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Anemia

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the body does not have enough healthy red blood cells

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Hemorrhage

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a rapid and uncontrolled loss of blood

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Erythropoietin

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is a glycoprotein - it acts on the bone marrow to increase the production of red blood cells

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Iron Deficiency Anemia

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Low red blood cells - insufficient dietary intake and absorption of iron

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Causes of Anemia

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Hemorrhage, Nutritional deficiency, Aplastic Anemia, inherited disorders

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Hemorrhage

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after a hemorrhage, there will be a period of time when the patient will be anemic due to blood loss.

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Erythropoietin production

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would correct the anemia by stimulating erythrocyte production and maturation

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Weakness and syncope

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the person's blood oxygen carrying capacity is diminished because of the hemorrhage, resulting in weakness.

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Hemorrhage

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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

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Nutritional deficiency

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red blood cells fail to mature.

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Iron deficiency anemia

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microcytic hypochromic anemia - they are small and pale in color, hemoglobin cannot be formed and erythrocyte production slows

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Megaloblastic anemias

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pernicious anemia

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pernicious anemia

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Vit. B12, instrinsic factor; dietary lack

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pernicious anemia

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: lack of vit. B12 in the diet; this stems from the inability to produce the molecule needed to transport B12

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Intrinsic Factor

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- the inability to produce intrinsic factor may result from gastritis, gastric carcinoma, gastrectomy

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Macrocytic or megaloblastic anemia

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normal RBC maturation is dependent on adequate amount of B12 for the synthesis of DNA molecules.

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anisocytosis

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RBC size

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poikilocytosis

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RBC shape

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Hyperbilirubinemia and jaundice

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ineffective RBC formation and increased erythroblast destruction leads to excess bilirubin in the blood

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Bilirubin

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the waste product from breakdown of hemoglobin

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Neutropenia and thrombocytopenia

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decreased white cell count and decreased platelet count. This occurs because white blood cells and megakaryocytes are rapidly dividing cells

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parasthesias

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tingling in the extremities

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ataxia

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inability to move muscles

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Folic acid

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Folic acid is a necessary cofactor for the synthesis of both DNA and RNA. common in alcoholism, chronic malnutrition and pregnancy

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Aplastic Anemia

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underproduction of red blood cells Bone Marrow destruction

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aplastic anemia

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the result of reduced red bone marrow function, which causes a drop in levels of all blood elements.

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Weakness, pallor, syncope

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common to all forms of anemia; due to decreased hemoglobin production and thus oxygen carrying capacity of the blood

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Genetic Anemia

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hemolytic

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Spherocytosis

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hereditary disorder of the red blood cell membrane autosommal dominant disorder

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Spherocytosis

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it results in excessively fragile red blood cells which are spherical, rather than the doughnut-shape or normal cells.

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Spherocytosis

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these spherical cells still contain hemoglobin and carry oxygen, BUT ARE EASILY BROKEN

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Hereditary hemoglobinopathies

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thalassemias, sickle cell anemia

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Hemoglobinopathy

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a disorder caused by abnormal hemoglobin. The red blood cells containing this hemoglobin are deformed and very fragile

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Inherited enzyme defect

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glucose-6-phosphate deficiency

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Glucose-6-phosphate

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an X-linked recessive disorder a hemolytic disorder

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General manifestation of anemia

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weakness, pallor, syncope

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Hyperbilirubinemia and jaundice

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hemolytic disorders cause this

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Splenomegaly

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the spleen becomes enlarged because it is the primary site for destruction of old or diseased erythrocytes

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Hemoglobinemia and hemoglobinuria

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excessive red blood cell destruction causes free hemoglobin to be present in both the blood and the urine.

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Immune destruction

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immune destruction of erythrocytes also causes hemolytic anemia

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Chronic Renal Disease

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causes anemia because of decreased production of erythropoietin by the diseased kidney

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Polycythemia

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excessive erythrocyte volume of the blood which causes increased hematocrit.

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Relative polycythemia

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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

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Absolute polycythemia

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an abnormally high hematocrit without low plasma volume, caused by excessive numbers of red blood cells.

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Primary polycythemia

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caused by excessive growth of bone marrow stem cells

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Secondary polycythemia

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caused by erythropoietin production

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increased blood viscosity

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(increased cell numbers, blood becomes more viscous or thick. This increases workload on the heart

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hypertension

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increased blood viscosity causes an increase in blood pressure

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stasis and hypercoagulability

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viscous blood has a tendency to pool; stasis. When blood is pooled, clots form more easily. Results in thrombus or thromboembolism

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Hypercoagulability

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where blood clots abnormally; too fast and too much * Increased platelet numbers or abnormally reactive platelets * atherosclerosis

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Thrombocytopenia

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a decrease in the number of circulating platelets

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Platelets or thrombocytes

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ARE NOT cells. They are cell fragments produced by megakaryocytes in the bone marrow.

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Defective platelet production

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Aplastic anemia can cause absence of platelet production. Leukemia can cause abnormal megakaryocytes to form

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Autoimmune Disorder

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Idiopathic thrombocytopenic purpura (ITP) - a disorder in which the body's own antibodies destroy platelets.

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Secondary thrombocytopenia

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caused by destruction of platelets in response to an external drug, chemical.

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cause platelet destruction.

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Acetaminophen, heparin, antihistamines, alcohol, aspirin, antidepressants,Viral, bacterial and protozoan infections

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Platelets - Normal Range

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between 150,000 and 400,000/mm of blood

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Platelet count <50,000

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there is a potential for hemorrhage associated with trauma (surgery, accidents)

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Platelet count <20,000

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thrombocytopenia is manifested as petechiae, ecchymoses and bleeding from the mucous membranes. Will cuase fatal hemorrhage throughout GI tract or CNS

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Hemophilia

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the clotting factor protein is missing.

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Hemophilia A

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this form is an inherited lack of FACTOR VIII protein in the clotting pathway. It is X-linked and primarily affects males

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Hemophilia B

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FACTOR IX is deficient in this form. It is X-linked and primarily affects males

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Von Willebrand Disease

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this factor activates platelets and causes them to adhere to blood vessel walls in the area of an injury.

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- instrinsic and extrinsic

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two mechanisms that start blood clotting

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Bleeding into the brain or skull

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trauma to the skull can cause a hemorrhagic stroke

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Bleeding into joints

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destruction of the entire joint can occur if bleeding fills the joint capsule

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Vitamin K Deficiency

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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

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Obstructive liver disease

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having this would block the flow of bile necessary for the absorption of fat soluble vitamins

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Massive Transfusion Syndrome

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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.

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In order to prevent clotting

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banked blood contains sodium citrate, which combines with soluble calcium.

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Patechiae

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pinpoint hemorrhages

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ecchymoses

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bruising

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Epistasix

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nosebleeds

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Hemorrhage

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if platelet concentration is too low, excessive bleeding will result.

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Disseminated Intravascular Coagulation

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a disorder that first causes widespread clotting that diminishes all clotting factors. Once clotting factors are absent, a sever hemorrhage follows

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Bacterial Sepsis

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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

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Lacking the clotting factors

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the patient suffers a massive hemorrage

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Acute onset of DIC

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dyspnea, cynaosis, hypoxia, decreased consciousness uncontrolled bleeding - because of consumption of clotting factors

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I-VI autoimmune disorders

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Allergy Rheumatoid athritis Systemic Lupus erythemotosus Myasthenia Gravis

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First line of Defense

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Mechanical Barriers Chemical Barriers

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Mechanical Barriers

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skin, mucous membranes and conjuctiva of the eye from the mechanical barriers to infection.

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Mechanical Barriers

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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.

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Chemical

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Body secreation also deter infectious agents

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First line of Defense

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Mechanisms include: Epihelial barriers Chemical barriers

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Second Line of Defense

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Fever and inflammation are responese to tisue damage and/or infection Macrophages in tissue, destroy microorganisms by phagocytosis.

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Natural Killer cells, or NK cells

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, are non-specific lymphocytes that first drill holes into an invading cell, then inserts enzymes that destroy cell proteins

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Third Line of Defense

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Specific Immune Response (adaptive or acquired response

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Cell Mediated Immunity

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Cell Medicated Immunity - lymphocytes that directly attack the infectious organism. is controlled by thymal-derived (T) lymphocytes.

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Cell Medicated Immunity

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other lymphocytes produce proteins called antibodies (Ab), also called immunoglobulins

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Antibodies

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immunoglobulins

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immunoglobulin proteins

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The immunoglobulin proteins assault specific proteins called antigens (Ag) on the infectious organism

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Cell Medicated Immunity

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B lymphocytes are responsible for this form of immunity

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non-self antigen

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a specific molecule (or pathogen) that is recognized as foreign by immune system cells. it initiates an immune reponse from lymphocytes.

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immune memory

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to retain cells that can respond immediately whenever the same non-self antigen is introduced.

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Third Line of Defense - Specific Response

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Attacks specific microbes (antigens) Developes after exposure to the specific antigen

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Humoral immunity

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antibody proteins in the blood that attack the specific antigen

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Cell-mediated immunity

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phagocytic cells that attack the specific antigen

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Species-specific immunity

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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

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Acquired Immunity

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Passive Active

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Passive

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the transfer of specific antibodies into a person. The antibodies are not made by that person

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Natural

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passive immunity can occur naturally when antibodies cross the placenta into a baby.

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Artificial

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Artificial - consists of an injection of an antibody - containing solution. example - Hepatitis shot to protect again Hep B

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Active

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initiating the individual's own immune response

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Natural

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Memory B and T lymphocytes will be formed during the initial infection. These cells "remember" the particular disease-causing agent

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Artificial

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Vaccinations

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B-Lymphocyte/Humoral Immunity

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This type of immunity is controlled by B lymphocytes which indirectly attack non-slf antigen via antibodies

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Development of Bursal derived (B) lymphocytes

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B-cells mature in the bursal equivalent tissue

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Precursor (stem) cells

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all lymphocytes and other blood cells arise from a common stem cells in the bone marrow

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immunocompetent B cells

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After completion of the maturation process, immunocompetent B cells move into secondary lymphoid organs (spleen, lymph nodes, tonsils

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Activiation of stem cells

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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.

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Immunocompetent B cells

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exposed to an antigen demonstrate clonal selection. A particular intigen triggers one or memory B cellsparticular B cell to transform into plams

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plasma cells

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they secreate a specific antibody tailored to destroy the antigen.

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Memory Cells

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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

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Activated B Cells Divide into Two Kinds of Cells:

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Memory B cells Plasma Cells

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Memory B cells

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Memory B cells - remain in the body, they fight off the antigen without a T helper cell telling them to do so

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response to the antigen immediately

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plasma antibody levels rise within days

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Plasma Cells

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create antibodies, special proteins designed to attach to that antigen and destroy it.

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Booster Shots

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cause a secondary immune response so antibody levels will be high before the diease is encountered

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B cell function - Antibody production

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B cells tranform into plasma cells upon exposure to non-self antigens

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B cell function - Antibody production

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Plasma cells secrete proteins called antibodies or ummunoglobulins, which mount an attack on a specific non-self antigen

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immunoglobulin's (antibody's) primary action

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is to bind to a specific antigen. This combination is called an antibody-antigen (Ag-Ag) complex

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The Ag-Ag complex

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initiates agglutination or precipitation; processes that neutralize the antigen

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Agglutination

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the clumping together of individual antigen molecules

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Precipitation

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occurs when a soluble antigen turns insoluble (like when water mist converts to snow and "precipitates from the sky as a solid

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Neutralization of an antigen

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is a result of either agglutination or precipitation

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neutralized antigen

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is powerless

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Immunoglobulins

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directly neutralize bacterial toxins, viruses or bacteria

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Bacterial toxin

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antibodies neutralize bacterial toxins by attaching to the toxin molecules. examples of bacterial toxins include those produced by tetanus and diphtheria bacteria.

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Viruses

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viruses infect cells by attaching to body cells. Antibodies neutralize the virus by attaching and completely covering it.

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Bacteria

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bacteria is also neutralized by antibody attachment

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Opsonization

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the process of neutralizing a bacterial cell

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Inflammatory response

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Ab -Ag complexes trigger the inflammatory response. Macrophages, neutrophils and monocytes are summoned via chemical messenger to the Ag-Ag complex.

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Classes of Immunoglublins (Ig)

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this class is primarily based on protein structure but also relate to function and tissue from where they are secreted

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IgA

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is secreted primarily from mucous membranes and glands. This class of immunoglobulins are found in many body secretions; tears, saliva, breast milk, etc

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IgD

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located on the surface of developing B lymphocytes, where it functions as an antigen receptor. It is needed for maturation of B cells

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IgE

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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

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IgG

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is both a systemic antibody found in the blood and also in secretions from the mucous membranes and glands.

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IgG

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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.

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IgG

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Is a major initiator of the immune response

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IgM

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the first immunoglobulin to process non-self antigen during the primary immune response.

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IgG

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circulates in body fluids, attacking antigens; crosses placenta, most common type

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IgM

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first antibody circulated by an infant, first made in any new infection. Circulates in body fluids; pull antigens together into clumps

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IgA

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found in secretions on mucus membranes; most common form secreated in breast milk, prevents antigens frolm entering the body

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IgD

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found on the surfaxce of B cells; acts as an antigen receptor

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IgE

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parasitic infections, found on mast cells in tissues; starts an inflammation, allergic reaction

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Cell Mediated Immunity

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This type of immunity is controlled by T lymphocytes, which direct or carry out attacks on non-self antigen

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T lymphocytes

answer

are important to activate all aspects of the specific immune response, and to control infections

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Development of Thymal derived (T) lymphocytes

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T helper cells (CD4+) T cytotoxic cells (CD8+)

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T helper cells (CD4+)

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attach to self proteins; start an immune response

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T cytotoxic cells (CD8+)

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attach to self proteins, kill infected cells

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Precursor (stem) cells

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three main populations of mature T cells - CD4+ (helper), CD8+ (cytotoxic) and regulatory or suppressory T cells

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Role of antigen-presenting cell

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immature T cells can only recognized foreign proteinantigens, and those antigens must be presented by another cell

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Antigen-presenting cells (APCs)

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destroy an antigen, then place its piecews on it own cell membrane.

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the pieces are attached to an MCH protein

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a "self" protein that allows immune system cells to double-check to recognize what is "you" and what is foreign

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T-cell function - cell - mediated immunity

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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.

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Helper T cell (Th

answer

they posses CD4 proteins, they are the chief regulators of the immune response

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TH1 cells

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stimulate phagocytosis of microbes by macrophages

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TH2 cells

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stimulate the B cells to create antibodies against the antigen

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Cytotoxic T cell (Tc

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have the presence of CD8 proteins. These cells directly attack and destory infected body cells by injecting cytotoxic proteins into the cell

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Regulatory (Suppressor) T cell (Ts

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inhibit the immune response by secreting cytokines that decrease reproduction of other lymphocytes

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inhibit the immune response by secreting cytokines that decrease reproduction of other lymphocytes

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occurs due to an altered immune response upon initial exposure to an antigen

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subsequent exposure

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additional exposures to the same antigen result in a pathological over-reaction of the immune response

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anaphylaxis

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immune reaction occurs very quickly during anapylaxis

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Catagories of Hypersensitivity

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Allergy Alloimmunity Autoimmunity

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Allergy

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caused by an axaggerated immune response to an environemtnal antigen; pollen, hay feber, penicillin, gluten, poison ivy

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Alloimmunity

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an immune reponse against beneficial non-self antigen. Ex. Tissue rejection after organ transplant and blood transfusion reactions

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Autoimmunity

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a misdirected immune reponse against self-antigen in the patients own body.

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Autoimmunity

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Grave's disease, systemic lupus erythemotosus, rheumatoid arthiritis, myasthenia gravis, Crohn's disease

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Sequestered antigen

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develop in areas of the body never "exposed" to the developing immune system; eyes and tests.

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Infectious disease and molecular mimicry

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Infectious disease and molecular mimicry - infectious disease can trigger an autoimmune response. Streptococcus; the immune resposne ultimately attacks the streptococcus

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Suppressor T cell dystunction

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decreased function decreases > cells iniatiate an immune response against self antigen

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Autoimmune Diseases

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Immune system attacks self-antigens

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Type I-Ige mediated (Anaphylactic)

answer

exposure to environmental allergens mold spores, pollen, animal dander drug reaction (penicillin) bee stings food (milk, chocolate, citrus, eggs, wheat, nuts, fish)

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Histamine is released to interact with Type I hypersensitivity

answer

skin, blood, vessels, mucous membranes

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Histamine

answer

makes blood vessels more permeable

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Skin - (hives)

answer

histamine on cutaneous blood vessels cause urticaria - due to increase blood flow and vessel permeability causes itching

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Respiratory

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causes smooth muscle contraction of the bronchioles - bronchoconstriction Increased mucous secretion - causes Rhinitis and Conjuctivitis

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Digestive

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Nausea and vomiting - food allergies Malabsorption - nutrients can't be absorved due to irritation in the gut

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Type I Hypersensitivity

answer

commonly called "allergic reactions" Systemic or anaphylactic reactions

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Type II - Tissue specific (cytotoxic)

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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

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Type II Hypersensitivity

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Cytotoxic IgG or IgM attack antigens on cell surfaces Usually involves antigens on red or white blood cells Transfusion reactions Rh disease Drug reactions

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Type III - Immune Complex

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Formation of Ab-Ag complex which triggers extreme inflammatory response

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Arthus reaction

answer

Arthus reaction - blood vessels - causes edema, hemorrhage and blood clotting fever, rash, pain are common symptoms

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Examples of type III hypersensitivities

answer

chronic low-grade infections glomerulonephritis - the filtering capillaries in the kidnes are inflammed systemic lupus erythematosis Rheumatoid arthritis vaccine reactions

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Type IV - cell mediated

answer

manifestation: occurs within hours to days

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Type IV - cell mediated

answer

Inflammation: T cell cytokine secretion Macrophage mediator secretion examples: contact dermatitis - poison ivy, metals (jewelry), Tuberculin reactions - TB skin test, transplant rejections

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Rheumatoid Arthritis

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Chronic disease with periods of execerbations and remissions. Usually seen in middle-age and elderly patients

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Rhemumatoid Factor (RF)

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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.

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Rheumatoid Arthritis

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The immune complexes deposit in synovial membranes of joints.

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Type III hypersensitivity

answer

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.

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Rheumatoid Arthritis

answer

fingers - bilateral, symmetric (joint deformities of the fingers), occur in both hands

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Rheumatoid Arthritis

answer

wrists, knees, elvows, ankles and feet - partial dislocations (subluxation) appear due to destruction of the joint capsule

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Vasculitis

answer

decreases blood supply to the fingers and toes, causing them to tingle (Raynaud phenomena)

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Pericarditis, pleuritis, scleritis

answer

Rheumatoid module formation and infrlammation can inflame and damage the pericardium of the heart, the pleurae and the whites (sclerae) fo the eyes

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Neurapathy

answer

tingling and loss of sensation in the hands and feet is due to inflammation of peripheral nerves.

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Systemic Lupus Erythematosis

answer

The cause of SLE is antibody formation to self-antigens located primarily in capillary basement membranes.

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Systemic Lupus Erythematosis (SLE)

answer

Triggers: Light,Stress, Strep or viral infection, immunication, pregnancy, abnormal estrogen metabolism drugs

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Systemic Lupus Erythematosis (SLE)

answer

Facial (malar) rash - a distinctive "butterfly" rash across the cheeks. This is a unique sign to lupus.

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Systemic Lupus Erythematosis (SLE)

answer

Discoid rash - raised, scaling skin Photosensitivity - rash due to sunlight exposure Oral and Nasopharyngeal ulcers Arthritis - in two or more joints Serositis

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Pericarditis

answer

* Pericarditis - inflammation of serous membrane around heart

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hemolytic anemia

answer

low red blood cell count due to cell destruction

question

leukopenia

answer

low white blood cell count

question

thrombocytopenia

answer

low platelet count

question

low platelet count

answer

Ab to self protein

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Myasthenia Gravis

answer

Neuromuscular juctions of one or more of the 12 cranial nerves - weakness and paralysis

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Myasthenia Gravis

answer

caused by antibody formation against acetylcholine repceptors on the motor end-plates of skeletal muscle

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Myasthenia Gravis

answer

Onset of the disease is sometimes associated with pregnancy, postpartum

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Myasthenia Gravis

answer

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

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Myasthenia Gravis

answer

Neuromuscular junctions of other nerves Major muscle groups - weakness and fatique after exercise Respiratory muscles - low tidal volume and vital capacity

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Myasthenic Crisis

answer

major muscle group paralysis - complete paralysis, quadriplegia respiratory failure - complete paralysis, death by asphyxiation

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Primary Immunodeficiency

answer

Direct - developmental ro inherited defect of immune system prior to birth

question

congential

answer

developmental defect of immune system prior to birth

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Genetic

answer

inherited deficiency of immune system development Sex-linked or autosomal

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Secondary Immunodeficiency

answer

Indirect Acquired

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Neuroendocrine

answer

Neuroendocrine - stress induces ACTH and glucocorticoid secretion. Steriods are frequently used to treat autoimmune disease. The side affect of cortisone, cortisol, glucocorticoids = anti-inflammatory

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Secondary Immunodeficiency - Acquired

answer

HIV infects and eventually destroys helper T cells, as well as other CD4 cells

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Secondary Immunodeficiency - Acquired

answer

Once a certain number of these cells are destroyed , the patient develops HIV.

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Immunodeficiency

answer

Primary Aquired

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Immunodeficiency- Primary

answer

B Cell deficiencies Ig deficiencies T cell deficiencies Combined innunodeficiences

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Immunodeficiency - Acquired

answer

AIDS

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opportunistic infection

answer

The ultimate manifestion of all immunodefiency disease

question

opportunistic infection

answer

They are cuased by microorganisms are found normal flora of the skin and mucous

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Opportunistic infectons

answer

caused by organisms which can cause disease

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Opportunistic microorganisms include bacteria

answer

Pseudomonas, Staphylococcus and Haemophilus, or varicells, vaccinia, herpes, cytomegalovirus

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SCID - Severe Combined Immunodeficiency

answer

Caused by genetic defects. Genetic diseases are caused by errors in the DNA

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SCID - Severe Combined Immunodeficiency

answer

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

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Reticular dysgenesis

answer

an enzyme needed for the development of a common stem cell is defective.

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Reticular dysgenesis - manifestations

answer

Reticular dysgensis * systemic oral candidiasis or thrush candidiasis - diaper rash otitis media - middle ear infection Pneumonia diarrhea - digestive tract Sepsis - blood Meningiti - cerebrospinal fluid

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DiGeorge Syndrome

answer

caused by a congenital midline defect due to abnormal development of the third and fourth pharyngeal pouches during the 12 week of pregnancy

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DiGeorge Syndrome

answer

Pathophysiology - the midline results in thymic hypoplasia, underdevlopment of the thymus gland.

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IgA deficiency

answer

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.

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Chronic Mucocutaneous Candidiasis

answer

pathogenesis - T cells are normal except for an inability to recognize non-self antigen on the yeast.

question

pathogenesis - T cells are normal except for an inability to recognize non-self antigen on the yeast.

answer

is spread by fluids containing the AIDS virus. The virus can be found in blood, semen, and vaginal secretions.

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Human Immunodeficiency Virus

answer

Pathogenesis: Replication of virus in cells with CD 4 marker, including helper T cells

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Human Immunodeficiency Virus

answer

HIV atttaches to any cell with CD4 surface receptor antigens. The virus then enters and infects the cell.

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Destruction of virus infected cells

answer

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.

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Immune deficiency due to decreased helper T cell count

answer

when there are low levels of Th cells, this allow opportunistic infections and even cancerous cells to develop

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HIV - Infection Period

answer

Infection Period - after primary infection, the patient develops an inllness that resembles influenza headache, fever, sore throat, muscle and joint pain

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HIV - Latency Period

answer

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

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AIDS Related Complex

answer

Classification of the severity of the patient's infection

question

Stages 1-3

answer

defined by the patient's signs and symptoms

question

Stage 1

answer

flulike symptoms, or no symptoms at all

question

Stage 2

answer

immune deficiency is present, but not serious

question

Stage 3

answer

serious immune deficiency with one or more AIDS defining illnesses.

question

Stages 1-2-3:

answer

based upon the CD4 T-cell count

question

Stage 1 - AIDS Related Complex

answer

greater than 500 cell/microliter

question

Stage 2 - AIDS Related Complex

answer

between 200-499 cells

question

Stage 3 - AIDS Related Complex

answer

fewer than 200 cells

question

Stage 2

answer

A patient who is Stage 2 is said to have AIDS-related complex - but not overt disease.

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Overt AIDS

answer

patient has a category 3 cell count and a Category C AIDS-defining illness

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Decreased CD4 cells

answer

increased opportunistic infections

question

Decreased CD4 cells

answer

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.

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Overt AIDS - CNS

answer

crytococcal meningitis, toxoplasmosis encephalitis

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Opportunistic infections of the CNS

answer

lead to headaches, memory loss, and demential eyes: cytomegalovirus retinitis - can cause blindness

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Kaposi's sarcoma

answer

purplish-brown lesions just under the skin-unique to AIDS. Cancer cachexia (weight loss and anorexia

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