Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
52 Cards in this Set
- Front
- Back
|
innate defenses |
fast response two barricades: 1st line (skin and mucosae) 2nd line (internal defense -- microbial proteins, phagocytes) |
|
|
events of phagocytosis |
|
|
|
Major histocompatibility complex (MHC) proteins |
glycoproteins that identify a cell as "self" each MHC protein has a deep groove that holds a peptide, either a self-antigen or a foreign antigen |
|
|
Natural killer (NK) cells |
kills infected cells (not displaying MHC I) via apoptosis by secreting chemicals that enhance inflammatory response |
|
|
benefits of inflammation |
prevents spread of damaging agents disposes cells debris alerts adaptive immune system sets the stage for repair |
|
|
4 cardinal signs of acute inflamamtion |
redness, heat, swelling, pain Redness and local heat are both caused by vasodilation of arterioles, which increases the flow of blood (warmed by the body core) to the affected area. The swelling (edema) is due to the release of histamine and other chemical mediators of inflammation, which increase capillary permeability. This increased permeability allows proteins to leak into the interstitial fluid (IF), increasing the IF osmotic pressure and drawing more fluid out of blood vessels and into the tissues, thereby causing swelling. The pain is due to two things: (1) the actions of certain chemical mediators (kinins and prostaglandins) on nerve endings (2) the swelling, which can compress free nerve endings. |
|
|
satges of inflamamtion |
inflammatory chemical release (histamines, cytokines) vasodialtion increases vascular permiability phagocyte mobilization |
|
|
most important antimicrobial proteins are |
interferons and complement proteins |
|
|
interferons |
small proteins secreted by infected cells to help protect cells that have not yet been infected by viruses they interfere with viral replication in healthy cells |
|
|
characteristics of adaptive immune system |
1) it is specific 2) it is systemic 3) it has memory note: this takes a long term (2 weeks) |
|
|
antibodies |
large Y-shaped proteins that function to identify and destory pathogens the antigen-binding site binds to the same place on the pathogen (antigen) |
|
|
most antigens have several different antigentic determinants |
antigen are collection of antigenic determinants |
|
|
how do antibodies destroy pathogens? |
1) neutralization (masks dangerous parts of bacterial exotoxins) opsonization "to make tasty" 2) agglutination 3) precipitation 4) complement activation |
|
|
allele |
different version of a gene. dominant alleles mask phenotype of recessive alleles |
|
|
homologous pairs have certain characteristics |
same length and centromere location both carry similar types of genes alternate forms of a gene are called alleles |
|
|
genotype |
all of an individuals genetic material |
|
|
physical trait can mask a genotype |
knowing the phenotype does not always tell you the genotype Type A blood: IAIA (homo) IAi (hetero) both these genotypes result in Type A blood however type O blood has only one genotype |
|
|
codominance |
when both alleles are expressed Individuals with AB blood are codominant |
|
|
PKU |
no expression of phenylalanine hydroxylase, which converts phenylalanine to tyrosine as a result, causes brain damage |
|
|
incomplete dominance |
blending inheritance heterozygous individuals have intermediate phenotype: they may have symptoms, but usually not as intense as homozygous individuals example: sickle cell disease SS = normal HB made Ss = sickle cell trait -- both mutated and normal HB are made (person can suffer sickle-cell crisis under prolonged reduction in blood O2) ss = sickle-cell anemia -- makes only mutated Hb. person is more prone to sickle-cell crisis |
|
|
multiple-allele inheritance |
some genes exhibit more than 2 allele forms ABO blood groups have 3 alleles any one person only inherits 2 of the 3 alleles in the population |
|
|
sex-linked inheritance |
inherited traits determined by genes on sex chromosomes genes found only on the X chromosome are X-linked genes |
|
|
What is the difference between the innate and adaptive defense systems? |
The innate defense system is always ready to respond immediately, whereas it takes considerable time to mount the adaptive defense system.
The innate defenses consist of surface barriers and internal defenses, whereas the adaptive defenses consist of humoral and cellular immunity, which rely on B and T lymphocytes. |
|
|
What is the first line of defense against disease? |
Surface barriers (the skin and mucous membranes) constitute the first line of defense.
|
|
|
macrophages |
WBCs that ingest and digest foreign invaders |
|
|
opsonization |
to make tasty process of making pathogens more susceptible to phagocytosis by decorating their surface with molecules that phagocytes can bind Antibodies and complement proteins are examples of molecules that act as opsonins. |
|
|
NK cells |
large granular lymphocytes that can lyse cancer cells and virus-infected cells before the adaptive system is activated non-specific, non-phagocytic initiate apoptosis enhance inflammatory response |
|
|
inflammatory chemical release |
chemicals are released into the ECF by injured tissues, immune cells, or blood proteins example: mast cells release histamine macrophages release cytokines all inflammatory chemicals dilate locate arterioles |
|
|
hyperemia |
congestion with blood occurs when local arterioles dilate |
|
|
exudate |
fluid containing clotting factors and antibodies seeps from the blood into the tissue spaces when local capillaries are more permeable causes local swelling and pain |
|
|
How does aspirin relieve pain? |
it is an anti-inflamatory. inhibits prostaglandin synthesis |
|
|
benefits of inflammation |
surge of protein-rich fluids into the tissue spaces sweeps foreign material into lymphatic vessels for processing in he lymph nodes delivers complement proteins and clotting factor to the ECF |
|
|
phagocyte mobilizaton |
phagocytes can remove cell debris and pathogens |
|
|
antimicrobial prteins |
enhance innate defense by attacking microorganisms directy or by hindering their ability to reproduce interferons and complement proteins are most important |
|
|
first line of defense (surface barrier) |
physical barrier to most microorganisms keratin is resistant to weak acids and bases, toxins, and bacterial enzymes acidity of the skin inhibits bacterial growth enzymes in saliva, respiratory tract, tears, and in stomach destroy microorganisms sticky mucin in respiratory tract trap microorganisms defensins -- proteins that inhibit growth sebum and sweat |
|
|
second line of defense (cells and chemicals) |
if microorganisms invade deeper tissues: Fever - high body temperature inhibits microbes from multiplying and enhances body repair processes Phagocytes Antimicrobial proteins Inflammation NK cells |
|
|
complement system |
group of <20 plasma proteins that normally circulate in blood in inactive state major mechanism for destroying foreign substances in the body activation enhances inflammation directly destroys bacteria |
|
|
complement activation (3 ways) |
3 ways: classical pathway -- when antibodies bind to pathogens, they can also bind complement components lectin pathway -- bind to specific sugars on the surface of microorganisms, which then activates complement alternative pathway -- microorganism lack inhibitors any of these pathways involves a cascade in which proteins are activated C3 is split into C3A and C3B. C3A amplifies inflammation via stimulating mast cells to the area C3B binds to target cells surface and triggers the insertion of MAC (membrane attack complex -- group of complement proteins) |
|
|
Under what circumstances might NK cells kill our own cells? |
when they have been infected by viruses or when they have become cancerous |
|
|
adaptive defenses |
specific defense system eliminates nearly any pathogen/abnormal cell in bidy amplifies inflammatory response activates complement must be primbed by initial exposure, so it takes longer than innate defense |
|
|
3 characteristics of adaptive immunity |
it is specific -- recognizes antigens it is systemic -- not restricted to initial infection site it has memory -- mounts even stronger attack to previously encountered pathogens |
|
|
2 main branches of adaptive system |
humoral (antibody-mediated) immunity: antibodies bind, inactivate, and mark extraceullar targets (bacterial, toxins, viruses) for destruction (complement or phagocyte) cellular (cell-mediated) immunity: lymphocytes act against cellular targets (infected cells, cancer cells) |
|
|
antigen |
antibody generator large complex molecules that are the ultimate targets of all adaptive immune responses not normally in the body intruders |
|
|
antigenic determinants |
parts of antigen that antibodies or lymphocyte receptors bind to most naturally occurring antigens have numerous antigenic determinants that either form different kinds of antibodies against them or mobilize several different lymphocyte populations chemically simple molecules (plastic) have little or no immunogenicity |
|
|
What marks a cell as "self" as opposed to "nonself"? |
Self-antigens, particularly MHC proteins, mark a cell as self
|
|
|
lymphocyte development, maturation, and activation |
lymphocytes develop in the bone marrow. B cells mature in bone marrow T cells mature in thymus |
|
|
antigen-presenting cells (APCs) |
engulf antigens and then present fragments of them (like signal flags) on their own surfaces where T cells can recognize them |
|
|
fertilization |
sperm has digestive enzymes to penetrate into the ovum sperm deposits genetic material at the plasma membrane of ovum |
|
|
primary function of gonads |
produce gametes produce sex hormones |
|
|
sustenocytes |
produces androgen binding protein binds testosterone |
|
|
interstitial cells |
produces testosterone |
|
|
hypothalamic pituitary gonadal axis |
neurons producing gonadotropin releasing hormone (GnRH) secretes into portal system GnRH stimulates the pituitary gland to secrete FSH and LH FSH stimulates sustenoctyes to produce ABP LH stimuates interstitial cells to produce testotone, which inibits FSH and LH release excess spersm stimultes sustenoctyes to produce inhibin which stops GnRH |
