Test 1 Flashcards
how is patho related to nursing
it is the foundation upon which all nursing is built
pathophysiology
the study of what happens when normal anatomy and physiology goes wrong
what does understanding patho provide us with?
insight to why patients look the way they do when they have a certain disease, why medicines we give them work, why the side effects of treatment occur, why complications transpire, will assist the nurse to better anticipate situations, correct issues, and provide appropriate care
why does cellular adaptation occur?
in an effort to maintain homeostasis, so the cell can survive
decrease in cell size, usually to decreased work load
atrophy
what things cause atrophy?
decreased work load, ischemia, decreased nutrition, decreased hormone stimulation in some organs
where is atrophy common?
in skeletal muscle
increase in cell size
hypertrophy
what are the two types of hypertrophy and what is an example of each?
normal or physiologic - muscle enlargement with working out
abnormal or pathologic - hypertension enlarging the heart
what happens to the size of the structure when it goes through hypertrophy?
usually, the entire structure size is increased
increase in the number of cells
hyperplasia
what are common reasons for hyperplasia?
wound healing and liver regineration
not a true adaptive change. causes changes in the size, shape, and organization
dysplasia
type of cellular adaptation that is considered “precancerous”
dysplasia
is dysplasia reverisble?
yes if the stimulus is removed, some changes can be reversed
where is dysplasia common?
in the respiratory and reproductive tracts
reversible replacement of one mature cell by another?
metaplasia
where is metaplasia common and why?
common in the respiratory tract because pcce can’t withstand the harsh environment so the pcce cells are replaced with epithelial cells that are tougher and more protective. this can become a problem because the epithelial cells don’t have mucous or cilia
what is the rule for metaplastic changes?
changes will stay within the same cell type. epithelial cells won’t change into nervous system cells
do metaplastic changes lead to cancerous changes?
no, but they will likely occur if the stimulus is not removed. pathological changes.
when does cellular injury or death occur?
when the cell is unable to maintain homeostasis
what are some causes of cellular injury?
chemicals, decreased oxygen supply, infection, radiation, nutritional problems, many more
programmed cell death/ cell suicide. cells shrink up and die
apoptosis
is apoptosis a normal process?
yes it needs to happen
decreased blood flow to tissue or organs that causes cellular injury and death.
ischemia
cellular death in which the cells swell
necrosis
what is cancer?
a disease of problems with cellular growth, division, and differentiation
new growth or neoplasm
tumor
are all tumors cancerous
no
what types of tumors are cancerous and which types are not?
malignant tumors are cancerous tumors
benign tumors are not cancerous
can benign tumors cause the body problems?
yes, they can still be detrimental depending on their placement and size
malignant tumor or neoplasm
cancer
what are the differences between benign tumors and malignant tumors with regards to growth?
benign tumors grow relatively slow, they are an expanding mass that is frequently encapsulated
malignant tumors grow rapidly, cells do not adhere and they infiltrate other tissues, they are not encapsulated
what are the differences in the cells in benign and malignant tumors?
benign tumor cells are similar to normal cels, differentiated and mitosis is fairly normal
malignant tumor cells are varied in size and shape, many are undifferentiated, mitosis is increased and atypical
what is the difference between benign tumors and malignant tumors in the way they spread?
benign tumors remain localized
malignant tumors invade nearby tissue or metastasize to distant sites through blood and lymph vessels
what are the systemic effects of benign tumors vs malignant tumors?
with benign tumors, systemic effects are rare because they usually stay where they are
with malignant tumors systemic effects are common
when are benign tumors life threatening?
when they are in certain locations like the brain
are malignant tumors life threatening?
yes, through tissue destruction and spread
what are the seven warning signs of cancer?
change in bowel or bladder habits, a sore that does not heal, unusual bleeding or discharge, thickening lump, indigestion or difficulty swallowing, obvious change in wart or mole
nagging cough or hoarseness
are the seven warning signs of cancer used to diagnose cancer?
no, but they are an indicator that further investigation is needed
what are the clinical manifestations of cancer?
pain, fatigue, cachexia, anemia, leukopenia, infection
what can cause pain in cancer patients?
pressure on other structures, blocking or obstructing of flow of normal body fluids and content
why is fatigue seen in cancer patients?
can be the result of the disease process or the treatments
what is cachexia, who is it most often seen with?
severe wasting away, often due to malnutrition in terminal cancer patients. characterized by dropping weight very quickly
what is anemia and why is it seen in cancer patients?
it is a lack of red blood cells that causes the body to not get the oxygen that it needs. can be related to the cancer process depending on the type or to the treatment of the cancer.
leukopenia
decreased white blood cell count
thrombocytopenia
decreased platelents
what can leukopenia and thrombocytopenia cause?
infection
what does the staging of cancers have to do with?
its spread
does one staging system work for all types of cancer?
no, many different types have their own unique staging systems
what are the four stages of cancer?
stage 1 - confined to the organ of origin, hasn’t metastasized
stage 2 - locally invasive, has spread, but not much
stage 3 - spread to regional structures, such as lymph nodes
stage 4 - cancer has spread to distant sites
what is the tumor staging system?
T - tumor spread. number indicates size of tumor and its local extent
N - node involvement. number indicates how many nodes are involved
M - metastasized. number indicates extent of spread
substances produced by both benign and malignant tumor cells
tumor cell markers
what are tumor cell markers used for?
to screen and identify individuals at risk for cancer, to help diagnose the specific type of tumors in individuals, to follow the clinical course of cancer
how do tumor cell markers tell people who are at risk for cancer?
those who have elevated levels are at risk
how do tumor cell markers hep diagnose the specific type of tumors in individuals?
by guiding us to where the cancer may be
what do tumor cell markers have to do with the clinical course of cancer?
positive treatment should cause levels of them to go down
what are some treatment options for cancer?
chemotherapy, radiation, surgery, immunotherapy, hormone therapy, hyperthermia, stem cell transplant, lasers
the study of heredity
genetics
basic units of inheritance, blueprints of proteins in the body
genes
what are the three components of DNA
deoxyribose
phosphate molecule
nitrogenous base
what is a nucleotide made of?
sugar, phosphate and a base
how many chromosomes do humans have?
46 chromosomes in 23 pairs
22 pairs of autosomes, 1 pair of gametes
what types of cells are gametes?
sperm and ovum
which cells are haploid and which are diploid
gametes are haploid
autosomes are diploid
visualization of a persons chromosomes
karyotype
is it possible to have an abnormal genotype, but a normal phenotype
yes
carries a gene for a disease without having the disease
carrier
is it possible to be a carrier of a dominant disease process?
no. if the gene for that disease is there, it will be manifested no matter what
do homozygous people have worse cases of autosomal dominant disorders than heterozygous people?
they tend to because it is like they have a “double dose” of the disease
what causes Marfan Syndrome?
single gene mutation on chromosome 15
what does the gene mutation in Marfan syndrome cause?
causes elastin and collagen defects which lead to ocular, skeletal, and cardiovascular disorders
what are the clinical manifestations for Marfan Syndrome?
increased height, long extremities, arachnodactyly, sternum defects (funnel chest or pigeon breast), chest asymmetry, spine deformities (scoliosis or kyphosis), flat feet, hypotonia and increased joint flexibility, high arched palate, crowded teeth, small lower jaw, thin, narrow face, nearsightedness and lens displacement, valvular defects, coarctation of the aorta
what is the most life threatening clinical manifestation of Marfan syndrome?
coarctation of the aorta
what are the valvular defects that occur with Marfan syndrome?
redundancy of leaflets, stretching of the chordae tendinae, mitral valve regurgitations, aortic regurgitations
what does lens displacement mean and what is it seen with?
the lens is not in the normal position on the eye. seen with Marfan syndrome
what is coarctation of the aorta?
narrowing of a portion of the aorta - most life threatening problem seen with Marfan syndrome
what are the complications that can occur with Marfan syndrome?
weak joints and ligaments that are prone to injury, cataracts, retinal detachment, severe mitral regurgitation, spontaneous pneumothorax, inguinal hernia
how is Marfan syndrome diagnosed?
through a thorough history and physical exam that would reveal lens displacement and other symptoms of the disease, skin biopsy that would be positive for fibrillin, x-rays to confirm skeletal abnormalities, an ecg to reveal cardiac abnormality, dna analysis for the gene.
is Marfan syndrome usually present in the patient’s family history?
yes, but as many as 30% of cases are spontaneous
what are the treatments for Marfan syndrome?
usually focus on alleviating symptoms. surgical repair of aneurysms and valvular defects, surgical correction of ocular deformities, steroid and sex hormone therapy to aid in closure of long-bones and limit height, beta-adrenergic blockers to limit complications from cardiac deformities, bracing and physical therapy for mild scoliosis and surgical correction for severe cases
disease that involves neurogenic tumors that arise from schwann cells
neurofibromatosis
what are the types of neurofibromatosis and what is the difference?
type 1 - involves the skin, cutaneous lesions that may include raised lumps, cafe au lait spots, and freckling. caused by mutation on chromosome 17
type 2 - bilateral acoustic tumors (8th cranial nerve) that cause hearing loss. caused by a mutation on chromosome 22
is there a cure of neurofibromatosis?
no
is neurofibromatosis inherited?
yes, but 30-50% of cases occur spontaneously
what are issues that may develop with type 1 neurofibromatosis?
small risk that the lesions may develop into cancer, ocular problems, scoliosis, and bone defects may also be problems
an increased incidence of what is associated with neurofibromatosis?
learning disabilities and seizure disorders
do homozygous dominant people have an autosomal recessive disease?
no. nor are they carriers
how can you be a carrier for an autosomal recessive disorder?
if you are heterozygous. you have the trait, but your more influential allele is normal
how can a person have an autosomal recessive disorder?
if they are homozygous recessive for the disease
what are some examples of autosomal recessive disorders?
PKU and sickle cell anemia
PKU is due to a mutation on what chromosome?
chromosome 12
an inherited metabolic disorder in which the person cannot metabolize phenylalanine?
phenylketouria
why is it a problem that people with PKU cannot metabolize phenylalanine
it is an essential amino acid that is obtained through eating. if we cannot metabolize it, it cannot be broken down and levels start to accumulate leading to toxic levels of phenylalanine in the blood, causing central nervous system damage
if untreated, what can PKU lead to?
severe intellectual disability
why are newborns screened for PKU?
because symptoms develop slowly and can go undetected. untreated cases almost always lead to intellectual disability
how are newborns screened and when?
shortly after birth by testing for high serum phenylalanine levels
what are the clinical manifestations of PKU?
failure to meet milestones, microcephaly, progressive neurological decline, seizures, hyperactivity, electrocardiograph abnormalities, learning disability, mousy smelling urine skin hair and sweat, eczema
treatment for PKU
diet low in phenylalanine - avoid proteins and minimize starches, oral medications to lower phenylalanine, gene therapy
who needs to be educated on diet regulations for a child with PKU?
both the parents and the child
most sex-linked disorders are linked to what chromosome?
the x chromosome
who is more often affected by sex-linked disorders and why?
men are more often effected because they only have one X, so if it is present, it will be manifested. women are more often carriers because they have two Xs
X-linked dominant disorder associated with a single trinucleotide gene sequence (FMR1) on the X chromosome, which leads to failure to express a protein necessary for neural tube development
fragile X syndrome
what are the clinical manifestations of fragile x syndrome, and which one is the most common?
intellectual, behavioral, and learning disabilities; prominent jaw and forehead; long, narrow face with long or large ears; connective tissue abnormalities; large testes; hyperactivity; siezures; speech and language delays; tendency to avoid eye contact
mental retardation is the most common manifestation
what is the most common form of inherited intellectual and developmental disabilities?
fragile x syndrome
what disease is fragile x syndrome most like?
autism
what does diagnosis of fragile x syndrome consist of?
identification of clinical manifestations and a positive genetic test
is there a cure for fragile x syndrome?
no, treatment focuses on controlling individual symptoms
what supportive interventions are recommended for fragile x syndrome?
behavioral and psychological support for parents and child. speech, physical, and occupational therapy
what happens to the chromosomes in fragile x syndrome?
areas on the chromosomes develop breaks and gaps
what do chromosomal disorders result from most often?
alteration in chromosomal duplication or number
when are chromosomal disorders most often caused?
in utero due to some environmental influences (maternal age, drugs, and infections)
what is another name for trisomy 21?
down syndrome
what causes down syndrom?
three copies of chromosome 21
who is trisomy 21 most likely to affect?
the offspring of women over 35
what increases the risk of trisomy 21?
greater maternal age and environmental teratogen exposure
when are the clinical manifestations of trisomy 21 apparent?
at birth
what are the clinical manifestations of Down syndrome?
hypotonia (low muscle tone), distinctive facial features, single crease on the palm (simean crease), white spots on the iris, intellectual disability, congenital heart defects, strabismus (lazy eye) and cataracts, poorly developed genitalia and delayed puberty, tend to be shorter
what are the distinctive facial features that occur with Down syndrome?
low nasal bridge, epicanthal folds, protruding tongue, low-set ears, small,open mouth, eyes tend to slant upward
what number of patients with Down syndrome also have cardiac abnormalities?
1/3 to 1/2 of patients
what is there an increased likely hood of developing with Down syndrome?
leukemia
what are some chromosomal disorders?
trisomy 21 (Down syndrome), monosomy x (turner’s syndrome), polysomy x (klinefelter’s syndrome)
the result of deletion of part or all of an X chromosome
turner’s syndrome
monosomy x
turner’s syndrome
how many births does turner’s syndrome affect, what gender does it affect, and why?
affects 1 in 2,000 live births. only affects females because a male baby cannot live with only a Y chromosome and survive - there is very little genetic material on the Y chromosome
are most babies with turner’s syndrome carried to term?
no, most don’t survive. usually ends in a miscairrage, or spontaneous abortion.
what are the clinical manifestations of turner’s syndrome?
gonadal streaks instead of ovaries - no menstruation, short stature, lymphedema (swelling) of the hands and feet, broad chest with widely spaced nipples, low-set ears, small lower jaw, drooping eyelids, increased weight, small fingernails, webbing of the neck, coarctation of the aorta, horseshoe kidney, visual disturbances, ear infections, hearing loss, reduced bone mass which increases risk for fractures
how is turner’s syndrome usually treated?
through administration of female sex hormones to promote development of secondary sex characteristics and skeletal growth, growth hormones may be administered to improve skeletal growth
when is turner’s syndrome usually identified when symptoms are more subtle? what can confirm the diagnosis?
usually not identified until late childhood or early adolescence, chromosomal analysis can confirm the diagnosis
what does early treatment of turners syndrome allow for?
early hormone replacement to minimize problems and detect complications
polysomy x is also called…
klinefelter’s syndrome
what is klinefelter’s syndrome
a chromosomal abnormality that results in an extra X chromosome so that a person has XXY
does klinefelter’s syndrome affect men or women?
men because of the presence of the Y chromosome
when does klinefelter’s syndrome usually become apparent, and why?
usually becomes apparent at puberty because the testicles fail to mature. boys are rendered infertile because of this
how many chromosomes do a person with turner’s syndrome have? klinefelter’s syndrome?
turner’s syndrome - 45
klinefelter’s syndrome - 47
what are the clinical manifestations of klinefelter’s syndrome?
small penis, prostate gland, and testicles; sparse facial and body hair; gynecomastia (female-like breasts); sexual dysfunction (impotence, decreased libido); long legs with a short, obese trunk; tall stature; behavioral problems; learning disabilities; increased incidence of pulmonary disease and varicose veins; tend to have high-pitched voice; usually sterile
what are some problems that can develop with klinefelter’s syndrome?
osteoporosis and breast cancer
what are the diagnostic procedures for klinefelter’s syndrome?
history, physical exam, hormone levels, and chromosomal testing.
treatments for klinefelter’s syndrome
male hormone replacement to promote secondary sex characteristics, mastectomy in cases of gynecomastia and breast cancer. psychological counseling may helpful for patient and parents
general adaptation syndrome
a cluster of systemic manifestations that represent an attempt to cope with a stressor
what are the three stages of the general adaptation syndrome?
alarm stage, resistance stage, exhaustion stage
what occurs during the alarm stage of the general adaptation syndrome?
generalized stimulation of the sympathetic nervous system resulting in the release of catecholamine and corisol - fight or flight response initiated
what occurs during the resistance stage of the general adaptation syndrome?
the body chooses the most effective or advantageous defense. sympathetic system returns to normal and fight or flight disappears, body either adapts or alters its workings in an attempt to limit problems or become desensitized to the stressor. - stress management techniques can help here
what occurs during the exhaustion stage of the general adaptation syndrome?
the stressor is prolonged or overwhelms the body. body becomes depleted and damage may appear because homeostasis cannot be maintained. disease or death results due to the utilization of the body’s defenses
what are some diseases/ailments that have been attributed to stress?
anxiety, depression, headaches, insomnia, infections, cardiovascular disease
what is the local adaptation syndrome?
a localized version of the general adaptation syndrome in which the body attempts to limit the damage associated by the stressory by confining it to one location
what is an example of the local adaptation syndrome?
inflammatory reactions to tissue trauma
what are factors that affect the stress response?
genetics, age, gender, life experiences, dietary status, social support
what can help to limit or eliminate the negative aspects of stress?
implementation of one or more positive coping strategies
an antibody made by the immune system that attacks an individual’s own proteins
autoantibodies
what does the body’s first line of defense consist of?
physical and chemical barriers - skin and mucous membranes
what are the physical aspects of the first line of defense?
skin - way cells are pushed to the surface when they die, waterproof, normal flora that resides on the skin
mucous membranes
what are the chemical aspects of the body’s first line of defense?
perspiration. hydrochloric acid protects against ingested microorganisms. skin is slightly acidic which prevents bacterial growth, tears and saliva contain lysozyme which is an enzyme that destroys bacterial walls
is the first line of defense specific against pathogens?
no, doesn’t distinguish between them or give a different response based on the type of pathogen present
how does the first line of defense distinguish cell from nonself?
it allows normal flora to be present on the skin, while getting rid of pathogens that are not normal
what is the body’s second line of defense?
inflammation
when does inflammation occur?
immediately after there has been a breach in the body’s first line of defense
what things, other than inflammation are included in the body’s second line of defense?
pyrogens, interferons, and complement proteins
what things trigger the body’s second line of defense?
injuries and trauma, the presence of microorganisms
is inflammation specific to the microorganism?
no
what triggers the inflammation response?
a set of mediators or mast cells - histamines and prostaglandins
what is the role of histamines?
they are a potent vasodilator that cause vessels to open up, and increase the permeability of vessels so that cells and fluid can leak out into the tissues. they contain a chemotactic factor that attracts white blood cells to where they need to be
what are the steps of inflammation?
mast cells trigger a response, arterioles in the area vasoconstrict to limit bleeding and the extent of injury, vasodilation immediately follow to allow essential immune cells, nutrients and oxygen to enter the area and to dilute toxins. capillary permeability increases. endothelial cells react to biochemical mediators that cause vessels to retract allowing leukocytes enough room to enter the interstitial fluid. leukocytes begin phagocytizing foreign substances and cellular debris in order to clean the area up. fibrinogen is formed into fibrin which walls off the area and keeps the foreign invaders contained. a meshwork of new cells form to provide support for the healing process. blood clotting begins if any vessels have been damaged
what are the classic symptoms of inflammation?
erythema, edema, heat, pain, and loss of function - can be due to pain or edema
what are the white blood cells that participate in inflammation?
neutrophils, monocytes, and eosinophils
what are the first WBCs to enter an area of injury or invasion?
neutrophils
what is the neutrophil’s life span and what happens to them after they die?
a few hours - a few days. when they die they usually become part of pus or exudate from the wound
what are macrophages?
mature monocytes
at what point during the inflammatory process do monocytes and macrophages usually enter the area?
about 24 hours in
what WBC levels would we expect to be higher in an infection that has been going on for a while?
monocytes and macrophages
WBC that is usually present during an allergic reaction or parasitic infection.
eosinophil
what are the benefits of inflammation?
limit and control tissue damage by preventing the spread of foreign substances to healthy tissues, keeps the damage contained. prevents and limits further infection and damage - immediately starts to take care of it and start the healing process. initiates adaptive immune response, innate healing
what are pyrogens?
proteins released by macrophages that have been exposed to bacteria. they travel to the hypothalamus and raise it’s set point causing a fever
why are fevers helpful?
mild fevers can cause the spleen and liver to remove iron from the blood which is necessary for bacterial reproduction, increases metabolism which facilitates healing and phagocytosis accelerates
what can happen if a fever becomes too high? what is considered a dangerous level for a fever?
high fevers can denature proteins, especially enzymes needed for biochemical reactions. 105 is considered a dangerous fever
what are interferons?
small proteins released from cells infected by viruses. they travel to neighboring cells and let them know there is an invasion going on. by binding to the uninfected cells they trigger the synthesis of enzymes that are capable of breaking down viral messenger RNA, and so they inhibit viral replication. when the virus enters the cell it cannot replicate or spread
do interferons protect cells that are already infected with a virus?
no, only uninfected cells
when do complement proteins become activated?
when foreign substances enter the body
what are some functions of complement proteins?
plasma protein embeds in the membrane of bacterial cells, allowing fluid to enter the cell and causing them to lyse, some stimulate vasodilation, some increase the permeability of vessels, some trigger chemotaxis, some bind to microbes and create a rough coat to aid in phagocytosis
what is the body’s third line of defense? is it specific or nonspecific?
the body’s immune system. specific.
why are immunizations given prior to flu season?
because the immune system is slower to respond, but has memory
what are the two major types of T cells?
regulator and effector/killer cells
what are the two types of regulator T cells and what are their purposes?
helper cells - activate or call up B cells to produce antibodies
suppressor cells - turn antibody production off
what is the purpose of effector/killer/cytotoxic cells?
destroy cells infected with viruses by releasing lymphokines that degrade cell walls
what type of cells are responsible for hypersensitivity and transplant rejections?
T cells
which cells participate in cell mediated immunity and which ones participate in humoral immunity
cell mediated immunity - T cells
humoral immunity - B cells
where are T cells produced and where do they mature? what about B cells?
T cells are produced in the bone marrow and mature in the thymus
B cells are produced in the bone marrow and mature there
what type of cell produces antibodies?
plasma B cells