Hematology

Question 1

erythroblastosis fetalis why doesn’t it occur in first pregnancy?

Answer 1

When the mother—who was likely Rh negative—first gave birth to an Rh-positive fetus, the fetal red blood cells (RBCs) entered the mother’s circulation. The mother’s body then recognized the Rh antigen as foreign and produced antibodies against it. The initial anti-Rh antibodies made by the mother were immunoglobulin M (IgM) in nature and thus could not cross the placenta and harm the fetus. This resulted in her uncomplicated first pregnancy, during which the fetus did not develop erythroblastosis fetalis.

However, the maternal anti-Rh antibodies are eventually replaced with immunoglobulin G (IgG) antibodies, which can freely cross the placenta. Therefore any subsequent Rh-positive fetus is at risk for hemolytic disease, as occurred in the second child.

Question 2

hydrops fetalis symptoms

Answer 2

gross hepatosplenomegaly and ascites, as well as peripheral edema and purpura. The placenta is pale, thickened, and enlarged.

Question 3

Birbeck granules

Answer 3

organelles found within Langerhans cells, which provide cell-mediated immunity in the skin. However, cell-mediated immunity is not the primary host response to cutaneous larva migrans.

Question 4

Major Basic Protein

Answer 4

In Eosinophils

Question 5

How do parasites die from eosinophils?

Answer 5

Interleukin (IL) -5 is produced by T-helper 2 cells and mast cells, which stimulates further eosinophil proliferation. Eosinophils then react to IgG and IgE on the surface of parasites, which triggers the release of major basic protein and oxygen intermediates contained within eosinophils and destroys the parasites. This antibody-mediated destruction of parasites by eosinophils is referred to as antibody-dependent cell-mediated cytotoxicity.

THIS IS NOT HYPERSENSITVITY I

Question 6

Immediate (Type 1) hypersensitivity reactions

Answer 6

reactions are triggered by mast cells and basophils and are a classic cause of anaphylactic shock. Although parasites can cause a type 1 hypersensitivity reaction, this is a late-phase reaction mediated by eosinophils and would present as a chronic allergy (rash, wheezing, cough).

Question 7

Complement activation

Answer 7

has a role in type 2 hypersensitivity (antibody-mediated) and type III (immune complex) reactions. These reactions are not part of the immune response to parasites. Classic examples of type 2 and type 3 reactions include rheumatic fever or acute post-streptococcal glomuleronephritis, respectively.

Question 8

Abundant secondary lysosomes

Answer 8

are seen in macrophages which require significant amounts of hydrolytic enzymes for digestion of phagocytes cell debris

Question 9

Abundant peroxisomes

Answer 9

Found in fatty acid metabolism

Question 10

Abundant mitochondria

Answer 10

are seen in cells with high adenosine triphosphate requirements, such as myocytes.

Question 11

Langerhans cell histiocytosis

Answer 11

Collective group of proliferative disorders of langerhans cells. presents in a child a lytic bone lesions, and skin rash or as a recurrent otitis media with a mass involving the mastoid bone.

Cells are functionally immature and do not effectively stimulate primary T cells, via antigen presentation. Cells express S-100 mesodermal origin, and Cd1a. Birbeck granules (tennis racket)

Question 12

Plasma Cells Vs B Cells?

Answer 12

B cells are APC MHC II that present to T cells that secrete IL4 IL5
to make Plasma B cell secreting cells

Question 13

bilobed nucleus and numerous blue to purple granules on hematoxylin and eosin stain

Answer 13

basophils, which are elevated in the blood in the setting of some parasitic infections.

Question 14

Bilobed nuclei with bright pink granules on hematoxylin and eosin stain

Answer 14

eosinophils

Question 15

CD5

Answer 15

is found on most T cells (and also on the cells of chronic lymphocytic leukemia)

Question 16

“warm” IgG autoimmune hemolytic anemia

Answer 16

Direct coombs Test: They demonstrate spherocytes- lack of central pallor) Splenic macrophages take chunks of membrane from IgG coated red cells. As a result surface area of RBC decrease and cells take spherical shape. Mean corpuscular hemoglobin concentration therefore increases!

Question 17

When would you do blood smear test for anemia hemolysis?

Answer 17

malaria and babesiosis, an intraerythrocytic parasitic infection that causes systemic symptoms and hemolytic anemia. Babesia microti is found in the northeastern and midwestern United States and is transmitted to humans through a tick bite.

Question 18

Eosin-5 maleimide binding test

Answer 18

screen red cells for hereditary spherocytosis. The eosin-5 maleimide fluorescent dye binds to band-3, a major structural protein in red blood cells.

Question 19

Cold agglutinin disease can lead to IgM-mediated hemolytic anemia.

Answer 19

The binding of IgM to red blood cells results in C3 complement fixation. Cells are then removed extravascularly via splenic macrophages. As a result, these patients have a positive direct Coombs test for C3 complement. Note that the hemolysis tends to be extravascular as RBC surface proteins protect cells from complement-mediated damage.

C3 think macrophage –> Spleen clearance –> Extravascular

C3b and IgG are the two 1° opsonins in bacterial defense; enhance phagocytosis. C3b also helps clear immune complexes. (like IgG in type 2 Hypersensitivity reaction cytotoxic antibody related killing)