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CUA / Nursing and Health Science / NURS 371 / What is a disorder of connective tissue that creates hyper elasticity

What is a disorder of connective tissue that creates hyper elasticity

What is a disorder of connective tissue that creates hyper elasticity


School: Catholic University of America
Department: Nursing and Health Science
Course: Pathophysiology
Professor: Sandra o'brian
Term: Fall 2016
Tags: adaptive immunity, Innate Immunity, immunodeficiency, cancer, and Hypersensitivity
Cost: 50
Name: NURS 371 Pathophysiology Study guide exam 1
Description: These notes are a rough fill in of the skeleton of the study guide Dr. O'Brian posted. Use this as a way to focus on what to study in your notes.
Uploaded: 09/15/2016
13 Pages 169 Views 1 Unlocks

40 multiple choice items similar to the quizzes

What is a disorder of connective tissue that creates hyper elasticity in connective tissue?

Additional study hints

Use the content guides included in the course outline

Review the study guides produced by your class mates

Reflect on the material in the quizzes

Know and be able to apply terms:

Chromosomal translocations are large changes in chromosome structure in which a  piece of one chromosome is translocated to another chromosome. Can be reciprocal or Robertsonian translocation

∙ Reciprocal translocation occurs when breaks take place in two different  chromosomes and the broken material is exchanged. The carrier with this  translocation is usually normal, but his or her offspring could have  duplications or deletions We also discuss several other topics like How do we assess psychological functioning?

∙ Robertsonian translocation- the long arms of two nonhomologous  chromosomes fuse at the centromere, forming a single chromosome. Usually  confined to chromosomes 13, 14, 15, 21, and 22 because their short arms are very small and contain no essential genetic material

What is autosomal recessive?

o The short arms are usually lost during cell divisions, but the carrier is  usually normal since the small arms are non-essential. Their offspring,  however, may have serious monosomies or trisomies.  

o Responsible for 3-5% of Down syndrome

 Ex: long arm of 21 and 14 fuse. An off spring who receives this  fusion through a gamete can receive an extra copy of the long  If you want to learn more check out What is an atomic symbol with dots placed around it to indicate the number of valence electrons?
We also discuss several other topics like What do you call kinship?

arm 21 and develop Down syndrome  

Breakage- during meiosis and mitosis, chromosomes usually maintain their  structural integrity, however chromosome breakage occasionally occurs. Some of  these break aren’t repaired in the correct way, or just remain, and can result in  altering the chromosome’s structure.

∙ Risk of breakage increases with exposure to harmful agents called clastogens (e.g. ionizing radiation, viral infections, or some types of chemicals)

What is phenylketonuria?

We also discuss several other topics like How blacks came to english colonies?

Fragile areas- an area of a chromosome that tends to break. A number of areas on  chromosomes develop distinctive breaks and gaps when cells are cultures. These  fragile sites do not appear to be related to disease, however one fragile site on the  X chromosome is associated with fragile X syndrome.  

∙ Fragile X syndrome is the second most common genetic cause of intellectual  disability (1st is Down syndrome). Females who inherit this condition may not  express it, but they can pass it on to offspring who can express it. Ordinarily a male who inherits a disease gene on the X chromosome expresses the  condition., because he only has one X.

o Males express this disorder more severely than females.

X linked recessive- will cause disease in the male, but 2 copies are needed in the  female because it is recessive and she has 2 X chromosomes. Therefore more males are affected by X linked recessive traits than females.

∙ Ex: red-green color blindness, Duchenne muscular dystrophy, hemophilia A  and B 

Autosomal aneuploidy- the presence of an abnormal number of chromosomes in a  cell (ex: person having 45 or 47). Trisomy, having an extra copy of a chromosome,  can occur for any chromosome. The best know example is trisomy of chromosome  21, which causes Down Syndrome. We also discuss several other topics like What are the 3 ways to examine relationship between technology and society?

∙ X linked aneuploidy example: Klinefelter X linked aneuploidy- individual has  at least 2 X and 1 Y chromosomes in each cell that can lead to physical and  mental impairments in males they develop female-like breasts, they are  sterile, and gynecomastia  

Autosomal dominant- diseases caused by this are rare. Affected offspring usually  produced by the union of a normal parent with an affected heterozygous parent.  Heterozygous for the disease Half the children will be heterozygous and will express the disease and half will be normal





















∙ Ex: Marfan syndrome- disorder of connective tissue that creates hyper  elasticity in connective tissue. Affected are usually tall and thin with long  extremities, largest concern is aortic rupture. We also discuss several other topics like What is deviation score?

Autosomal recessive- expression rare, but there can be numerous carriers. Some  are characterized by delayed are of onset, incomplete penetrance, and variable  expressivity.  

∙ Examples: sickle cell anemia, cystic fibrosis, PKU, Tay Sachs Diagram  below: HbA HbS= trait













o Tay Sachs disease- cause by a deficiency of the lysosomal enzyme  HexA. Onset occurs in infants aged 4-6 months. Symptoms:  

exaggerated response to loud noises, seizures, developmental  

regression, dementia and blindness. Death is almost universal at 5yrs  of age.

o Phenylketonuria (PKU)- inability to metabolize the amino acid  phenylalanine. They need a special diet in which they avoid  

phenylalanine (milk, dairy products, meat, fish, chicken, eggs, beans,  and nuts. If left untreated it can cause irreversible brain damage, if you follow the diet you can prevent brain and intellectual damage

Epigenetic changes- chemical modifications that alter the expression of genes. A  major cause of epigenetics is DNA methylation, or the attachment of a methyl group to a cytosine base. When heavy methylation is located near a gene, that gene is les  likely to be transcribed (aka silenced).  

Beckwith-Wiedemann syndrome- caused by insulin-like growth factor 2 (IGF-2)on  chromosome 11 is inherited twice from the father and none from the mother.  Manifestation would be identifiable at birth because the baby is larger than  gestational age, hypoglycemic, have a large tongue, creases in earlobes,  incomplete closure in the abdominal cavity risk for kidney tumor ∙ Upregulation of IGF-2= overgrowth  

Russell-Silver syndrome- characterized by growth retardation, proportionate short  stature, leg length discrepancy, and a small, triangular face.

∙ About 1/3 of Russell-Silver syndrome cases are caused by imprinting  abnormalities on chromosome 11p15.5 that lead to down regulation of IGF-2  and therefore diminished growth.

o Down regulation of IGF-2= undergrowth

Cellular components of Inflammation (second line of defense) and their functions

∙ Vascular epithelium becomes a principle coordinator of blood clotting and the passage of cells and fluid into tissue.

∙ Mast cells- probably the most important activators of inflammation o Mast cells are cellular bags of granules locate in the loose connective  tissues close to blood vessels Contain histamine, cytokines, and  chemotaxic factors

o Degranulation- The release of the contents of mast cell granules  o Synthesis- the new production and release of mediators in response to  a stimulus

∙ Dendritic cells- connect the innate (1st line of defense) and acquired (3rd line  of defense) immune responses

o Migrate through lymph vessels to lymph tissue and interact with T  lymphocytes to generate and acquired immune response

∙ Erythrocytes (RBC) carry oxygen to the tissues

∙ Platelets are involved with clotting

∙ Leukocytes- fight pathogens

o Granulocytes- most common leukocyte, can be three different types  Basophils

 Eosinophils- defend against parasites and regulation of vascular  mediators

 Neutrophils- predominant in early inflammation, ingests  

bacteria, dead cells, and cellular debris

o Monocytes- precursors to macrophages that are found in the tissue o Lymphocytes- participate in the innate immune response and the  acquired immune response

∙ Plasma proteins

o Complement (Produces biologically active fragments that recruit  phagocytes, activate mast cells, and destroy pathogens)  

o Coagulation (prevents the spread of infection)

o Kinin (Causes dilation of the blood vessels, pain, and smooth muscle  contraction, increases vascular permeability)

∙ Cell receptors, products

o Cytokines-intercellular signaling molecules that are secreted, bind to  specific cell membrane receptors, and regulate innate or adaptive  immunity

o Can be pro-inflammatory or anti-inflammatory in nature depending on  whether they tend to induce or inhibit the inflammatory response

Key players in immunity

∙ B lymphocytes- bone marrow derived, leave the bone marrow as incompetent in that they have the capacity to respond to antigens, but they are naïve in  that they have not yet encountered an antigen, they migrate to secondary  lymphoid organs (spleen, lymphnodes). They it goes through the clonal  selection whch is initiated when infection occurs antigens are processed by  phagocytic cells (dendritic), then they present the antigen to the B  lymphocyte, cytokines are released and then the B lymphocyte differentiates  into a plasma protein that creates antibodies.

∙ T lymphocytes- go through this same process but they can turn into T helper  cells, T regulator cells, T cytotoxic cells, or memory cells.  

∙ IgG- monomer (has just one Y)

o Most abundant class at 80-85% of the antibodies are IgG second on  scene after IgM

o Accounts for most of the protective activity against infections o Transported from mother to fetus across the placenta

o 4 different classes (1-4)

∙ IgA- dimer with a J chain (has 2 Y’s)

o Has 2 classes

 IgA- found predominantly in the blood

 IgA-2 (secretory IgA) molecules are found predominantly in  

bodily secretions (most important)- part of the secretory system ∙ IgM- pentomer (has 5 Y’s)

o Largest of the immunoglobulins

o Pentomer stabilized by a j chain

o First antibody produced during primary response to an antigen o Synthesized early in an neonatal life

∙ IgE- monomer

o Least concentrated because they defend against parasites

 It initiates an inflammatory response which attracts the  


o When produced against innocuous environmental antigens, they are a  common cause of allergies

o Accounts for allergic responses

 Process

∙ B cells interact with IGE, parasite antigen degranulates  

the mast cells which releases ECF which attaches to the  

eosinophils, the capillaries open which allows the  

eosinophils out which then attach the parasite.

∙ IgD- monomer

o Low concentration in the blood and functions as one type of B cell and  antigen receptor

Three types of immunity:

∙ Innate- natural and you’re born with it

o Includes natural barriers (physical, mechanical, and biochemical) that  form the first line of defense at the body’s surfaces

o Also includes the second lie of defense: inflammation which is  programmed to respond to tissue damage, whether the tissue is septic  or sterile.

o Includes wound healing

∙ Adaptive/Acquired immunity- third line of defense

o Active- includes the production of antibodies after the recognition of a  foreign, or even local , antigen

o Passive- when the body receives preformed antibodies or T cells from  another source.  

 Could be from maternal transmission in which the fetus receives  some immunity from the mother, but this only lasts for the first  6 months of the baby’s life.

∙ Artificial- receiving immunoglobulin  

o She gave an example where she use to have to get immunoglobulin  shots for Hep A  

o She also gave an example of if a person gets bitten by an animal who  potentially has rabies, then they get the immunoglobulin that will  prevent them from getting rabies.

Four types of Hypersensitivity reactions

1. Type 1- IgE hypersensitivity

a. Against environmental antigens (allergens) after initial exposure.  b. IgE binds to Fc receptors on surface of mast cells

c. Histamine released from mast cell degranulation

d. Most common allergic reactions are type 1 (remember IgE has to do  with allergie-e-e-es)

i. GI allergies result in nausea, vomiting, diarrhea, and abdominal  pain

ii. Skin manifestations include urticarial (hives)

iii. Mucosal allergens manifest as conjunctivitis, rhinitis, asthma  iv. Lung allergens anifest as bronchospasms, edema, and thick  secretions

2. Type 2- Tissue-Specific Hypersensitivity reactions

a. Generally reactions against a specific cell or tissue (IgM or IgG) certain cells and tissues have their own unique group of antigens b. What happens: on the surface of the specific cell type is an antigen to  which the body thinks is an invader.  

c. Environmental allergens can also bind to a specific cell and then that  cell becomes a target for type II reaction  

d. 5 mechanisms by which type II can affect cells

i. The cell is destroyed by antibodies and complement

ii. Cell destruction through phagocytosis

iii. Soluble antigen may enter the circulation and deposit on tissues, tissues destroyed by complement and neutrophil granules

iv. Antibody-dependent cell-mediated cytotoxicity (ADCC)

v. Target cell malfunction (EG graves- targets thyroid)

3. Type 3 Immune Complex- Mediated Hypersensitivity reactions a. Antigen-antibody complxes are formed in the circulation and are later  deposited in vessel walls or extravascular tissues

i. Large release of lysosomal enzymes

b. Not organ specific (differs from 2)

c. Ex: serum sickness and Arthus reaction

4. Type 4 Cell-Mediated Hypersensitivity reaction

a. Mediated by T lymphocytes and do not involve antibodies!  

b. Cytotoxic T cells attack ad destroy cellular targets directly

c. Th1 and Th17 cells produce cytokines that recruit and activate  phagocytic cells, especially macrophages

i. Examples: graft rejection, kin test for TB, allergic reactions  

resulting from contact with substances such as poison Ivy and  


ii. Can also be the cause of some autoimmune diseases

Hashimotos (usually in older women and leads to  

hyperthyroidism, goiters, and even some heart problems)

Composition of antibodies and their functions

∙ Antibodies kind of look like a Y

∙ The antigen binding fragments create the recognition sites (receptors) for  antigen determinants

∙ Fc Crystalline fragment is responsible for biologic function- can vary and  determines the function of the antibody

∙ Polypeptide chains are the top two segments of the Y

o The light chain is the outer green portion

o The heavy chain is the inner purple portion  

∙ Antigenic determinant (epitope) area of the antigen is where the antigen is  recognized by the antibody

o Once again, it is on the antigen

∙ Antigen binding site (paratope) is the place where the antigen fits into the  antibody like a lock and key (between the light and heavy chains) o Once attached, the antigen is held in place by noncovalent chemical  interactions

Primary (congenital) immune deficiency  

∙ Most are the result of a single gene defect and are generally not inherited  this means epigenetic!

∙ May appear early or late in life, and is rare but rates are increasing ∙ May lead to recurrent life-threatening infections.

∙ 3 most common deficiencies:

o Common variant

o Selective IgA

o IgG subclass

∙ Combined deficiencies result from underdevelopment of T and B lymphocytes o Ex: severe combined immunodeficiency (SCID)- results in few  detectible lymphocytes, underdeveloped thymus and absent or  reduced IgM and IgA levels

o Wiskott-Alldrich Syndrome and DiGeorge Syndrome are examples ∙ Predominantly antibody deficiencies have a defective B cell development  which may affect only one class of Antibody or several

∙ Phagocyte defects lead to Chronic Granulomatous Disease (CGD) which  causes deficient production of hydrogen peroxide and oxygen products  needed for phagocytic killing

∙ Defects in innate immunity is a defect in capacity to produce immune  responses. Can lead to chronic Mucocutaneous candidiasis (severe recurrent  yeast infections) because macrophages cannot be activated

∙ Lastly, Complement deficiencies- C3 deficiency is severe because of the  critical role C3 plays in the complement cascade results in recurrent life threatening infections

Secondary (Acquired ) immune deficiencies

∙ More common than primary deficiencies, but not often clinically relevant  because of how minor they are.

∙ Due to complications of other physiologic or pathophysiologic conditions. ∙ The immune system may be substantially suppressed, but only for a short  duration manifestations include frequent infections

o Children normaly have 6-12 infections in a year

o Adults have 2-4 infections annually when beyond these ranges, or  there is a recurrence of a rare condition, that’s when a clinician  suspects a problem.

∙ T cell deficiencies would manifest as viral, fungal, yeast, and atypical  microorganisms

o AIDS is an example it is caused by a viral disease (HIV) which  depletes the body’s T helper cells and destroys the CD4 T helpers ∙ B cell and phagocyte deficiencies  

∙ Complement deficiencies

Apoptosis vs necrosis

∙ Apoptosis- programmed cellular death and is generally how cells die at the  end of their lifecycle, they are then replaced by new cells.

o The normal way a cell breaks down is by disassembling the internal  components of the cell and the cytoskeleton. The cell then shrinks and  forms small buds and the cellular membrane does not break!

o Pathophysiological way is when the body basically consumes itself  (autophagy)

 If a person goes through starvation the body will break itself  down and recycle its nutrients.

∙ Necrosis – final result of irreversible cell damage which is more problematic  than apoptosis

o When you can’t make ATP, the Na+/K+ pump fails. Na will try to enter  the cell, water enters the cell (vacuolation) and K will rush out. Calcium enters the cell and will activate enzymes that damage the cell  

membranes and the cell will burst.

Wound healing

∙ The conclusion of inflammation

∙ Two types:

o Primary intention- wounds that heal under conditions of minimal tissue  loss and almost all of it is resolved (cut in the skin)

o Secondary intention- wounds that require a great deal more tissue  replacement (usually an open wound)

∙ The steps to wound healing

1. Inflammation- begins almost immediately. There iscoaulation in which the  bleeding stops, infiltration in which wound healing cells move into the area,  and angiogenesis in which new capillaries are formed in the area

2. Proliferation and New tissue formation- this begins 3-4 days after the incident and takes up to 2 weeks to complete

a. Granulation – red granular appearance of the wound bed due to  invasive cells, new lymphatic vessels, and new capillaries

b. Epithelialization- new cells migrate from surrounding healthy tissue starts under the clot or scab and undergoes cell differentiation to  match the cells around it

c. Requires fibroblast proliferation, collagen formation, and wound  contraction (this is when the itchiness happens

3. Remodeling and Maturation

a. This occurs a couple of weeks after the injury and may take up to 2  years to complete

b. There is a continuation of cell differentiation  

c. Sometimes scar tissue forms if the wound is avascular

∙ Sometimes wound healing doesn’t go as planned. This is what we call  Dysfunctional wound healing

o Can occur at any stage of wound healing due to many influences o Ischemia ay deprive the wound of oxygen which prolongs inflammation and there is also not enough energy being made which leads to  collagen synthesis

o Excessive bleeding increases the amount of space that must be filled  in, or a bacterial infection could occur

o Excessive fibrin deposition- fibrin isn’t reabsorbed so there are fibrin  adhesions

o There could be excessive production of collagen which lead to  hypertrophic scar (normal scar) or Keloid scar (raised and past the  boundaries of the wound)

o Dehiscence- when the wound pulls apart at suture line

o Impaired contraction in which there is excessive contraction- can leave  joints hard to move

Autoimmunity and alloimmunity

∙ Autoimmunity is a disturbance in the immunologic tolerance ofsel-antigens body recognizes itself as foreign.

o They occur when the immune systemsreactsto its own self-antigen to  such a degree that autoantibodies or autoreactive T cells damage the  individual’s tissues more prevalent in women

∙ Alloimmunity occurs when the immune sytem of one individual produces an  immunologic reaction against tissues of another individual i.e. transfusions,  r fetus during pregnancy

ABO and Rh

∙ Blood type A has A antigens on the erythrocyte and Anti B antibodies floating  around.

∙ B had B antigens and anti-A antibodies

∙ AB expresses both A and B antigens but has no antibodies  

o Because this blood type lacks both anti-A and anti-B antibodies, they  are known as universal recipients

∙ O expresses neither A or B antigen and has both anti-A and anti-B antibodies  in the serum.

o Because people with this blood type lack both antigens, they are  considered universal donors

∙ Rh blood group is a group of antigens expressed only in erythrocytes. Those  who express the D antigen are Rh-positive, and those who do not are Rh negative.

o Rh-negative individuals can make an IgG antibody to the D antigen  (anti-D) if exposed to Rh-positive blood type

 Hemolytic disease of the newborn is when anti-D antibodies are  made by Rh-negative mothers against erythrocytes of their Rh

positive fetuses


∙ Cancer- mutations in a single cell that grows out of control  



Grow slowly

Grow rapidly

Well-defined capsule

Not encapsulated

Not invasive


Well differentiated

Poorly differentiated

Low mitotic index

High mitotic index

Do not metastasize

Can spread distantly  (metastasis)

∙ Cancer is predominantly a disease of aging and multiple mutations are  required before cancer can develop

o 2 genetic events give rise to genetic mutations that may result in  cancer (uncontrolled cell proliferation

 1) genetic overstimulation (sustained proliferative signaling) of  a dominant gene, called a proto-oncogene

∙ Proto-oncogenes regulate normal cell processes and  

promotes growth. If there is a mutation in these genes,  

they act as oncogenes- mutations may result from  

carcinogenesis of oncogenic viruses

 2) inhibited oncogenes process

∙ Normally tumor suppressor genes suppress tumor growth.

∙ As a result of mutations in the tumor suppressor gene  

mutations, they lose the ability to suppress this growth

The 10 Hallmarks of cancer

∙ Sustained Proliferative signaling

∙ Avoiding immune destruction

∙ Evading growth suppressors- mutation (inactivation) of tumor-suppressor  genes which allows unregulated cellular growth

∙ Enabling cell immortality- telomeres are protective caps on each chromosome and are held in place by telomerase. Cancer cells activate telomerase so that  they go through unlimited cell divisions and proliferation.

∙ Tumor promoting inflammation- chronic inflammation is an important factor in the development of cancer

∙ Activating invasion and metastasis

∙ Genomic instability- increased tendency for genomic mutations during life  cycle of the cell so the risk for cancer increases

o There are mutations in caretaker genes which are involved in repairing  damaged DNA

o Instability may result from increased silencing or modulation of gene  functioning’

o Chromosome instability

∙ Inducing angiogenesis- advanced cancer cells can secrete angiogenic factors  (VEGF) Vascular endothelial GF, platelet-derived GF, basic fibroblast GF  which helps form capillaries and vessels in the cancer

∙ Resisting cell death- cancer cells ignore signaling for programmed cell death ∙ Deregulating cellular energetics- Warburg effect activated by oncogenes and mutant tumor suppressors. Some cancer cells have developed mechanisms  to use oxidative phosphorylation and glycolysis.


Environmental factors and behaviors associated with cancer

∙ Tobacco use- cigarette smoking is carcinogenic and remains the most  important cause of cancer.

o Causes cancer in more than 15 organ sites, and exposure to  secondhand smoke (or environmental tobacco smoke) and parental  smoking causes cancer in other people.

o It is the largest preventable cause of cancer!

o Linked to cancer of the lung, upper aerodigestive tract (oral cavity,  pharynx, larynx, nasal cavity, paranasal sinus, esophagus, and  

stomach), the lower urinary tract, kidney, pancreas, cervix, and uterus, as well as myeloid leukemia  

∙ Diet and nutrition- affect development of cancer due to the variety of foods  eaten, the many constituents of food, the metabolic consequences of eating,  and the temporal changes in the pattern of food use.

o Dietary sources of carcinogenic substances comes from cooking of fat,  meat, or protein and naturally occurring carcinogens associated with  pant food substances, such as alkaloids or mold byproducts.

o Nutrition has a large effect on the cell cycle, the balance between cell  death and cell proliferation, cell differentiation, genes, cell signaling,  and much more.

∙ Obesity- risk factor for cancers of the endometrium, colorectum, kidney,  esophagus, breast, and pancreas.

o Also a poor prognostic factor for most cancers

o Influences insulin-like growth factor 1, sex hormones, and adipokines all linked to metabolic dysregulation of adipose tissue and endocrine  and paracrine altered signaling of adipose tissue in obesity.

∙ Alcohol consumption- linkage between excessive alcohol consumption and  cancers of the mouth, pharynx, larynx, esophagus, liver, colorectum, and  breast.

∙ Physical Activity- reduces the risk of breast and colon cancers and may  reduce the risk of other cancers including endometrial, lung, and prostate  cancers.

o Due to decreasing IGF levels, decreasing obesity, increasing free radial  scavenger systems, decreasing levels of circulating sex and other  hormones

o There are still many questions as to the frequency and intensity of  physical activity that has a positive effect on cancer prevention

∙ Other environmental factors: radiation (xray and ultraviolet), infection, sexual and reproductive behavior, air pollution, chemical and occupational health

Patterns of cancer in children and adolescents

∙ Rare but leading case of death from disease in children

∙ More than 15,500 children under the age of 19 were estimated to be  diagnosed with cancer in the US in 2014 slightly more prevalence in boys  than girls.

∙ Most originate from the mesodermal germ layer (layer that gives rise to  connective tissue, bone, cartilage, muscle, blood, blood vessels, gonads,  kidneys, and lymphatic system

∙ Usually sarcomas vs carcinomas in adults and usually discovered during peak growth periods

o Most childhood cancers are leukemias, sarcomas, and embryonic  tumors

 Embryonic tumors originate during intrauterine life which results in immature embryonic tissue unable to mature or differentiate  into fully developed cells

∙ Most do not demonstrate predisposing environmental factors, so it is usually  due to

o Genetic factors- chromosome abnormalities including neudoploidy,  amplification, deletions, translocations, and fragility

 Certain congenital syndromes and cancers occur together

Wilms tumor and urogenital abnormalities, Downs syndrome and leukemia

o Issues with Oncogens and tumor-suppressor genes which can lead o  Fanconi anemia and bloom syndrome

o Environmental factors usually include prenatal exposure to  drugs/tobacco smoke and ionizing radiation (x-rays, CT scans,  radioisotopes, etc.) and also childhood exposure to drugs, EMFs and  viruses

∙ Prognosis- more than 0% of children are cured, survival rates are higher in  children under 15 years because younger children are more likely to be  enrolled in clinical trials

o Survivors have an increased risk of cancer later in life* due to lingering effects of chemotherapy and radiation.

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