Blood & Immunology Flashcards
Blood Antigens
Surface molecules that act as promoters of agglutination and have co-dominance of IA & IB genes as well as i (recessive)
Agglutinogens
Antigen found at the blood cell surface
Agglutinins
Antibodies for the antigen NOT found on blood cell surface. For A and B antibodies, humans will synthesize these at birth. No prior exposure needed.
Whole blood transfusion
Transfusion with all blood components including donor antibodies
Packed red blood cell transfusion
-Transfusion of blood with plasma and white blood cells removed
-No plasma = No donor antibodies
Universal Recipient
Type AB. Host makes no antibodies to attack donor blood
Universal Donor
Type O: No antigens on RBC surface for host antibodies to target
Rhesus Factor
-Forms D antigen that will denote +/-
-Antibodies not preformed in the fetus. Will only be made following exposure
Donor cells in incompatible blood transfusion
-Donors cells are attacked by recipient plasma agglutinins
-Blood agglutinates and clogs small vessels
-Rupture and release hemoglobin into bloodstream
Erythroblastosis Fetalis
-Rh- mom exposed to Rh+ blood of fetus during delivery of first baby causes mother to synthesize anti-Rh antibodies
-During another pregnancy with an Rh+ baby, mother’s anti-Rh antibodies will cross placenta and destroy RBC’s of fetus
Result of incompatible blood transfusion
-Diminished oxygen-carrying capacity
-Diminished blood flow beyond blocked vessel
-Hemoglobin in kidney tubules causing kidney failure
Rho-GAM
Received antibodies that come in a drug in a low enough quantity to react with Rh of fetus in order to mask the fetus blood from the mother’s immune system that would eventually attack the fetus.
Antibody-Antigen complex
Signal for destruction for the immune system
Adaptive immunity
Specific defense system
Innate immunity
Nonspecific defense in cells
First line of defense
External body membranes such as skin and mucosae
Second line of defense
Antimicrobial proteins, phagocytes, and other cells to prevent infection, inhibit spread of invaders, and promote inflammation
Adaptive defense system
Third line of defense to attack specifically a particular foreign substance
-Takes longer to react than innate system
-Specific and Highly Effective
Surface barriers warding off invading pathogens
-Physical barrier to most microorganisms
-Acid secretion
-Phagocytes & dendritic cells
-Enzymes-lysozyme of saliva, respiratory mucus, and lacrimal fluid
-Defensins
Internal defenses (Second line) of the body
-Phagocytic cells
-Natural killer cells
-Antimicrobial proteins
-Fever
-Inflammatory response
Neutrophils
Most abundant phagocytic cells but often die fighting. Become phagocytic on exposure to infectious materials
Macrophages
Phagocytic cells that develop from monocytes. Act as the chief phagocytic cells
-Free macrophages wander through tissue spaces
-Fixed macrophages permanent residents of some organs
Phagocytic cells of the body
Neutrophils and Macrophages
Antibacterial proteins (Interferons, complement proteins, defensins)
-Attack microorganisms directly
-Hinder microorganisms ability to reproduce
Natural Killer Cells
-Derived from lymphocytes
-Non-phagocytic large granular lymphocytes
-Attack cells that lack cell-surface receptors that indicate “Self” or belonging to host
-Induce apoptosis in cancer cells and virus-infected cells
-Enhance inflammatory response
Fever
-Sysetmic increase in body temperature to increase metabolism, proliferation and mobility of WBS, phagocytosis promotion, and impairment of pathogen proliferation
Pyrogens
Substances that induce fever
Triggers of inflammatory response
-Injured body tissue
-Extreme heat
-Infection
Goal of inflammatory response
-Prevents spread of damaging agent
-Disposes of cell debris and pathogens
-Alerts adaptive immune system
-Sets stage for repair
4 main signs of inflammatory response
-Redness
-Heat
-Swelling
-Pain
First phase of inflammation
-Injured tissue or immune cells release chemical signals
-Macrophages identify invaders
-Vessels dilate to increase heat and redness of area
-Histamine causes higher capillary permeability causing exudate (blood components) to enter tissue which leads to swelling (Edema) and pain
Second phase of inflammation
Phagocytes arrive in mass
4 steps for phagocyte arrival
1.Leukocytosis: Neutrophils enter blood from marrow
2. Margination: Neutrophils cling to capillary wall
3. Diapedesis: Neutrophils flatten and squeeze out of capillary
4. Neutrophils follow chemical trail to damaged site
Effects of histamine
-Higher capillary permeability causing tissue exudation, swelling and pain
-Vasodilation causing more blood to tissue leading to redness and increased metabolism that leads to heat.
Adaptive Defense/Acquired Immunity
-Specific response: Antigens produced
-Systemic
-Can have memories
-Both humoral and cellular immunity
Humoral Immunity
-Antibodies produced by plasmocytes, circulating freely in the body
-Bind temporarily to target cell antigen to temporarily inactivate and mark for destruction
-Humoral immunity has extracellular targets
IgM
-Primary response: 1st Ig secreted
-Complement activating
-Highly agglutinating
-Mostly in intravascular fluid
-B cell receptor if membrane bound
-Isohemagglutinin in ABO blood types
-Does not pass placenta
-B cells producing IgM’s can switch to produce IgG and memory cells
IgA
-Major Ig in bodily secretions
-Prevents pathogens & infection
-Highly agglutinating to promote innate immune response
IgD
-B cell receptor
-Unclear function
IgG
-Most abundant Ig in plasma
-Main Ig for secondary response
-Complement activation via IgG-Ag complexes
-Activated Ab-dependent cell mediated cytotoxicity through NK cells
-Passes placenta barrier
-Passive immunization
IgE
Fce binds to receptor on mast cells and basophils to release heparin, histamine, leukotrienes, etc. Causes immediate hypersensitivity
Cytotoxic T cells
Attack and kill infected cells
Cellular immunity
-Lymphocytes act against target cell
-Cellular immunity has cellular targets
-Mostly triggered by T-lymphocytes
Helper T cells
Activate B and T cells and induce proliferation
Regulatory T cells
Suppress immune response
