Tuesday Flashcards
Male and Female reference ranges for WBC’s
4.0-11.1
Male ref. range for RBC’s
4.76-6.09
Female ref. range for RBC’s
4.18-5.64
How do you know it’s an RBC?
Biconcave dis, no nucleus, eosinophiic cytoplasm and central area of pallor which should be less than 1/3 of the diameter
Male ref. range for HGB
14.3-18.1
Female ref. range for HGB
12.1-16.3
Male ref. range for HCT %
39.2-50.2
Female ref. range for HCT%
35.7-46.7
What is the formula for HCT?
HCT = RBC x MCV
Male and Female ref. range for MCV
80-100
Low MCV means
Microcytosis, iron deficiency anemia, or thalassemia
High MCB means
Macrocytosis, megaloblastic anemia
What are the thresholds for microcytic, normocytic and macrocytic anemia?
MCV100
MCH (mean cell hemoglobin) parallels which other important measure?
MCV
What is the formula for MCH?
MCH=HGB /RBC
What does low MCH mean?
hypochromatic, iron deficiency anemia
What does high MCH mean?
Hyperchromatic, megaloblastic anemia
What is the female and male reference range for MCH?
27.5-35.1
What is the formula for MCHC?
MCHC = HGB/HCT or MCHC = MCH/MCV
What does high MCHC mean?
hereditary spherocytosis
What does low MCHC mean?
moderate to severe microcytic anemia
What are the male and female ref. ranges for RDW?
11.7-14.2
Neutrophil info
Cytoplasm acidic, many fine granules, 2.5 nuclear segments/lobes
What is the threshold for Neutropenia and some possible causes?
decreased absolute neutrophil count ANC <1.5 x 10^9/L
Causes: Infections, drugs, marrow disease, autoimmune disease and congenital
What is the threshold for Neutrophilia and some possible causes?
ANC>11.1 x 10^9/L
Causes: Physiologic, acute inflammation, endocrine, myeloproliferative neoplasms, malignant diseases and drugs
Eosinophil info
Numerous large, round and red-orange granules 1-4 nuclear lobes
Eosinopenia
<0.01x 10^9
Causes: Drug induced, acute inflammation ro infection
Eosinophilia
> 0.4x 10^9/L
Causes:
Primary stimulating cytokines-IL-5 and IL-3
Infections, allergic disorders, loffler’s syndrome, leukemias and malignant diseases
Basophil info
Numerous large round purple-block granules, two nuclear lobes often covered by granules
Basopenia
<0.01 x 10^9/L
Causes: Acute hypersensitivity reactions, administration of progesterone
Basophilia
> 0.2 x 10^9/L
Causes: Mastocytosis, lots of leukemias
Monocyte info
large and eccentric nucleus, kidney/horshoes-shaped, lacey appearance, lots of cytoplasm, few granules, may have intracytoplasmic vaculoes
Monocytopenia
<0.2x10^9/L
Causes: aplastic anemia, hemodialysis, thermal injury, AIDS, hairy cell leukemia
Monocytosis
> 1.0 x 10^9L
Causes: physiologic, infants, infections, marrow disease, Hodgkin’s
Lymphocyte info
Mostly small, nucleus round or slightly indented, condensed chromatin, scanty bluish cytoplasm, a few granules
Lymphopenia
<1.0 x 10^9/L
Causes: Dependent on CD4+ T-cells, DiGeorge syntome, ataxia telangiectasia, Acquired, HIV,
Lymphocytosis
> 5 x 10^9/L
Causes: Physiologic, viral infections, pertussis, Post-splenectomy
Platelet info
Small fragments of megalokaryocytes, irregular outline, light blue cytoplasm, lots of small granules
Thrombocytopenia
<140 x 10^9/L
Caues: Peripheral destruction, sequestration in the spleen, inadequate production, inherited i.e. Wiskott-Aldrich syndrome
Thrombocytosis
> 400 x 10^9/L
Causes: Primary marrow neoplasm, reactive
Hallmarks of iron deficiency anemia
Small RBC’s, larger central pale area, target cells, all parameters decrease except RDW
How do you identify spherocytes?
Spherical, no central pallor, due to decreased cell membrane, increased MCHC
What are bite cells?
Bite-size defect due to removal to Heinz body in spleen and associated with G6PD Deficiency
What are schistocytes?
Fragmented RBC’s helmet cells, HUS, TTP, DIC, burns, HELLP, mechanical heart valves
What are target cells?
Central hemoglobin and target shape, thalassemia, hemoglobin C, iron deficiency, liver disease
Sickle cell
Bipolar, spiculated shape, banana shape
What is basophilic stippling?
Morphology- evenly dispersed fine blue granules, content: aggregated ribosomes
Causes: Lead poisoning, porphyria, hemoglobinopathies, infection
Howell-Jolly bodies
Morphology- single, dense, blue dot
Content: Nuclear DNA remnant
Causes: Post-splenectomy, functional asplenia, megaloblastic anema, myelodysplasia
Heinz body
Not visible on a Wright-Giemsa stain, need to stain with supravital dye, causes by G6PD deficiency and associated with bite cells
Dohle Body
Pale blue inclusion at the periphery of the cytoplasm, infection, inflammation, burns or pregnancy
contents: condensed RNA
Toxic granulation
lots of granules doe to rapid cell division and often associated with Dohle bodies and toxic vacuolization
causes: bacterial infection, marrow recovery
Hypersegmented neutrophils
More than five lobes, associated with megaloblastic anemia
What are the three things that innate immunity recognizes?
PAMP- pathogen associated molecular patterns
DAMP- damage associated molecular patterns
the absence of normal cell surface molecules
TLR receptors activate the IRAK pathway and what is the net effect?
Activation of the inflammatory transcription factor NF-KB
The cell that unifies the innate and adaptive immune system is:
the dendritic cell
It’s impossible to have a good adaptive response without. . .
an innate response
What is the name of the piece of the antigen that fits into the lymphocyte?
antigenic determinant or epitope
Type 1 Helper T cells
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.
Th17 Helper T cells,Th17
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
Type 2 Helper T cells
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
Follicular Helper T cells
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.
Regulatory T cells
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
Cytotoxic or killer T cells
CTL for short, destroy any body cell they identify as bearing a foreign or abnormal antigen on its surface.
Th1, Th2, Th17, Tfh, and Treg have which molecular marker on their surface?
CD4
Killer T cells have which molecular marker on their surface?
CD8
IgG
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
IgM
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
IgD
is a form of antibody inserted into B cell membranes as their antigen receptor
IgA
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.
IgE
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
Type I immunopathology, immediate hypersensitivity
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%
Type II immunopathology
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
Type III immunopathology
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
Type IV immunopathology is T cell mediated
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.
