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89 Cards in this Set

  • Front
  • Back
Inflamation has three purposes
1. neutralize and destroy invading and harmful antigens
2. to limit the spread of harmful agents
3. to prepare damage tissue for repair
Inflamation increases capillary permeability so
Phagocytic cells, complement and antibodies can leave the blood stream and enter tissue were neede.
Acute inflammation
Short duration, lasting less than 2wks, and involves a discrete set of events.
Cronic inflammation
More diffuse
Extended over longer periodes
May result in the formation of scar tissue and deformity
Inflammatory process
Increased vascular permeability
Recruitment and emigration of leukocytes
Phagocytosis of antigens and debris
Interact with neutrophils (macrophages) to increase binging affinity of integrin receptors on leukocytes.
Endothelial cells express binding molecules on the cell surface
Leukocytes have selectins, can bind to endothelial adhesion proteins.
-causes leu to stick and roll
Intigrins facilitate
Firm attachment and diapedesis thru capillary wall, this allows neutrophils to bind to endothial cells and EC matrix and then pull themselves into tissue.
Systemic effect of inflammation
Three macrophages derived cytokins
IL-1, IL-6, and TNF-alpha
TNF-alpha and IL-1
Raises temp, induces sleep, and suppress appetite
Cytokines conservation heat
Thru vasoconstriction and shivering
Stimulating release of neutrophils from bone marrow storage sites, thus productinf neutrophilia
Cytokines enhance protein catabolism
Act on skeletal muscle
An available pool of aa for efficient antibody production by plasma cells.
Acute phase proteins
IL-1, IL-6, and TNF-alpha
induce liver to release proteins
Include complement components, clotting factors and protease inhibitors.
Increase in fibrinogen
C-reactive protein (CRP) and serum amyloid A
In controlling inflammation to prevent excess tissue damage

Coats surface of red blood cells and reduces their charge so that the surface of red blood cells and reduces their charge so they aggregate more readily.
Erythrocyte sedimentation rate
Measure levels of inflamtion
Increase ESR increase inflamtion
CRP activity
Nospecific indicator of inflamtion
T helper
can recognize and bind antigen in association w/ major histocompatibility complex (MHC) class II molecules
T-cell receptor (TCR) on the helper T cell binds to the antigen, and the CD4 protein recognizes the MHC class II protein
Binding is specific b/c the TCR must match the antigen fragment precisely.
CD3 and gamma proteins assocaitae w/ the TCR and activated to initiate intracellular enzyme cascade
T-helper cell recognizes antigen in the MHC II class
CD4 proteins is needed to enable T-helper cell to bind the MHC II protein
TCR recognizes specific antigen
TCR binds to antigen signals a cascade in the T –helper cell
TCR is linked to this signaling cascade through a protein called CD3
Activation of kinase enzymes in the cytoplasm that mediate production of two 2nd messangers
Isositol triphosphate
Isositol triphosphate
Increase intracellular Ca+
Ca+ acts as second messenger to change cell behavior
Protein Kinase
Turns on cytokines
IL-2, IFN-alpha, others), IL-2 receptors and other proteins
Il-2 activates
Helper and cytotoxic T cells, NK cells and macrophages
Secreted by TH1 cells
IFN-Alpha activates
Secreted by TH1 cells
TH2 stilmulate B cells
IL-4, IL-5, IL-6, IL-3
serve as
an antigen presenting cell
T-cells help B cells through direct cell-cell contact by receptor proteins
Antigen recognition by B-cell
Bone marrow B-cells express BCR on there surface
They have two distict gene
-variable region-antigen-binding sites
-Constant region-same for all antibodies
Selective splicing variable-region genes
Allows for greater diversity of BCR binding specificities
Activevation of B-cells
B-cells must engulf some antigen, process it, present it to T-helper
-inactivate cell-cell contact b/w B-cell and T-helper cells
contact b/w B-cell and T-helper cells
Cell to cell binding interactes and stimulates intracellular signaling pathway in the B cell (and T-helper) that promote clonal expansion and differentiation.
They require certain cytokines to proliferate and begin antibody syn.
T-cell and B-cell and MHC-II-TCR interactions
Include B7-cd28 and CD40L-CD40
Primary response
B cells are dependent on T-cell help during initial exposure to antigens
Primary response
B cells are dependent on T-cell help during initial exposure to antigens
BCR bind to noprotein antigens
Bacterial sugars and lipids
Bcell response is independent
Complement fragment C3d on the antigen
Costimulation to achieve B-cell response and antibody production
Cytotoxic T cells
They recognize antigen displayed in associations w. MHC class I protein
CD8 protein is necessary to bind MHCI
TCR recognizes the presented antigen
Binding of TCR triggers reponses in cytotoxic T cells
Signal transduction thru CD3
By IL-2 ctokines
IL-2 is primary secreated by activated TH1
Cytotoxic cell proliferate into memory cells as well as effector
Effector cells
Porforins thru CD95
Proteins manufactured in cytotoxic T cell and stored in granules (vesicles w/in the cytoplasm.
Degrade DNA and trigger target cell death
CD95 protein on Cytotoic cell is called CD95L or FAS ligand.
It binds to complemntary CD95 protein (FAS) found on surface of the targeted cell
BAD cell express CD95
CD95L to CD95 trigger programmed cell death
Active immunity
Protects body thru active infection or immunization
Second response
Antiboby is greater and more rapid
Immune system must be exposed to the antigen long enough and sufficient fose to stimulate and immune response
Primary response
Take much loner to develop and falls of rapidly
Neurophiles, macrophages and NK cells receptors bind
Complement opsonin and molecules expressed on microbes
Lipopolysacharide and mannose
NK cell release cytokins on target
Mac, neu, phagocytose digest their targets
The physical and biochemical attributes of an individual that are outwardly apparent
Phenotype are a result of the expression of the individuals unique genetic makeup
The x-shaped chromosome is really made up of two identical linear chromosomes units
The point at the middle of the X at which the two sister chromatids are joined together
Human chromosomes
They occur in pairs
One member pairs come from mother and the other member pair come from the father
Members of the pair appear to be identical although they are different in DNA sequence.
Of the 23 pairs of chromosomes, 22 are homologous
Sex chromosomes
Differ in male and female
The female receives an X chromosome from each parent (homologous), where the other receive and X chromosome from their mother and a Y chromosome from the father (hemizygous). Thus, the genotype is a result of the union of 23 maternal and 23 paternal chromosomes at conception.
Refers to this special form of cell division, which results in germ cells that are haploid
They have half of the normal number of chromosomes
The gene code for a particular trait, such as eye color, are located at a particular position (locus) on the chromosome and comes together and forms
If both alleles for a trait are identical
Two different alleles are present
22 pairs of the autosomes and 2 sex chromosomes (euploid). It resfers to an abnormal number of chromosomes- in humans, either more of less than 46.
Cause of aneoploidy
Nondisjunction and anaphase lag
That the pair of homologous chromosomes fail to separate normally during either the first of second meotic division. The resulting germ cells than have an abnomal number of chromosomes: one will have 22 chromosomes and one will have 24.
-deficient by one chromosome (45) or have an extra chromosome (47)
Anaphase lag
One daughter cell with the normal number of chromosomes and one with a deficiency of one chromosome called monosomy
Having two many chromosomes
Down syndrome
Autosomal disorder
Having an extra 21st chromosome
Rare form of down syndrome
Chromosomal translocation of the long are of the chromosome 21 to another chromosome.
Effects of down syndrome
Mental retardation
Epicanthal folds
Poor muscle tone
Short stature
Congenital heart deformities
Respiratory infections
Klinefelter syndrome
Sex chromosome
Extra X chromosome (an XXY genotype)
The extra X chromosome determines the sex of these individuals to be male, however results in abnormal sextual development and ferminization
Effects of klinfelter syndrome
Testicular atrophy
Tall stature
Long arms and legs
Feminie hair
High pitched voice
Impaired intelligence
Turner syndrome
Monosomy X
Presence of only one normal X chromosome and no Y chromosome
Results in female phenotype
Ovaries fail to develop (sterile)
Missing or damage X chrom is the paternal origin and maybe result to advanced age of father.
Effects of turner’s syndrome
Short stature
Webbing of the neck
Fibrous ovaries
Wide chest
Congenital heart defects

Autosomal dominant disorder
Mutation of a dominant gene located on one of the autosomes
It is involved in structural proteins or regulatory proteins such as membrane receptors.
Disorder of connective tissue
Also called arachnodactyly
Trace mutation in the fidrillin 1 gene chromosome 15. Fibrillin 1 is a glycoprotein secreated by fibroblasrs in the EC matrix
Provides important scaffolding ie elastin
Proteolytic degradation than normal fibrillin
Huntington disease
Affect neurological function
Localized to chromosome 4, where an abnormally large number of triplet repeat (CAG)
More than 39 are reliably associated with the development of the disease.
Huntington disease

Mental deterioration and involuntary movement
Autosomal recessive disorders
Mutation of a recessive gene located on one of the autosomes.
Only expressed when both alleles for a particular gene are mutant (homozygous), they are often associated w/ consaguinty- the matting of relative individuals.
Involve abnormal enzymatic function
Lack of pigment
Lack of enzyme tyrosinase, which catalyzes the formation of dopa from tyrosine.
Dopa is the presusor of the pigment melanin
Inability to metabolize the aa phenylalanine due to lack of the enzyme phenylalanine hydroxylase.
Buildup of phenylalanine causes nervous damage
Urine in form of phenylketones “sweet urine”
Low phenylalnine diet
Cystic fibrosis
Single gene disorder
Defect in the membrane transporter Cl ion in epithelial cells.
Adnormal secreation in glandular tissue
Chromosome 7
Detection of 3 necleotide that are normally code for phenylalanine at position 508
Absence of protein causes fod abnormally, preventing release from ER. And causes degradation.
Cystic fibrosis transmembrnae conductance regulator protein (CFTR)
ABC transporter that binds to ATP hydrolyse
Sex-linked (x-disorder)
Mutation in the sex chromosome
Nearly all X-linked disorders are recessive
Almost always male
A is a bleeding disorder associated w/ deficiency of factor VIII, a protein necessary for blood clotting.
Royal disease
Genomic imprinting
Parental origin of a gene does not matter to the cell that inherits them.
Parental and maternal chrom are marked differntaly w/in the cell.
Two syndromes
Prader-Willi and Angelman syndrome
(results from the same chromosomal defect)
-deletion at the same location on chrom 15.
Prader-Willi effects
-Parentally derived
Short stature
Poor muscle tone
Angel effects
-maternally derived
Metal retarded, but they have ataxia and tend to laugh inappropriately
Parental diagnosis and counseling
1. Maternal age of 35 yrs or greater
2. having borne a child w/ chrom disorder (trisomy 21)
3. know family history of X-linked disorder
4. know family history of inborn errors of metabolism
5. occurrence of neutral tube abnormalities in the previous pregnancy
6. known carrier of recessive genetic disorder
Noninvasive procedure that uses sound waves to produce a reflected image of the fetus.
Ultra sound determines
Gestational age
Fetal position
Placenta location
Spina bifida
Heart defects
Malformations face, head, body and limb
Determines genetic and development disorders
Alpha- fetoproteins- may indicate neural tube defects
Chorinoic villus sampling
Removing bit of tissue from chorion
Visualizes of the embryo as early as the first trimester of pregnancy.
Diagnoses structural anomalies