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Hematology > WBC abnormalities (Exam III) > Flashcards

WBC abnormalities (Exam III) Flashcards

1
Q

Leukocytosis

A

increase in WBC

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2
Q

Leukopenia

A

decrease in WBC

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3
Q

Left shift / shift left

A

Increase in slightly immature neutrophils
- band neutrophils
- metamyelocytes
- **BM releasing sooner **(accelerated)

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4
Q

Terminology based on indention of nuclei

A
  • myelocyte
  • metamyelocyte (increase)
  • band (increase)
  • segmented
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5
Q

Leukemoid reaction

A

Exaggerated response to infections and inflammation

  • Leukocytosis
  • Shift Left
  • Nonmalignant (Not leukemia)
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6
Q

Leukocytosis (WBC count)

A

WBC count: 20,000-50,000 ul

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7
Q

Leukocyte Alkaline Phosphatase Stain (LAP)

Leukemoid vs. leukemia

A

Stains neutrophilic granules containing LAP enzyme
- present in segmented neutrophils, bands, and metamyelocyte

Positive stain - blue intensified granules

Used to differentiate
- leukemoid rxn = High LAP score
- Chronic Myelogenous Leukemia (CML) = Low LAP

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8
Q

Low LAP score

A

CML

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9
Q

High LAP score

A

Leukemoid Reaction

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10
Q

LAP score

A

count and grade 100 mature neutrophils or band neutrophils based on their LAP staining intensity

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11
Q

LAP Score =

A

sum of 100 graded mature neutrophils and bands

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12
Q

Normal range of LAP

A

11-95.

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13
Q

Grade 0

A

Stain: 0

Granules: 0

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14
Q

Grade 1+

A

Stain: fine + diffuse

Granules: occasional

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15
Q

Grade 2+

A

stain: moderate

granules: moderate

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16
Q

grade 3+

A

stain: strong

granules: many

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17
Q

grade 4+

A

stain: brilliant

granules: nucleus obscured

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18
Q

Quantitive changes

Neutrophils

A

Increase: infections/inflammation

decrease: chemotherapy

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19
Q

Quantitative changes

Eosinophils

A

Increase: parastic infections

decrease: ACTH hormone

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20
Q

Quantitative Changes

Basophils

A

Increase: hypersensitivity

Decrease: steroid treatment

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21
Q

Quantitative changes

Monocytes

A

increase: chronic infections (TB)

decrease: autoimmune processes

22
Q

Quantitative Changes

Lymphocytes

A

increase: viral infection

decrease: chemotherapy

23
Q

Qualitative abnormalities

A

Toxic granulation
- primary granules persisting

Dohle Bodies
- RNA remnant of RER aggregated

Toxic vaculoziation
- Phagocytisis

24
Q

Phagocytosis - Chemotaxis and Diapedisis

A

Marginating pool neutrophils roll along vessel endothelium

Cytokines are released from sites of inflammation

Neutrophils are attracted to these sites (follws trails to highest concentration) = chemotaxis

Neutrophil then squeezes between endothelial cells to enter tissue = diapedesis

25
Q

chemotaxis

A

Neutrophils are attracted to inflammation sites (follows trail to highest concentration).

26
Q

Diapedesis

A

Neutrophil squeezes between endothelial cells to enter tissue

27
Q

Phagocytosis - Opsonization and recognition

A

Neutrophils cannot efficiently recognize most microorganisms

Requires opsonins
- promotes interaction of surface of microorganisms with receptors on neutrophil plasma membrane

Microorganisms coated in immunoglobin (antibodies) or complement = opsonization

Opsonin is recognized by the neutrophil
- receptors for Fc fragment of antobody or complement attach

28
Q

Opsonization

A

Microorganism coated in immunoglobulin (antibodies) or complement.

29
Q

Phagosome (ingestion and killing)

A

Pseudopods extend around microbe forming a vacuole

30
Q

Phagolysosome (ingestion and killing)

A

lysosomes with cytoplasmic granules fuse with phagosome

31
Q

In phagolysosome, granules degranulate…

A

realeasing lytic elements and leads to drop of pH

  • non oxygen dependent mechanism
  • Able to cleave bacterial cell wall
32
Q

Phagocytosis finale - Respiratory burst

A

NADPH converts oxygen into lethal metabolites including:
- H2O2 - hydrogen peroxide
1. causes major microorgnaism injury
2. accelerates the destructiion process

Oxygen dependent mechanism

Any remnant are removed through exocytosis

33
Q

Diseases of improper phagocytosis

A

Disease can occur due to

Ingestion by cell has normal enzyme activity, BUT…
- Thing ingestied is resistant to being killed
- Cell is overzealous in amount it has ingested

Actual deficiency of lysosomal enzymes

34
Q

Symptoms of improper phagocytosis

A

Accumulation of unmetabolized material in lysosomes

Undigested metabolic products accumulate in cells

Metabolic enzyme deficiency -> Undigested metabolic product

35
Q

Chronic Granulomatous Disease

A

Most cases - X linked
- primarily males

Problem: Deficiency in Cytochrome B
- Needed for Respiratory Burst
- H2O2 of respirary burst needs to kill catalase positive organisms
1. Staphylococcus aureus, Mycobacteria, Serrita
2. Fungus: Asperigillus

Granulomas accumulate

Average life span: 10 years

Prone to recurrent infections

36
Q

Chediak Higashi Syndrome

A

Rare, Fatal, autosomal recessive disorder

Problem: Defective fusion protein
- lysosomes will not secrete and release enzymes properly
- creates giant azurophilic granules in cytoplasm

Found in granulocytes, lymphocytes, and monocytes

Susceptible to recurrent infections (S. auereus)

Additional clinical features: Neutropenia, albinism, photophobia, thrombocytopenia, PLT dense granule deficiency

37
Q

Gauchers Disease

A

Most common lipid storage disease

Autosomal Recessive

Problem: deficiency of betaglucocerebrosidase
- Glucocerebroside (a glycolipid waste product) accumulates. Gaucher cell

Additional clinical features: Neutropenia, anemia, thrombocytopenia, hepatomegaly

Classified into 3 types
- Type II: infantile form is the most severe

38
Q

Niemann-Pick Disease

A

2nd most common lipid (lysosomal) storage disease

Autosomal Recessive

Problem: Deficiency og sphingomyelinase
- Sphingomyelin and Cholesterlol accumuates in cytoplasm of macrophages
- foamy Histiocytes = Niemann Pick cells

Additional Clinical Features
- Mental retardation, delayed structural development - lipids accumulate in nervous tissue

Hepatosplenomegaly

39
Q

Tay Sachs - aka Gangliosidosis

A

Autosomal Recessive

Problem: Deficiency in hexosaminidase A
- lipids and gangliosides accumulate - leads to nercous and eye tissue damage

Life expectancy less than 4 years

No abnormal morphological characteristics

40
Q

Alder-Reilly Anomaly - aka “Alders Anomaly”

A

Autosomal Recessive

Problem: Deficiency in alpha-L-iduronidase
- Mucopolusaccharides accumulate
- creayes large granules in neutrophils, lymphocytes, monocytes, eosinophils, basophils
1. can give a clearing (halo) around the granule
2. can be misinterpreted as toxic granulatpion

Additional clinical features: Dwarfism, skeletal problem (humped back), frontal bossing

Average life expectancy: 6-10 years

Formerly called Gargolyism

41
Q

Lymphocyte Review

A

WBC differential: 20-44%

1.Resting small lymphocyte
- small (8-12 um), scanty cytoplasm, with round nucleus

Reactive lymphocyte
- Large (9-30 um), abundant cytoplasm, round to irregular nucleaus, and possible nucleoli
- Can be confused with malignant conditions

42
Q

Viral infections (Causes of reactive lymphocytosis)

A

Chickenpox, cytomegalovirus, EBV (infectiousmononucleosis)

43
Q

Bacterial infection (causes of reactive lymphocytosis)

A

Brucellosis
Perussis (whooping cough)
Tuberculosis

44
Q

Drug reactions (reactive lymphocytosis)

A

Due to medications for infections

45
Q

Miscellaneous (causes of reactive lymphocytosis)

A

Allergic reactions, auto immune disease, malnutrition

46
Q

Infectious mononucleosis - NOTHING to do with monocytes

A

**Vast majority are caused by Epstein Barr Virus (EBV) **

**EBV infects B lymphocytes

**T lymphocytes (CD8) react becoming reactive lymphocytes. **

Virus is transmitted through bodily fluids, espeially saliva
- increased prevalence in young adults (17-25 years old)
1. correlates to prime dating and social interaction years

-Usually self-limiting, general symtpoms: sore throat, and flu like symptoms
1. lymph nodes become enlarged (possible hypersplenism)

47
Q

Lab findings infectious mononucleosis

A

Usually diagnosed on symptoms only

Screening test - Monospot test
- detects heterophile antibodies produced against EBV

48
Q

heterophile antibodies

A

antibodies that crossreact either with other antigens that did not stimulate its formation or proteins across species lines

Test against Sheep or horse RBCs

49
Q

Infectious Mononucleosis
Peripheral smear

A
  • Increased reactive lymphocytes
  • T lymphocytes working against the infection
  • Cytoplasm tends to stain darker and morph arounf RBC - “ballerina skirt”
50
Q

Infectious Mononucleosis

Additional sereoly tests detects antibodies to:

A
  1. Viral capsid antigen (IgM and IgG)
  2. EBV nuclear antigen
  3. EBV early antigen complex

Using this combination, we can judge the time frame of a current infection or historical infection.

Hematology (36 decks)

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