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Advanced Patho Test 1 > TEST 2: Hematology > Flashcards

TEST 2: Hematology Flashcards

1
Q

$ RBC function and main component

A

Function: O2 transport from lungs to body and & CO2 transport from tissue to lungs
Main component: hemoglobin (binds O2)
-Catalyzes the reversible reaction between C02 and H20

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2
Q

WBC function and types

A

Function: Infection defense
Types: several types (neutrophils, lymphocytes, monocytes, eosinophils and basophils) where each type has a specific role

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3
Q

Platelets and main function

A

Crucial role in blood clotting and wound healing
Main function: aggregate to form a temporary plug at the site of blood vessel injury and release chemicals that activate further clotting processes.

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4
Q

Plasma function and main components

A

Function: liquid component of blood transports blood cells, nutrients, waste, and other substances throughout the body
Main component: water, electrolytes, protein (albumin, clotting factors), hormones and waste.

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5
Q

$$ Anemia Types (8)

A
  1. Iron Deficiency
  2. Vit B 12 deficiency (Pernicious)
  3. Folate Deficiency
  4. Aplastic
  5. Sickle Cell
  6. Hemolytic
  7. Anemia of chronic disease
  8. Acute blood loss
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6
Q

$Lymphoma definition?
Types (2)
What tissues does it affect?

A

Def: cancer of lymphatic system
Types:
1. Hodgkin lymphoma (~75% survival)
2. Non-hodgkin lymphoma

Tissues: lymphoid such as spleen, marrow and thymus. Typically starts in lymph nodes.

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7
Q

$Myeloma definition and symptoms

A

Def: cancer of plasma cells in bone marrow
Sx: bone pain, anemia, renal dysfunction, recurrent infections,
LONG BONE FRACTURE

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8
Q

$$Hemophilia definition, types (2) and symptoms

A

Def: genetic disorder impairing the body’s ability to make blood clots
Types:
1. Hemophilia A (factor 8 deficiency)
2. Hemophilia B (factor 9 deficiency)

Sx: prolonged bleeding, spontaneous bleeding into joints and muscles

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9
Q

*What is a blood smear

A

Microscopic exam of stained blood cells to evaluate their morphology

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10
Q

*What is flow cytometry

A

A test analyzing the physical and chemical characteristics of cells or particles

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11
Q

$$ Hematologic medication treatments (4) and the condition they treat

A
  1. Anti-coagulants (prevent clotting)
  2. Clotting factor concentrates (hemophilia)
  3. Immunosuppressants (autoimmune anemia)
  4. Erythropoiesis-stimulating agents (anemia of chronic disease)
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12
Q

What is erythropoiesis

A

Development of RBCs

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13
Q

*What hormone regulates erythropoiesis? Where is it produced?
Under what conditions (most common one)?
Using what factor?

A

Hormone: Erythropoietin (Epo)
Where: kidneys
Condition: Hypoxia
Factor: Hypoxia inducible factor-1 (HIF-1)

Bonus Info: hypoxia such as anemia or high altitude the kidneys release Epo, which stimulates the bone marrow to produce more RBCs

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14
Q

*Where are RBCs developed in adults (tissue and location)

A

Hematopoietic tissue, primarily found in flat bones such as pelvis, vertebrae, cranium, and mandible.

Bonus: these bone house hematopoietic bone marrow

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15
Q

$$ Where are RBCs developed in Infants (prenatal & post natal)

A

Prenatal: yolk sac in early gestation, then liver in second gestational month

Postnatal & last month of gestation: bone marrow
Marrow of all bones make RBCs until around 5yo

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16
Q

*In cases where additional RBCs are needed what occurs?
Is there a difference in children?

A

Extra RBC production takes place in extramedullary erythropoiesis outside the bone marrow. Can take place in the liver and spleen.

Children: This entire process is more common in children than adults

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17
Q

*What are Hematopoietic Stem Cells (HSCs)? What (2) types of cell can they become?

A

Multipotent cells found in the bone marrow that have the unique ability to self-renew and differentiate into all types of blood cells.

Can become:
1. Common lymphoid progenitors (CLPs)
2. Common myeloid progenitors (CMPs)

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18
Q

*What are precursor cells?
Examples?

A

Immature cells derived from committed progenitor cells that undergo further differentiation and maturation into specific blood cell types.

-BLAST CELLS

Examples: erythroblasts, myeloblasts, monoblasts, and megakaryoblasts

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19
Q

What is the platelet precursor cell?

A

Megakaryloblasts

Bonus Info: when megakaryocytes are mature they release small fragments of their cytoplasm into the blood stream as platelets.

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20
Q

$$ What are the (5) triggers for RBC production?

A
  1. Anemia/Hypoxemia
  2. Low blood volume
  3. Poor blood flow
  4. Pulmonary Disease
  5. Increased androgens
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21
Q

**How does an increase in androgens trigger erythropoiesis?

A

Androgens including testosterone have been shown to upregulate erythropoiesis by modulating erythropoietin productions.

Bonus: elevated androgens, either due to medical conditions or testosterone supplementation, can enhance RBC production.

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22
Q

$$ How does the Kreb’s cycle influence hematopoiesis?

A

Krebs plays a role in the synthesis of Succinyl Co-A (an intermediary in cellular energy)-> Binds with glycine -> pyrrole

-4 pyrroles bind to make protoporphyrin IX that combine with Iron to make a HEME

ADDITIONAL ORGANIZER INFO: Krebs is not directly involved in hemoglobin synthesis it does play a role in generating components essential for cellular metabolism indirectly supporting the energy requirements for hematopoiesis, including the production of hemoglobin.

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23
Q

$$ What are the 4 polypeptide chains that comprise ADULT hemoglobin?

A
  1. Alpha globulins (x2)
  2. Beta globulins (x2)

Bonus: the four polypeptide chains are arranged as two pairs of identical chains. The chains are proteins known as globulins and consist of two alpha globin chains and two beta globin chains.

-The combination of alpha and beta globin chains is crucial for the structural integrity and proper function of the hemoglobin molecule, enabling it to effectively bind and release O2 as needed.

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24
Q

$$ What are Iron-Protoporphyrin Complexes (hemes)

A

For each hemoglobin there are 4 iron-protoporphyrin complexes known as hemes, with each group associated with a polypeptide chain.

Bonus: It is a critical component of hemoglobin that can bind one molecule of oxygen facilitating O2 transport.

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25
Q

$$ What does a heme group consist of?

A

-Protoporphyrin ring with a centrally bound ferrous iron (Fe2+ OR Fe3+) depending on O2 status.

Heme combines with globin to make HEMOGLOBIN

BONUS: When oxygen binds to the heme group the ferrous iron (Fe2+) is oxidized to the ferric state (Fe3+) leading to the formation of oxyhemoglobin which enhances O2 transport.

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26
Q

$What is the STRUCTURAL ROLE of alpha and beta globin chains in the hemoglobin molecule?

A

alpha and beta globin chains are integral components of the hemoglobin tetramer, which consists of two alpha chains and two beta chains. This quaternary structure is essential for the stability and proper functioning of hemoglobin as an oxygen carrying protein.

-composition and arrangement influence the O2 binding affinity of hemoglobin.

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27
Q

$What is the OXYGEN BINDING ROLE of alpha and beta globin chains in the hemoglobin molecule?

A

alpha and beta globin chains contain heme groups, each within an iron atom at its core. The heme groups bind to and transport O2.

-There are 4 Iron molecules meaning up to 2 molecules of O2 can be transported.

Bonus: the cooperative binding and release of O2 by hemoglobin depends on the interaction between the heme groups and globin chains.

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28
Q

$What is the effect of alterations to the alpha and beta globin genes?

What does this cause?

A

Vatiations in the sequences can lead to the production of different hemoglobin variants that affect the STRUCTURE AND FUNCTION of the alpha or beta globin chains.

-the balanced production of alpha and beta are CRITICAL for the proper assembly of functional hemoglobin molecules.

Results: sickle cell anemia or thalassesmias (can be alpha or beta) that both affect the shape and function of RBCs.

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29
Q

What is the Bohr Effect?

A

Refers to the phenomenon where low pH and high CO2 in the tissues enhance the release of O2 from hemoglobin. It supports O2 unloading in active tissues.

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29
Q

What is the Haldane Effect?

A

Describes how deoxygenation of blood in tissues results in an increased capacity to carry CO2 and H2CO3 back to the lungs. This assist in the removal of CO2 and waste products of cellular metabolism from tissues.

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30
Q

$$ What is Fetal Hemoglobin (HbF) composition and function?

A

Composition: HbF is composed of 2 alpha globin chains and two gamma globin chains giving it the formula: α₂γ₂

(Alpha, beta, gamma, delta and fetal globins possible types)

Function: HbF has a higher affinity for O2 than adult hemoglobin, which facilitates O2 transfer from mother to fetus across the placenta.

Bonus: levels increase in beta thalassemia

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31
Q

What is polycythemia and what causes it?

A

What: increase in RBC count, hemoglobin and hematocrit.

Cause: Can occur as a normal response in fetuses and newborns due to the lower oxygen environment in utero which stimulates erythropoiesis.

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32
Q

$$ What INCOMPATIBILITY causes hemolytic disease of the newborn?

What is the effect on hemoglobin?

A

Incompatibility of blood types between mother and baby, such as Rh incompatibility.

Effect: hemolysis of fetal RBCs leads to increase in erythropoiesis, raising Hb levels initially. However, severe cases can lead to anemia.

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33
Q

$$The effect of lower testosterone in men (aging) on erythropoiesis?

A

Decrease in testosterone levels lead to decreased stimulation of erythropoiesis.

Unlike other physiologic changes this reduction is not considered a normal physiological variation but rather a consequence of hormonal decline associated with aging.

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34
Q

$$ What is the lifespan of RBCs.

A

90- 120 days

-With aging membrane becomes fragile and rbcs can lyse

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35
Q

$What are the (3) steps in RBC destruction at the end of their lifespan?

A
  1. Globin breakdown: broken down into amino acids, which are reused.
  2. Heme breakdown: Iron is recycled from heme, is oxidized to form methemoglobin and eventually recycled into new RBCs.
  3. Porphyrin ring breakdown: broken down into unconjugated bilirubin. The liver conjugates the bilirubin to make it water soluble and it is then excreted into the bile.
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36
Q

*What role do mononuclear phagocytes have in iron management?

A

They can store iron within tissues

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37
Q

$$ What role do hepatic cells have in iron management?

A

liver is primary storage site for iron in the body

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38
Q

$$ What two forms can iron be stored?

A
  1. Ferritin
  2. Hemosiderin
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39
Q

$$ What is Ferritin?

A

Primary form of stored iron within cells. Ferritin is a protein complex that can store up to 4,500 iron atoms, making it a key iron reservoir. It released iron in a controlled fashion according to need.

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40
Q

$$ What is Hemosiderin?

A

a form of stored iron that is formed when there is an excess of iron. It is less readily available than ferritin and can be seen in conditions of iron overload.

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41
Q

*What ways can iron be lost?

A
  1. Urine: very minor amounts
  2. Seat: some
  3. Bile: can contain small amounts of iron
  4. Sloughing of epithelial cells: like those lining the GI tract and skin. They die and are shed naturally removing some iron.

CLINICAL GEM: THERE IS NO ACTIVE EXCRETORY PATHWAY TO REMOVE EXCESS IRON IN THE BODY!!!

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42
Q

What is Iron Toxicity? Why is it a problem?

A

What? Without a excretory pathway excess iron can become toxic in large quantities.

Problem? It can cause damage to organs and tissues by catalyzing the formation of free radicals, which can result in oxidative stress and cellular damage.

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43
Q

What is Hemochromatosis?

A

a genetic disorder that causes the body to absorb an excessive amount of iron from the diet.

Overtime this can lead to iron accumulation in organs such as the liver, heart, and pancreas causing damage.

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44
Q

How does frequent blood transfusions affect iron balance?

A

Can lead to iron overload if not properly managed.

Example: thalassemia or sickle cell anemia where frequent transfusions are required.

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45
Q

What 2 tests help monitor iron status?

A
  1. Serum ferritin
  2. transferrin saturation
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46
Q

What is Chelation therapy?

A

a therapy that can be used to bind excess iron and facilitate its removal from the body in cases of iron overload.

-Can be used for other heavy metals as well (lead, mercury, or arsenic)

NOT needed for test but relevant to our practice: can be oral or IV. Oral takes several days to weeks with doses taken at regular intervals. IV given over 1-4 hrs depending on the agent being used. Frequency and duration of treatment based on iron levels.
Rough on kidneys.

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47
Q

What are the (4) clinical implications that require understanding the oxygen-hemoglobin dissociation curve?

A
  1. Respiratory conditions: alter breathing and can change the shape of the curve and affect O2 delivery.
  2. Anemia: Hgb concentration impact on O2 carrying capacity
  3. CO poisoning: CO binds to Hgb with much greater affinity than O2 shifting the curve to the LEFT and making it difficult for O2 to unload at the tissues.
  4. Exercise physiology: during exercise, factors like increased CO2 production and body temp shift the curve to the RIGHT, facilitating O2 unloading into muscles.
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48
Q

$$ What is Mean Corpuscular Volume (MCV)? How is it calculated and what units is it reported?

A

What: MCV measures the average volume or size of a single RBC.

Calculation: MCV= (Hct% x10)/RBC count (in Millions/μL)

Reported Units: fL (femtoliters) or (one quadrillionth of a L)

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49
Q

$$ What is the interpretation of MCV (Mean Corpuscular Volume)?

A

-CYTIC

LOW (MCV < 80fL)= MICROCYTIC anemia: smaller than normal RBCs

NORMAL (MCV 80-100 fL) = NORMOCYTIC anemia: normal RBCs

HIGH (MCV > 100fL)= MACROCYTIC anemia: larger than normal RBCs. Seen in Vit B12 deficiency, folate deficiency, and certain types of liver disease or hypothyroidism.

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50
Q

$$ What is Mean corpuscular hemoglobin concentration (MCHC)? How is it calculated and what units is it reported?

A

What: MCHC measures the average concentration of Hgb in a given volume of packed RBCs.

Calculation: MCHC- (Hgb (g/dL) x 100)/Hct%

Reported Units: g/dL (grams per deciliter)

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51
Q

$$ What is the interpretation of MCHC (mean corpuscular hemoglobin concentration)?

A

-CHROMIC

LOW (MCHC < 32 g/dL)= HYPCHROMIC: RBCs with less Hgb (paler color). Common in iron deficiency anemia and thalassemia.

NORMAL (MCHC 32-36 g/dL)= NORMOCHROMIC: Normal Hgb concentration. Normocytic anemias like anemia of chronic disease or acute blood loss.

HIGH (MCHC > 36 g/dL)= HYPERCHROMIC: Rare! indicates spherocytosis or other RBC membrane disorders where cells are densely packed with Hgb.

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52
Q

$$ What is Red Cell Distribution Width (RDW)? How is it calculated and what units is it reported?

A

What: measures the variation in the size (volume) of RBCs.
NEW ARE BIGGER get smaller over time

Calculation: RDW= (Standard deviation of MCV/Mean MCV) x 100

Reported Units: Percent %

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53
Q

$$ What is the interpretation of RDW (red cell distribution width)?

A

HIGH (RDW > 14.5%): indicated larger variation in RBC size (anisocytosis). Often seen in mixed anemias (such as iron deficiency anemia combined with Vit B12 or folate deficiency) and conditions where RBCs are being created and destroyed at uneven rates.

NORMAL (RDW 11.5%-14.5%)= uniform size of RBCs, typical in chronic anemia without significant variation in cell size.

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54
Q

What is Anisocytosis?

A

Presence of RBCs of varying size

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55
Q

$$ What lab values would be consistent with microcytic, hypochromic anemia? What are common causes?

A

MCV LOW
MCHC LOW
RDW High IF combined with another anemia

Causes: iron deficiency, thalassemia

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56
Q

$$ What lab values would be consistent with normocytic, normochromic anemia? What are common causes?

A

MCV NORMAL
MCHC NORMAL
RDW NORMAL OR HIGH

Causes: acute blood loss, hemolytic anemia, anemia of chronic disease, aplastic anemia.

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57
Q

What lab values would be consistent with macrocytic anemia? What are common causes?

A

MCV HIGH
MCHC NORMAL OR HIGH
DRW OFTEN HIGH

Causes: Vit B12 or folate deficiency, liver disease, hypothyroid

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58
Q

$ What studies (3) appropriate to evaluate for suspected iron deficiency anemia?

A

Serum iron, ferritin, TIBC (total iron binding capacity)

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59
Q

What studies (2) are appropriate to evaluate for suspected macrocytic anemia?

A

Vit B12 and folate levels

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60
Q

$$ What studies (3) are appropriate to evaluate for suspected hemolytic anemia?

A

LDH
Haptoglobin
Bilirubin

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61
Q

$$What studY is appropriate to evaluate for suspected aplastic anemia? What would the common studies show?

A

Bone marrow biopsy

Normal studies: pancytopenia, normal iron studies.

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62
Q

What does serum iron assess?

A

Amount of circulating iron bound to transferrin

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63
Q

$$ What would abnormal values on a serum iron mean? High and low.

A

High: may indicate hemochromatosis, hemolytic anemia, or iron poisoning.

Low: potential iron deficiency anemia, chronic blood loss, or anemia of chronic disease

64
Q

What does ferritin assess?

A

the amount of stored iron in the body. Also an acute phase reactant

65
Q

What would abnormal values on a ferritin test indicate? High and low.

A

High can indicate iron overload (hemochromatosis) or elevated due to inflammation, infection, or malignancy as it acts as an acute phase reactant.

Low: strongly suggests iron deficiency as it reflects depleted iron stores.

66
Q

What does Transferrin assess?

A

a protein that transports iron in the blood stream

67
Q

What would abnormal values on a Transferrin test indicate? High and low.

A

High: typically iron deficiency as the body produces more transferrin in an attempt to increase iron transport

Low: may indicate malnutrition, chronic liver disease or inflammation.

68
Q

$ What does Total iron binding capacity (TIBC) study assess?

A

measures the bloods capacity to bind and transport iron

69
Q

$ What would abnormal values on a TIBC (total iron binding capacity) test indicate? High and low.

A

High: common in iron deficiency anemia, reflecting the body’s increased need for iron.

Low often seen in chronic inflammatory conditions, malignancies, or liver disease as the body’s iron binding capacity is reduced.

70
Q

What does a transferrin saturation study assess?

A

percent of transferrin that is saturated with iron. calculated as (Serum iron/TIBC) x100.

71
Q

What would abnormal values on a transferrin saturation study indicate? High and low.

A

High: may indicate iron overload disorders like hemochromatosis.

Low: indicates iron deficiency anemia

72
Q

$$ What is the mechanism of Chronic illness anemia?

A

proinflammatory cytokines:
-inhibit erythropoietin production
-destroy immature erythroblasts
-stimulate release of hepcidin (controls iron absorption and blocks iron release, reducing iron availability despite normal or increased iron stores)

73
Q

$$ What is Chronic illness anemia? What study patterns would you expect to see?

A

What: second most common anemia, seen in chronic infections or inflammatory conditions and chronic disease.

Studies:
Serum Iron: LOW
Ferritin: Normal or HIGH
TIBC: LOW or Normal
Transferrin Saturation: LOW

74
Q

$$ What are the causes of hemolytic anemia?

A

destruction of RBCs due to genetic disorders, autoimmune diseases (lupus, RA), drug reactions (NSAIDS, PCN, cephalosporins) and NEONATAL hyperbilirubinemia HEMOLYSIS BUT IS NOT ANEMIA

75
Q

$$ What study patterns would you expect to see with hemolytic anemia?

A

Serum Iron: Normal or HIGH (increased iron release from destroyed RBCs)
Ferritin: Normal or HIGH
TIBC: Normal
Transferrin Saturation: CAN be high
Other: Elevated Bilirubin & hemoglobinuria, decreased haptoglobin

76
Q

$$What is Sickle cell anemia? What is the prevalence?

A

What: genetic autosomal recessive hemolytic anemia characterized by the presence of hemoglobin S (HbS)

Prevalence: 1:500 African Americans

77
Q

$$What study pattern would you expect to see in Sickle cell anemia?

A

Serum Iron: Typically normal
Ferritin: Typically normal
TIBC: Typically normal
Other: HgS identified, low O2 capacity, crises can be triggered by infection, dehydration, hypoxia, leading to vaso-occlusive events and increased risk of complications like MI, stroke, and pulmonary injury.

78
Q

$$What is Pernicious Anemia? What causes it?

A

Vit B12 deficiency anemia due to impaired DNA synthesis and shortened RBC lifespan, NOT due to hemolysis.

Causes: inability to absorb B12 (lack of intrinsic factor), dietary insufficiency, autoimmune destruction of gastric mucosal cells.

79
Q

$$What study pattern would you expect in Pernicious Anemia?

A

Serum Iron: normal
Ferritin: normal
TIBC: normal
Other: elevated homocysteine, sx like paresthesia, balance issues and oral pain. Associated with macrocytic RBCs and megaloblastic anemia.

80
Q

$$What is Folate deficiency anemia? What are the causes?

A

Anemia due to impaired RNA/DNA synthesis, leading to ineffective erythropoiesis.

Causes: dietary deficiency (lack of fruits and veggies), poor absorption, drug interference (e.g. ASA), maternal deficiency leading to fetal neural tube defects.

81
Q

$$What study pattern would you expect in folate deficiency anemia?

A

Serum iron: normal
Ferritin: normal
TIBC: normal
Other: megaloblastic anemia noted on blood smears

82
Q

$$What study pattern would you expect in iron deficiency anemia?

A

Serum iron: LOW
Ferritin: LOW
TIBC: HIGH
Transferrin saturation: LOW

83
Q

What are hematopoietic stem cells (HSCs)?

A

Multipotent stem cells that give rise to ALL blood cell types including WBCs

84
Q

$What is a neutrophil? What does it do?

A

Mature granulocyte. Most abundant type.

Involved in phagocytosing pathogens.

85
Q

$What is an eosinophil? What does it do?

A

Mature granulocyte.

Combat multicellular parasites and involved in allergic responses.

86
Q

$What is a basophil? What does it do?

A

Mature granulocyte.

Release histamine in allergic reactions and inflammatory responses.

87
Q

$Where do B Cells (B-lymphocytes) develop and what do they do?

A

Develop: primarily bone marrow
Do: mature into plasma cells that produce antibody. Involved in humoral immunity (antibody-mediated response)

88
Q

$Where do T Cells (T-lymphocytes) develop and what do they do?

A

Develop: Initially in bone marrow, mature in thymus.
Do: central players in cell-mediated immunity

89
Q

Where to Natural Killer Cells (NK) develop and what do they do?

A

Develop: from CLPs, final maturation in bone marrow and other lymphoid tissues.

Do: target and kill virally infected cells and tumor cells without prior sensitization

90
Q

$$ What cell (3) types are Lymphocytes (agranulocytes)?

A
  1. T cells
  2. B cells
  3. NK cells
91
Q

How do interleukins affect leukopoiesis?

A

Promote the differentiation and proliferation of specific WBCs

92
Q

*What is Leukopenia? Causes (6)?

A

Low WBC (< 4)

Causes:
-bone marrow suppression: marrow aplasia or myelodysplastic syndromes, leukemia or lymphoma where marrow is infiltrated with malignant cells.

-severe infections: viral infections such as HIV/AIDS, hepatitis and influenza can suppress bone marrow. Severe bacterial sepsis can lead to depletion of WBCs.

-autoimmune diseases: Lupus where immune system attacks WBCs or their precursors.

-certain medications: chemo/radiation, some antipsychotics or antithyroid can damage bone marrow

-Nutrient deficiency: B12, folate, or copper can impair bone marrow function.

-Genetic conditions: Kostmann syndrome (severe congenital neutropenia)

93
Q

What is leukocytosis? Causes (6)?

A

High WBC (> 11)

Causes:
-infections: generally bacterial, though some viral and fungal infections can cause leukocytosis (less common)

-inflammation: chronic inflammation such as RA or IBS

-stress responses: physical or emotional stress, intense exercise or seizure.

-malignancies like leukemia: rapid proliferation of abnormal wbcs

-Allergic reactions: anaphylaxis can cause transient leukocytosis.

-Drugs: Corticosteroids or adrenaline can increase wbcs, some other drugs and toxins can stimulate the release of wbcs.

94
Q

How are pathogens detected by the immune system?

A

Immune cells sense and recognize the presence of bacteria, viruses and fungi through pattern recognition receptors (PRRs)

PRRs detect pathogen associated molecular patterns (PAMPs) on the surface of the pathogen, triggering an immune response.

95
Q

How is the immune system activated when a pathogen has been detected?

A

The immune system initiates an inflammatory response releasing chemical signals such as cytokines (e.g. Interleukin) and chemokines that attract immune cells to the site of infection.

Inflammation helps to contain and eliminate pathogens.

96
Q

Once the immune system has detected a pathogen and the inflammatory response has begun, how does the immune system proceed to elimination? (3 steps)

A

Cytokine Signaling: cytokines (e.g. interleukin-1 or IL-1, or IL-6) and granulocyte colony stimulating factor (G-CSF) already released act on hematopoietic stem cells in the bone marrow.

Mobilization: cytokines and chemokines activate signaling pathways that direct migration of immune cells, such as neutrophils and monocytes, from the bone marrow to the infection.

Phagocytosis: these cells actively engage in phagocytosis, engulfing and destroying pathogens.

97
Q

What is the significance of band cells or a “left shift” in the differential count?

A

In response to acute infection bone marrow may produce and release immature forms of WBCs called band cells and metamyelocytes, indicating a “left shift” in the differential count.
–The increased presence of immature cells reflects an accelerated neutrophil production to combat the infection.

98
Q

Symptoms of Leukopenia?

A

Increased susceptibility to infections
Frequent, severe bacterial, viral or fungal infections
Fever, chills and other signs of infection

99
Q

How is leukopenia diagnosed?

A

CBC with Diff
Bone marrow biopsy if suppression or infiltration is suspected
Serological tests for infections and autoimmune markers

100
Q

How is leukopenia treated?

A

-Fix underlying cause (infection, medication, treat autoimmune disease)
-Use of growth factors G-CSF to stimulate wbc production
-Antibiotics or antifungal sto prevent or treat infection

101
Q

What are the symptoms of leukocytosis?

A

Depend on underlying cause.
-Fever, swelling, pain from inflammation
-Signs of leukemia such as fatigue and bruising
-Severe cases hyperviscosity such as blurry vision, headaches and dizziness.

102
Q

How is leukocytosis diagnosed?

A

-CBC with diff
-Diff necessary to determine which type of wbcs are elevated)
-additional tests based on suspected underlying cause e.g. cultures for infection, imaging for inflammation, bone marrow biopsy for leukemia.

103
Q

How is leukocytosis treated?

A

-Manage underlying cause
–abx for infection
–antiinflammatory drugs for inflammation
–chemo for leukemia
–address complications such as hyperviscosity syndrome.

104
Q

$$What are neutrophils? What is their normal range?

A

What: most abundant type of wbc and play a critical role in fighting BACTERIAL infections

Range: 40-60% of total wbc count

105
Q

$What causes altered levels of neutrophils? High and low

A

High: bacterial infections, inflammation, stress or certain medications.

Low: viral infections, bone marrow disorders, or autoimmune conditions.

106
Q

$$ What are lymphocytes? What is their normal range?

A

What: key players in adaptive immune response, including antibody production and immune memory.

Range:20-40% wbcs

107
Q

$$ What causes altered levels of lymphocytes? High and low

A

High: viral infection, chronic infection, some cancers, or autoimmune disease.

Low: immune deficiencies or immune suppressing medication

108
Q

$$ What are monocytes (agranulocytes)? What is their normal range?

A

What: involved in immune response, engulfing pathogens and debris as part of the body’s defense system

Range: 2-8% wbcs

109
Q

$$ What causes altered levels of monocytes? High and low

A

High: chronic infection, inflammatory conditions or some blood disorders

Low: less common but may occur in severe infections or bone marrow disorders.

110
Q

$$ What are eosinophils? What is their normal range?

A

What: play a role in combating parasitic infections and are involved in allergic reactions.

Range: 1-4% wbcs

111
Q

$$ What causes altered levels of eosinophils? High and low

A

High: allergies, asthma, parasitic infections and certain autoimmune diseases

Low: less common but can be stress or severe infections

112
Q

$$ What are basophils? What is their normal range?

A

What: involved in allergic and hypersensitivity reactions releasing histamine and other chemicals in response to allergens.

Range: <1% wbcs

113
Q

$$What causes altered levels of basophils? High and low

A

High: allergic reactions, chronic inflammation or certain hematological disorders.

Low: generally not clinically significant but may occur in some conditions like severe infections.

114
Q

What does “shift” mean in a hematologic context?

A

A qualitative change in the composition of wbcs specifically the distribution of immature and mature forms.

115
Q

“Left shift” definition?

A

increase in the proportion of immature neutrophils (band forms and metamyelocytes) in the peripheral blood.

-normally only a small % of precursor cells are found in circulation

116
Q

Causes and interpretation for LEFT shift

A

Causes:
-acute bacterial infection
-severe inflammation
-other conditions requiring a large number of neutrophils

Interpretation:
-Accelerated production/demand for neutrophils
-acute infection
-Inflammatory response
-BAND forms indicate an ONGOING response to infection

117
Q

“Right Shift” definition

A

Decrease in proportion of mature neutrophils and an increase in hyper segmented neutrophils. Can suggest issues with neutrophil maturation or function.

118
Q

Causes and interpretation for RIGHT shift

A

Causes: less common
-megaloblastic anemia (VitB/folate def.) where bone marrow produced abnormally large and immature neutrophils.

Interpretation:
-problems with neutrophil maturation due to underlying nutritional deficincies or bone marrow disorders.

119
Q

$$Leukemia symptoms general and specific

A

General: fatigue, weakness, weight loss, frequent infections, easy bruising and bleeding

Specific: enlarged spleen or liver, swollen lymph nodes bone and joint pain, pale skin, night sweats.

120
Q

$$ What testing should be done for leukemia, and what treatment?

A

CBC with diff
Bone marrow biopsy
cytogenic studies

Treatment: chemo, often in cycles.
–targeted therapy
–bone marrow transplant (MORE COMMON WITH SOME TYPES)

121
Q

Lymphoma general and specific symptoms

A

General: enlarged lymph nodes, fever, weight loss, night sweats, fatigue.

Specific- Hodgkin: reed-sternberg cells, enlarged lymph nodes in a specific pattern.

Specific- Non-Hodgkin: FAILED TO INCLUDE IT!! {Insert eye roll here}

122
Q

What studies should be done if lymphoma is suspected?

A

Lymph node biopsy
CT/PET scans to determine extent of disease
Bone marrow biopsy

TYPICAL PRESENTATION IS WITH ENLARGED LYMPH NODES

123
Q

What is the treatment for lymphoma?

A

Chemo (both Hodg & Non)
Radiation (localized)–COMMON
Immunotherapy: some types

124
Q

$$ Pathology of Acute Lymphoblastic Leukemia (ALL)

A

overproduction of immature lymphoid cells (lymphoblasts) in bone marrow. Lymphoblasts fail to mature properly and proliferate uncontrollably, inhibiting the production of normal blood cells.

LEAST COMMON SUBTYPE BUT MOST COMMON IN PEDIATRIC CANCER

125
Q

$$ Mechanisms of ALL (leukemia)

A

Chromosomal abnormality/genetic mutation
Dysfunctional tumor suppressor genes and oncogenes

126
Q

$$ Clinical presentation of ALL (Leukemia)

A

Related to bone marrow failure: anemia, fatigue, pallor, thrombocytopenia, bruising/bleeding, and neutropenia/infection

Extramedullary manifestations: lymphadenopathy (swollen lymph glands), hepatosplenomegaly and bone pain.

127
Q

$$ How is ALL (Leukemia) diagnosed?

A

Blood test: high WBCs with increased lymphoblasts
Bone marrow biopsy and aspiration
Flow cytometry and cytogenetic analysis to classify subtypes and detect genetic abnormalities.

128
Q

$How is ALL (leukemia) treated?

A

Intensive chemo
Targeted therapy for specific genetic abnormalities
Hematopoietic stem cell transplant (specific cases)

129
Q

*Pathology of Chronic Lymphocytic Leukemia (CLL)

A

Clonal proliferation of mature but functionally incompetent lymphocytes (primarily B cells) that accumulate in the blood, bone marrow and lymphoid tissues.

130
Q

*Mechanism of CLL (leukemia)

A

-Genetic and epigenetic changes in B cells such as genetic deletions
-dysregulation of apoptosis, leading to prolonged cell survival
-altered interaction with tumor microenvironment

131
Q

*Clinical presentation of CLL (leukemia)

A

Asymptomatic at diagnosis common
May have: lymphadenopathy, hepatosplenomegaly, fatigue, night sweats, weight loss, increased susceptibility to infections.

132
Q

*How is CLL (Leukemia) diagnosed?

A

Peripheral blood smear: presence of mature lymphocytes
Flow cytometry: characteristic surface markers
Genetic testing for chromosomal abnormalities and mutations

133
Q

*How is CLL (Leukemia) treated?

A

-Often “watch and wait” approach for asymptomatic cases.
-Chemo & immunotherapy for symptomatic or advanced cases
-Targeted therapy

134
Q

$Pathology of Acute Myeloid Leukemia (AML)

A

rapid proliferation of myeloid precursor cells (myeloblasts) in the bone marrow, leading to impaired differentiation and accumulation of these immature cells.

135
Q

$Mechanism of AML (leukemia)

A

chromosomal translocations or gene mutation
disruption of normal hematopoietic pathways leading to blocked differentiation and increased proliferations

136
Q

$Clinical presentation of AML (leukemia)

A

-Bone marrow failure: anemia, thrombocytopenia, neutropenia
-High blast count: fatigue, fever, bruising, recurrent infections.
-Organ infiltration: skin, gums, central nervous system

137
Q

$How is AML (leukemia) diagnosed

A

-Blood test: presence of myeloblasts in peripheral blood
-Bone marrow: hypercellular marrow with increased myeloblasts
-Cytogenetic and molecular testing to identify specific mutations and chromosomal changes.

138
Q

$How is AML (Leukemia) treated

A

-Induction chemo to achieve remission
-consolidation therapy, including further chemo or hematopoietic stem cell transplantation
-targeted therapy

139
Q

$$ Pathology of Chronic myeloid Leukemia (CML)

A

presence of Philadelphia chromosome, a result of the translocation between chromosomes 9 & 22, leading to uncontrolled cell division

Three phases:
-Chronic: slow progressing with increased mature myeloid cells
-Accelerated: increased blast cells, worsening sx
-Blast crisis: resembles acute leukemia with high number of blast cells

140
Q

$$ Mechanism of CML (leukemia)

A

tyrosine kinase activity drives uncontrolled proliferation and reduced apoptosis in myeloid cells

141
Q

$$Clinical presentation of CML (leukemia)

A

-often asymptomatic in chronic phase, with incidental discover of leukocytosis
-Advanced: fatigue, weight loss, splenomegaly, anemia, bleeding

142
Q

$$ How is CML (leukemia) diagnosed?

A

Blood: elevated wbc with increased basophils and eosinophils
Bone marrow: biopsy and cytogenetic analysis
Genetic: detection of fusion gene by PCR (BCR-ABL)

143
Q

$$ How is CML (leukemia) treated?

A

tyrosine kinase inhibitors (imatinib, dasatinib etc.) are the primary treatment
Hematopoietic stem cell transplant for refractory or advanced cases

144
Q

What are the characteristics of NON-Hodgkin lymphoma?

A

More common the hodgkin, encompasses a diverse group of lymphomas with varying behaviors and treatment options. A

Arises from T & B cells, or natural killer cells in the lymphatic system

145
Q

What are the treatment options for Lymphomas?

A

GENERAL: Varies by subtype

Chemo, immunotherapy, radiation and stem cell trans.

146
Q

What is Primary Mediastinal B-cell Lymphoma (PMBCL)

A

Rare involving thymus and mediastinal lymph nodes
More common in young women
Treated with chemo

147
Q

What is Primary CNS Lymphoma?

A

Arises in the brain, spinal cord or eyes
Most are diffuse large b cell lymphomas
treatment includes high dose methotrexate based chemo and radiation

148
Q

$$ Pluripotent Cells

A

Pleuripotential hematopoietic stem cells in the bone marrow differentiate:

Committed stem cells become -> Colony forming units (CFU) for RBCs they are CFU-E (erythroblasts)

Blastocyte-> Erythroblast-> Reticulocytes-> Erythrocytes

149
Q

$$ What happens to RBCs after lysis?

A

Macrophages phagocytized

-Liver Kuppfer cells, spleen and marrow

150
Q

$$ Iron Deficiency Anemia, common causes, when most prevalent in children?

A

Causes: chronic blood loss (most common)
Diet deficiency
Malabsorption- Crohns/Gastric bypass
Pregnancy

INCREASED IN CHILDREN DURING PERIODS OR RAPID GROWTH (TODDLER AND ADOLESCENTS)

151
Q

$$ Thalassemia what? Treatment?

A

Autosomal recessive disorder: alpha and beta types (mutation of HBB) A less severe (usually)

Effects synthesis of Hgb-A

Treat with transfusions

152
Q

$$ What is multiple Myeloma?
What are the two primary manifestations?

A

Plasma cell malignancy (genetic mutation that inactivate tumor supports)

Manifestations:
1. Slow proliferation of immunoglobulin (IgG usually), BENCE JONES PROTIEN (light chain in urine)
2. Lytic bone lesions, increased serum Ca, fractures and renal failure.

153
Q

$$ Which lymphomas are linked to the epstein barr virus?

A

Hodgkin
Burkitt’s
Primary Central Nervous

154
Q

Microcytic

A

smaller than normal cells

155
Q

Macrocytic

A

larger than normal cells

156
Q

Hypochromic

A

less than normal pigmentation

157
Q

normochromic

A

normal pigmentation

NO HYPERCHROMIC

Advanced Patho Test 1 (20 decks)

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