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206 Cards in this Set
- Front
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a change or mutation in the DNA sequence of one gene. The code for protein is not correct and protein is abnormal and nonfuctional |
single gene disorders |
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what are four example of single gene disorders? |
sickle cell anemia, cystic fibrosis, marfans syndrome, huntingtons disease |
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what are four ways that single gene disorders occur? |
gene deletion, duplication, insertion, and translocation |
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__ occurs when there are missing portions of genes. |
gene deletion |
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what are two examples of gene deletion? |
velocardiofacial syndrome, cystic fibrosis |
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cleft palate, craniofacial anomalies, ventricular septal defect and retardation caused by a deletion in chromosome 22 |
velocardiofacial syndrome |
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a deletion of a gene hat makes a protein that transports chloride across the cell membrane |
cystic fibrosis |
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what is an example of gene duplication? |
alzhemiers and downs syndrome both show duduplication of parts of gene 21 |
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what are two examples of gene insertion? |
huntingtons disease, fragile X syndrome |
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what are two examples of gene translocation? |
burkitts lymphoma, chronic myelogenous leukemia |
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gene translocation in chronic myelogenous leukemia occurs on teh __ chromosome |
philadelphia |
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what is the normal number of chromosomes in a human? |
46 |
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changes in chromosomal nuber, size, or arrangement occur during __ and are inherited at __ |
meiosis, conception |
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occurs when a normal 46 chromosome cell splits into two cells with 23 chromosomes |
disjunction |
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gives a "map" of a persons chrmosomes |
karotype |
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describe the two kinds of downs syndrome |
mosaic: extra copy of chromosome 21 (47 total)
translocation: chromosome 21 placed on chromosome 14 |
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__ is expressed by overexpression of genes for premature aging, mental retardation, heart defects, skeletal abnormalities, DNA synthesis, cataracts, and immune fuction |
downs syndrome |
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where a male has an extra X chromosome (XXY) giving 47 chromosomes in each cell. these patients have failure to develop decondary sexual characteristics (no male genetalia), are tall in stature, have learning disabilities, personality impariments, and a single palm crease |
kleinfelter syndrome in males |
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when females only have 1 X chromosome. appear short in stature, lack ovarian development, have webbed neck and arms that turn out slightly at the elbow, have a low hairline in teh back of the head, are prone to CV problems, skeletal disorders like scoliosis or dislocated hips and have hearing disturbances |
turner syndrome |
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the ability to a genetic disease or abnromality to present ( explains why some disorders have mild expressions and some skip a generation. |
penetrance |
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method of gene transmission where: a person needs only one abnromal gene to have the disease, each generation is affected, the disease occurs in both genders |
autosomal dominant |
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method of gene transmission where: a person must have two copies of the abnromal genen to express the disease. persons with only one abnromal gene are called "carriers" |
autosomal recessive |
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describe how X linked dominant diseases are transmitted |
affected males transmit trait to all of the daughters but none of their sons
affected females (with one gene) transmit to 1/2 of children
affected females (with 2 genes) transmit to all children |
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how do X linked recessive gene disorders work? |
nearly all affected persons are male
all daughters of affected males are carriers
carrier females transmit traits to 1/2 of sons |
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kind fo inheritence that depends on genetics, the environment, and ones own personal conditions. examples are neural tube defects, heart anomalies, epilepsy, cleft lip/palate, hyperension, arteriosclerosis, diabetes, cancer, and arthritis |
multifactorial inheritence |
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what are two examples of inborn errors of metabolism? |
abnormalities in synthesis or catabolism of proteins, carbs and fats caused by defective enzymes or transportation proteins
mitochondrial disorders that cause faulty production of energy |
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what does the "dogma of DNA replication" mean? |
DNA replication must be done in proper order: DNA is transcribed to RNA, proteins are transcripted from proteins |
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when a cell divides into two identical copies of iteself called daughter cells |
mitosis |
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what three things need to occur for mitosis to happen? |
DNA needs to be copied without error
organelles must be evenly split
cytoplasm must be split to create 2 cells |
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newly divided chromosomes are called __ |
chromatids |
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what are the 4 phases of mitosis? |
prophase (spindle fibers form from centrioles, chromosomes compact)
metaphase (nucleus dissolves, chromosomes attach)
anaphase (chromatids separate and move)
telophase (chromatids are portioned into new nuclei) |
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How is DNA replicated? |
DNA helicase breaks the H bond of DNA seperating it into single strands
New nucleotide bases (adenine-thyamine, guanine-cytosine) are added by DNA polymerase creating a new strand of DNA
DNA polymerase proofreads the DNA |
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the site of protein synthesis is the __ |
ribosome |
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describe the role of RNA in protein synthesis (3) |
ribosome binds to an inititaiton site on mRNA sequence
robosome binds tRNA to its surface so base pairing can occur between tRNA and mRNA
ribosome moves along mRNA processing codons and translates AA into protiens |
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how does base pair substitution cause mutations in DNA sequence? |
one base substitutes for another |
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__ pedigrees are represented in every generation and are seen in both sexes. |
autosomal dominant |
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__ pedigrees have both sexes affected but tend to skip generations. there are carriers marked throughout generations. in x linked pedigrees ther __ are teh carriers and the __ express the traits |
recessive trait; females, males |
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huntingtons disease is an __ disease |
autosomal dominant |
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cystic fibrosis is an __ disease |
autosomal recessive |
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coffin-lowry syndrom is an __ disease |
X linked dominant |
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hemophilia is a __ disease |
X linked recessive |
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why is the risk of any genetic disease is the same for all children born to the same parents? |
all genes are thrown into the gene pool at every conception making the odds the same every time |
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what kinds of studies are helpful for genetic diseases? |
twin/adoption studies |
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how does hypersensitivity type I occur in allergic people and non allergic people? |
in allergic people: release IgE and causes mast cell degranulation and synthesis of later phase reactors
in non-allergic people: release IgG
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explain the 4 kinds of hypersensitivity reactions |
type I due to production of IgE (classic allergic diseases)
type II due to binding of antibodies (hemolytic drug reactions, Rh disease)
type II due to deposits of soluble antigen-antibody complexes on organs (rheumatoid arthritis)
type IV due to sensitized T cells (TB, sarcoidosis, leprosy) |
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explain the part IgE plays with allergic reactions |
first exposure to allergin produces IgE
IgE binds to mast cells
at the next exposure the mast cell degranulates causing an allergic reaction |
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describe anaphylaxis |
the most severe from of Type I hypersensitivity
presentation is immediate (severe bronchoconstriction and hypotension) |
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allergic diseases like hay fever, asthma, and urticaria that have a strong familial predisposition |
atopic diseases |
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what causes atopic diseases? |
failure of T cell regualtion that causes too much IgE production, mutations of interleukins, target tissues have excess receptors |
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what are the two most common drugs that cause hypersensitive reactions? |
penicillin and asprin/NSAIDS |
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how do drug reactions happen? |
Haptens bind to antipbodies causing an allerigcl reaction |
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what are three symptoms of latex allergy? |
irritant contact dermatitis (gradual onset over days)
allergic contact dermatitis (type IV, over 6-48 hours)
immediate type I hypersensitivity |
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kind of allergic reaction with gradual onset, over days, caused by hand washing, occlusion, antisepics, and glove chemicals; symptoms include redness, cracks, fissures and scaling |
irritant contact dermatitis |
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allergic reaction with onset of six to 48 hours after contact, caused by chemicals; symptoms include erythema, vesicles, papules, pruritus, blisters, crusting |
Type IV hypersensivity |
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allergic reaction characterized by onset within minutes, very rarely longer than two hours, caused by latex; symptoms include local and generalized urticaria, feeling of faintness, feeling of impending doom, angioedema, nausea, vomiting, abdominal cramps, rhinoconjunctivitis, bronchospasm, anaphylactic shock |
immediate type I hypersensitivity |
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children with repeated surgeries early in life especially spina bifida and urogenital disorders are suseptible to __ allergies |
latex |
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why is asthma on the rise? |
decrease in parasites makes IgE more available for allergies |
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does reducing sensitization reduce allergies? |
NO |
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describe type II hypersensitivity |
its a cytotoxic hypersensitivity caused by blood transfusion reaction, pemphigus, and goospastures syndrome
mediated by IgG, IgM, adn complement
cell is destroyed and ineffective (myasthenia, diabetes) |
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how doe hemolytic transfusion reactions occur? |
antibodis are directed against antigens on donor cells.
symptoms are due to a destruction of RBC and complement |
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what is the most frequent cause of hemolytic transfusion? |
ABO icnompatibility |
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how hemolytic transfusion reactions occur with multiple transfusions? |
antibodies become amplified over time cause RBC's to be tagged for removal by splenic macrophages |
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describe type II hypersensitivity |
an immune complex hypersensitivity where IgG or IgM bind to an antigen to form soluble immune complexes. damage occurs from neutrophils and platelets attacking tissues bound with complexes |
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describe post-streptococcal glomerulonephritis |
after infection of group A beta hemolytic strep infection (often necrotizing faciaiatis)
eynzyme on strep alters IgG
IgG combines with strep antigen depositied on teh basement membrane and activates complement |
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describe how type IV delayed hypersensitivity reactions occur |
cell mediated (cytoxitc cells directly damage, helper T cells activate cytotoxic T and macrohpages, macropahges are major cause of damage).
small molecules of hapten bind to proteins and become antigens sensitizing patients
next exposure response is over days |
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TB reactions to monotoux testinging, posion ivy, and allergy to metals, soaps, cosmetics, and topical meds are all examples of type __ allergies |
IV |
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what are three different kinds of autoimmune diseases? |
generalized (attacks many tissue types ie. SLE)
tissue specific (myasthenia gravis destroys the myoneural junction, MS destroys myelin)
Organ specific (thyroid/adrenals) |
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describe the normal immune response |
lymphocytes recognize anitgens, presents them to helper T cells which secretes cytokines to signal cytotoxic T cells to destroy the antigen |
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what are 7 features of autoimmune disease? |
tissue reponse varies, young people diseases, non-neonatal disease, mostly seen in women, non genetic, not contagious, can have vertical transmission |
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what kind of pathogen usually is thought to be a trigger of an autoimmune disease? |
viruses |
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what are three ways pathogenesis occurs in autoimmune disesase? |
T cells bypass: some antigens are able to activate the B cells primarily
T cell and B cell miscommunication: B cells may be responding to the wrong informatoin on T cells
Feedback to B cell errors: B cells become over reactive and supress the normal feedback loop |
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how does molecular mimicry cause autominnue diseases? |
antigens are very structurally similar to body tissues or cells which causes immune cells kill both the agent and teh cells. this is prolonged if the antigen can't be killed |
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what are three contoroversies about mimicry? |
infections are common, infections have become less common since hygiene and vaccinations have increased, antibotics can treat or cure infection. despite all this autoimmune diseases have increased |
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autoimmune disease that effects the ACh recepotrs on teh PSN. presents with eyelid weaknress, blurred vision, difficulty in swallowing, impaired speech, unstable gait, and respiratory failure |
myasthenia gravis |
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describe the pathogeneisis of myasthenia gravis |
tymus contains cells that resemble skeletal muscle and have receptors for ACh on their surfaces
antibodies to the receptors are produced and block reception, complement damages receptors (reduces number of ACh receptors and flattens the synaptic cleft) |
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describe the pathogenesis of guillian barre |
molecular mimicry of anti-myelin IgG antibodies directed toward infecting virus misidentifies nerves as anitgens. cuases inflammation which stimulates complement |
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__ presents as ascending tingling in hands and feet, weakness in arms and legs days to weeks after a respiratory or GI virus. children show exercise intolerance and muscle pain with exercise |
guillan barre |
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inflammatory demylinating disease of teh CNS caused by infliltration of monocytes, lymphocytes in teh parenchyma of the CNS. penetrate theBBB, elevated IgG in CSF, B cell activation |
mulitple sclerosis |
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what is one possible cause of MS? |
molecular mimicry by EBV or herpes simplex virus |
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MS is predominante in __ climates |
temperate |
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what is the pathogensis of MS? |
viral infection cuases inflammation due to interleukins and cytokines. T cels clones react with myelin destroing it |
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tingling, numbness, loss of balance, weakness in one or more limbs, and blurred/double vision are sympotms of __ of MS
fatigue, heat sensitivity, spasticity, dizziness, impaired thinking, abonrmal sensation, altered giat, tremors, difficulty, and swallowing/chewing problems are symptoms of __ of MS |
early presentation, late presentation |
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what is the pathogenesis of rheumatoid arthritis? (6) |
T cells are activated by an antigen (mycoplasma, EBV, parovirus, rubella)
cells with CD4 receptors are foudn in the synovial membrane. they cause a prolonged iflammatory response.
B cells are activated aginst the synovium forming antigen-antibody complexes which are depositied in the synovium
TNF is produced activated osteoclasts to reabsorb bone
a pannus is created in the bone composed of osteoclasts and fibroblasts
synovium thickens making it harder to supply nutrients to cartilage |
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morning stiffness, arthritis of the hands, symmetric arthritis, arthritis in 3 or more joints. (all needed)
subcutatneous nodules on bony prominenences or extensor surfaces, elevated RF, and erosioins or decalcificatoin in involved jionts on X ray area |
Reumatoid arthritis |
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how does systemic lupus erythematousus work? |
microvascular inflammation caused by defects in apoptosis. increased cell death releases contents of cell, body recognizes these as "forigen" antigens and attacke them. antigen-antibody complexes are deposeted in the skin and kidneys causing red butterfly rashes and kidney failure |
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a foreign protein that initiates an allergic reponse |
allergen |
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a foreign protein that initiates an inflammatory repsonse |
antigen |
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type II hypersensitivity is an __ response where histamine binds to teh H1 receptors in teh nose, lungs, skin, GI tract, and blood vessels. the later resonse (>6 hours is cased by stimulation of leukotrieines and prostoglandins which signal neutrohils and eosinophils keeping the allergic response going |
immediate |
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what kind of allergic reaction is anaphylactic shock? |
type I |
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how do eosinophils cause allergic reactions? |
release lytic enxymes causing damage to the epithelium and endothelium |
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who are at risk for drug allergies? |
females, adults if they have many medicaitons, have HIV, or asthma |
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feeling faint, feeling of impending doom, angioedema, nausea, vomiting, rhinoconjunctivitis, bronchospasm, and anaphylactic shock are all symptoms of a __ reaction |
type I |
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a later response 24-48 hours caused by a T driven response as they body sees chemicals as allergens. causes erythema, vesicles, pupules, pruritus, blisters, and crusting |
type IV syndrome |
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what does atopic mean? |
inheritied/predisposed allergy response having a family history.
ie. hay fever, asthma, urticaria, eczema, ectopic dermatitis
due to failure of T cell to regulate IgE causing too much IgE, mutated interluekins, and target cells having too many IgE recepotrs |
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what seperates Type IV reactions from other allergic reactions? |
type IV is not antibody mediated |
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what are the 3 kinds of "tolerance" |
autoimmune: immunological intolerance inability to discriminate between self and non-self. attacks self because it doesn't see a difference. occurs more typically in women
central: developed during ebryonic period when autoreactive lymphoctes are either eliminated or suppressed in teh primary lymphoid organs during differentiation and proliferation of immature T and B lymphocytes
peripheral tolerance: maintained in secondary lymphoid organs through teh action of regulatory T lymphoctes or antigen presenting dendritic cells |
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how does T cell education occur? |
in the thymus T cells are exposed to nonself antigens and self molecules. if they don't destroy the nonself or destory self they are destoryed. |
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describe primary immunodeficiences |
they're congenital (often sex linked)
can be from defects in stem cells causing failure to produce T and B cells
Can be caused by thymus deficiencys (failure to educate)
often suspected with sever recurrent inffections |
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sever combined immunodeficiency (SCID) is a more __ form of immunodeficiency, caused by a fialure of __ different genes. almost 50% of cases are __ linked |
severe, 8, X |
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__ causes a complete failure of lymphoid and myeloid stem cells during fetal development, is not compatible with life (fetal development is usually normal but infant is severely affected by decreased B and T lymphoctes and other phagocytes and develop severe Candidiasis, otitis, and pneumocystis) |
severe combined immunodeficiency |
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describe the primary disorders of B cell immunity |
selective genetic IgA deficiency (prone to respiratory, GI infections, milk allergies seen)
lack of normal bursal equivalent tissues (normal B differentiation and antibody production after 6 months of age)
suseptible to infections of encapsulated bacteria |
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describe primary disorders of T cell immunity |
occurs before 6 monthes of age (DiGorge syndrome from genetic thymic hypoplasia)
see failure to thirve and severe oral thrush |
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you may see post vaccination paralytic polio (with live oral poliovirus vaccine) with __ immunodeficiency |
B cell |
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describe phagocytic disorders |
inability of phagocyte to engulf and kill the pathogen
usually severe infections by common pathogens
see granuloma formation and poor wound healing |
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an acquired immunodeficiency cuased by reduced T cells |
malnutrition of protein or zinc |
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an acquired immunodeficiency cuased by chemotherapy, stroids, and antibiotics |
iatrogenic |
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an acquired immunodeficiency cuased by loss of primary defense and supression of T and B cells |
burns |
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an acquired immunodeficiency cuased by supression of T and B cells |
stress response |
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an acquired immunodeficiency cuased by decreased IgM and antibodies, reduced reponse to encapsulated bacteria |
splenectomy |
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how is HIV transmitted? |
unprotected sexual intercourse (especially anal) risk increases when gonorrhea, chlamidia, syphilis, and genital herpes are also present
shared intravenous drug needles
mother to child during birth or breastfeeding |
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with HIV co-infection is common with viruses that share the same route of infection like __ and __ |
hepatitis B or C, kaposi sarcoma |
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describe the two species of HIV |
HIV-1: orginated from chimps in Africa, common in developed world, subtypes are common (B clade)
HIV-2: lower risk of transmission, infection progresses more slowly to AIDS, rare in the developed world |
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describe the pathogenesis of HIV |
HIV virus attaches to CD4 receptor cell
HIV fuses to the cell membrane, sheds its protein coat, and unloads all the viruses its carrying.
Viral RNA is turned into DNA by reverse transcriptase
Viral DNA makes new viruses
Viruses migrate to cell surface and bud off in part of the CD4 cells membrane to exit as a new HIV virus |
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describe the pathophysiology of HIV and how it causes immunodeficency |
HIV depeletes helper T cells by killing the cell directly, having killer T cells kill it, and increasing apoptosis by natural killer cells
HIV causes increased CD4 cell turnover and defects in replication making the helper T cells less able to recognize antigens and altered B cell production |
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opportunistic infections liek cyrptococcal meningitis, toxoplasmosis, and histoplasmosis, odd bacterial infections like tuberculosis, and neoplasms like kaposis sarcoma or non-hodgkins lymphoma are all examples of infections commonly seen in people with __ |
HIV |
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how do macrophages help spread HIV? |
macrophages are the first cells infected by HIV. it hides the virus and spreads it directly to helper T cells. |
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with the help of macrophages direct contact with T cells, T cells can be infected as quickly as __ |
1 T cell every 6 hours |
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how does the gut play a role in HIV transmission |
the GI tract contains the largest immune compartment in the body (60% of lymphocytes) and is heavily affected by HIV when spread through anal sex |
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how does HIV cross the GI tract? |
direct breach, movement through epithelial cells, movement through M cells, or transport through dendritic cells |
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how is HIV spread through vaginal intercourse? |
HIV is taken into the mucosa by langerhan cells. from there its taken into the genital lymph nodes and then infects T cells |
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explain teh steps of HIV infection |
step 1: acute seroconverion langerhans cells in the skin are the 1st cellular targets of HIV, these fuse with CD4 cells and migrate deeper
a proviral reservoir is established mainly by the macrophages
the viral load is high (as CD4 count falls), symptoms in 50% of people
Step 2: asymptomatic HIV infection lasts an average of 10 years with persistent lymph nodes and skin rash, viral replication continues and HIV is infectious during this stage
Step 3: AIDS low CD4 and T cell counts, you see opportunistic infections and cancers |
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tumor of blood vessels caused by herpes virus (many times seen with people with AIDS) |
karpis sarcoma |
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what are three cancers seen with AIDS? |
burketts lymphoma, kaposis sarcoma, and anal/cervical cancer (caused by by HPV which is an AIDS defining condition) |
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what is the untreated moltality rate of AIDS? |
90% |
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wat is the general time from infectin to death of individuals with HIV |
8-10 years |
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once infection has progressed to AIDS, survival is usually less than __ if untreated |
2 years |
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what is the leading cancer in men? |
lung and bronchus |
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what are the 5 charactersitics of cancer? |
where cells continue to produce, ignore cell signals for contact inhibition, have no adhesion and b/c of that migrate, remain immature and provide no function, they don't die if they move to antoerh part of the body |
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cancer of the endothelial or ectodermal tissue or epithelial lining of organs and glands |
carcinoma |
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cancer of a mesodermal connective tissue |
sarcoma |
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cancer to lympohid tissue |
lymphoma |
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cancer of hematopoeitc cells |
leukemia |
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most cancers occur __ in life |
later |
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cancers begin as a __ |
single mutated cell |
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how do proto-oncogenes work? |
makes teh cell divde without contrls by destroying signals between the membrane and nucleus and sending out continuous signals to grow. |
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for cancer to occur you need both __ and __ |
a proto-oncogenes and an inactive tumor suppressor genes |
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genes that cause malignant transformations (either cellular or viral) |
oncogenes |
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cancer usually requries the activation of more than one __ to induce |
oncogene |
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G-quadruplex which causes a faulty replicatin of daughter cells is an example of an __ |
oncogene |
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viral oncogenes account for only __% of cancers |
20 |
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what was the first retroviral oncogene? |
src |
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__ is the retroviral oncogene that causes lymphoblastic leukemia, __ is the one that causes hairy cell leukemias, and __ is associated with B lymphocyte cancers and proliferation of kapsois sarcoma via the TAT protein |
HTLV 1, HTLV II, HTLV III |
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a viral DNA oncogene that has 80% of DNA sequences in cervical cancer |
human papilloma virus |
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cuases impaired immunity from malaria which allows the virus to alter DNA via translocations of chromosomes |
epstin barr virus |
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epstein barr virus leads to __ |
burkitts lymphoma |
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caues acute liver failure and chronic liver failure and then liver cancer in alomst all cases |
hepatitis B |
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__ viral DNA is found in virtually all cases of liver failure |
hepatitis B |
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what is the normal role of the tumor suppressor genes (p53) |
inhibit cell prliferation |
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cancers deactivated __ |
tumor suppressor genes (p53) |
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normally senses DNA damage during G1 and G2 phases. |
P53 |
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__ impairs p53 |
smoking |
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what are three cancers due to failure of suppressor genes? |
breast cancer (BRCA1 and BRCA2) pancreatic cancer (DPC4) colon cancer (APC and MADR4) |
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the breast cancer gene that can be genetically tested for |
BRACA-2 |
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what are the 6 properties of cancer cells |
excessive autonomous growth, promoting their own blood supply, failure to differentiate/dedifferentiation, ability to metastasize, ability to live forever, genetic instability |
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explain three things that give cancer cells excessive autonomous growth |
tumor cells produce growth factor, abnormal receptors signal cell division, loss of inhibitory factors |
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how does cancer promote its own blood supply? |
uses the growth factor VEGF to cause angiogensis |
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blood vessels formed via VEGF are __ |
leaky |
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when cancer cells "reverse" cellular maturation to become an earlier form of teh cell that does not have a specific function |
dedifferentiation |
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OAT cell lung cancer cells producing ACTH is an example of __ in cancer cells |
dedifferentiation |
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when cancer cells loose the ability to adhere to parent tissues and basement membranes (lack cell to cell contact inhibition) |
metastasize |
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production of __ degrades proteins in blood veessels and lymph to help cancer cells metastasize |
collagenase |
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how do cancer cells "live forever"? |
they have defective dedifferentiation causing cancer cells to perform no function and have no apoptosis |
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how do cancer cells have genetic isntability? |
there are high frequency of mutations in cell reproduction due to DNA plymerase (tumors become heterogenous) |
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what are 6 things cancer can do to a patient? |
pressure in tissues, high metabolic rate, imparied immune response, production of hormone liek tissues, invasion of tissue, destruction of tissues |
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how does are body response to cancer? |
recognize altered self cells (only certain surface antigens can be seen, killing cells that express this protien allow tumor cells without to grow) |
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__ and __ are cells that can lyse a wide variety of tumor cells |
NK and macrophages |
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what are two ways cancer cells avoid detection? |
cover surface antigens, suppress anti-tumor immune reponses |
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what is a way to detect cancers? |
teh presence of oncofetal tumor antigens (CEA) |
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what are internal factors that affect cancer |
genes and proteins |
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what are extrenal factors that affect cancer? |
enviornmental factors (UV, asbestos, cigarette smoke, life style patters) |
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only __% of cancers are heridited |
5-10 |
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inhereted cancers inovle an inheridted __ and display a __ |
single gene disorder/mutation, medelian pattern of inheritance |
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what are 4 charactersitics of hereditary cancer? |
most are caused by mutated tumor suppressor genes
most follow an autosomal dominant pattern of inheritance
occur at a younger age than expected
may be bilaterality in paired organs |
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with hereditary cancer there may be more than one __ in the same individual |
primary |
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in __ there may be a clustering of rare or unusual cancers in a family |
hereditary cancer |
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in __ there may be unique tumor sites comibnations in a family |
herediatry cancer |
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hereditary breast and ovarian cancers, familial adenomatous polyposis, neurofibibomatosis, von hippele-lindau syndrome, and li fraumeni syndrome are all examples of __ that cause hereditary cancers |
tumor suppressor gene mutations |
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what are the three germline mutations that cause hereditary cancer? |
hereditary papillary renal cell cancer (MET gene), multiple endocrine neoplasia type 2 (RET gene), familial melanoma (CDK4 gene) |
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the inadequate ingestion of protein and calories to support metabolic/growth/healing needs or loss of nutrients |
protein-energy malnutrition |
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what are three main reasons for proein energy malnutrition (PEM) |
decreased oral intake (anorexia, nausea, pain)
increased nutrient losses (malabsorption, diarrhea, bleeding)
increased nutrient needs (fever, infection, cancers, surgery/wound healing) |
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what are three results of PEM? |
consumption of stored CHO and fat, catabolism of protein |
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weight loss, slow/absent wound healining, and low albumin after 20 days, prealbumin after 5 days and total lymphocytes counts are signs and sympotoms of __ |
PEM |
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one of teh causes of increased mortality in nursing home patients |
unintentional weight loss of the elderly |
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who are at high risk for unintentional weight loss of teh eldery? |
demented who are dependent upon others for care, dpressed |
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what are three physiologic reasons for unintentional weight loss of the elderly |
incrased amounts of cholecystokinin, increased TNF, interleukins |
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less lean body mass, decreased basal metabolic rate, loss of taste, smell, and teeth, lower socioeconomic status and functional disabilities are all sings and sympotms of __ |
weight loss int eh elderly |
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what are 4 cuases of weight loss in the elderly? |
psychiatric disorders, polypharmacy, poor oral intake, cancer and benign GI disorders |
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what are 8 effects of malnutrition |
affects every organ system
slow replacement of injured itssues (dietary protein)
decreased lean muscle
decreased immunocompetence
diabetes
osteoporosis/vitamin deficincies
loss of fiber (diverticualr disease/constipation)
depression |
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a severe lack of calories, called second child disease where the second child gets breastfed, kids look like skeletons |
marasmus |
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a malnutrtion of children that is a severe lack of proteins, develop in teh 1st child where the second child is born. the child is thin but has a swollen belly |
kwashiorkor |
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what are two effects of starvation on the digestive tract? |
decreased HCl, loss of intestinal villi |
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what is an effect of starvation on the cardiovascular system? |
reduced heart size |
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what are two effects of starvation on the respiratory system |
reduced lung capacity, respiratory failure |
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what are on effect of starvation on the immune system |
loss of all cells |
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what are three effects of starvation on the reproductive system |
reduced gonad size, ammenorrhea, loss of libido |
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what are two effects of starvation on the nervous system? |
apathy/irritability, mental retardation |
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starvation can cause muscle __ |
wasting |
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what are two effects of starvation on the metabolic system |
decreased BMR, low oncotic edema |
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thin, dry, sparse skin is an affect of __ |
starvation |
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what is the ideal weight formula for men and women? |
men=106 lbs (first 5 feet) + 6 lbs for each inch +/- 1-% of body frame
women: 100 lb (first 5 feet) + 5 lbs for each inch +/- 10% of body frame |
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obesity is defined as a BMI of >__ |
25 |
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__% of obesity has genetic causes |
25-35% |
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other than genetics, what two things cause obesity? |
increased food intake, decreased energy expenditure |
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fat cells are used as a __, the cell count is constant even with weight changes. |
reservoir of energy |
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males accumulate fat __, females __ |
above the waist, below the waist |
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there are __ calories in a lb of fat |
4000 |
