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Blood and Lymph week 1 > Tuesday > Flashcards

Tuesday Flashcards

1
Q

Male and Female reference ranges for WBC’s

A

4.0-11.1

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2
Q

Male ref. range for RBC’s

A

4.76-6.09

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3
Q

Female ref. range for RBC’s

A

4.18-5.64

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4
Q

How do you know it’s an RBC?

A

Biconcave dis, no nucleus, eosinophiic cytoplasm and central area of pallor which should be less than 1/3 of the diameter

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5
Q

Male ref. range for HGB

A

14.3-18.1

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6
Q

Female ref. range for HGB

A

12.1-16.3

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7
Q

Male ref. range for HCT %

A

39.2-50.2

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8
Q

Female ref. range for HCT%

A

35.7-46.7

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9
Q

What is the formula for HCT?

A

HCT = RBC x MCV

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10
Q

Male and Female ref. range for MCV

A

80-100

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11
Q

Low MCV means

A

Microcytosis, iron deficiency anemia, or thalassemia

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12
Q

High MCB means

A

Macrocytosis, megaloblastic anemia

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13
Q

What are the thresholds for microcytic, normocytic and macrocytic anemia?

A

MCV100

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14
Q

MCH (mean cell hemoglobin) parallels which other important measure?

A

MCV

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15
Q

What is the formula for MCH?

A

MCH=HGB /RBC

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16
Q

What does low MCH mean?

A

hypochromatic, iron deficiency anemia

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17
Q

What does high MCH mean?

A

Hyperchromatic, megaloblastic anemia

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18
Q

What is the female and male reference range for MCH?

A

27.5-35.1

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19
Q

What is the formula for MCHC?

A

MCHC = HGB/HCT or MCHC = MCH/MCV

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20
Q

What does high MCHC mean?

A

hereditary spherocytosis

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21
Q

What does low MCHC mean?

A

moderate to severe microcytic anemia

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22
Q

What are the male and female ref. ranges for RDW?

A

11.7-14.2

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23
Q

Neutrophil info

A

Cytoplasm acidic, many fine granules, 2.5 nuclear segments/lobes

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24
Q

What is the threshold for Neutropenia and some possible causes?

A

decreased absolute neutrophil count ANC <1.5 x 10^9/L

Causes: Infections, drugs, marrow disease, autoimmune disease and congenital

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25
Q

What is the threshold for Neutrophilia and some possible causes?

A

ANC>11.1 x 10^9/L

Causes: Physiologic, acute inflammation, endocrine, myeloproliferative neoplasms, malignant diseases and drugs

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26
Q

Eosinophil info

A

Numerous large, round and red-orange granules 1-4 nuclear lobes

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27
Q

Eosinopenia

A

<0.01x 10^9

Causes: Drug induced, acute inflammation ro infection

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28
Q

Eosinophilia

A

> 0.4x 10^9/L
Causes:
Primary stimulating cytokines-IL-5 and IL-3
Infections, allergic disorders, loffler’s syndrome, leukemias and malignant diseases

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29
Q

Basophil info

A

Numerous large round purple-block granules, two nuclear lobes often covered by granules

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30
Q

Basopenia

A

<0.01 x 10^9/L

Causes: Acute hypersensitivity reactions, administration of progesterone

31
Q

Basophilia

A

> 0.2 x 10^9/L

Causes: Mastocytosis, lots of leukemias

32
Q

Monocyte info

A

large and eccentric nucleus, kidney/horshoes-shaped, lacey appearance, lots of cytoplasm, few granules, may have intracytoplasmic vaculoes

33
Q

Monocytopenia

A

<0.2x10^9/L

Causes: aplastic anemia, hemodialysis, thermal injury, AIDS, hairy cell leukemia

34
Q

Monocytosis

A

> 1.0 x 10^9L

Causes: physiologic, infants, infections, marrow disease, Hodgkin’s

35
Q

Lymphocyte info

A

Mostly small, nucleus round or slightly indented, condensed chromatin, scanty bluish cytoplasm, a few granules

36
Q

Lymphopenia

A

<1.0 x 10^9/L

Causes: Dependent on CD4+ T-cells, DiGeorge syntome, ataxia telangiectasia, Acquired, HIV,

37
Q

Lymphocytosis

A

> 5 x 10^9/L

Causes: Physiologic, viral infections, pertussis, Post-splenectomy

38
Q

Platelet info

A

Small fragments of megalokaryocytes, irregular outline, light blue cytoplasm, lots of small granules

39
Q

Thrombocytopenia

A

<140 x 10^9/L
Caues: Peripheral destruction, sequestration in the spleen, inadequate production, inherited i.e. Wiskott-Aldrich syndrome

40
Q

Thrombocytosis

A

> 400 x 10^9/L

Causes: Primary marrow neoplasm, reactive

41
Q

Hallmarks of iron deficiency anemia

A

Small RBC’s, larger central pale area, target cells, all parameters decrease except RDW

42
Q

How do you identify spherocytes?

A

Spherical, no central pallor, due to decreased cell membrane, increased MCHC

43
Q

What are bite cells?

A

Bite-size defect due to removal to Heinz body in spleen and associated with G6PD Deficiency

44
Q

What are schistocytes?

A

Fragmented RBC’s helmet cells, HUS, TTP, DIC, burns, HELLP, mechanical heart valves

45
Q

What are target cells?

A

Central hemoglobin and target shape, thalassemia, hemoglobin C, iron deficiency, liver disease

46
Q

Sickle cell

A

Bipolar, spiculated shape, banana shape

47
Q

What is basophilic stippling?

A

Morphology- evenly dispersed fine blue granules, content: aggregated ribosomes
Causes: Lead poisoning, porphyria, hemoglobinopathies, infection

48
Q

Howell-Jolly bodies

A

Morphology- single, dense, blue dot
Content: Nuclear DNA remnant
Causes: Post-splenectomy, functional asplenia, megaloblastic anema, myelodysplasia

49
Q

Heinz body

A

Not visible on a Wright-Giemsa stain, need to stain with supravital dye, causes by G6PD deficiency and associated with bite cells

50
Q

Dohle Body

A

Pale blue inclusion at the periphery of the cytoplasm, infection, inflammation, burns or pregnancy
contents: condensed RNA

51
Q

Toxic granulation

A

lots of granules doe to rapid cell division and often associated with Dohle bodies and toxic vacuolization
causes: bacterial infection, marrow recovery

52
Q

Hypersegmented neutrophils

A

More than five lobes, associated with megaloblastic anemia

53
Q

What are the three things that innate immunity recognizes?

A

PAMP- pathogen associated molecular patterns
DAMP- damage associated molecular patterns
the absence of normal cell surface molecules

54
Q

TLR receptors activate the IRAK pathway and what is the net effect?

A

Activation of the inflammatory transcription factor NF-KB

55
Q

The cell that unifies the innate and adaptive immune system is:

A

the dendritic cell

56
Q

It’s impossible to have a good adaptive response without. . .

A

an innate response

57
Q

What is the name of the piece of the antigen that fits into the lymphocyte?

A

antigenic determinant or epitope

58
Q

Type 1 Helper T cells

A

Th1, recognize antigen and make a lymphokine that attracts thousands of macrophages, the heavy-duty phagocytes, to the area where antigen has been recognized. This intense inflammation can wipe out a serious infection—or a transplanted kidney.

59
Q

Th17 Helper T cells,Th17

A

are similar to Th1 in that their main role is to cause focused inflammation, although they are more powerful than Th1. They help resist some very tough infectious organisms, but they have been implicated in many serious forms of autoimmunity

60
Q

Type 2 Helper T cells

A

Th2, stimulate macrophages to become ‘alternatively activated,’ and then function in walling-off pathogens and promoting healing, a process that usually takes place after the pathogen-killing Th1 response. They are very important in parasite immunity

61
Q

Follicular Helper T cells

A

Tfh,are stimulated by antigen and migrate from T cell areas of lymph nodes into the B cell follicles, where they help B cells get activated and make the IgM, IgG, IgE and IgA antibody subclasses.

62
Q

Regulatory T cells

A

Treg, make lymphokines that suppress the activation and function of Th1,Th17, and Th2 cells, so they keep the immune response in check. They are part of the Th family

63
Q

Cytotoxic or killer T cells

A

CTL for short, destroy any body cell they identify as bearing a foreign or abnormal antigen on its surface.

64
Q

Th1, Th2, Th17, Tfh, and Treg have which molecular marker on their surface?

A

CD4

65
Q

Killer T cells have which molecular marker on their surface?

A

CD8

66
Q

IgG

A

Immunoglobulin G, is the most abundant antibody in blood. Two adjacent IgG molecules, binding an antigen such as a bacterium, cooperate to activate
complement, a system of proteins that enhances inflammation and pathogen destruction. IgG is the only class of antibody that passes the placenta from mother to fetus in humans, and so
is critical in protecting the newborn until it can get its own IgG synthesis going

67
Q

IgM

A

IgMis a large polymeric immunoglobulin. It’s even better at activating complement than is IgG,
and is the first antibody type to appear in the blood after exposure to a new antigen. It is replacedby IgG in a week or two

68
Q

IgD

A

is a form of antibody inserted into B cell membranes as their antigen receptor

69
Q

IgA

A

is the most important class of antibody in the secretions like saliva, tears, genitourinary and
intestinal fluids, and milk. In these secretions
it’s associated with another chain called Secretory
Component, which it acquires from epithelial cells during the process of being secreted.
Secretory Component makes it resistant to digestive enzymes. IgA plays an important role as the first line of defense against microorganisms trying to gain access to the body through the mucous membranes.

70
Q

IgE

A

is designed to attach to mast cells in tissues. Thus attached, when it encounters antigen, it
will cause the mast cell to make prostaglandins, leukotrienes, and cytokines, and release its
granules which contain powerful mediators of inflammation like histamine. These mediators
produce the symptoms of allergy, which range from hay fever and hives to asthma and
anaphylactic shock, depending on the site of antigen entry and dose. The real role of IgE is in
resistance to parasites, such as worms

71
Q

Type I immunopathology, immediate hypersensitivity

A

is seen in patients who make too much
IgE to an environmental antigen, which is often innocuous like a pollen or food. About 10% of
the population has allergic symptoms. Although usually a nuisance, asthma can be life-
threatening, and several people die each year of anaphylactic shock, in which the mast cells
throughout the body are suddenly degranulated and release their histamine. A bee sting or certain
foods can do it. We don’t know why some people are allergic; it is partly genetic, and if both
your parents are allergic your risk of developing allergies goes up to over 60%

72
Q

Type II immunopathology

A

is autoimmunity due to antibodies which react against self. There are a number of ways this can come about: For example, if a foreign antigen happens to look like a self molecule, the response to the antigen may accidentally “cross-react” with self. And if an antigen sticks to certain cells in the body, the immune response may destroy the cells as innocent bystanders. The mechanism is what we observed in normal antibody immunity: antibody binds,complement is activated, phagocytes are attracted, and they attempt to eat the antigen. We treat these diseases with immunosuppressive and anti-inflammatory drugs

73
Q

Type III immunopathology

A

can occur whenever someone makes antibody against a soluble antigen. Immune complexes of antigen and antibody are usually eaten by phagocytes, but if they are a bit too small for that, they may instead get trapped in the basement membranes of capillaries they circulate through. This will happen mostly where there is net outward movement of fluid from blood to tissues, such as in the kidneys, joints, pleura and skin. The trapped
complexes activate complement and the usual inflammatory response occurs, with the tissue
damaged as an innocent bystander. No matter what the antigen is, the symptoms tend to be the
same: arthritis, glomerulonephritis, pleurisy, rash. Foreign antigens that cause Type III include
drugs like penicillin when given in large doses, and foreign serum, such as horse antiserum to
rattlesnake venom (in fact, the syndrome is often called serum sickness.) More troublesome is
when the antigen is internal, as part of an autoimmune process. Thus people with systemic lupus erythematosus, SLE, make antibody to their own DNA, some of which can always be found free
in blood, and people with rheumatoid arthritis make antibody… to antibody

74
Q

Type IV immunopathology is T cell mediated

A

and can be autoimmune, or more commonly
innocent bystander injury. For example, in tuberculosis most of the cavity formation in lungs is T cell-mediated, not bacterium-mediated. In acute viral hepatitis, most of the liver destruction is
by killer T cells, just doing their job.

Blood and Lymph week 1 (1 decks)

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