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Hem Yr 2 Sem 2 > Week 3 > Flashcards

Week 3 Flashcards

1
Q

What is monocytosis

A

-absolute count greater than 1.0 x 10^9/L in adults and greater than 3.5 x10^9/L in neonates

-seen after neutropenia or overwhelming infection can be sign of recovery from acute infection
-TB
-malaria

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2
Q

What is monocytopenia

A

absolute monocyte count of less than 0.2 x 10^9/L

-rare
-aplastic anemia
-chemotherapy induced cytopenia
-Hairy Cell leukemia HCL

Absolute monocytopenia can be found in
-pt with steroid therapy or hemodialysis
-pts with sepsis
-pt with viral infections - EBV

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3
Q

What are qualitative changes in monocytes

A

-immature monocytes can be seen in PBS as a response to infection or inflammation not as common as a neutrophilic left shift

hematologic neoplasms

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4
Q

What are some reactive changes that you would see in monocytes

A

reactive changes can be seen during infection, recovery from BM aplasia or post GM-CSF

nuclear contortion
increased cytoplasmic volume
increased cytoplasmic granules
-phagocytic activity (cytoplasmic vacuolation, intracellular debris, and irregular cytoplasmic borders)
-thin band like segmentation

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5
Q

Functional abnormalities in mono and macro

Lysosomal storage diseases
what can they be classified into

A

mucopolysaccharide storage disease
lipid storage disease

-represent group of inheritied enzyme deficiencies that cause flawed degradation of phagocytized material resulting in buildup of that partially digested material in that phagocyte

-seen in macrophages and monocytes found in the BM and in the spleen

Inherited condition that affects mucopolysaccharide storage that also affects the neutrophils- Alder Riley

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6
Q

lipid storage diseases that affects macrophages

Gaucher disease

A

-most common lysosomal lipid storage disease
-defect/deficiency of an enzyme responsible for glycolipid metabolism so unmetabolized lipid accumulates in macrophages through out the body
-BM has Gaucher cells which are macrophages that have a fibrillar blue gray cytoplasm with wrinkled appearance
-pts asymp and others have neurological def
-anemia and thrombocytopenia

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7
Q

lipid storage diseases that affects macrophages

neimann pick disease

A

-mutation to genes controlling enzymes responsible for lipid metabolism and flow of lipids into and out of the cell.
-causes build up of lipids in cellular lysosomes of organs and macrophages = impairs function depending on the organ that is affected
-niemann pick cells found in BM
-macrophages with a foamy cytoplasm packed with lipid filled lysosomes that look like vacuoles after staining

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8
Q

What are the three types of Niemann Pick Disease

A

Type A - in infancy = failure to thrive death by age 4

Type b - from 1st decade to adulthood no neruocognitive impairment

Type c - heterogenous

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9
Q

What are age related qualitative differences in lymphs

A

Reverse ratio in childhood
lymphocytosis compared to adults
-need to use age related RI
-in children age related lymphocytosis is an absolute count greater than 10.0 x 10^9/L but in adults it is a count greater than 4.5 x 10^9

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10
Q

When looking at smear from a child what do you have to pay attention to

A

-dont assume they are all lymphs
-look at morph - can be blasts
-lymphs have a higher N:C ratio than myeloblasts and can be smaller

Acute lymphoblastic leukemia is most common cancer in childern

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11
Q

What is lymphocytopenia

A

age dependent
in children - absolute lymph count under 2.0 x 10^9/L but in adults it is a count below 1.0 x 10^9/L

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12
Q

Lymphocytosis without morphologic alterations

A

-bordetella pertussis
-acute infectious lymph - smaller lymph

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13
Q

Lymphocytosis with morphologic alterations

most common cause

A

infectious mononucleosis - larger lymphs
-infectious hepatitis
cytomegalovirus infection
viral influenza
lymphoid malignancies

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14
Q

Lymphocytopenia most common cause

A

steroid therapy
strenuous exercise
morphine administration
HIV
genetic abnormalities

inherited vs acquired

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15
Q

What do large granular lymphs look like

A

-expanded nucleus with clumped chromatin
-increased cytoplasmic volume but the color is still pale blue
-azurophilic cytoplasmic granules

normal cytotoxic T cells or NK cells

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16
Q

How is the change in morphology related to function in lymphs

A
  • small lymphs are not end cells = resting lymphs
    -reactions to AG can be enlargement or blastogenesis
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17
Q

What happens when an lymphocyte interacts with the correct ag

A

-turns into active cell = blastogenesis (converting from resting to active cell - BLAST)
-cell enlarges, chromatin changes - homogenous and nucleoli are more distinct
-increase in cytoplasm and it becomes more blue because of increased RNA and protein production
-divides by mitosis making more memory and effector cells

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18
Q

Depending on the stage of blastogensis what variations would you see in
nuclear shape

A

Small, round, central
Oval, extended
Enlarged, irregular, clings to inner membrane
Clefting

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19
Q

Depending on the stage of blastogensis what variations would you see in chromatin
cell shape
color

A

Dark, clumped
Delicate, homogenous
Nucleoli

20
Q

Depending on the stage of blastogensis what variations would you see in
cell shape

A

Round or oval
Enlarged, ‘squarish’
Very enlarged, spreading around RBCs
Increased cytoplasm

21
Q

Depending on the stage of blastogensis what variations would you see in
color

A

Pale blue
Darker blue
Extremely basophilic
Azurophilic granules

22
Q

What are reactive lymphocytes

A

-activated lymph
-<10% of total lymph count
-have many shapes and sizes

variation in
N:C ratio
nuclear shape
chromatin pattern
visible nucleoli
increased cytoplasm being blue to dark blue
-spreading cytoplasm and peripheral basophilia (Edges of cytoplasm darker blue where it touches red cells)

dont confuse with monocytes because reactive lymphs have regular shaped nuclear membrane (round or oval) and blue cytoplasm (hugging the RBC)

23
Q

infectious monoculeosis caused by

A

EBV
-affects mostly young children
-infection occurs in childhood and goes unnoticed because youre asymp
-it becomes symp when teens and adults get it

24
Q

What are the symptoms of IM

A

-3-7 week incubation
Sore throat- dysphagia
Lymphadenopathy
Fever/chills
Excessive fatigue
Headache

splenomegaly
hepatomegaly

25
Q

Etiology of IM

and how is the infection control through a cellular response

A

-virus infects B lymphs during incubation by attaching to the CD21 receptors
-EBV infects epithelial cells of pharynx, cervical lymph nodes and THEN B lymphs

activation of natural killer (NK) lymphocytes, CD4+T cells, and CD8+memory cytotoxic T cells in response to B cell infection

26
Q

What is the IM immune response

A

Th cells secrete cytokines to activate normal, un-infected B-cells

circulating reactive lymphs are activated T cells

non infected Host plasma cell produce anti EBV AB

27
Q

What can PT IM caused by EBV produce

A

-EBV stimulates infected host plasma cells to produce non EBV AB

A non specific heterophil antibody
-AB that reacts with an AG from a species that is different than the AG that stimulated its production

Patients with I.M. caused by the EBV produce an antibody (IgM) to the virus but ALSO produce Heterophile antibodies that react with sheep or horse RBCs

28
Q

What are the two types of antibodies that are being produced within a patient with mono

A

One, it’s the anti Epstein Barr IgG antibody made by the healthy plasma cells. Two is the heterophile antibody made by the infected plasma cells.

not everyone makes this heterophile AB - young kids dont

29
Q

What do reactive lymphs in IM look like

A
  • pleomorphic , large, blue
    -each cell looks different
    -lots of blue cytoplasm
    -Round, oval or irregular nucleus - may have nucleoli
    -Irregular margins – cytoplasmic projections ‘hug’ red cells
    Peripheral basophilia
30
Q

lesser found clinical manifestation of IM

A

Mild Cold Autoimmune HA

-caused by auto Anti i which react best at 4 degrees but can start to bind at 30 C.
-Low Titer, IgM , narrow thermal range
so extravascular hemolysis is mild

wide thermal range = intravascular hemolysis through full complement activation

31
Q

what would we see in the lab when you think we have mono

A

-elevated WBC count 10-30 x 10^9/L
-absolute lymphocytosis
-variation in lymph morphology
-increased reactive lymphs - HALLMARK OF IM - diagnostic if age and symps match
-reactive lymphs are activated cytotoxic CD8+ T cells ( can be T or B)
-cells seen in blastogenesis
-variation in cells

if >10% of reactive lymphs = increased
some, many in WBC morph

32
Q

What are some testing strategies used for testing of IM

A

PT may have primary EBV = Monospot test
-Monospot repeated incase it was too early to detect AB
Monospot negative but EBV is still suspected = EBV specific serology performed by PHOL

32
Q

How can heterophile AB be used for screening tests

A

-tests with IgM AB

Monospot - IM latex agglutination test
-latex particles coated with AG from bovine red cells
-pt AB agglutinates latex particles = positive

Screening test
-can have false positives
-negative in IM patients that dont make AB

33
Q

if you have a confirmed IM diagnosis what do you have

A

WBC 10-30 x 10^9/L because of absolute lymphocytosis
-reactive lymph morphology
-positive heterophile AB
-positive EBV specific AG and AB test

34
Q

What are examples of leukocyte artifacts

A

-Necrotic cells- dead cell

-“Denuded nucleus”- when cytoplasm has disappeared so the nucleus is the only thin that remains - falsely high N:C ratio

-Smudge cells aka basket cell

Broken down cells:
degenerated cells
crushed cell

Anti-coagulant changes

35
Q

What happens when Granulocytes (neutrophils) sit in EDTA for too long

A

-necrotic -looking
-increase in artifact smudge cells

-nuclear swelling
-chromatin changes
-loss of structure of lobes
-cytoplasmic rim looks ragged
-increased vacuolization
-loss of granules
-necrotic changes

36
Q

What happens when mononuclear cells sit in EDTA for too long

A

cytoplasmic vacuolization
-irregular nuclear lobulation/nuclear budding
-homogenously staining chromatin
-partial nuclear disintegration

37
Q

how can anticoagulant changes be avoided

A

-make smears on fresh samples
-put sample in the fridge right after assessment

new sample can be requested if morphological info is required by the physician

38
Q

What are smudge cells

A

No nucleus or membranes
-pathological if seen in large numbers
Associated with chronic lymphocytic leukemia (CLL) where lymphocytes are ‘delicate’

-Artifact
Ignore unless suspect CLL – then count separately

39
Q

What are immunodeficiency states

A

-conditions were parts of the immune system is defective

Hereditary lymphocyte disorders
T cell like AIDS
B cell
Combined B & T cell

40
Q

How do you diagnose immunodeficiency disorders

A

Flow cytometry – quantitative & qualitative:
T – cells
B – cells

SPE and IFE – immunoglobulin

CBC & Smear:
Often a Lymphopenia is seen
Response to infection

41
Q

What is DiGeorges Syndrome

A

Defect in T cells
-low t cells
-underdeveloped Thymus, thyroid and parathyroid resulting reduced production of t cells and impaired response to stimulus (cytokines)
-Cardiac and neurological disorders

-thymus is were t cells develop

Susceptible to infections with opportunistic pathogens
Fungi
Pneumocystis carinii
Viruses

42
Q

What is AIDS

A

Human immunodeficiency Virus (HIV)

-CD4 T-cells (Helper T) destroyed
causing Host to be immunocompromised
-Chronic infection, chronic inflammation, chronic anemia

last phase of HIV is AIDS

CBC PBS of someone with HIV:
-Pancytopenia with dysplastic marrow
-Normochromic/Normocytic Anemia
-AZT (drug used to treat HIV) can cause Macrocytosis, Megaloblastic changes and marrow Erythroid hypoplasia.

43
Q

What is Bruton’s Agammaglobulinemia

A

B cell disorder

-X-linked caused by a mutation in BTK
-This Defect is in B cell lineage (pre-B cells) causes a block in B cell development
-No mature B cells therefore no plasma cells
-No antibody formed
-Major consequence is infections (bacterial)

Treatment:
Intravenous Immunoglobulin (TSML)
IV Ig replaces missing immunoglobulins

44
Q

IgA Deficiency

A

hypogammaglobulimia where the pt does not produce or decreased IgA

-Thought to arise after a maturation defect of B cells
-Frequently asymptomatic or
Increased ear, throat, lung infections (since iga is found in mucosal secretions)
upper respiratory
gastrointestinal

-Lab Diagnosis – IFE
-DECREASE in IgA band
-Treat as needed with antibiotics and with IgA deficient blood products

why are blood products IgA deficient
30 - 40% develop anti-IgA AB so if you give them something with IgA then they can have an allergic reaction

45
Q

Severe Combined Immunodeficiency (SCID)

A

Severe dysfunction of both T & B cells

Two types :
X-linked is most common
Autosomal recessive
-Both types leads to T cell lymphopenia, B cell dysfunction and a lack of NK cells

Severe infections and death by 2 yrs.

Symptoms show by 2 months
Flow-cytometry essential in Dx

gene therapy - causes risk of leukemic transformation with this procedure.

Hem Yr 2 Sem 2 (6 decks)

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