Body Defenses Flashcards
Lysis?
cell membrane is attacked in some way so cell loses control of its contents and ruptures
Phagocytosis?
engulfment by neutrophil/macrophage then goes under intracellular digestion by lysosomes
Adaptive Defense Systems?
Specific, develop after birth upon exposure to foreign antigens
What are surface barriers and what do the include?
first line of defense
physical and chemical barriers
What are all WBC formed from and where?
Red bone marrow stem cells(hemocytoblasts)
What are characteristics of physical barriers?
Intact skin, keratin resists abrasion, tearing, weak acids and bases and bacterial toxins
intact mucosal membranes protect internal orgs/cavities
What are the two mechs in which foreign orgs are destroyed?
Phagocytosis
Lysis
Innate Defense System?
Nonspecific, born with, activate against any invader
Leukocytosis?
inducing factors from damaged cells stimulate
Chemical barrier characteristics? Skin: Stomach: Saliva and Tears: Mucus:
Skins acidic secretions which inhibit bacterial growth
stomach has hcl and protein digesting enzymes
saliva and tears - lysozymes defensins
Mucus traps organisms
What are internal defense?
Second line
What types of WBC can phagocytosize?
Macrophages
Neutrophils
Eosinophils
What do macrophages develop from?
What are characteristics of them?
What are example of free/fixed?
Monocytes
can phagocytize lots without damage
kill also by releasing a respiratory burst of oxidizing chems/ acids
Heavy hitters
Free - dendritic cells in epidermis and alveolar in lungs
fixed - kupffer cells in liver
Whats the most common WBC?
What is there role?
When do they migrate from blood to tissues?
What are they considered?
Neutrophil
first responders @ infection
Upon chemical clues
suicide killers
What kind of granules do eosinophils contain?
What kind of phaocytes are they considered?
How do they attack large paracites
pink cytoplasmic granules
weak
release hydrolytic enzymes externally
How to phagocytosis occur?
ahattach to pathogen engulf into phaosome fusion with lysosome --> phagolysosome Hydrolysis by enzymes killing by burst of free radicals/oxidizing chems killing by defensins Exocytosis of residual body
Margination?
WBCs move along caps and cling to CAMs on cap walls`
CAMS?
Cell adhesion molecules mark the sites of damage or infections
Diapedesis?
WBC squeeze between endothelial cells toward injurt by amoeboid motion
Positive Chemotaxis?
WBC follow increasing concentration gradient of inflamm chems to site of injury
What is the order of WBC into response of infection?
Neutrophils
monocytes which then convert to macrophages
Pus?
evidence of phagocytosis
Abscess?
Infection not completely cleared, walled of by collagen fibers
Lysis by natural killer cells? What are NK? Where are the found? How to they work? How do they kill cancer and virus cells?
Large type if granular T lymphocyte, involved in non specific defense
Blood, lymph vessels, and other tissues
crawl over surface of cells looking for abnorm marker proteins
perforin and granzymes
Anitmicrobial Proteins?
Enhance defense, attack microorganisms directly, hinder MO’s ability to reproduce
How do perforins work?
insert into membrane of target cells, polymerize and form pores
how do granzymes work?
Enter through pores and attack membranes destroy nucleus and cell undergoes apoptosis
What does inflammation triggered by?
What does it prevent?
what does it prepare for?
What are the four cardinal Signs?
when body tissues are injured or infected
prevents spread of infection, disposes of debris and pathogen
Repair
Red Heat Swelling Pus
What are stimulus’ that trigger inflamm responses?
Histamines - released by mast cells in loose CT
Toll like Receptors - on macrophages and in boundary epithelial tissues recognize specific classes of microbes which trigger release of cytokines
Kinins, Prostglandins, Leukotrienes, complement - released by injured tissue, phagocyte, lymphocyte and basophils
What is the process of inflammation?
Chems released into extracellular fluids–> arteriole dilation–> increased Blood flow –>red/heat–>permeability of caps increase –> exudate leaks out–>pressure –>swelling/pain –>walls off damaged area providing framework for tissue repair –>foreign material into lymphatics –> more pain –> damage to mucosa(secretion of defensins increases)
Two types of antimicrobial proteins?
Interferons
Complement
Interferons are produced by what? What do they act against? What do they do? What do they activate? What do they reduce?
cells infected by viruses
a range of viruses
macrp[hages & NK cells
inflammation
What is complemet?
What does it assist in?
what is it a major mechanism for?
20+ inactive plasma proteins
specific and no defense
destroying antigens
What is complement activated by?`
.
What is complements classical PW?
complement fixation - c1 binds to antigen-antibody complex
What is complements alt pw?
Exposure of factors to bacterial cell wall
What dies cleavage of C3 into C3a and C3b cause?
causes cell lysis, enhanced phagocytosis and inflammation, production c reactive protein
Fever?
In response to pyrogens
Too high=denature of enzymes
Moderate increase inhibits bacterial growth
Also speeds up metabolism increasing repair
What does the third line of defense do?
It recognizes, immobilizes, neutralizes and destroyed specific antigens
Protects against pathogens and abnormal cells
Amplifies inflamm
Carries out complement fixation
What do both classical and alt pws of complement lead to?
Formation of C3
Characteristics of the third line of defense?
Systemic
Specific
Memory
Humoral and cellular component
Humoral component?
B cells release antibodies which immobilize bacteria, toxins and free viruses
mark destruction by phagocytes and complemement
Cellular Component?
t Lymphocytes act directly against infected cancerous or foreign cells lyse cells(direct) release chemicals (indirect)
What is the difference between complete antigens and incomplete antigens?
Complete antigens are antigenic and reactive
Incomplete antigens are not antigenic