255 terms

Hematologic Diseases

the body does not have enough healthy red blood cells
a rapid and uncontrolled loss of blood
is a glycoprotein - it acts on the bone marrow to increase the production of red blood cells
Iron Deficiency Anemia
Low red blood cells - insufficient dietary intake and absorption of iron
Causes of Anemia
Hemorrhage, Nutritional deficiency, Aplastic Anemia, inherited disorders
after a hemorrhage, there will be a period of time when the patient will be anemic due to blood loss.
Erythropoietin production
would correct the anemia by stimulating erythrocyte production and maturation
Weakness and syncope
the person's blood oxygen carrying capacity is diminished because of the hemorrhage, resulting in weakness.
if blood volume becomes too low, so does blood pressure. To compensate, arterioles at the surface of the body will restrict the amount of flood that travels through them the blood will be diverted to vital organs
Nutritional deficiency
red blood cells fail to mature.
Iron deficiency anemia
microcytic hypochromic anemia - they are small and pale in color, hemoglobin cannot be formed and erythrocyte production slows
Megaloblastic anemias
pernicious anemia
pernicious anemia
Vit. B12, instrinsic factor; dietary lack
pernicious anemia
: lack of vit. B12 in the diet; this stems from the inability to produce the molecule needed to transport B12
Intrinsic Factor
- the inability to produce intrinsic factor may result from gastritis, gastric carcinoma, gastrectomy
Macrocytic or megaloblastic anemia
normal RBC maturation is dependent on adequate amount of B12 for the synthesis of DNA molecules.
RBC size
RBC shape
Hyperbilirubinemia and jaundice
ineffective RBC formation and increased erythroblast destruction leads to excess bilirubin in the blood
the waste product from breakdown of hemoglobin
Neutropenia and thrombocytopenia
decreased white cell count and decreased platelet count. This occurs because white blood cells and megakaryocytes are rapidly dividing cells
tingling in the extremities
inability to move muscles
Folic acid
Folic acid is a necessary cofactor for the synthesis of both DNA and RNA.
common in alcoholism, chronic malnutrition and pregnancy
Aplastic Anemia
underproduction of red blood cells
Bone Marrow destruction
aplastic anemia
the result of reduced red bone marrow function, which causes a drop in levels of all blood elements.
Weakness, pallor, syncope
common to all forms of anemia; due to decreased hemoglobin production and thus oxygen carrying capacity of the blood
Genetic Anemia
hereditary disorder of the red blood cell membrane
autosommal dominant disorder
it results in excessively fragile red blood cells which are spherical, rather than the doughnut-shape or normal cells.
these spherical cells still contain hemoglobin and carry oxygen, BUT ARE EASILY BROKEN
Hereditary hemoglobinopathies
thalassemias, sickle cell anemia
a disorder caused by abnormal hemoglobin. The red blood cells containing this hemoglobin are deformed and very fragile
Inherited enzyme defect
glucose-6-phosphate deficiency
an X-linked recessive disorder
a hemolytic disorder
General manifestation of anemia
weakness, pallor, syncope
Hyperbilirubinemia and jaundice
hemolytic disorders cause this
the spleen becomes enlarged because it is the primary site for destruction of old or diseased erythrocytes
Hemoglobinemia and hemoglobinuria
excessive red blood cell destruction causes free hemoglobin to be present in both the blood and the urine.
Immune destruction
immune destruction of erythrocytes also causes hemolytic anemia
Chronic Renal Disease
causes anemia because of decreased production of erythropoietin by the diseased kidney
excessive erythrocyte volume of the blood which causes increased hematocrit.
Relative polycythemia
Relative polycythemia - develops if there is an excessive loss of plasma. Erythrocytes appear concentrated because they are "floating" in a decreased volume of liquid.
Restoring the liquid volume returns hematocrit to normal
Absolute polycythemia
an abnormally high hematocrit without low plasma volume, caused by excessive numbers of red blood cells.
Primary polycythemia
caused by excessive growth of bone marrow stem cells
Secondary polycythemia
caused by erythropoietin production
increased blood viscosity
(increased cell numbers, blood becomes more viscous or thick. This increases workload on the heart
increased blood viscosity causes an increase in blood pressure
stasis and hypercoagulability
viscous blood has a tendency to pool; stasis. When blood is pooled, clots form more easily. Results in thrombus or thromboembolism
where blood clots abnormally; too fast and too much
* Increased platelet numbers or abnormally reactive platelets
* atherosclerosis
a decrease in the number of circulating platelets
Platelets or thrombocytes
ARE NOT cells. They are cell fragments produced by megakaryocytes in the bone marrow.
Defective platelet production
Aplastic anemia can cause absence of platelet production.
Leukemia can cause abnormal megakaryocytes to form
Autoimmune Disorder
Idiopathic thrombocytopenic purpura (ITP) - a disorder in which the body's own antibodies destroy platelets.
Secondary thrombocytopenia
caused by destruction of platelets in response to an external drug, chemical.
cause platelet destruction.
Acetaminophen, heparin, antihistamines, alcohol, aspirin, antidepressants,Viral, bacterial and protozoan infections
Platelets - Normal Range
between 150,000 and 400,000/mm of blood
Platelet count <50,000
there is a potential for hemorrhage associated with trauma (surgery, accidents)
Platelet count <20,000
thrombocytopenia is manifested as petechiae, ecchymoses and bleeding from the mucous membranes. Will cuase fatal hemorrhage throughout GI tract or CNS
the clotting factor protein is missing.
Hemophilia A
this form is an inherited lack of FACTOR VIII protein in the clotting pathway. It is X-linked and primarily affects males
Hemophilia B
FACTOR IX is deficient in this form. It is X-linked and primarily affects males
Von Willebrand Disease
this factor activates platelets and causes them to adhere to blood vessel walls in the area of an injury.
- instrinsic and extrinsic
two mechanisms that start blood clotting
Bleeding into the brain or skull
trauma to the skull can cause a hemorrhagic stroke
Bleeding into joints
destruction of the entire joint can occur if bleeding fills the joint capsule
Vitamin K Deficiency
this disorder is caused by a deficiency of fat soluble Vitamin K.
Its produced by the microbes that inhabit the large intestine.
Is needed for synthesis of FACTORS II,VII, IX, X
Obstructive liver disease
having this would block the flow of bile necessary for the absorption of fat soluble vitamins
Massive Transfusion Syndrome
caused by administration of a large volume of blodd over a short peiod of time.
Banked blood is deficient in both factor VIII and platelets.
In order to prevent clotting
banked blood contains sodium citrate, which combines with soluble calcium.
pinpoint hemorrhages
if platelet concentration is too low, excessive bleeding will result.
Disseminated Intravascular Coagulation
a disorder that first causes widespread clotting that diminishes all clotting factors. Once clotting factors are absent, a sever hemorrhage follows
Bacterial Sepsis
Bacterial Sepsis - a blood-borne bacterial infection. Viruses and parasites can also cause DIC
Pregnancy - rare, amniotic fluid enter the mother's bloodstream, can trigger DIC
Lacking the clotting factors
the patient suffers a massive hemorrage
Acute onset of DIC
dyspnea, cynaosis, hypoxia, decreased consciousness
uncontrolled bleeding - because of consumption of clotting factors
I-VI autoimmune disorders
Rheumatoid athritis
Systemic Lupus erythemotosus
Myasthenia Gravis
First line of Defense
Mechanical Barriers
Chemical Barriers
Mechanical Barriers
skin, mucous membranes and conjuctiva of the eye from the mechanical barriers to infection.
Mechanical Barriers
sloughing of the skin, mucous production, slaivation, swallowing, urination and defecation help remove potential infectious agents.
Normal bacterial living in the skin and gut also make it difficult for infectious agents to cross mechanical barriers.
Body secreation also deter infectious agents
First line of Defense
Mechanisms include:
Epihelial barriers
Chemical barriers
Second Line of Defense
Fever and inflammation are responese to tisue damage and/or infection
Macrophages in tissue, destroy microorganisms by phagocytosis.
Natural Killer cells, or NK cells
, are non-specific lymphocytes that first drill holes into an invading cell, then inserts enzymes that destroy cell proteins
Third Line of Defense
Specific Immune Response (adaptive or acquired response
Cell Mediated Immunity
Cell Medicated Immunity - lymphocytes that directly attack the infectious organism.
is controlled by thymal-derived (T) lymphocytes.
Cell Medicated Immunity
other lymphocytes produce proteins called antibodies (Ab), also called immunoglobulins
immunoglobulin proteins
The immunoglobulin proteins assault specific proteins called antigens (Ag) on the infectious organism
Cell Medicated Immunity
B lymphocytes are responsible for this form of immunity
non-self antigen
a specific molecule (or pathogen) that is recognized as foreign by immune system cells.
it initiates an immune reponse from lymphocytes.
immune memory
to retain cells that can respond immediately whenever the same non-self antigen is introduced.
Third Line of Defense - Specific Response
Attacks specific microbes (antigens)
Developes after exposure to the specific antigen
Humoral immunity
antibody proteins in the blood that attack the specific antigen
Cell-mediated immunity
phagocytic cells that attack the specific antigen
Species-specific immunity
all species have innate resistnace to some infectious diseases of other species.example: humans cannot contract Marek's Disease - it is aviral disease of chickens
Acquired Immunity
the transfer of specific antibodies into a person. The antibodies are not made by that person
passive immunity can occur naturally when antibodies cross the placenta into a baby.
Artificial - consists of an injection of an antibody - containing solution.
example - Hepatitis shot to protect again Hep B
initiating the individual's own immune response
Memory B and T lymphocytes will be formed during the initial infection. These cells "remember" the particular disease-causing agent
B-Lymphocyte/Humoral Immunity
This type of immunity is controlled by B lymphocytes which indirectly attack non-slf antigen via antibodies
Development of Bursal derived (B) lymphocytes
B-cells mature in the bursal equivalent tissue
Precursor (stem) cells
all lymphocytes and other blood cells arise from a common stem cells in the bone marrow
immunocompetent B cells
After completion of the maturation process, immunocompetent B cells move into secondary lymphoid organs (spleen, lymph nodes, tonsils
Activiation of stem cells
B lymphocyte antigen receptors are actually antibodies attached to the cell membrane.
they can recognize both the shape of all classes of normal body molecules, as well as those of a foreign invader.
Immunocompetent B cells
exposed to an antigen demonstrate clonal selection.
A particular intigen triggers one or memory B cellsparticular B cell to transform into plams
plasma cells
they secreate a specific antibody tailored to destroy the antigen.
Memory Cells
responsible for the secondary immune response. The next time your body encounters the same antigen from an infectious agent, B memory cells transform very quickly
Activated B Cells Divide into Two Kinds of Cells:
Memory B cells
Plasma Cells
Memory B cells
Memory B cells - remain in the body, they fight off the antigen without a T helper cell telling them to do so
response to the antigen immediately
plasma antibody levels rise within days
Plasma Cells
create antibodies, special proteins designed to attach to that antigen and destroy it.
Booster Shots
cause a secondary immune response so antibody levels will be high before the diease is encountered
B cell function - Antibody production
B cells tranform into plasma cells upon exposure to non-self antigens
B cell function - Antibody production
Plasma cells secrete proteins called antibodies or ummunoglobulins, which mount an attack on a specific non-self antigen
immunoglobulin's (antibody's) primary action
is to bind to a specific antigen. This combination is called an antibody-antigen (Ag-Ag) complex
The Ag-Ag complex
initiates agglutination or precipitation; processes that neutralize the antigen
the clumping together of individual antigen molecules
occurs when a soluble antigen turns insoluble (like when water mist converts to snow and "precipitates from the sky as a solid
Neutralization of an antigen
is a result of either agglutination or precipitation
neutralized antigen
is powerless
directly neutralize bacterial toxins, viruses or bacteria
Bacterial toxin
antibodies neutralize bacterial toxins by attaching to the toxin molecules. examples of bacterial toxins include those produced by tetanus and diphtheria bacteria.
viruses infect cells by attaching to body cells. Antibodies neutralize the virus by attaching and completely covering it.
bacteria is also neutralized by antibody attachment
the process of neutralizing a bacterial cell
Inflammatory response
Ab -Ag complexes trigger the inflammatory response. Macrophages, neutrophils and monocytes are summoned via chemical messenger to the Ag-Ag complex.
Classes of Immunoglublins (Ig)
this class is primarily based on protein structure but also relate to function and tissue from where they are secreted
is secreted primarily from mucous membranes and glands. This class of immunoglobulins are found in many body secretions; tears, saliva, breast milk, etc
located on the surface of developing B lymphocytes, where it functions as an antigen receptor. It is needed for maturation of B cells
IgE - attaches to basophils and mast cells located in perpheral tissue. When the antigen binds to the bound IgE, the cells release histamine and other chemicals of the inflammatory response.
responds to infections by parasites
is both a systemic antibody found in the blood and also in secretions from the mucous membranes and glands.
Is the only class of immunoglobulin which crosses the placenta into fetal circulation; this makes IgG the primary source of acquired passive immunity in the fetus and neonates.
Is a major initiator of the immune response
the first immunoglobulin to process non-self antigen during the primary immune response.
circulates in body fluids, attacking antigens; crosses placenta, most common type
first antibody circulated by an infant, first made in any new infection. Circulates in body fluids; pull antigens together into clumps
found in secretions on mucus membranes; most common form secreated in breast milk, prevents antigens frolm entering the body
found on the surfaxce of B cells; acts as an antigen receptor
parasitic infections, found on mast cells in tissues; starts an inflammation, allergic reaction
Cell Mediated Immunity
This type of immunity is controlled by T lymphocytes, which direct or carry out attacks on non-self antigen
T lymphocytes
are important to activate all aspects of the specific immune response, and to control infections
Development of Thymal derived (T) lymphocytes
T helper cells (CD4+)
T cytotoxic cells (CD8+)
T helper cells (CD4+)
attach to self proteins; start an immune response
T cytotoxic cells (CD8+)
attach to self proteins, kill infected cells
Precursor (stem) cells
three main populations of mature T cells - CD4+ (helper), CD8+ (cytotoxic) and regulatory or suppressory T cells
Role of antigen-presenting cell
immature T cells can only recognized foreign proteinantigens, and those antigens must be presented by another cell
Antigen-presenting cells (APCs)
destroy an antigen, then place its piecews on it own cell membrane.
the pieces are attached to an MCH protein
a "self" protein that allows immune system cells to double-check to recognize what is "you" and what is foreign
T-cell function - cell - mediated immunity
Three subspecies of T cells develop upon exposure to a non-self Ag. Each type of T cell plays a role in mounting and controlling a cell-mediated immune response.
Helper T cell (Th
they posses CD4 proteins, they are the chief regulators of the immune response
TH1 cells
stimulate phagocytosis of microbes by macrophages
TH2 cells
stimulate the B cells to create antibodies against the antigen
Cytotoxic T cell (Tc
have the presence of CD8 proteins. These cells directly attack and destory infected body cells by injecting cytotoxic proteins into the cell
Regulatory (Suppressor) T cell (Ts
inhibit the immune response by secreting cytokines that decrease reproduction of other lymphocytes
inhibit the immune response by secreting cytokines that decrease reproduction of other lymphocytes
occurs due to an altered immune response upon initial exposure to an antigen
subsequent exposure
additional exposures to the same antigen result in a pathological over-reaction of the immune response
immune reaction occurs very quickly during anapylaxis
Catagories of Hypersensitivity
caused by an axaggerated immune response to an environemtnal antigen; pollen, hay feber, penicillin, gluten, poison ivy
an immune reponse against beneficial non-self antigen. Ex. Tissue rejection after organ transplant and blood transfusion reactions
a misdirected immune reponse against self-antigen in the patients own body.
Grave's disease, systemic lupus erythemotosus, rheumatoid arthiritis, myasthenia gravis, Crohn's disease
Sequestered antigen
develop in areas of the body never "exposed" to the developing immune system; eyes and tests.
Infectious disease and molecular mimicry
Infectious disease and molecular mimicry - infectious disease can trigger an autoimmune response.
Streptococcus; the immune resposne ultimately attacks the streptococcus
Suppressor T cell dystunction
decreased function decreases > cells iniatiate an immune response against self antigen
Autoimmune Diseases
Immune system attacks self-antigens
Type I-Ige mediated (Anaphylactic)
exposure to environmental allergens
mold spores, pollen, animal dander
drug reaction (penicillin)
bee stings
food (milk, chocolate, citrus, eggs, wheat, nuts, fish)
Histamine is released to interact with Type I hypersensitivity
skin, blood, vessels, mucous membranes
makes blood vessels more permeable
Skin - (hives)
histamine on cutaneous blood vessels cause urticaria - due to increase blood flow and vessel permeability
causes itching
causes smooth muscle contraction of the bronchioles - bronchoconstriction
Increased mucous secretion - causes Rhinitis and Conjuctivitis
Nausea and vomiting - food allergies
Malabsorption - nutrients can't be absorved due to irritation in the gut
Type I Hypersensitivity
commonly called "allergic reactions"
Systemic or anaphylactic reactions
Type II - Tissue specific (cytotoxic)
Opsonization and then phagocytosis of cells with specific alloantigen or autoantigen
Cell lysis of cells with specific alloantigen or autoantigen
overstimulatio of cells with specific autoantigen
cell dysfunction caused by antibodies
Type II Hypersensitivity
IgG or IgM attack antigens on cell surfaces
Usually involves antigens on red or white blood cells
Transfusion reactions
Rh disease
Drug reactions
Type III - Immune Complex
Formation of Ab-Ag complex which triggers extreme inflammatory response
Arthus reaction
Arthus reaction - blood vessels - causes edema, hemorrhage and blood clotting

fever, rash, pain are common symptoms
Examples of type III hypersensitivities
chronic low-grade infections
glomerulonephritis - the filtering capillaries in the kidnes are inflammed
systemic lupus erythematosis
Rheumatoid arthritis
vaccine reactions
Type IV - cell mediated
manifestation: occurs within hours to days
Type IV - cell mediated
T cell cytokine secretion
Macrophage mediator secretion
examples: contact dermatitis - poison ivy, metals (jewelry), Tuberculin reactions - TB skin test, transplant rejections
Rheumatoid Arthritis
Chronic disease with periods of execerbations and remissions.
Usually seen in middle-age and elderly patients
Rhemumatoid Factor (RF)
Rhemumatoid Factor (RF) is an antibody which is found in 70-80% of affected individuals.
This antibody reacts with IgG to form immune complexes which deposit in the joint synovial membrane and elsewhere.
Rheumatoid Arthritis
The immune complexes deposit in synovial membranes of joints.
Type III hypersensitivity
In severe cases, this Type III hypersensitivity reaction can lead to formation of Rheumatoid nodules.
The nodules are collections of inflammatory cells around fibrin and cellular debris.
Rheumatoid Arthritis
fingers - bilateral, symmetric (joint deformities of the fingers), occur in both hands
Rheumatoid Arthritis
wrists, knees, elvows, ankles and feet - partial dislocations (subluxation) appear due to destruction of the joint capsule
decreases blood supply to the fingers and toes, causing them to tingle (Raynaud phenomena)
Pericarditis, pleuritis, scleritis
Rheumatoid module formation and infrlammation can inflame and damage the pericardium of the heart, the pleurae and the whites (sclerae) fo the eyes
tingling and loss of sensation in the hands and feet is due to inflammation of peripheral nerves.
Systemic Lupus Erythematosis
The cause of SLE is antibody formation to self-antigens located primarily in capillary basement membranes.
Systemic Lupus Erythematosis (SLE)
Light,Stress, Strep or viral infection, immunication, pregnancy, abnormal estrogen metabolism drugs
Systemic Lupus Erythematosis (SLE)
Facial (malar) rash - a distinctive "butterfly" rash across the cheeks. This is a unique sign to lupus.
Systemic Lupus Erythematosis (SLE)
Discoid rash - raised, scaling skin
Photosensitivity - rash due to sunlight exposure
Oral and Nasopharyngeal ulcers
Arthritis - in two or more joints
* Pericarditis - inflammation of serous membrane around heart
hemolytic anemia
low red blood cell count due to cell destruction
low white blood cell count
low platelet count
low platelet count
Ab to self protein
Myasthenia Gravis
Neuromuscular juctions of one or more of the 12 cranial nerves - weakness and paralysis
Myasthenia Gravis
caused by antibody formation against acetylcholine repceptors on the motor end-plates of skeletal muscle
Myasthenia Gravis
Onset of the disease is sometimes associated with pregnancy, postpartum
Myasthenia Gravis
Cranial Nerves affected:
extraocular muscles - diplopia
facial muscles - blank, expressionless face
Muscles of mastication - difficult chewing
Muscles of involved in swallowing - nasal regurgitation of fluids
Week neck muscles - head bobs, patient tilts head hack
Myasthenia Gravis
Neuromuscular junctions of other nerves
Major muscle groups - weakness and fatique after exercise
Respiratory muscles - low tidal volume and vital capacity
Myasthenic Crisis
major muscle group paralysis - complete paralysis, quadriplegia
respiratory failure - complete paralysis, death by asphyxiation
Primary Immunodeficiency
Direct - developmental ro inherited defect of immune system prior to birth
developmental defect of immune system prior to birth
inherited deficiency of immune system development
Sex-linked or autosomal
Secondary Immunodeficiency
Neuroendocrine - stress induces ACTH and glucocorticoid secretion. Steriods are frequently used to treat autoimmune disease. The side affect of
cortisone, cortisol, glucocorticoids = anti-inflammatory
Secondary Immunodeficiency - Acquired
HIV infects and eventually destroys helper T cells, as well as other CD4 cells
Secondary Immunodeficiency - Acquired
Once a certain number of these cells are destroyed , the patient develops HIV.
Immunodeficiency- Primary
B Cell deficiencies
Ig deficiencies
T cell deficiencies
Combined innunodeficiences
Immunodeficiency - Acquired
opportunistic infection
The ultimate manifestion of all immunodefiency disease
opportunistic infection
They are cuased by microorganisms are found normal flora of the skin and mucous
Opportunistic infectons
caused by organisms which can cause disease
Opportunistic microorganisms include bacteria
Pseudomonas, Staphylococcus and Haemophilus, or varicells, vaccinia, herpes, cytomegalovirus
SCID - Severe Combined Immunodeficiency
Caused by genetic defects.
Genetic diseases are caused by errors in the DNA
SCID - Severe Combined Immunodeficiency
1) disordered genes code for cell receptor that cause T-lymphocytes to develop.
2) reticular dysgenesis - an enzymes needed for white blood cell development of while blood cells
Reticular dysgenesis
an enzyme needed for the development of a common stem cell is defective.
Reticular dysgenesis - manifestations
Reticular dysgensis
* systemic
oral candidiasis or thrush
candidiasis - diaper rash
otitis media - middle ear infection
diarrhea - digestive tract
Sepsis - blood
Meningiti - cerebrospinal fluid
DiGeorge Syndrome
caused by a congenital midline defect due to abnormal development of the third and fourth pharyngeal pouches during the 12 week of pregnancy
DiGeorge Syndrome
Pathophysiology - the midline results in thymic hypoplasia, underdevlopment of the thymus gland.
IgA deficiency
a genetic disease in which B cells can't transform into IgA secreting plasma cells
since B cells can't transform into IgA secreting plasma cells, no IgA is produced. IgA is the major immunoglobulin secreted from mucous membranes.
Chronic Mucocutaneous Candidiasis
pathogenesis - T cells are normal except for an inability to recognize non-self antigen on the yeast.
pathogenesis - T cells are normal except for an inability to recognize non-self antigen on the yeast.
is spread by fluids containing the AIDS virus.
The virus can be found in blood, semen, and vaginal secretions.
Human Immunodeficiency Virus
Replication of virus in cells with CD 4 marker, including helper T cells
Human Immunodeficiency Virus
HIV atttaches to any cell with CD4 surface receptor antigens. The virus then enters and infects the cell.
Destruction of virus infected cells
thousands of replicate copies of HIV are released to infect other cells with CD4 receptors.
The levels of Th cells decrease to the point where non-self antigen is not properly processed.
Immune deficiency due to decreased helper T cell count
when there are low levels of Th cells, this allow opportunistic infections and even cancerous cells to develop
HIV - Infection Period
Infection Period - after primary infection, the patient develops an inllness that resembles influenza
headache, fever, sore throat, muscle and joint pain
HIV - Latency Period
after infecton, the patient experiences a latent period during which he/she has not symptoms.
The average latency time is 10 years, during which the patient is infectious
AIDS Related Complex
Classification of the severity of the patient's infection
Stages 1-3
defined by the patient's signs and symptoms
Stage 1
flulike symptoms, or no symptoms at all
Stage 2
immune deficiency is present, but not serious
Stage 3
serious immune deficiency with one or more AIDS defining illnesses.
Stages 1-2-3:
based upon the CD4 T-cell count
Stage 1 - AIDS Related Complex
greater than 500 cell/microliter
Stage 2 - AIDS Related Complex
between 200-499 cells
Stage 3 - AIDS Related Complex
fewer than 200 cells
Stage 2
A patient who is Stage 2 is said to have AIDS-related complex - but not overt disease.
Overt AIDS
patient has a category 3 cell count and a Category C AIDS-defining illness
Decreased CD4 cells
increased opportunistic infections
Decreased CD4 cells
the decreased CD4 cells leads to immunodeficiency and incerased opportunistic infection.
an opportunistic infection is caused by an organism that is harmless in a healthy individual, but serious or deadly in one with a weakened immune system.
Overt AIDS - CNS
crytococcal meningitis, toxoplasmosis encephalitis
Opportunistic infections of the CNS
lead to headaches, memory loss, and demential
eyes: cytomegalovirus retinitis - can cause blindness
Kaposi's sarcoma
purplish-brown lesions just under the skin-unique to AIDS. Cancer cachexia (weight loss and anorexia