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Patho > Heme And Immunity > Flashcards

Heme And Immunity Flashcards

1
Q

What is DIC?

A

Overactivation of coagulation factors

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2
Q

What is thrombotic thrombocytopenia purpura (TTP)?

A

Clotting and bleeding at the same time.
Blood disorder where the platelets abnormally clump together causing blood clots which will reduce # of platelets b/c they are being used to form clots.

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3
Q

What does it mean to have a hypersensitivity?

A

When the immune system is reacting in a way that damages the body instead of protecting it.

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4
Q

What antibodies are associated with type 2 hypersensitivities?

A

IgM and IgG

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5
Q

Which hypersensitivity has an environmental antigen IgE?

A

Type 1

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6
Q

What is a type 3 hypersensitivity?

A

When antigen-antibody complexes deposit in blood vessel walls leading to inflammation and tissue damage.

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7
Q

What is a type 4 hypersensitivity?

A

When inflammation and tissue damage is caused by T cells.

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8
Q

What are the 3 different types of anemia?

A

Blood loss, hemolytic, and deficient RBC production

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9
Q

What will labs look like in a patient with anemia?

A

decreased Hbg/Hct and RBC count.

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10
Q

What does microcytic and hypochromic RBC mean?

A

Cell is too small and too pale

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11
Q

What happens to the RBCs in sickle cell disease?

A

RBC’s sickle to a crescent shape when the hemoglobin is deoxygenated

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12
Q

What is the characteristic of the RBCs in iron deficiency anemia?

FAST

A

microcytic and hypochromic

F= iron deficiency
A= anemia of chronic disease
S= seroblastic anemia
T=thalassemia

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13
Q

What are megaloplastic anemias?

A

B12 and folic acid deficiency

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14
Q

What is B12 deficiency anemia called?

A

Pernicious anemia

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15
Q

What is the cell shape and color of cells in pernicious anemia?

Big Fat Pig

A

macrocytic and normochromic (big w/ normal color)

B= B-12
F= folate
P= pernicious
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16
Q

What is aplastic anemia?

A

When there is a reduction in RBC, WBC, and platelets.

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17
Q

impaired bone marrow can cause what type of anemia?

A

Aplastic anemia

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18
Q

What is the normal lifespan of RBCs?

A

120 days

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19
Q

Why is erythropoietin important?

A

It is required to stimulate the bone marrow to create RBCs

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20
Q

What is (primary) polycythemia vera?

A

Increased in all 3 blood cells (RBC, WBC, platelets) caused by overproduction of the bone marrow d/t neoplastic disease.

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21
Q

What is a hematocrit level?

A

The % of total blood volume occupied by RBCs.

I.e : 45% of blood volume is made up of erythrocytes

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22
Q

Where is erythropoietin produced?

A

in the kidneys

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23
Q

What are the 3 types of polycythemia?

A

primary or polycythemia vera, secondary , and relative.

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24
Q

What is polycythemia?

A

Increased RBCs with a hematocrit level greater than 50% which increases blood viscosity.

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25
Q

What is secondary polycythemia?

A

Increase in erythropoietin as a compensatory response to hypoxia. Only RBC levels will be high and WBC and platelets will be normal.

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26
Q

What is relative polycythemia?

A

Only blood volume has been lost, but no cells. There is less of the water component of plasma, concentrating the RBCs.

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27
Q

Hypercoagulability can be caused by what 2 factors?

A

increased platelet function or clotting activity

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28
Q

How does endothelial damage increase risk for blood clots?

A

greater chance for platelets to adhere and aggregate on damaged walls releasing growth factors

*think atherosclerosis

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29
Q

What is thrombocytosis?

A

Increased platelet #

30
Q

How does polycythemia increase the risk of blood clots?

A

high hematocrit increases blood viscosity

31
Q

Where are clotting factors produced?

A

In the liver

32
Q

Where are clotting/coagulation factors produced?

A

In the liver

33
Q

What are the 4 causes of thrombocytopenia?

A

ITP, TTP, splenic sequestration, and dilution

34
Q

What is a splenic sequestration?

A

When the spleen is enlarged, platelets will get trapped inside and the # of platelets in the serum will decrease.

35
Q

How can ASA and NSAIDs cause a decrease in platelets?

A

they impair synthesis of thromboxane needed for platelet aggregation.

36
Q

How do ASA and NSAIDs affect platelets differently?

A

ASA permanently alters the platelets and NSAIDs only affect platelets as long as the life cycle of the drug

37
Q

Why is vitamin K important for coagulation factors?

A

it is required for activation of factors II, VII, IX, X, and prothrombin.

38
Q

Which clotting factors is calcium required for?

A

All of them except the first 2

39
Q

How can DIC lead to thrombocytopenia?

A

Too much clotting uses a lot of the platelets so there will be a reduced amount. This will cause excessive bleeding because there will be less clotting in other areas of the body where platelets can’t be found.

40
Q

What labs confirm DIC?

A

↑ PT, PTT, and D dimer

41
Q

What activates the intrinsic pathway of DIC?

A

Endothelial injury

42
Q

What activates the extrinsic pathway of DIC?

A

Tissue injury

43
Q

What does a high PTT mean?

A

The higher it is the slower it is for the blood to clot

44
Q

What lab values will be abnormal if the extrinsic pathway is affected?

A

PT and INR

45
Q

Does heparin affect the intrinsic or extrinsic pathway?

A

Intrinsic

46
Q

Does coumadin/warfarin affect the intrinsic or extrinsic pathway?

A

Extrinsic

47
Q

Hemophilia A has a deficiency in which coagulation factor?

A

Factor VIII

48
Q

What is ITP?

A

When life cycle of platelets is shortened d/t an autoimmune disorder where the body produces anti-bodies that destroys it’s own platelets.

May seen easy bruising in patients

49
Q

What causes infectious mononucleosis?

A

Epstein Barr virus infecting B lymphocytes

50
Q

What are the s/sx of infectious mononucleosis?

A

Swollen lymph nodes, fever, malaise, and enlarged liver and spleen.

51
Q

What causes the enlarged lymph nodes in infectious mononucleosis?

A

B cells mature in the lymph nodes so if they are infected they will cluster in the area

52
Q

lymphocytic and myelogenous are acute or chronic leukemias?

A

both

53
Q

Which cells does Acute lymphocytic leukemia (ALL) affect?

A

Natural killer, B, and T cells

54
Q

Which cells does Acute myelogenous leukemia (AML) affect?

A

myeloid precursor cells in the bone marrow such as neutrophils, basophils, eosinophils, and monocytes

55
Q

Which acute leukemia primarily occurs in children?

A

ALL

56
Q

What is pancytopenia?

A

Reduction or absence of all three blood cell types

57
Q

What are the 2 types of chronic leukemias?

A

CLL and CML

58
Q

CLL affects which cells primarily?

A

B cells

59
Q

Presence of Reed-Sternberg cells indicates what type of lymphoma?

A

Hodgkin’s

60
Q

What is multiple myeloma?

A

proliferation of malignant plasma cells in the bone marrow and osteolytic bone lesions throughout the skeletal system

61
Q

What are the manifestations of multiple myeloma?

A

pathologic fx, hypercalcemia, hyperviscosity of blood, osteolytic lesions, compression fx

62
Q

A blood type has what kind of antibodies?

A

B antibodies

63
Q

B blood type has what kind of antibodies?

A

A antibodies

64
Q

AB blood type has what type of antibodies?

A

None

65
Q

O blood type has what type of antibodies?

A

A and B

66
Q

Can type A blood donate to type AB?

A

yes

67
Q

Can AB blood donate to type B?

A

No

68
Q

Who is the universal blood type donor?

A

Type O

69
Q

Who is the universal blood type receiver?

A

AB

70
Q

Does AML mostly occur in children or adults?

A

Older adults

71
Q

Which cells are involved in CML?

A

Pluripotent hematopoietic progenitor cell such as bone marrow granulocytes, erythroid precursors, and megakaryocytes.

Patho (11 decks)

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