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Hematopoietic Function Flashcards

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1
Q

RBCs make up what % of blood? What is the average life span?

A

45% and 120 days

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2
Q

Neutrophils

A

Inhibit bacterial and fungal infections. Most abundant WBC in adults followed by lymphocytes.

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3
Q

Eosinophils

A

Allergies and parasitic infections

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4
Q

Basophils

A

Release histamine and defend against parasitic infections

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5
Q

Monocytes

A

Phagocytic cells that engulf bacteria or worn out cells

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6
Q

Lymphocytes

A

Give humoral and cellular immunity

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7
Q

Most abundant WBC in infants

A

Eosinophils and monocytes

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8
Q

Water makes up what % of plasma? What is the most abundant protein in plasam?

A

92%. Albumin.

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9
Q

Where are WBCs formed?

A

In the bone marrow and partially in the lymphatic system

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10
Q

What are the two types of progenitor cells that form WBCs?

A

Lymphoid and myeloid

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11
Q

Components of blood

A

55% plasma, 45% formed elements

Formed elements: >99% erythrocytes. 1% thrombocytes and <1% leukocytes.

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12
Q

What is needed for the production of RBCs?

A

Erythropoietin, Vitamin B12, folic acid, and iron.

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13
Q

What is needed for vitamin B12 absorption

A

Intrinsic factor secreted by gastric parietal cells

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14
Q

What is the oxygen-carrying protein of RBCs. What is made of?

A

It consists of a heme portion (iron and porphyrin ring) and 2 alpha and two beta globin chains

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15
Q

How does iron get transported around blood? How does it cross cell membranes?

A

transferrin (in ferric 3+ state). And ferroportin (in ferrous 2+ state)

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16
Q

Where is iron found?

A

75% is bound to Hgb. Iron can be found in the liver/spleen/bone marrow stored as ferritin, and some circulates as transferrin.

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17
Q

What is hepcidin?

A

It’s a protein in the liver that regulates the uptake of iron. It acts as a ferroportin inhibitor. When iron levels are high, hepcidin increases and binds to ferroportin. When iron levels are low, hepcidin decreases.

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18
Q

Give examples of clinical conditions that can alter hepcidin levels?

A

Chronic kidney disease, chronic Hep C infection, alcoholism

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19
Q

What is the difference between methemoglobin and normal hemoglobin?

A

Methemoglobin is in a noncarrying oxygen ferric (3+ state). Iron is heme must be in ferrous (2+) form.

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20
Q

Which two substances which normally block platelet adhesion are diminished with endothelial injury?

A

Nitric oxide and prostacylin

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21
Q

vWF serves what purpose in hemostasis?

A

It acts as a glue to allow adherence of platelets.

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22
Q

What two substances are required to activate clotting factors II, VII, IX, and X?

A

calcium and vitamin K

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23
Q

How does prothrombin become thrombin?

A

Through the activation of factor X

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24
Q

What substance converts soluble fibrinogen to insoluble fibrin?

A

Thrombin

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25
What is a leukemoid reaction?
When the need for neutrophils increases beyond the supply, immature neutrophils (banded neutrophils) are released into the blood.
26
Causes of neutropenia
Prolonged infection. Decreased production. Reduced survival. Abnormal distribution or sequestration as seen with hemodialysis, autoimmune d/o, or splenic d/o.
27
What is the most common site of infection with neutropenia?
Respiratory tract
28
Role of eosinophils and basophils in allergic reactions.
Eosinophils are released with allergic d/o (seasonal allergies) and basophils are released during IMMEDIATE hypersensitivity reaction (food allergies, hives)
29
Lymphocytosis is usually caused by what?
Acute viral infections
30
What are the primary lymphoid tissues? What are the secondary lymphoid tissues?
Bone marrow and thymus. Spleen, tonsils, lymph nodes, and Peyer patches of the small intestine.
31
What are B symptoms?
Fever, night sweats, and unexplained weight loss.
32
Clinical manifestations of Hodgkins lymphoma
Painless, enlarged lymph node in neck/supraclavicular area. Mediastinal mass seen on CXR. B symptoms.
33
What types of cells are seen in Hodgkins lymphoma?
Reed Sternberg cells (abnormal B cells)
34
Most common types of non-Hodgkins lymphoma (NHL)?
Burkitts lymphoma, lymphoblastic lymphoma, and large cell lymphoma.
35
Burkitt lymphoma
most common type of NHL in children. May be caused by EBV. Very fast growing tumor of jaw and facial bones. B-cell tumor.
36
Multiple myeloma
Cancer of plasma cells (type of NHL). Abnormal immunoglobulin called M proteins. CRAB manifestations (hypercalcemia, renal failure, anemia, and bone lesions. Bence Jones proteins in urine (amyloid deposits)
37
myelodysplastic syndrome
Considered a preleukemia. Mostly found in the elderly. The result of multiple somatic mutations in multipotent myeloid progenitor cells. Cells defective and don't mature properly. Blasts 5-19%.
38
Difference between acute and chronic leukemias?
Acute leukemia involves immature cells and are more aggressive. Chronic leukemia involves more mature cells and are more insidious.
39
What chromosomal alteration is found in 95% of CML cases?
Philadelphia chromosome, translocation at 9 and 22 (BCR-ABL fusion gene)
40
3 phases of CML
chronic phase blasts < 10% accelerated phase 10-19% blasts blast crisis >20% blasts
41
targeted therapy for CML
tyrosine kinase inhibitors (block BCR-ABL)
42
MCV
average volume of RBC
43
Reticulocyte count
number of immature erythrocytes. Will be high when there is an increased need for RBCs (blood loss). Will be low when there is a problem with production of RBCs.
44
Serum ferritin
Store iron. Low in iron deficiency.
45
TIBC
Total iron binding capacity (amount of iron capable of binding to transferrin). High in iron deficiency. Low with excess iron.
46
transferrin
transports iron. High in iron deficiency. Low with excess iron.
47
Anisocytosis
red cells are present in different sizes
48
poikilocytosis
red cells are present in various shapes
49
Severe symptoms of anemia
syncope, chest pain, angina, heart attack
50
microcytic-hypochromic anemias
iron deficiency and thalassemia
51
What is the most common blood d/o of infancy and childhood?
iron deficiency anemia
52
Lab results seen in iron deficiency anemia
Low serum ferritin Low serum iron Low transferrin saturation (not enough iron to bind) High TIBC (so more iron can be delivered) High transferrin (body tries to compensate by increasing transport)
53
Megaloblastic anemia-macrocytic
Vitamin B12 deficiency and folic acid deficiency. impaired DNA synthesis. Large cells but normal hemoglobin concentration.
54
Folic acid deficiency
Water-soluble B vitamin. Normally from inadequate dietary intake. Very small amounts stored in body, deficiency can happen very quickly. Most common reasons for deficiency are chronic alcoholism and malnourishment.
55
Why is it important for childbearing/pregnant women to have adequate folate?
To prevent neural tube defects.
56
Vitamin B12 deficiency.
Usually from absorption issues. More abundant stores in body so deficiencies take longer to develop. Associated with neurological symptoms. Beefy red tongue (atrophic glossitis)
57
Pernicious anemia
autoantibodies involving CD4+ helper T cells destruction of intrinsic factor necessary for the absorption of B12.
58
Lab results for folic acid and vitamin b12 deficiency.
Homocysteine levels will be increased in both as well as low Hgb, high MCV, and low retic. Anti-IF antibodies highly specific to Vit B12 deficiency. Methylmalonic acid (B12 cofactor) will b elevated in b12 deficiency but normal in folate deficiency.
59
Normoytic-normochromic anemias
insufficient in number of RBCs. 1. anemia of chronic disease 2. aplastic anemia 3. posthemmorhagic anemia 4. hemolytic anemias
60
Anemia of chronic disease
second most common after iron deficiency. Causes include malignancy, chronic kidney disease, upregulation of hepcidin, inflammatory cytokine inhibition of erythropoietin
61
Iron studies in anemia of chronic disease
low serum iron, normal or increased ferritin, low TIBC, normal transferrin saturation,
62
Aplastic anemia
Main characteristic is PANCYTOPENIA as a result of BONE MARROW STEM CELL FAILURE.
63
Difference between aplastic anemia and myelodysplastic syndrome (MDS).
MDS is an abundance of immature cells. There is a shortage of stem cells in AA, but the cells that are present are mature, normocytic, and normochromic.
64
Posthemmorhagic anemia
ACUTE blood loss from vascular space. CHRONIC blood loss leads to iron deficiency anemia.
65
Sickle cell disease
abnormality in genes coding for globin portion of hemoglobin. Mutation of HBB gene.
66
SCD HbSS
2 sickle cell genes. Most severe from of disease.
67
SCD Hb SC
One sickle cell gene from one parent and from the other parent a gene for an abnormal Hgb called "C". Milder form of disease.
68
SCD Hb S beta-thalassemia
One sickle gene from one parent and one beta-thalassemia gene from the other parent. Two types of beta-thalassemia, 0 and +. Those with 0 will have more severe type and no beta globin production and those with + will have a milder form and reduced beta globin production.
69
What labs distinguish thalassemia from iron deficiency anemia?
iron and rbc count in high in thalassemia major and may be normal in minor whereas in iron deficiency iron and rbc count is low.
70
What distinguished polycythemia vera from other causes of increased RBCs?
erythropoietin levels are low. Mutation in JAK2 gene.

Advanced Pathophysiology (2 decks)

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