Test 1 Flashcards
(472 cards)
0
Q
how is patho related to nursing
A
it is the foundation upon which all nursing is built
1
Q
pathophysiology
A
the study of what happens when normal anatomy and physiology goes wrong
2
Q
what does understanding patho provide us with?
A
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
3
Q
why does cellular adaptation occur?
A
in an effort to maintain homeostasis, so the cell can survive
4
Q
decrease in cell size, usually to decreased work load
A
atrophy
5
Q
what things cause atrophy?
A
decreased work load, ischemia, decreased nutrition, decreased hormone stimulation in some organs
6
Q
where is atrophy common?
A
in skeletal muscle
7
Q
increase in cell size
A
hypertrophy
8
Q
what are the two types of hypertrophy and what is an example of each?
A
normal or physiologic - muscle enlargement with working out
abnormal or pathologic - hypertension enlarging the heart
9
Q
what happens to the size of the structure when it goes through hypertrophy?
A
usually, the entire structure size is increased
10
Q
increase in the number of cells
A
hyperplasia
11
Q
what are common reasons for hyperplasia?
A
wound healing and liver regineration
12
Q
not a true adaptive change. causes changes in the size, shape, and organization
A
dysplasia
13
Q
type of cellular adaptation that is considered “precancerous”
A
dysplasia
14
Q
is dysplasia reverisble?
A
yes if the stimulus is removed, some changes can be reversed
15
Q
where is dysplasia common?
A
in the respiratory and reproductive tracts
16
Q
reversible replacement of one mature cell by another?
A
metaplasia
17
Q
where is metaplasia common and why?
A
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
18
Q
what is the rule for metaplastic changes?
A
changes will stay within the same cell type. epithelial cells won’t change into nervous system cells
19
Q
do metaplastic changes lead to cancerous changes?
A
no, but they will likely occur if the stimulus is not removed. pathological changes.
20
Q
when does cellular injury or death occur?
A
when the cell is unable to maintain homeostasis
21
Q
what are some causes of cellular injury?
A
chemicals, decreased oxygen supply, infection, radiation, nutritional problems, many more
22
Q
programmed cell death/ cell suicide. cells shrink up and die
A
apoptosis
23
Q
is apoptosis a normal process?
A
yes it needs to happen
24
decreased blood flow to tissue or organs that causes cellular injury and death.
ischemia
25
cellular death in which the cells swell
necrosis
26
what is cancer?
a disease of problems with cellular growth, division, and differentiation
27
new growth or neoplasm
tumor
28
are all tumors cancerous
no
29
what types of tumors are cancerous and which types are not?
malignant tumors are cancerous tumors
| benign tumors are not cancerous
30
can benign tumors cause the body problems?
yes, they can still be detrimental depending on their placement and size
31
malignant tumor or neoplasm
cancer
32
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
33
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
34
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
35
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
36
when are benign tumors life threatening?
when they are in certain locations like the brain
37
are malignant tumors life threatening?
yes, through tissue destruction and spread
38
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
39
are the seven warning signs of cancer used to diagnose cancer?
no, but they are an indicator that further investigation is needed
40
what are the clinical manifestations of cancer?
pain, fatigue, cachexia, anemia, leukopenia, infection
41
what can cause pain in cancer patients?
pressure on other structures, blocking or obstructing of flow of normal body fluids and content
42
why is fatigue seen in cancer patients?
can be the result of the disease process or the treatments
43
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
44
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.
45
leukopenia
decreased white blood cell count
46
thrombocytopenia
decreased platelents
47
what can leukopenia and thrombocytopenia cause?
infection
48
what does the staging of cancers have to do with?
its spread
49
does one staging system work for all types of cancer?
no, many different types have their own unique staging systems
50
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
51
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
52
substances produced by both benign and malignant tumor cells
tumor cell markers
53
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
54
how do tumor cell markers tell people who are at risk for cancer?
those who have elevated levels are at risk
55
how do tumor cell markers hep diagnose the specific type of tumors in individuals?
by guiding us to where the cancer may be
56
what do tumor cell markers have to do with the clinical course of cancer?
positive treatment should cause levels of them to go down
57
what are some treatment options for cancer?
chemotherapy, radiation, surgery, immunotherapy, hormone therapy, hyperthermia, stem cell transplant, lasers
58
the study of heredity
genetics
59
basic units of inheritance, blueprints of proteins in the body
genes
60
what are the three components of DNA
deoxyribose
phosphate molecule
nitrogenous base
61
what is a nucleotide made of?
sugar, phosphate and a base
62
how many chromosomes do humans have?
46 chromosomes in 23 pairs
| 22 pairs of autosomes, 1 pair of gametes
63
what types of cells are gametes?
sperm and ovum
64
which cells are haploid and which are diploid
gametes are haploid
| autosomes are diploid
65
visualization of a persons chromosomes
karyotype
66
is it possible to have an abnormal genotype, but a normal phenotype
yes
67
carries a gene for a disease without having the disease
carrier
68
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
69
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
70
what causes Marfan Syndrome?
single gene mutation on chromosome 15
71
what does the gene mutation in Marfan syndrome cause?
causes elastin and collagen defects which lead to ocular, skeletal, and cardiovascular disorders
72
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
73
what is the most life threatening clinical manifestation of Marfan syndrome?
coarctation of the aorta
74
what are the valvular defects that occur with Marfan syndrome?
redundancy of leaflets, stretching of the chordae tendinae, mitral valve regurgitations, aortic regurgitations
75
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
76
what is coarctation of the aorta?
narrowing of a portion of the aorta - most life threatening problem seen with Marfan syndrome
77
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
78
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.
79
is Marfan syndrome usually present in the patient's family history?
yes, but as many as 30% of cases are spontaneous
80
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
81
disease that involves neurogenic tumors that arise from schwann cells
neurofibromatosis
82
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
83
is there a cure of neurofibromatosis?
no
84
is neurofibromatosis inherited?
yes, but 30-50% of cases occur spontaneously
85
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
86
an increased incidence of what is associated with neurofibromatosis?
learning disabilities and seizure disorders
87
do homozygous dominant people have an autosomal recessive disease?
no. nor are they carriers
88
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
89
how can a person have an autosomal recessive disorder?
if they are homozygous recessive for the disease
90
what are some examples of autosomal recessive disorders?
PKU and sickle cell anemia
91
PKU is due to a mutation on what chromosome?
chromosome 12
92
an inherited metabolic disorder in which the person cannot metabolize phenylalanine?
phenylketouria
93
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
94
if untreated, what can PKU lead to?
severe intellectual disability
95
why are newborns screened for PKU?
because symptoms develop slowly and can go undetected. untreated cases almost always lead to intellectual disability
96
how are newborns screened and when?
shortly after birth by testing for high serum phenylalanine levels
97
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
98
treatment for PKU
diet low in phenylalanine - avoid proteins and minimize starches, oral medications to lower phenylalanine, gene therapy
99
who needs to be educated on diet regulations for a child with PKU?
both the parents and the child
100
most sex-linked disorders are linked to what chromosome?
the x chromosome
101
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
102
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
103
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
104
what is the most common form of inherited intellectual and developmental disabilities?
fragile x syndrome
105
what disease is fragile x syndrome most like?
autism
106
what does diagnosis of fragile x syndrome consist of?
identification of clinical manifestations and a positive genetic test
107
is there a cure for fragile x syndrome?
no, treatment focuses on controlling individual symptoms
108
what supportive interventions are recommended for fragile x syndrome?
behavioral and psychological support for parents and child. speech, physical, and occupational therapy
109
what happens to the chromosomes in fragile x syndrome?
areas on the chromosomes develop breaks and gaps
110
what do chromosomal disorders result from most often?
alteration in chromosomal duplication or number
111
when are chromosomal disorders most often caused?
in utero due to some environmental influences (maternal age, drugs, and infections)
112
what is another name for trisomy 21?
down syndrome
113
what causes down syndrom?
three copies of chromosome 21
114
who is trisomy 21 most likely to affect?
the offspring of women over 35
115
what increases the risk of trisomy 21?
greater maternal age and environmental teratogen exposure
116
when are the clinical manifestations of trisomy 21 apparent?
at birth
117
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
118
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
119
what number of patients with Down syndrome also have cardiac abnormalities?
1/3 to 1/2 of patients
120
what is there an increased likely hood of developing with Down syndrome?
leukemia
121
what are some chromosomal disorders?
trisomy 21 (Down syndrome), monosomy x (turner's syndrome), polysomy x (klinefelter's syndrome)
122
the result of deletion of part or all of an X chromosome
turner's syndrome
123
monosomy x
turner's syndrome
124
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
125
are most babies with turner's syndrome carried to term?
no, most don't survive. usually ends in a miscairrage, or spontaneous abortion.
126
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
127
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
128
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
129
what does early treatment of turners syndrome allow for?
early hormone replacement to minimize problems and detect complications
130
polysomy x is also called...
klinefelter's syndrome
131
what is klinefelter's syndrome
a chromosomal abnormality that results in an extra X chromosome so that a person has XXY
132
does klinefelter's syndrome affect men or women?
men because of the presence of the Y chromosome
133
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
134
how many chromosomes do a person with turner's syndrome have? klinefelter's syndrome?
turner's syndrome - 45
| klinefelter's syndrome - 47
135
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
136
what are some problems that can develop with klinefelter's syndrome?
osteoporosis and breast cancer
137
what are the diagnostic procedures for klinefelter's syndrome?
history, physical exam, hormone levels, and chromosomal testing.
138
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
139
general adaptation syndrome
a cluster of systemic manifestations that represent an attempt to cope with a stressor
140
what are the three stages of the general adaptation syndrome?
alarm stage, resistance stage, exhaustion stage
141
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
142
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
143
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
144
what are some diseases/ailments that have been attributed to stress?
anxiety, depression, headaches, insomnia, infections, cardiovascular disease
145
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
146
what is an example of the local adaptation syndrome?
inflammatory reactions to tissue trauma
147
what are factors that affect the stress response?
genetics, age, gender, life experiences, dietary status, social support
148
what can help to limit or eliminate the negative aspects of stress?
implementation of one or more positive coping strategies
149
an antibody made by the immune system that attacks an individual's own proteins
autoantibodies
150
what does the body's first line of defense consist of?
physical and chemical barriers - skin and mucous membranes
151
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
152
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
153
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
154
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
155
what is the body's second line of defense?
inflammation
156
when does inflammation occur?
immediately after there has been a breach in the body's first line of defense
157
what things, other than inflammation are included in the body's second line of defense?
pyrogens, interferons, and complement proteins
158
what things trigger the body's second line of defense?
injuries and trauma, the presence of microorganisms
159
is inflammation specific to the microorganism?
no
160
what triggers the inflammation response?
a set of mediators or mast cells - histamines and prostaglandins
161
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
162
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
163
what are the classic symptoms of inflammation?
erythema, edema, heat, pain, and loss of function - can be due to pain or edema
164
what are the white blood cells that participate in inflammation?
neutrophils, monocytes, and eosinophils
165
what are the first WBCs to enter an area of injury or invasion?
neutrophils
166
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
167
what are macrophages?
mature monocytes
168
at what point during the inflammatory process do monocytes and macrophages usually enter the area?
about 24 hours in
169
what WBC levels would we expect to be higher in an infection that has been going on for a while?
monocytes and macrophages
170
WBC that is usually present during an allergic reaction or parasitic infection.
eosinophil
171
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
172
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
173
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
174
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
175
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
176
do interferons protect cells that are already infected with a virus?
no, only uninfected cells
177
when do complement proteins become activated?
when foreign substances enter the body
178
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
179
what is the body's third line of defense? is it specific or nonspecific?
the body's immune system. specific.
180
why are immunizations given prior to flu season?
because the immune system is slower to respond, but has memory
181
what are the two major types of T cells?
regulator and effector/killer cells
182
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
183
what is the purpose of effector/killer/cytotoxic cells?
destroy cells infected with viruses by releasing lymphokines that degrade cell walls
184
what type of cells are responsible for hypersensitivity and transplant rejections?
T cells
185
which cells participate in cell mediated immunity and which ones participate in humoral immunity
cell mediated immunity - T cells
| humoral immunity - B cells
186
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
187
what type of cell produces antibodies?
plasma B cells
188
what is the difference between T cells and B cells with regards to the way they attack the antigen?
T cells directly attack the antigen through cytotoxic T cells, while B cells indirectly attack the antigen by secreting antibodies to attack the antigen
189
what is the purpose of memory B cells?
allow faster recognition and response to an antigen
190
what are immunoglobulins used in?
humoral immune responses
191
what is IgG?
the most common antibody - 80-85% of plasma antibodies. main defense against bacteria.
192
why is IgG the main antibody found in fetal blood?
it crosses the placenta
193
which antibody is tested to see if a person has an immunity to something?
IgG
194
what is IgM?
the largest immunoglobulin. it is the first one produced in the initial response to an antigen. first antibody made by the fetus
195
which immunoglobulin tells us whether you have a current infection of something or have a recent infection with something?
IgM
196
antibody present in body secretions such as tears, saliva, and perspiration
IgA
197
least understood antibody. present in small amounts in blood serum and B cell surfaces. is a receptor for antigens and helps anchor cell membranes.
IgD
198
antibody that protects the body through its presence in mucous membranes and skin. triggers allergic reactions. also important for parasitic infections.
IgE
199
what is the difference between primary and secondary response to something, and what antibodies are most common during each?
primary response is when the antigen first enters the body. IgM levels are higher at this time
secondary response is an anamnestic immune response. IgG levels are higher
200
what are the three different T cell classifications?
helper T cells (Th)
cytotoxic T cells (Tc)
suppressor T cells
201
destroy cells with viruses or tumor cells
cytotoxic T cells
202
what two T cells do we need a balance between and what happens if there is not one?
helper T cells and suppressor T cells. if helper T cells function more than suppressor T cells, exaggerated responses occur. if suppressor T cells function more than helper T cells, the immune system weakens
203
immunity that is gained after birth
acquired immunity
204
immunity produced by the host after either a natural exposure to an antigen or immunization. long lasting or short term?
active acquired immunity - long lasting
205
immunity obtained by the transfer of preformed antibodies to the recipient passed to the individual or the host. short term or long term?
passive acquired immunity - short term
206
what are the two types of active immunity and what are the differences between them?
natural active - pathogens enter the body and cause illness. antibodies are formed.
artificial active - vaccine is injected into the body. no illness results, but antibodies are formed.
207
what are the two types of passive acquired immunity?
natural passive - antibodies are passed directly from mother to child to provide temporary protection
artificial passive - antibodies are injected into the body to provide temporary protection or to minimize the severity of an infection
208
what type of immunity has memory and what type does not?
active acquired immunity has memory, passive acquired does not
209
what is hypersensitivity?
when the immune system doesn't respond as it should
210
what are some common types of altered immune responses?
allergy, autoimmunity, alloimmunity
211
exaggerated response against environmental agents
allergies
212
what things can be environmental agents?
food, medications, pollen, doesn't just have to be something occurring in nature
213
immune response directed at one's own cells. when the immune system starts fighting the persons own body
autoimmunity
214
who are autoimmune disorders most common in?
women
215
immune response directed against beneficial foreign tissues. transfusion reactions, and when a mother's body tries to attack the fetus
alloimmunity
216
what is the difference between immediate and delayed hypersensitivity reactions?
immediate occur within minutes to hours following exposure
| delayed may take several hours
217
what is type I hypersensitivity, and what is it mediated by?
IgE mediated immediate reaction that most of our allergic reactions come from (hay fever, food allergies, anaphylaxis), IgE binds to mast cells and upon a second exposure, the antigen binds to the IgE antibodies on the mast cells, causing the mast cells degranulate and release histamine and other mediators of the inflammatory response
218
what are the clinical manifestations for type I hypersensitivity?
hives (erdecaria), itching (pruritis), angioedema (soft tissue swelling) immediate
219
what are treatments of type I hypersensitivity?
epinephrine, antihistamines, corticosteroids, ad desensitizing injections which suppress all inflammatory activity
220
what is type II hypersensitivity?
tissue or cells specific immediate reaction that has to do with IgG and IgM antibodies. these antibodies react with an antigen on the cell activating the compliment system. cell lysis and phagocytosis result.
221
what are some examples of type II hypersensitivity?
blood transfusion reactions and erythroblastosis fetalis
222
what are some treatments for type II hypersensitivity?
focus on prevention. includes insuring blood compatibility prior to infusions and administering medication to suppress immune activity and prevent maternal antibody development
223
what is type III hypersensitivity?
immune complex-mediated hypersensitivity reaction. circulating antigen-antibody complexes accumulate and are deposited in the tissue. the body then tries to destroy these complexes triggering the complement system which causes inflammation locally to wherever they were deposited, due to vasodilation, more complexes accumulate. autoimmune condition (systemic lupus)
224
what is treatment for type III hypersensitivity dependent on?
the disease
225
what is type IV hypersensitivity?
delayed reaction because it is cell mediated tissue reactions rather than antibody mediated. delayed processing of the antigen by macrophages. once processed, the antigen is presented to the T cells resulting in the release of lymphokines that cause inflammation and antigen destruction
226
what is type IV hypersensitivity seen with and what does treatment depend on?
transplant reactions, TB reactions (why you have to wait to have a TB test read), contact dermatitis. treatment is disease specific
227
what are the four types of transplant possibilities and what is each?
allogenic - tissue comes from same species as host and is of similar tissue type, but not identical - what most transplants are
autologous - host and donor are same person
syngenic - from identical twin of host
xenogenic - tissue transplant from another species
228
what are transplant rejections classified based on?
their timing
229
when do hyperacute tissue rejections occur and why?
occur immediately to three days after transplant. a complement response where the host has antibodies against the donor tissue. triggers a systemic inflammatory reaction
230
with hyperacute tissue reactions, often times the rejection occurs so fast that the new tissue did not have a chance to do what?
establish vascularization, so the tissue becomes permanently necrotic
231
what is the most common and treatable type of tissue rejection?
acute tissue rejections
232
when do acute tissue rejections occur and why?
occur four days up to three months after the transplant. cell mediated reactions result in tissue destruction or necrosis. exhibit signs and symptoms of the inflammatory response. may experience impaired function of the transplanted organ
233
when and why does chronic tissue rejection occur?
occurs four months to years after the transplant. most likely due to antibody mediated immune response where antibodies and complement molecules become deposited in the transplanted tissue walls decreasing blood flow and causing ischemia
234
what is the difference between host-vs-graft rejections and graft-vs-host rejections? which is the most common?
host-vs-graft the host is fighting the graft - most common
| graft-vs-host the graft is fighting the host
235
how and where do graft-vs-host reactions occur?
only occur with bone marrow transplants. the graft cells recognize the host cells as foreign and launch an attack. the host is usually immunocompromised and unable to fight back
236
what is crucial to reversing a rejection?
identifying it quickly by assessing manifestations of a health and unhealthy transplant
237
what are the diagnostic procedures for recognizing a transplant rejection?
lab tests to identify immune and inflammatory activity and specific tests to determine the function of the transplanted organ
238
treatment for transplant rejections
usually begins with prevention by ensuring tissue match and initiating immunosuppressive therapy. once the transplant is suspected to be rejected, immunosuppressive therapy is intensified to try and reverse it
239
occurs when the body's defenses lose the ability to recognize self and become self destructive, attacking the host
autoimmune disorders
240
what gender is most often affected by autoimmune disorders?
females
241
what are autoimmune diseases characterized by?
frequent periods of exacerbations and remissions
242
what things can trigger exacerbations?
physical and emotional stress
243
what triggers autoimmune disorders?
the mechanism that triggers the response is unclear
244
how do genetics play a role in autoimmune disorders?
if a family member is affected by an autoimmune disease, an individual has increased chances of having the disease, but it is not known to be passed down
245
what is the frequent cause of autoimmune diseases?
an abnormal stressor, either physical or psychological
246
what is do treatments for autoimmune diseases usually entail?
they are usually disease specific, but often include coping and stress management strategies to prevent exacerbations
247
chronic, inflammatory, autoimmune disorder that can affect any connective tissue
systemic lupus erythematosus
248
what is thought to happen with SLE?
B cells are thought to be activated for unknown reasons to produce autoantibodies and autoantigens which then combine to form immune complexes that fight against the body's own tissues. hyperactive T cells helper T cells and subdued suppressor T cells are thought to create a prime environment for B cells to overproduce.
249
which systems are most likely to be harmed with SLE
heart, joints, skin, lungs, blood vessels, liver, kidneys, and nervous system
250
how much more likely are women to be affected by SLE than men?
9x more likely in women than in men
251
who are the most likely to get SLE?
women, ages 15-50, Asians and African Americans
252
When is the diagnosis of SLE strongly suggested?
when the person has four or more of the 11 criteria
253
what are the 11 criteria of SLE
butterfly rash over the cheeks, skin rash of patchy redness with hyper and hypo pigmentation that can cause scarring, photosensitivity, mucous membrane ulcers, arthritis, pleuritis or pericarditis, renal abnormalities, brain irritation, blood abnormalities, immunologic disorder, immunologic disorder, antinuclear antibody
254
what is pleuritis or pericarditis?
inflammation of the lining around the heart or lungs
255
how are renal abnormalities associated with SLE detected?
abnormal amounts of urine protein or clumps of cellular elements, alled casts are detectable with a urinalysis. renal abnormalities due to lupus are the main cause of renal transplants
256
how is brain irritation manifested with sle?
through seizures or psychosis
257
what are the blood abnormalities of SLE?
low counts of white or red blood cells or platelets
258
in addition to the 11 criteria of SLE, what other tests can be helpful in evaluating patients with SLE?
tests to determine the severity of organ involvement. these tests include routine testing of the blood to detect inflammation, blood chemistry testing, direct analysis of internal body fluids, and tissue biopsies. abnormalities can further support the diagnosis
259
what does treatment for SLE consist of?
targeted at symptom management. stress reduction, exercise, and sleep. nonsterioidal anti-inflammatory drugs to reduce pain and inflammation in joints, muscle, and other tissues. corticosteroids. antimalarial drugs to treat fatigue, joint pain, rashes, and pleural inflammation by suppressing the immune system. plasmapheresis to remove antibodies and other immune substances from the blood to suppress immunity.
260
what is the difference between primary or secondary immunodeficiencies?
primary reflect a defect with the immune system
| secondary reflect an underlying disease or factor that is suppressing the immune system
261
what are the most common forms of immunodeficiency caused by?
viral infections or are iatrogenic reactions to therapeutic drugs
262
what do primary deficits involve?
developmental failures, many of which result from genetic or congenital abnormalities
263
what do secondary or acquired immunodeficiencies refer to?
a loss of immune function because of a specific cause like infection, splenectomy, hepatic disease, drug therapy, or stress
264
what are opportunistic infections?
infections caused by pathogens that do not usually cause disease in healthy individuals
265
what do opportunistic infections usually result from?
a disruption of normal flora. they are difficult to treat and can become life threatening
266
what does diagnosis of the immunodeficient state entail?
identification of recurrent or persistent infections. involve measurements of immunoglobulin levels, white blood cells, and T cell counts.
267
what does treatment of immunodeficient diseases entail?
individualized for the specific deficiency and may include gamma globulin, bone marrow transplants, or thymus transplants
268
which strain of HIV is the most common in the US, which is most common in Africa?
HIV 1 US
| HIV 2 Africa
269
how is HIV transmitted?
through direct contact with infected blood, blood products, or body fluids. it is not transmitted through saliva and kissing unless open sores are present
270
what is the chance of a mother passing HIV to their offspring , what can decrease this risk, by how much?
13-40% chance of passing it, antiretroviral therapy can decrease the risk by 68%. Retrovir is the most common drug and has a high safety index. C-section can further decrease the risk of transmission
271
how does HIV work?
once it gains access to the body it invades CD4 cells and uses an enzyme, reverse transcriptase, to convert the viral RNA to DNA. the viral DNA then becomes integrated into the CD4 cell's DNA as the infected CD4 cell reproduces, it inadvertently produces viral copies. meanwhile the CD4 cells reproduce in the cells until the point when the cell membrane is comprimised, releasing millions of viral copies into the blood stream, starting the cycle over.
272
what are the three forms that the HIV infectious process takes, what does each include?
immunodeficiency - includes opportunistic infections
autoimmunity - lymphoid interstitial pneumonitis, arthritis, and hypergammaglobulinemia
neurologic dysfunction - AIDS dementia complex, HIV encephaly, peripheral neuropathies
273
what is the first sign of HIV?
a brief period of flulike symptoms referred to as acute retroviral syndrome. may not have any more symptoms. as more and more CD4 cells are destroyed, the individual begins to have symptoms
274
how does the symptom process of HIV occur?
initial onset of flulike symptoms that disappear for a while until enought CD4 cells have been affected to begin showing symptoms (lymphopathy, diarrhea, weight loss, fever, cough, shortness of breath). over the next 10 years, serious clinical manifestations begin appearing as the individual moves into the late stage of infections
275
what manifestations can children have that are infected with HIV?
difficulty gaining weight, difficulty growing normally, problems walking, delayed mental development, severe forms of common childhood illnesses such as ear infections (otitis media), pneumonia, and tonsillitus
276
once HIV/AIDS is confirmed, what is done?
a test to predict the probable disease progression, or viral load (number of viral particles per milliliter) is done. the higher the viral load, the further the progression
277
what is the aim of antiretroviral therapy?
to reduce the viral load to a point that the body's immune system can keep the virus in check.
278
what can be an indicator of treatment success in HIV/AIDS?
an indicator of treatment success, along with other indicators
279
what two systems is the HIV infections progression classified on?
CD4 count and symptom presentation - these are used to track progression and treatment
280
what is antiretroviral therapy used for?
to control the reproduction of HIV and slow the progression of the disease to help try to prevent AIDS from developing
281
HAART
highly active antiretroviral therapy
282
what are the five approved classes of antiretroviral therapy?
nucleoside/nucleotide reverse transcriptase inhibitors, non-nucleoside reverse transcriptase inhibitors, protease inhibitors, integrase inhibitors, fusion inhibitors
283
can resistance occur to HAART?
yes if a patient does not strictly adhere to the prescribed regimen
284
what are treatments other than HAART that can treat HIV?
medications to treat specific opportunistic infections as they arise, manage the numerous drug sid effects and prevent reexposure
285
what can continued reexposure to HIV cause?
it can increase the viral load and introduce another strain - this can increase the disease's progression
286
what does prevention for HIV include?
avoiding contact with bodily fluids, avoiding activities that increase the risk to exposure to bodily secretions (drug use and multiple sexual partners) education, using condoms every time, preexposure to prophylaxis (daily antiretroviral therapy for people at high risk), male circumcision reduces male-to-female risk of transmission
287
what are at risk individuals and states that put individuals at risk for developing an impaired immune system?
very young and old, poor nutrition, impaired skin integrity, circulatory issues, alterations in normal flora due to antibiotic therapy, chronic diseases especially diabetes mellitus, corticosteroid therapy, chemotherapy, smoking, alcohol consumption, immunodeficiency states
288
what are stragegies to build a healthy immune system?
increased fluid intake, eating a well-balanced diet, increasing antioxidants and protein intake, getting adequate sleep, avoiding caffeine and refined sugar, spending time outdoors, reducing stress
289
when does disease occur with blood?
when there are too few, too many, or dysfunctional blood components
290
the process of blood formation. occurs primarily in the bone marrow.
hematopoiesis
291
plasma is a transport medium that carries what?
blood cells, antibodies, nutrients, electrolytes, hormones, lipids, and waste products
292
what does the shade of the color of blood tell us?
the hemoglobin saturation. the brighter the shade of red, the more blood that is saturated with oxygen
293
refers to how much of the blood volume comprises erythrocytes
hematocrit
294
the release of this causes a quick chain reaction that ends in clotting
thromboplastin
295
what do platelets containing contractile proteins do?
they pull the edges of a wound together
296
enzyme that dissolves clots once healing has occured
plasmin
297
what are the granulocytes?
neutrophils, basophils, and eosinophils
298
what are the normal levels of neutrophils?
3000-7000
299
what are the normal levels of eosinophils?
100-400
300
what are the normal levels of basophils?
20-50
301
what are the normal levels of monocytes?
100-700
302
what are the normal levels of lymphocytes?
1500-3000
303
what are normal white blood cell levels?
5000-10,000 cells/mL3
304
increased WBC levels
leukocytosis
305
decreased WBC levels
leukocytopenia
306
what can leukocytosis indicate?
an active infectious process
307
what can leukocytopenia indicate?
an immune deficiency state
308
what do most leukocyte disorders result from?
originate from deficiencies of one or more of the varying leukocytes
309
which cells are the first to arrive on the scene of an infection?
neutrophils. they are attracted by various chemicals released by the infected tissue
310
what do neutrophils do when they get to a site of infection?
they phagocytize microorganisms and prevent the infection from spreading
311
what happens to the infected neutrophils that die?
the become part of yellowish wound drainage (pus)
312
neutropenia
a decrease in circulating neutrophils to less than 1500
313
how does a lower neutrophil count effect the body?
the lower the neutrophil count, the less the body's ability to fight infections
314
what are causes of neutropenia?
increased usage (infection and inflammation); drug suppression (immunosuppression and chemotherapies; radiation therapy; congenital conditions (periodic or cyclic); bone marrow cancers (leukemias and lymphomas); spleen destruction; vitamin deficiency
315
what are the clinical manifestations of neutropenia?
signs and symptoms of bacterial and fungal infections. mouth ulcerations, ulcerations of the skin, vagina, and GI tract
316
what antigens do each of the blood groups have on their surfaces, what antibodies do they produce?
type A - A antignes on surface, B antibodies
type B - B antigens on surface, A antibodies
type AB - A and B antigens on surface, no antibodies
type O - no antigens on surface, A and B antibodies
317
which blood group is the universal receiver and which is the universal donor?
universal receiver - type AB
| universal donor - type O
318
homozygous dominant or heterozygous for the Rh gene are positive or negative?
Rh+
319
homozygous recessive for Rh factor are positive or negative?
Rh-
320
which Rh factor is able to receive blood that is the other type?
Rh positive can receive blood from Rh negative because Rh negative has not antigens on its surface, so there is nothing for the Rh positive blood to see as foreign. Rh negative blood cannot receive Rh positive though because Rh positive has antigens for Rh negative to see as foreign
321
what are the indicators of infection?
malaise, fever, chills, body aches
322
what are the diagnostic procedures for neutropenia?
serum neutrophil levels and a bone marrow biopsy may be conducted to determine the cause of neutropenia
323
what are treatments for neutropenia
antibiotics therapy to treat infection.
324
what is crucial to a positive outcome with neutropenia?
identification and treatment of the cause
325
what causes infectious mononucleosis?
the Epstein-Barr virus
326
what family is EBV in?
the herpes family
327
do most people who are exposed to EBV develop infectious mononucleosis? explain.
no, because most people have been exposed to it as children, and because of this exposure, they have developed immunity
328
how does EBV work in the body?
it infects B cells by killing the cells or being incorporated into their genomes. once the disease is eliminated, a few B cells still remain altered, giving an individual an asymptomatic infection for life and the potential to occasionally spread ebv to others
329
how is infectious mononucleosis spread?
person-to-person through contact with saliva most commonly.
330
why is ebv transmission through drinking or eating after someone a risk?
it can survive for hours outside the body
331
what is the incubation period for infectious mononucleosis?
4-6 weeks
332
according to the CDC, depending on the method used to detect the virus, individuals who have recovered from infectious mononucleosis will continue to excrete the virus through their saliva for..... why?
years due to periodic reactivations of viral infection
333
who is the primary resevoir for ebv?
healthy individuals who secrete ebv particles are the primary reservoir for transmission among humans
334
onset of clinical manifestations of infectious mononucleosis are usually called what?
insidious symptoms
335
what are insidious symptoms?
a general feeling of being sick
336
what are the insidious symptoms that manifest with infectious mononucleosis?
malais, fever, chills, anorexia
337
what happens after the insidious symptoms that occur with infectious mononucleosis?
the manifestations intensify and include severe sore throat, fever, and lymphopathy.
338
how long does the acute phase of infectious mononucleosis usually last?
2-3 weeks
339
what are possible complications of mono?
ruptured spleen, hepatitis, and meningitis
340
why can mono cause an enlarged spleen?
it causes the spleen to become congested with blood cells. this puts the patient at risk for their spleen rupturing
341
how is mono diagnosed?
2-3 weeks post exposure, a heterophile antibody test is done. increased lymphocytes, increased monocytes, and atypical t lymphocytes in the blood will be present and can be identified and tested. leukocyte counts may also be increased
342
how common is lymphoma in children and how common is it in the adult?
6th most common cause of cancer in the adult
| 3rd most common cause of cancer in the child
343
what are the two types of lymphoma? which is the most common?
Hodgkin's lymphoma
| Nonhodgkin's lymphoma - most common
344
what are risk factors for both types of lymphomas?
HIV and EBV
345
what are risk factors, other than HIV and EBV, for non-Hodgkin's lymphoma?
the presence of an inherited immune or autoimmune condition and infection with helicobacter pylori or human T cell leukemia/lymphoma virus type 1 (HTLV-1)
346
least common and most treatable lymphoma
Hodgkin's lymphoma
347
in what lymph nodes does Hodgkin's lymphoma most commonly start?
the lymph nodes of the upper body - neck, chest, and upper arms
348
how do Hodgkin's lymphoma cancer cells usually spread?
from one lymph node to the next through the lymphatic vessels
349
which lymphoma has Reed-Sternberg cells?
Hodgkin's lymphoma
350
is metastasis to other parts of the body, other than lymph nodes, common in Hodgkin's lymphoma?
no, if it occurs it is usually late in the disease process
351
an abnormal type of b lymphocyte that is much larger than normal lymphocytes
Reed-Sternberg cells
352
are t lymphocytes affected with Hodgkin's lymphoma?
yes, they appear defected as well and the total number of lymphocytes in general decreases
353
what are the two types of Hodgkin's lymphoma and what are they differentiated depending on?
classic and nodular - they differ in the way the cells appear under the microscope and the way they grow and spread - they are usually treated differently
354
which type of Hodgkin's lymphoma makes up 95% of hodkin's cases?
classic Hodgkin's lymphoma
355
at what ages are you most likely to get Hodgkin's lymphoma?
adults 20-40, with a second peak of occurrence in men 50+
356
when is prognosis of Hodgkin's lymphoma improved?
when the disease is localized and treated early
357
those with Hodgkin's disease that are treated with radiation may be at further risk for what?
stroke and transient ischemic attack
358
what are the clinical manifestations of Hodgkin's disease?
swollen, painless lymph nodes; weight loss; persistent fever; night sweats; generalized pruritis; coughing, trouble breathing, or chest pain; malaise; recurrent infections; splenomegaly
359
what are the stages of Hodgkin's lymphoma?
stage 1: lymphoma cells are in one node group, or only one part of a tissue or organ
stage 2: lymphoma cells are in at least 2 lymph node groups or tissues on the same side of the diaphragm
stage 3: lymphoma cells are above and below the diaphragm in lymph nodes, may be in a tissue or organ near the lymph node and in the spleen
stage 4: in several parts of one or more organs or tissues and in distant nodes
360
what ethnic group is non-hodgkin's lymphoma most common in?
caucasians
361
how can non-hodgkin's lymphoma be divided?
aggressive (fast-growing) and indolent (slow-growing) types and they can arise form either B cells (80%) of cases, or T cells
362
how are hodgkin's and non-hodgkin's lymphomas the same and how are they different?
they are similar in their clinical manifestations, staging and treatment, but different in their spread and diagnosis. non-hodgkin's lymphoma contains no Reed-Sternberg cells
363
how does non-Hodgkin's lymphoma spread?
it involves multiple lymph nodes throughout the body and metastasizes in an unorganized manner. metastasis is often present at diagnosis
364
cancer of the leukocytes
leukemia
365
what occurs with leukemia?
the bone marrow makes abnormal leukocytes, or leukemia cells, which do not die when they should and so they begin crowding normal leukocytes, erythrocytes, and thrombocytes. this makes it difficult for normal blood cells to function properly
366
the most common blood cancer
leukemia
367
is the exact cause of leukemia known?
no
368
leukemia is the most common cancer in what age group?
although it affects 10x as many adults as it does children, it is the most common cancer among children
369
what gender is at more of a risk for leukemia?
men
370
what are risk factors for leukemia?
exposure to chemical, viral, and radiation mutagens; smokin; use of chemotherapies; certain disease conditions; immunodeficient disorders
371
what are the four most common types of leukemias?
acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), chronic lymphoid leukemia (CLL), chronic myeloid leukemia (CML)
372
type of leukemia that affects primarily children - it accounts for approximately 75% of all childhood cases of leukemia. responds well to therapy and contains a good prognosis
acute lymphoblastic leukemia
373
type of leukemia that affects primarily adults; responds fairly well to treatment and carries a good prognosis, but is a little worse than acute lymphoblastic leukemia
acute myeloid leukemia
374
type of leukemia that affects primarily adults; responds poorly to therapy, yet many patients live for many years after diagnosis
chronic lymphoid leukemia
375
type of leukemia that affects primarily adults; responds poorly to chemotherapy, but the prognosis is improved with allogeneic bone marrow transplants
chronic myeloid leukemia
376
what are the clinical manifestations of leukemia?
leukopenia - characterized by frequent infections; anemia - pallor, fatigue, dyspnea, and decreased activity tolerance; thrombocytopenia - petechiae, bleeding gums, hematuria, and prolonged bleeding time; lymphadenopathy; joint swelling; bone pain; weight loss; anorexia; hepatomegal; splenomegaly; central nervous system dysfunction
377
which types of leukemia respond better to chemotherapy?
the acute types
378
cancer of the plasma cells that most often affects older adults.
multiple myeloma
379
what is multiple myeloma characterized by?
BENCE JONES PROTEINS. excessive numbers of plasma cells accumulate in the bone marrow and crowd out blood-forming cells, causing bence jones proteins to be excreted in the urine. multiple bone tumors develop and bone destruction occurs leading to hypercalcemia and kidney impairment and neuromuscular issues. tumor cells can spread to lymph nodes and infiltrate organs
380
this is the second most common blood cancer
multiple myeloma
381
what people are at a greater risk for multiple myeloma?
men and african americans
382
is multiple myeloma curable?
no
383
because of the weakening of the bone, what are people with multiple myeloma more at risk for?
pathologic fractures
384
when is multiple myeloma usually diagnosed?
often when the malignancy is well advanced
385
what are the clinical manifestations of multiple myeloma?
anemia, thrombocytopenia, leukopenia, decreased bone density, bone pain, hypercalcemia, renal impairment, pathologic fractures
386
how is the diagnosis of multiple myeloma often made?
incidentally during routine blood tests for other conditions
387
pancytopenia
low numbers of erythrocytes, leukocytes, and platelets
388
what are most diseases of the RBCs related to?
the quantity or quality of the RBCs
389
anemia
a common acquired or inherited disorder of the erythrocytes that impairs the oxygen-carrying capacity of the blood
390
what are the three things that anemia can result from?
a decrease in the number of circulating erythrocytes; a reduction in hemoglobin content; the presence of abnormal hemoglobin
391
what do the clinical manifestations of anemia reflect regardless of the diseases cause, and what are these?
the decreased oxygen-carrying capacity of the blood - weakness, fatigue, pallor, syncope, dyspnea, tachycardia
392
what are hematocrit levels in order for anemia to be diagnosed?
less than 41% males
| less than 37% females
393
what are hemoglobin concentration levels for the diagnosis of anemia?
men - 13.5 g/dL
| women - 12 g/dL
394
what are normal hemoglobin and hematocrit concentrations for men and women?
men: 13.5-18 g/dL; 41-52%
females: 12-16 g/dL; 37-47%
395
why does syncope occur with anemia?
there are low blood oxygen levels and the brain isn't getting enough oxygen so the person passes out
396
why does dyspnea occur with anemia?
the body isn't getting enough oxygen, so its natural response is to make the body breath more
397
why does tachycardia occur with anemia/
compensatory mechanism to push as much oxygen as quickly as possible to the body
398
the most widespread anemia in the world
iron-deficiency anemia
399
who is iron-deficiency anemia most common in?
women of childbearing age, children younger than 2, and the elderly
400
when does iron deficiency anemia occur?
when the supply of iron necessary to produce hemoglobin is inadequate to meet the demand of hemoglobin production.
401
what are possible causes of iron-deficiency anemia?
low iron consumption, decreased iron absorption, increased bleeding (like what occurs with menstruation and as a result of some cancers), and pregnancy
402
how much of the ingested iron is actually absorbed into the blood stream?
only about 10%
403
what happens to erythrocytes when there is an iron deficiency?
they become pale and small
404
hypochromic
pale
405
microcytic
small
406
what are the clinical manifestations of iron deficiency anemia?
usual manifestations of anemia, cyanosis of the sclera, brittle nails, decreased appetite, headache, irritability, stomatitis, unusual food cravings (pica), delayed healing
407
what causes cyanosis of the sclera in iron-deficiency anemia?
oxygen deprivation
408
stomatitis
sores in the fissures of the mouth - inflammatory response
409
why are healing times prolonged with iron-deficiency anemia?
they body needs good oxygen supply to promote good healing
410
why should foods high in vitamin c be given to people with iron-deficiency anemia?
vitamin c promotes the absorption of iron
411
aka vitamin b12 deficiency and megaloblastic anemia
pernicious anemia
412
what is pernicious anemia characterized by?
large, immature erythrocytes
413
what does pernicious anemia usually result from and why does this occur?
a vitamin b12 deficiency that occurs due to a lack of intrinsic factor which is a protein produced by the stomach that is necessary for the absorption of vitamin b12
414
what does the lack of intrinsic factor in pernicious anemia result from?
autoantibodies, and the subsequent immune reaction leads to atrophy of the gastric mucosa and glands
415
what is vitamin b12 required for? what does too little b12 cause?
required for DNA synthesis of RBC and a deficiency leads to decreased cell division and maturation. too little b12 causes neurologic problems because it breaks down the myelin sheath.
416
what are the clinical manifestations of pernicious anemia?
usual manifestations of anemia, bleeding gums, diarrhea, impaired sense of smell, loss of deep tendon reflexes, anorexia, personality and memory changes, positive Babinski's sign, stomatitis, paresthesia of hands and feet, unsteady gait especially in the dark, confusion, pica, poor apetite, beefy red tongue that's swollen and sore
417
rare, but serious type of anemia that is the result of the bone marrow not making enough blood cells
aplastic anemia
418
is aplastic anemia temporary or permanent?
it may be either
419
causes of aplastic anemia:
autoimmune, idiopathic causes, medications and treatments (chemo), viruses, toxins, genetic abnormalities, infectious diseases, pregnancy, cancer, radiation
420
what are the clinical manifestations of aplastic anemia?
usual manifestations of anemia, leukocytopenia, thromboxytopenia, as blood cell levels decline clinical manifestations worsen
421
anemia that results from destruction of erythrocytes
hemolytic anemia
422
what are causes of hemolytic anemia?
idiopathic causes, autoimmune causes, genetics, develops secondary to an infection, blood transfusion reactions, and blood incompatibility in the neonate
423
what are the different types of hemolytic anemias?
sickle cell anemia and thalassemia and erythroblastosis fetalis
424
type of genetic anemia in which the erythroblasts have an abnormal, or sickle shape
sickle cell anemia
425
what is sickle cell anemia caused by?
an abnormal type of hemoglobin called Hemoglobin S which distorts the shape of erythrocytes, especially when the body's supply of oxygen is low. these cells deliver less oxygen to the body's tissues and clog easily into small vessels and break into pieces that disrupt flow
426
is sickle cell anemia recessive or dominant?
it is neither recessive or dominant, it is co-dominant. if the person inhereits the sickle cell gene from one parent and the normal erythrocyte from the other, both will be expressed
427
why do persons who only have one sickle cell allele (sickle cell trait) not have the symptoms of true sickle cell anemia?
fewer than half of their RBCs are sickled
428
when does a person have sickle cell disease?
when they are homozygous for hemoglobin s
429
why is sickle cell disease more severe than sickle cell trait?
almost all of the individual's erythrocytes are abnormal
430
who is sickle cell disease more common in?
people of african and Mediterranean descent, people from south and Central America, the carribean, and the Middle East
431
do clinical manifestations of sickle cell disease usually appear in newborns? why?
no because fetal hemoglobin protects the RBCs from sickling
432
when does a child start to show signs of sickle cell disease?
when the fetal hemoglobin is replaced with adult hemoglobin around the age of 4-5 months
433
what is usually the first symptoms of sickle-cell disease?
swelling in the hands and feet, often in conjunction with a fever. the swelling results from sickle cells occluding the blood vessels and blocking blood flow in and out of the hands and feet
434
crises
painful episodes with sickle cell anemia that can last for hours to days. these are caused by obstruction of small vessels as the sickled cells clog up the vessels leading to ischemia and necrosis. complications depend on location
435
what can episodes of crises be triggered by?
dehydration, stress, high altitudes, fever, and extreme temperatures
436
how long do most patients with sickle cell anemia live now?
into their 50's
437
what are the clinical manifestations of sickle cell anemia?
manifestations of anemia, abdominal pain, bone pain, dyspnea, delayed growth and development, fatigue, fever, jaundice, pallor, tachycardia, skin ulcers on the lower legs, angina, excessive thirs, frequent urination, painful and prolonged erection, vision impairment, frequent infections, acute chest syndrome, splenic sequestration, leg ulcers, stroke
438
what is acute chest syndrome?
a potentially life-threatening condition that causes chest pain, coughing, difficulty breathing, and fever
439
what is splenic sequestration?
a potentially life-threatening condition that causes sudden weakness, pale lips, tachypnea, extreme thirst, left quadrant abdominal pain, and tachycardia
440
what ar the complications of blood vessel occlusions in sickle cell anemia in the bone
susceptibility to osteomyelitis due to staph infection
441
what are complications of blood vessel occlusions in sickle cell in the papillae of the renal medulla?
gross hematuria and renal tubular concentrating defects
442
what are the complications of blood vessel occlusions of sickle cell in the eye?
retinopathy and blindness
443
what are the complications of blood vessel occlusions in sickle cell anemia in the sinus?
stroke
444
what are the complications of blood vessel occlusion in sickle cell anemia that occurs in the spleen, liver, and what are miscellaneous complications that occur?
spleen - hyposplenism and susceptibility to infections
liver - jaundice and hepatomegaly
miscellaneous - cardiomegaly and slow-healing leg ulcers
445
a rare disorder that is considered neoplastic. the bone marrow produces too many blood cells.
polycythemia vera
446
why is polycythemia vera considered neoplastic?
because of the uncontrolled proliferation of the cells
447
what gender is polycythemia vera most common in?
men
448
how do complications arise with polycythemia vera?
as blood cell numbers increase, so does the blood volume and viscosity. blood vessels become distended and blood flow is sluggish.
449
what complications can arise with polycythemia vera?
tissue ischemia and necrosis, thrombosis, hypertension, heart failure, hemorrhage, slpenomegaly, hepatomegaly, acute myeloblastic leukemia
450
why might hypertension occur with polycythemia vera?
the heart is trying to pump against the high pressure in the vessels, so blood pressure goes up. over time the heart muscle becomes stretched out and doesn't work well and congestive heart failure occurs
451
what are the clinical manifestations of polycythemia vera?
cyanotic or plethoric skin (bluish or reddish), high blood pressure, tachycardia, dyspnea, headaches, visual abnormalities
452
what are the normal platelet levels?
150,000-350,000 cells/mL3
453
thrombocytosis increases the risk of what?
thrombus formation
454
thrombocytopenia increases the risk for what?
bleeding and infection
455
X-linked recessive bleeding disorder that involves a deficiency or abnormality of clotting factor VIII
hemophilia A
456
what does the severity of hemophilia a depend on?
the amount of factor VIII present in the blood
457
what is the main symptom of hemophilia a
bleeding
458
what gender is affected more often with hemophilia a?
males
459
what are the clinical manifestations of hemophilia a?
hemarthrosis (bleeding into the joints; painful), hematuria, GI bleed, ecchymosis, epistaxis (nose bleeds). internal bleeding can happen anywhere
460
when does hemophilia a usually become noticed in people affected by it?
it can become noticed when the child starts walking or crying if it has not been detected before, mild cases can go unnoticed until trauma or surgery
461
the most common hereditary bleeding disorder. results from a deficit of Von Willebrand's factor which ordinarily causes platelets to aggregate and adhere to the vessel wall in times of injury
Von Willebrand's disease
462
the most common and mildest form of Von Willebrand's disease. occurs in 70-80% of patents and follows an autosomal dominant inheritance pattern. the level of von Willebrand factor in the blood is reduced and most cases go undiagnosed. does not usually cause spontaneous bleeding, but significant bleeding can occur with trauma or surgery
type 1
463
von Willebrand's disease that occurs in 15-20% of cases. autosomal dominant or autosomal recessive. has 5 subtypes. the building blocks that make up the von Willebrand's factor are smaller than usual or break down easily
type 2
464
von Willebrand's disease that follows an autosomal recessive pattern. severe bleeding problems with this type due to a lack of measurable von Willebrand's factor or factor VIII.
type 3
465
von willebran's disease that occurs in persons with Wilms' tomor, congenital heart disease, SLE, and hypothyroidism
acquired type
466
what are the clinical manifestations of von willebrand's disease?
abnormal bleeding
467
a life threatening disorder that occurs as a complication of other diseases and conditions.
disseminated intravascular coagulation
468
what occurs during disseminated intravascular coagulation?
normally during injury, clotting factors become activated and travel to the injury site to stop bleeding. however in persons with DIC these factors become abnormally active as an inappropriate immune reaction. small blood clots form within the blood vessel and some of these clots can occlude vessels. eventually, all of a person's clotting factors are used up and the person is at serious risk even from a minor injury
469
what are the typical triggers for DIC?
blood transfusion reaction, cancer, infection in the blood by bacteria/fungus, pregnancy complications (retained placenta after pregnancy, abruptio placentae, and eclampsia), recent surgery or anesthesia, sepsis, severe liver disease, severe tissue injury, cardiac arrest, poisonous snake bites
470
what are the clinical manifestations of DIC?
signs and symptoms of tissue and organ ischemia (angina, confusion, dyspnea) and abnormal bleeding (petechiae, epistaxia, and hematuria). indicators of complications such as shock and multiple organ failure will appear
471
DIC often causes necrosis where?
in the fingers and toes
