Test 4 Chapter 17 Flashcards
Tight Junctions
Doesn’t let anything between cells
Desmosomes
Strong, but flexible junctions
Gap Junctions
Allow small molecules (ions) to go directly between cells
Skin as a barrier
Multilayered. Surface dry and salty. Not favorable environment usually
Epidermis
Most external layer of skin. Dead keratinized cells. Dry, salty, and acidic.
Exfoliation
Sluff off the outer most layer of skin
Dermis
Depp to the epidermis. Connective tissue
Hypodermis
Deep to the dermis. Adipose tissue. Subcutaneous layer
Mucous Membranes
Mucus, Epithelium, basement membrane. Line passageways exposed to outside world.
Mucociliary Escalator
Trachea to the respiratory tract. Mucus cells and glands. Cilia propel mucus to the pharynx.
Digestive Tract Barrier
Lined by Mucous membrane. Numerous Goblet Cells - Produce Mucous.
Peristalsis
Oral to anal propulsion of ingested material. Moves mucus and ingesta through tract.
endothelia
Lines urogenital tract. blood vessels, and lymphatic vessels
Blood-Brain Barrier
Brain is a protected site. Endothelial cells of these blood vessels are specialized.
Crying
Tears physically wash the eyes
Urination
Washes away pathogens
Defecation
Removes pathogens, mucus, non-digestible food.
Microbiome
Normal resident microbiota in select locations. Compete for space and nutrients. Inhibit growth of primary and opportunistic pathogens.
Sebum
Has antimicrobial proteins, excreted from sebaceous glands
Earwax
Antimicrobial Proteins
Saliva
Antimicrobial proteins, non-specific proteins and some antibodies
Tears
Antimicrobial proteins, non-specific proteins and some antibodies
Mucus
Very sticky
Gastric Fluid
Hydrochloric acid produced by the stomach. pH 2 extremely acidic
Antimicrobial peptides (AMPS)
Broad-Spectrum antimicrobial properties.
Bacteriocins
Disrupt membranes
Defensins
Disrupt Membranes
Dermcidin
Disrupts membrane integrity and ion channels
Acute-Phase Proteins
Produced early in an infection. Produced mainly by the liver
C-Reactive Protein
Opsonization
Ferritin and Transferrin
Bind and sequester iron
Fibrinogen
Clotting Protein
Mannose-Binding Lectin
Activates complement system
Classic Pathway
First pathway discovered, involves antibodies, plays a role in adaptive immunity.
Activation of Classic Pathway
Antibody binds antigen and antibody, changes shape exposing C1 binding site. C1 binds to antibody and is activated.
Result of C1 binding to antibody
Activation of C2 and C4. Portions of C2 and C4 combine to form an enzyme to activate C3. C3 -> C3a and C3b
Alternative Pathway
Innate immunity. Less efficient that the classic pathway.
Alternative Pathway Activation
Activated spontaneously. Activates C3 -> C3a and C3b. when microbes are present they bind to and stabilize C3b
Lectin Pathway
Innate Immunity. Mannose-Binding lectin binds to mannose on microbial surface.
Mannose binding leads to (lectin pathway)
Triggers activation of C2 and C4. Portions of C2 and C4 combine to form an enzyme to activate C3. C3-> C3a and C3b
C3a Function
Inflammation
C3b Function
Opsonization and activation of C5 -> C5a and C5b
C5a Function
Chemotaxis - coordinates immune cells
C5b Function
Combines with C6, C7, C8, and C9 forming a membrane attack complex. Makes holes in bacterium
Autocrine
Cells talk to itself and the same type of cell
Paracrine
Nearby, but different cell types
Endocrine
Hormones, chemicals in the blood for intracellular communication.
Interleukins
Not only produced by white blood cells. Involved in almost all aspects of the immune system. Non-immune functions too.
Chemokines
Guide cells to a destination. Chemotactic factors. Recruit leyukocytes
Type 1 Interferons
Interferon-Alpha/Beta. Secreted by virally infected cells. Stimulate close cells to decrease mRNA synthesis, Destroy RNA, and reduce translation. Stimulate immune cells to be more aggressive.
Type 2 Interferons
Interferon-Gamma. Activates various immune cells
Histamine
Secreted by basophiles and mast cells
Leukotrienes
Secreted by white blood cells
Prostaglandins
Lots of different things some cause inflammation.
Bradykinin
Inflammation and pain
Neutrophils
Chief enemy of bacteria (kills everything). Granules contains defensins and hydrolytic enzymes (digestive enzymes). Contributor to purulent exudate (pus)
Neutrophil Extracellular Traps
Kind of contains damage
Eosinophils
Responds to Protozoa and helminths (parasites). Associated with allergy reactions.
Basophils
Pro-Inflammatory, blood and migrate to tissue.
Histamine
Basophil type. Stimulates inflammation. Vasodilator, brings blood to area
Heparin
Basophil type. Anticoagulant. Need to clot a little but not a lot
Natural Killer Cells (NKC)
Non-Specific, elegant killers. Secret perforins which make small holes in target cells. Send Granzymes into the cell which apoptosis in cell. Target cancer and virally infected cells.
Major histocompatibility complex (MHC) proteins
Located on cells. ID tags for your cells. prevents NKC from killing
Monocytes
Leave the bloodstream and differentiate.
Macrophages
A kind of monocyte. Fixed macrophages live in specific tissue
Dendritic Cells
A kind of monocyte. found on skin and mucous membranes.
Diapedesis
How white blood cells squeeze between endothelial cells.
Pathogen-Associated molecular patterns (PAMPs)
Peptidoglycan. Flagellin. LPS
Flagellin
Protein that makes the bacteria flagella
LPS
Outer membrane of gram-negative bacteria.
Toll-Like Receptors (TLR)
A type of pattern recognition receptor. Found on phagocytic cells. Binds to PAMPs.
Adhesion
Phagocytic cell sticks to pathogen
Phagocytosis
When a phagocytic cell internalizes a pathogen. process forms a phagosome.
Phagolysosome
Form when a lysosome fuses with a phagosome. Lysosomes contain various reactive oxygen species and digestive enzymes
Fina step of Phagocytosis
Degradation of phagocytized material. Exocytosis of undigested waste. Antigen presentation
Acute Inflammation
Develops quick and is short lived. Is typically beneficial. Is important to innate immunity.
Acute Inflammation Results
Dilation and increased permeability of the blood vessels. Migration of phagocytes. Tissue Repair. Contain Damage.
Four Cardinal Signs/Symptoms of Inflammation
Redness, more blood, histamine.
Swelling, more permeability, histamine.
Heat, More blood.
Pain, From damage.
Chronic Inflammation
Can continue for months or years. May have formation of granulomas. Tissue damage and degeneration
Why does inflammation become chronic?
Damage cannot be repaired or fixed, or nothing is telling the inflammation response to stop.
What part of the brain is the thermostat?
hypothalamus
What temperature is bad?
> 102.5
What causes fever?
Pyrogens. LPS, interleukins, Interferon-gamma, tumor necrosis factor, and prostaglandin E-2.
Crisis phase
when the fever breaks
Positives of Fever
Enhances innate response - Macrophages eat more. Inhibits growth of some viruses and bacteria. Increase metabolic rate of speed healing. Interferons work better during fever.
