
  • Pronóstico bueno (curación con QT: 80%)
    CLINICA:
  • Niños y adultos jóvenes
  • Afectación extraganglionar (60%)
A

LINFOMA ANAPLASICO DE CELULAS GRANDES

241
Q
  • Células anaplásicas grandes con núcleo en herradura y citoplasma voluminoso (hallmark cell)
  • Fondo inflamatorio
  • Crecimiento paracortical o sinusoidal
  • Afectando vénulas
  • Necrosis
  • INMUNO: ALK, CD30 +
A

LINFOMA ANAPLASICO DE CELULAS GRANDES

242
Q
  • Asociado a infección por HTLV-1
  • Endémico en Japón, Africa occidental y Caribe
    CLÍNICA: Linfoadenopatías generalizadas, hepatoesplenomegalia, linfocitosis en sistema pulmonar, hipercalcemia y lesiones cutáneas
    Rápidamente progresiva y mortal
A

LEUCEMIA / LINFOMA T DEL ADULTO

243
Q

Proliferación de linfocitos T CD4+ cooperadores en piel
3 etapas: Premicótica inflamatoria, en placas y tumoral
Progresión a afectación ganglionar y de MO

A

MICOSIS FUNGOIDE / SME DE SEZARY

244
Q
A

MICOSIS FUNGOIDE / SME DE SEZARY
Sme de Sézary: eritrodermia generalizada y linfocitos T circulantes en sistema pulmonar

245
Q
  • Surge en un único ganglio o cadena ganglionar
  • Se disemina primero hacia los tejidos linfoides continuos anatómicamente
A

LINFOMA DE HODGKIN

246
Q

LINFOMA DE HODGKIN
Características morfológicas distintivas:

A
  • Células de Reed Sternberg
  • Liberan factores que inducen la acumulación de linfocitos, macrófagos y granulocitos reactivos (representan el 90% de la celularidad tumoral)
247
Q

LINFOMA DE HODGKIN
Clínica:

A
  • Más frecuente en adultos jóvenes y adolescentes
  • Es curable en la mayoría de los casos (80% remisión completa)
248
Q

LH: clasificación

A
249
Q

Células de Reed Sternberg

A
  • Variante clásica: CD15+, CD30 +, CD20-
  • Su identificación es esencial para el diagnostico.
  • Son células grandes con múltiples núcleos o un solo núcleo con múltiples lóbulos nucleares, cada uno con un gran nucléolo a modo de inclusión con el tamaño aprox. de un linfocito pequeño.
250
Q
  • Forma mas frecuente (70%) de LH (Linfoma de Hodgkin).
  • Adolescentes y adultos jóvenes. Sexo femenino
  • GL mas afectados: cervicales, supraclaviculares y mediastínicos
  • Pronostico excelente
  • Afectación EG (extraganglionar): rara
A

LH ESCLEROSIS NODULAR

251
Q

LH ESCLEROSIS NODULAR

A
  • célula de RS variante lacunar sobre un fondo maduro con linfocito, eosinófilos, plasmocitos y macrófagos.
  • deposito de colágeno en blandas que dividen el ganglio en nódulos circunscriptos
  • Fibrosis
  • (+) para PAX5, CD15, y CD30
  • (-) para CD45
252
Q
  • 20-25%
  • > hombres, incidencia bifásica
  • Se presenta en estadio III o IV
  • Pronostico global es muy bueno
  • Relación con VEB
A

LH CELULARIDAD MIXTA

253
Q

LH CELULARIDAD MIXTA

A

Borramiento difuso de la arquitectura por un infiltrado células heterogéneo que contiene linfocitos T, eosinófilos, plasmocitos y macrófagos benignos, mezclados con CRS clásicas y mononucleares
Las CRS están infectadas por VEB (79%)

IHQ:
- (+) para PAX5, CD15, y CD30
- (-) para CD45

254
Q
  • Infrecuente
  • Más frecuente en varones
  • Adultos mayores
  • VEB 40%
  • Pronóstico muy bueno o excelente
A

LH RICO EN LINFOCITOS

255
Q
  • Linfocitos reactivos suponen la inmensa mayoría del infiltrado celular
  • Afectación difusa
  • CRS variante mononuclear
A

LH RICO EN LINFOCITOS

256
Q
  • LH menos frecuente (‹5%)
  • Ancianos, VIH +
  • Evolución menos favorable (estadios avanzados y síntomas sistémicos)
A

LH CON DEPLECIÓN LINFOCÍTICA

257
Q

LH CON DEPLECIÓN LINFOCITICA

A

MICRO: Escases de linfocitos y abundancia relativa de Células Reed Steinberg o variantes
INMUNO: idéntico al LH EN
- DD: LNH de células grandes
VEB 90%

258
Q
  • Variante “no clásica”
  • 5%
  • > hombres jóvenes
  • GL (ganglios linfaticos) cervicales o axilares
  • Afectación mediastinal y de MO rara
  • Pronostico excelente
  • No se asocia a VEB
A

LH DE PREDOMINIO LINFOCITICO NODULAR

259
Q
  • infiltrado nodular de linfocitos pequeños mezclados con macrófagos
  • CRS variante LH (linfocítica e histiocítica) que tiene un núcleos multilobulado que se semeja a una palomita de maíz
  • CRS (celulas de reed steinberg) clásicas ausentes
  • Eosinófilos y plasmocitos escasos o ausentes

Células RS expresan marcadores típicos de los linfocitos B del centro germinal (CD20 y BCL-6), negativo para CD15 y CD30.

A

LH DE PREDOMINIO LINFOCITICO NODULAR

260
Q

DIFERENCIAS LH Y LNH

A

Linfoma de Hodgkin
- Localizado en un solo grupo ganglionar axial (cervical, mediastínico, paraaórtico)
- Dispersión ordenada por contigüidad
- Ganglios mesentéricos y anillo de Waldeyer raramente afectados
- Presentación extraganglionar infrecuente

Linfoma NO de Hodgkin
- Afectación mas frecuente de múltiples ganglios periféricos
- Se disemina, pero no por contigüidad
- Afectación frec del anillo de Waldeyer y
ganglios mesentéricos
- Presentación extraganglionar habitual

261
Q

NEOPLASIAS MIELOIDES
Se originan de la célula hematopoyética progenitora mieloide.
Tres categorías:

A
  • Leucemia mieloide aguda
  • Síndromes mielodisplásicos
  • Trastornos mieloproliferativos
262
Q
  • Tumor de progenitores hematopoyéticos causado por mutaciones oncogénicas que provoca acumulación de blastos mieloides en MO.
  • Conduce a fracaso medular
  • 60 años o más
A

LEUCEMIA MIELOIDE AGUDA (LMA)

263
Q

LEUCEMIA MIELOIDE AGUDA (LMA)
Diagnóstico

A
  • Presencia de al menos 20% de blastos en MO
  • Mieloblastos o monoblastos
264
Q

CLASIFICACIÓN MORFOLOGICA LMA

A
265
Q

LEUCEMIA MIELOIDE AGUDA (LMA)
Citogenética:

A
  • Se correlacionan con el cuadro clínico. En jóvenes t[8;21] , inv(16) y t[15;17].
  • En adultos mayores generalmente es secundaria a Smes mielodisplásicos (del o monosomias cromosoma 5 y 7).

MOLECULAR
- CBF1α y CBF1β
- PML-RARα
- FLT3
- C-KIT
- NPM

266
Q

Enfermedad clonal del stem cell, con displasia y hematopoyesis inefectiva de 1 o más líneas. Frecuente evolución a LMA (leucemia mieloide aguda).
En >70 años.

A

SINDROMES MIELODISPLASICOS

267
Q

ETIOPATOGENIA
- Primaria (de novo)
- Quimioterapia – Radioterapia – Benceno
- Enfermedades hereditarias
CLÍNICA
- Síndrome anémico
- Petequias - hematomas
- Organomegalias - adenopatías (infrecuentes)
- Anemia, trombocitopenia, leucopenia. Reticulocitos normales o ↑
- ↑ ácido úrico y LDH.

A

SINDROMES MIELODISPLASICOS

268
Q

SINDROMES MIELODISPLASICOS
Diagnóstico

A
  • Citopenia > 6 meses en al menos 1 linaje celular y exclusión de otra causa de citopenia.
  • Displasia morfológica en > 10% células MO o anomalía CTG o 5-19% blastos.
269
Q

Son trastornos que presentan tirosina quinasas constitutivamente activadas que evitan los controles normales y producen proliferación y sobrevida de los progenitores de manera independiente.

A

TRASTORNOS MIELOPROLIFERATIVOS (NMPC)

270
Q

TRASTORNOS MIELOPROLIFERATIVOS (NMPC)
NMPC: neoplasias mieloproliferativas crónicas
Cuales son?

A
  • Leucemia mieloide crónica
  • Policitemia Vera
  • Trombocitemia esencial
  • Mielofibrosis primaria
  • Leucemia neutrofílica crónica
  • Leucemia eosinofílica crónica
271
Q
  • Proliferación células pluripotenciales y granulocitos con presencia de cromosoma Philadelphia t[9:22] o BCR/ABL
  • 15% de las leucemias (3% en infancia)
  • Edad 65. A > edad > mortalidad
A

LEUCEMIA MIELOIDE CRÓNICA (LMC)

272
Q

LEUCEMIA MIELOIDE CRÓNICA (LMC)

A

 Hipercelular, hiperplasia granulocítica
 Citogenético t[9;22] - Molecular BCR/ABL+

273
Q

LEUCEMIA MIELOIDE CRÓNICA (LMC)
Clínica:

A
  • Fatiga – intolerancia al ejercicio
  • Sudoración - Disminución de peso
  • Anorexia – Saciedad precoz
  • Palidez
  • Esplenomegalia (90% casos)
  • Hepatomegalia (10-15%)
  • Anemia NN – eritroblastos en SP
  • Leucocitosis (>25.000/mm3) Neutrofilia – basofilia
  • Trombocitosis (50%)
  • Hiperuricemia - LDH elevada (80%)
274
Q
  • Proliferación clonal de células hematopoyéticas a predominio serie eritroide
  • Edad 60 años
  • Predominio masculino
A

POLICITEMIA VERA (PV)

275
Q

ETIOPATOGENIA: Mutación V617F del gen JAK-2 (>90%)

A

POLICITEMIA VERA (PV)

276
Q

POLICITEMIA VERA (PV)
Clínica:

A
  • Astenia – disminución de peso
  • Sudoración – Prurito acuógeno - Eritromelalgia – facie pletórica
  • Trombosis venosa - arterial *TVP- Budd-Chiari – porta - esplénica
  • Sme de hiperviscosidad
  • Hepatomegalia (15%) Esplenomegalia (50%)
277
Q

LABORATORIO
- Hb >16,5 o 18,5g/dl
- Leucocitosis con neutrofilia – Trombocitosis
- Aumento uricemia, LDH
- EPO normal

A

POLICITEMIA VERA (PV)

278
Q
  • Trastorno clonal de progenitores con hiperplasia megacariocítica
  • Igual ambos sexos
  • Edad 50-60 años
  • En <40 años es más frec en mujeres
  • Asintomática en 50% de los casos
A

TROMBOCITEMIA ESENCIAL (TE)

279
Q

TROMBOCITEMIA ESENCIAL (TE)
Clínica

A
  • Eritromelalgia – isquemia digital – cianosis
  • Trombosis arterial (+frec) y venosa
  • Hemorragias (>1.500.000 plaquetas)
  • Esplenomegalia moderada (10%)
280
Q
  • Mutación JAK-2 + (50%)
  • Agregación plaquetaria anormal
A

TROMBOCITEMIA ESENCIAL (TE)

Sobrevida no difiere de la población general Evoluciona a:
- LMA espontánea <1%
- LMA asociada a tto 3-10%
- Mielofibrosis 3-10% a los 10 años

281
Q

Expansión clonal de célula hematopoyética con:
- Fibrosis medular
- Hematopoyesis extramedular
- Leucoeritroblastosis en Sistema Pulmonar

A

MIELOFIBROSIS PRIMARIA (MF)

282
Q

ETIOLOGIA: Benceno, radiaciones ionizantes
- Edad 65 años
- Sobrevida 5-6 años
- 1/3 de los ptes asintomáticos

A

MIELOFIBROSIS PRIMARIA (MF)

283
Q
  • Intensa displasia megacariocítica, fibrosis reticulínica en diferentes grados
  • Hematopoyesis intrasinusoidal
  • Nódulos linfoides
    MUTACIÓN: JAK-2+ (50%); MPL (5-10%)
A

MIELOFIBROSIS PRIMARIA (MF)

284
Q

MIELOFIBROSIS PRIMARIA (MF)
Clínica:

A
  • Anemia (80%)
  • Desconforto abdominal - anorexia
  • Sudoración - disminución de peso
  • Esplenomegalia severa (90%)
  • Hepatomegalia (50-60%)
  • Fenómenos autoinmunes: AR,CBP,
  • Sjögren
285
Q
  • Hb < 10g/dl, dacriocitos en SP
  • Leucoeritroblastosis (75%)
  • GB y plaquetas N, aumentadas o
    disminuídas
  • Aumento LDH, uricemia
A

MIELOFIBROSIS PRIMARIA (MF)

286
Q

MIELOFIBROSIS PRIMARIA (MF)
Causas de muerte:

A
  • Progresión a leucemia (31%)
  • Trombosis (14%)
  • Infecciones (10%)
  • Hemorragias (5%)
  • Hipertensión portal (4%)
    Unica opción de curación: trasplante alogénico de MO

3MED FB Pato Teorico (29 decks)

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