rrd 4 Flashcards
mech of defense: inflammation and immune fxn and disorders pt 2 (274 cards)
1
Q
non-medicinal interventions for inflammation include putting protected ice on the area of swelling. what is the mechanism of action?
A
- cold numbs pain
- coolness vasoconstricts the blood vessels of the area -> diminishing swelling and pain
2
Q
anti-inflammatory medications do what?
A
minimize the pain and swelling of inflammation (whether it is normal inflammation or too much inflammation)
- called antiinflammatories
3
Q
what is the mechanism of action of most anti-inflammatories?
A
- suppress PGs effects
- works well for suppressing inflammation, but can result in side effects
4
Q
two types of anti-inflammatories
A
- steroids
- NSAIDS “non-steroidal anti-inflammatory drugs”
5
Q
prostaglandins (PGs)
A
group of mediators that have a large variety of functions
6
Q
PGs are created in the ___ ____ of most cells in the body, in a series of steps called ____ ____.
A
cell membrane, arachidonic pathway
7
Q
PGs are generally categorized as either being _____ or _____.
A
protective, proinflammatory
8
Q
certain types of PGs ______ _____ inflammation by _____ vascular permeability and also _____ fever and pain. what are these PGs called?
A
stimulate further, increasing, induce
- pro-inflammatory
9
Q
other types of PGs have _____ characteristics that are important in many ways throughout the body. they are considered what type of PGs?
A
protective
- protective PGs
10
Q
what do the side effects of anti-inflammatory drugs have to do with?
A
- suppressing the protective PG effect and proinflammatory
- ideal effect would have to be specific and suppress proinflammatory only
11
Q
the arachidonic pathway is what process?
A
- birth pathway of prostaglandins
- process in cell membranes of most cells
- begins with generic phospholipids and ends with the creation of inflammatory mediators like prostaglandins and leukotrienes
12
Q
basic/simple map of the arachidonic pathway
A
- cell membrane phospholipids
- arachidonic acid
3(1). leukotrienes
3(2). prostaglandins
13
Q
what are phospholipases? where do they work in the arachidonic pathway?
A
- enzymes that catalyze the creation of arachidonic acid from the phospholipids of the cell membrane
- after cell membrane phospholipids, before arachidonic acid
14
Q
where do steroids work in the arachidonic pathway?
A
with phospholipases
15
Q
steroids are ____ ____. what is the most common steroid?
A
- naturally occurring
- cortisol
16
Q
synthetic examples of steroids are ____ based on the structure of ____. what are some examples?
A
- drugs, cortisol
- prednisone and solumedrol
17
Q
steroids are ______ in their inhibition of prostaglandins. they suppress both ____ and ____ types of prostaglandins.
A
non-specific, proinflammatory, protective
18
Q
how do steroids suppress both proinflammatory and protective types of prostaglandins?
A
suppress phospholipase
19
Q
steroids are the _____ and ____ anti-inflammatories because they work ____ ___ in the arachidonic pathway, thus blocking both ____ and ____.
A
- strongest, best
- high up
- prostaglandins and leukotrienes
20
Q
steroids are used for more ______ conditions such as?
A
- inflammatory
- acute back injuries, asthma, allergic rxns, bad rashes, lupus, other autoimmune dx
21
Q
downside of steroids working high up in the arachidonic pathway?
A
- steroids the worst of all anti-inflammatories in creating side-effects related to suppression of the protective roles of prostaglandins
22
Q
potential side effects of steroids
A
- stomach ulcers
- easier bleeding
- diminished kidney fxn
- diminished capacity to combat infection
- increased skin fragility
- HTN
23
Q
steroids nickname
A
a double-edged sword
24
Q
NSAIDs
A
non-steroidal anti-inflammatories
25
NSAIDs ____ inflammation, but do so at a ____ place in the arachidonic pathway compared to steroids.
suppress, lower
26
NSAIDs are ____ powerful compared to steroids because?
- not as
- work lower in the arachidonic pathway
27
T/F: NSAIDs do not have as bad of side effects as steroids.
- TRUE
- not as bad of side effects because they work lower in the arachidonic pathway
28
NSAIDs are used for problems such as? what are they not used for?
- headaches
- general aches and pains
- not used for suppressing more serious inflammatory conditons
29
examples of NSAIDs
- aspirin
- ibuprofen (Motrin)
- naproxen
30
leukotrienes
inflammatory mediators
31
prostaglandins 2 categories of fxn?
- proinflammatory
- protective
32
proinflammatory category of PGs
increase inflammatory response as needed
33
protective category of PGs
- have normal PLATELET clotting fxn
- maintain the integrity of the GASTRIC mucosa
- promote healthy RENAL fxn
- maintain appropriate VASOMOTOR tone
- maintain normal IMMUNOCYTE fxn
34
ProstaGlandins R Very Important
- P: platelet
- G: gastric
- R: renal
- V: vasomotor
- I: immunocyte
35
vasomotor tone
the ability of arteries to:
- constrict when your body needs less blood supply to an area
- dilate when your body needs more blood supply
- responsiveness is normal, healthy state of your arteries
36
third line of defense?
- normal immunocyte response
- acquired immunity
37
immunocyte response
a state of acquired defense
38
immunocyte response characterized by:
- involvement of immunocytes/lymphocytes
- being delayed and specific
39
types of lymphocytes involved in immunocyte response
- T-lymphocytes (T-cells)
- B-lymphocytes (B-cells)
40
t-lymphocytes (t-cells)
defend the body by direct attack against invading microbes
41
subtypes of t-lymphocytes
- CD4 cells
- CD8 cells
- memory t-cells
42
CD4 cells
- helper-T
- introductory cells
43
CD8 cells
- cytotoxic T-cells
- act as direct killers
44
memory t-cells
memorize microbe properties
45
b-lymphocytes (b-cells)
defend by a more complicated method
46
subtypes of b-lymphocytes
- b-cells
- plasma cells
- memory B cells
47
B-cells
differentiate into plasma cells
48
plasma cells
- create antibodies to the microbe that has attacked the body
- a particular set of antibodies now always remember and lay in waiting for specific microbe
49
immunocyte response being specific means?
immunocytes only respond fully to microbes that they recognize (have developed memory of)
50
immunocyte response being delayed means?
- takes time to develop the ability to recognize and destroy microbes
51
antigens
- a blood molecule that can stimulate immunocyte rxn against them
- response to antigens that are foreign to our bodies is normal
- response to our own self antigens is abnormal
52
antibodies
- IgG, IgE, IgA
- a group of blood proteins that are made by the immune system in response to and counteract a specific antigen
53
due to immunocyte involvement, the person develops?
ability to resist certain diseases and conditions
54
B and T lymphocytes, and various lymphatic tissues, are?
major players in the immune response
55
if the T cell is "in charge" of developing immunity, the person developed?
cell-mediated immunity
56
if the B cell is "in charge" of developing immunity, the person developed?
humoral immunity
57
no matter which type of immunity developed, it involves?
a primary and secondary response
58
the third line of defense is stimulated by?
the second line of defense, as needed
59
a meningitis bacterial microbe is inhaled and makes it way to the meninges. what line of defense did it breach?
1st line of defense - the mucous membranes of nose
60
when a meningitis bacterial microbe makes it way to the meninges, what happens next?
inflammation takes place as part of the body's normal healing process attempt
61
what happens when local inflammation cannot handle the meningitis bacterial microbe stimulating inflammation in the meninges?
systemic inflammatory mediators are released
62
_____ identifies that a microbe is present after systemic inflammatory mediators are released.
macrophage
63
once the macrophage identifies the microbe, the macrophage secretes chemotactic substances and calls in?
the 3rd line of defense: CD4 cell
64
after calling the CD4 cell, the macrophage displays the _____ remnant of the antigen on its membrane.
phagocytized
65
the CD4 ____ the remnant of the antigen that has been phagocytized by the macrophage and _____ the remnant on the _____ _____.
accepts, displays, T-cell membrane
66
CD4 decides which system is best to deal with the particular antigen it is displaying on the membrane, T-cells or B-cells. for the meningitis microbe, what system is best?
B-cell system because the microbe is a bacteria
67
the b-cell accepts the remnant from the t-cell once the CD4 decides which system is better to deal with the meningitis bacterial microbe. what happens next?
the b-cell differentiates into plasma cells and begins making antibodies against that specific meningitis microbe
68
if this is the first time (aka ?) that type of microbe has invaded the body, the b-lymphocytes cannot mount a ______ defense this first time around. they will get what?
- primary response
- full
- S&S of meningitis (probably will be pretty sick!)
69
even though the b-lymphocytes can't help much during the primary response, they begun to create and establish?
- memory/recognition of the meningitis microbe
70
the plasma cells are making ____ so that in the future, the person will be protected and won't have ____ again.
antibodies, S&S
71
the person who developed memory (antibodies) to the specific meningitis microbe has?
acquired immunity to that organism
72
if that _____ type of meningitis microbe ever invades the person again, the ___ will come out (aka ?) of the lymphatic system where they lay in wait and attack the microbe immediately.
specific, antibodies, secondary response
73
if the immunocytes already have _____ from previous exposure, the meningitis-specific antibodies will ____ destroy any meningitis microbe that enters the body in the future and the person will not "get" the disease.
memory, quickly
74
the 3rd line of defense (acquired immunity) can be categorized as?
- active vs passive FURTHER INTO:
- natural vs artificial
75
active acquired immunity
a persons own immunocyte system developed the antibodies that established immunity
76
natural active acquired immunity
person's plasma cells build up antibodies in response to a microbially-induced illness
77
artificial active acquired immunity
person's plasma cells build up antibodies in response to receiving inoculations/vaccinations of a much-weakened or inactive microbe
78
other names for vaccinations
- immunizations
- inoculations
79
example of artificial active acquired immunity
- child gets vaccinated with MMR vaccine
- weak mixture of actual live viruses given to child
- mix too weak to cause S&S but does mobilize the child's own immunocyte system to create antibodies specific to those virus
80
once immunized, a person has the _______ forever, but they may get ____ in strength & numbers. often, a _____ is given.
antibodies, weaker, booster
81
MMT given at age ___ to ____ months & booster at age ____ years.
12, 15, 5
82
tetanus boosters must be given every?
5 to 10 years
83
an ______ ____ test may be used to detect the presence of antibodies within the blood.
antibody titer
84
passive acquired immunity
- they had been given someone else's antibodies
- they did not develop the antibodies on their own
85
natural passive acquired immunity
transfer of antibodies from mom to baby via placenta or breast milk
86
natural passive acquired immunity via placenta
- antibodies that the mom has in her body (MatAb) crosses the placental membrane from her blood to fetus's
- MatAb disintegrate by the time baby is 2-3 months old
87
natural passive acquired immunity via breast milk
- some MatAbs can transfer during breast feeding
- soon after breast feeding stopped, the MatAbs disintegrate
- by then, baby has own antibodies or has been vaccinated
88
artificial passive acquired immunity
antibodies are injected during treatment, usually in emergencies or as a stop-gap measure until active immunity can develop
89
artificial passive acquired immunity is usually given as a ____ ____ of antibodies to disease that you have a high risk of contracting.
intramuscular injection
90
why is an IM injection of antibodies given in times of emergencies?
- microbe may have entered body via recent laceration, being coughed upon, sharing body fluids, etc.
- person never previously has the disease and has no antibodies to it
91
TIG - tetanus immunoglobulin - is made from what?
prior-formed antibodies against tetanus antigen
92
when is TIG given?
when a patient gets a dirty wound and has either never had tetanus vaccine or has not had a booster in a long time
93
advantage to artificial passive acquired immunity
can be a powerful, immediate way to fight disease bc disease-specific antibodies will immediately begin attacking microbes (if they have invaded your body)
94
disadvantage to artificial passive acquired immunity
passive immunity only lasts as long as the antibody lasts - after about 2 wks, the antibody degrades
95
TIG is given as a just in case because?
- don't know whether a tetanus microbe actually entered the wound
- TIG given gives temp immunity
- if tetanus bacterium present, antibodies will attack it then disintegrate
96
humoral immunity is acquired by?
actions of B-cells
97
B-cells action's that gives humoral immunity is triggered to do so by?
invasion of particular kinds of microbes
98
B-cells, once triggered, differentiate into ______ , which create ____ that are specific for those microbes.
plasma cells, antibodies
99
antibodies defeat microbes by?
- neutralization (inactivation)
- opsonization
100
neutralization
- neutralize bacterial toxins by binding to the toxins of bacteria, renders toxins unable to bind to host tissues
- neutralizes viruses by preventing attachment and entrance of viruses into host cells
101
opsonization
- coats bacteria, which promotes phagocytosis
- optimizes recognition and digestibility of antigen for phagocytes
102
hypersensitivities
- too much immunocyte response
- response that is supposed to help us goes too fat and harms us
103
subcategories of hypersensitivity responses based on the?
target antigen (the antigen that is attacked by antibodies or T-cells)
104
subcategories of hypersensitivity responses based on target antigen
- allergic response (allergic rxn)
- autoimmune response
- alloimmune response
105
basic definition of allergic response/rxn
hypersensitivity to a target antigen (environmental, medical, or pharmaceutical) called allergen
106
basic definition of autoimmune response
hypersensitivity to self-antigens (the target antigen)
- rxn of our body to our own antigens
107
basic definition of alloimmune response
hypersensitivity to another person's antigens (the target antigen), such as when an organ is transplanted
108
allergic hypersensitivity is also called?
IgE-mediated reaction
109
IgE (immunoglobin E) helps protect and defend against ______ but higher numbers of IgE indicate some of kind _______ response.
parasitic infections, allergic hypersensitivity
110
examples of allergen
- pollen
- animal dander
- meds like penicillin
- chems like household cleaners, soaps
111
how can a person be exposed to a substance in an allergic hypersensitivity rxn?
- inhalation
- ingestion
- injection
- skin contact
112
when the substance enters the body for the first time, what happens normally?
- primary response (sensitization) triggered, leads to creation of an antibody
- antibody stands down/hides out in lymph system for the second exposure
113
if an individual who is genetically programmed/predisposed to an allergic rxn, there is a _______ response to that substances that involves?
pathologic, IgE antibody
114
after the initial exposure to an allergen, ___ pathologically binds to _____ cells instead of "standing down." this does what to the cell?
IgE, mast, sensitizes the mast cell
115
on ___ exposure to that allergen, the allergen's receptors bind to the IgE on the _____ mast cell and quickly initiates ______ of mast cell.
repeated, sensitized, degranulation
116
upon degranulation of mast cell, what happens after?
1). histamine release
2). histamine binds to H1 receptors of surrounding tissue and causes systemic and/or local rxns
117
once a person is sensitized, the S&S appear immediately upon?
2nd or more exposures
118
S&S of localized rxn of allergic hypersensitivity
- dermatitis (skin rash that can cause itching/swelling)
- nasal allergic rhinitis
- conjunctivitis from histamine
- leukotriene
- prostaglandin release from mast cells
119
S&S of systemic reaction to allergic hypersensitivity
anaphylaxis - occurs when someone is more severely allergic to the antigen
120
____, ____, ____, and _____ such as complement system are overacted throughout body. all S&S for localized rxns become systemic.
- histamine
- leukotrienes
- PGs
- acute phase reactants
121
components of anaphylaxis
- urticaria
- angioedema
- N, V, D, cramps
- wheezing, dyspnea, possibly laryngeal edema
- hypotension + shock if bad enough
122
urticaria
itching all over; hives
123
angioedema
- abnormal vasodilation and edema of small blood vessels
- usually occurs in lips, tongue, hands
124
where does wheezing during anaphylaxis come from?
- from bronchial edema
- from leukotriene-induced bronchoconstriction
125
____ can be considered an allergic hypersensitivity. ____ are one of the inflammatory mediators that causes bronchoconstriction, causing dyspnea (___), wheezing, etc.
asthma, leukotrienes, SOB
126
what causes hypotension during anaphylaxis?
1). systemic vasodilation from large amts of acute phase reactants
2). blood pools in periphery instead of being part of circulation
3). BP drops
127
treatment for allergic hypersensitivity
- histamine: antihistamine
- inflammatory properties of PGs: steroids
- against bronchoconstrictive properties of leukotrienes: leukotriene blockers
128
antigens
proteins that can stimulate immunocyte rxn against them
129
a reaction against antigens that are foreign to our own bodies is?
normal
130
a reaction against out own, self antigens is?
abnormal
131
autoantibody
a pathologic antibody because it attacks self antigens (the antigens that are our cell membranes saying self)
132
rheumatic, rheumatism, rheumatologist are words that relate to?
inflammation, disturbance, or degeneration of connective tissue structures
133
many connective tissue disorders (ie, rheumatic disorders) are ______ in origin
autoimmune
134
reasons why our bodies' antibodies (or T-cells) sometimes react to own antigens
- sometimes after we fight off an infection, our system stays primed
- genetic factors are important in autoimmune dzs
- gender effect is a consideration
135
what does it mean when our system stays primed?
instead of standing down (sending post-attack immunocytes back to lymph tissue)
- immunocyte system begins attacking antigens on our own cells
136
example of system staying primed (autoimmune hypersensitivity)
rheumatic heart disease (an autoimmune, hyperinflammatory rxn)
137
the etiology of rheumatic heart disease
1). person gets strep throat + resolves bc antibodies killed streptococcus bacteria
2). antibodies look around for sumn that resembles strep antigen
3). heart valve cells close enuf match to strep antigen, cause autoantibodies to attack them
4). heart valve malfxn - floppy and leaking instead of opening/closing tight
138
possible sequela of strep throat is?
bad heart valves due to autoimmune attack, but usually doesn't occur if strep treated thoroughly by antibiotics
139
w/ genetic factors, presence of certain _______ in people with certain autoimmune dzs is statistically significant
HLA antigens
140
gender effect for autoimmune hypersensitivity
10:1 ratio females to males
141
autoimmune diseases often categorized according to 2 possible _____, which are?
- drivers
- autoantibody attack (humoral) VS
- auto T-cell response (cell-mediated
142
humoral autoimmune response
1). autoantibody attacks tissue cells
2). opsonize tissue cells + causing them to be phagocytized by macrophages as if they were bacteria
3). triggers inflammatory response
4). cause damage to target tissues + S&S of inflammation (S&s of disease)
143
cell-mediated autoimmune response
- instead of autoantibody, the attacker is our own T-cells
- attack our tissue and trigger damaging inflammation and S&S
144
examples of tissue-specific autoimmune diseases
- multiple sclerosis
- graves disease
- Goodpasture's syndrome
- myasthenia gravis
- type-1 diabetes
- celiac disease (sprue)
- autoimmune hemolytic anemia
145
multiple sclerosis
- t-lymphocytes destroy random patches of the myelin sheath that insulates the fibers of neurons in the brain
- results in asymmetric weakness and/or malfxn of various areas of the body
146
Graves disease
- disease that causes most cases of hyperthyroidism
- autoantibody stimulates thyroid gland cells to oversecrete thyroid hormone (TH) -> causes S&Ss of hyperthyroidism
147
Goodpasture's syndrome
- autoantibody attacks connective tissue in pulmonary and glomerular basement membrane
- results in pulmonary hemorrhage and glomerulonephritis
148
myasthenia gravis
- autoantibody attacks acetylcholine receptors on cells of muscles
- ACh would not have enuf effective post-syn gap receptor
- S&S of muscle weakness
149
type-1 diabetes
- t-cells destroy insulin-producing cells
- w/o insulin, glucose accumulates in blood and no energy source for cells
150
celiac disease (sprue)
- caused by individual's intolerance of protein gluten (found in wheat and other foods)
- gluten triggers attack by T-cells on own intestinal lining + cause diarrhea
151
autoimmune hemolytic anemia
- a trigger like a frug causes autoantibodies to attack RBCs
- result is abnormally high hemolysis (destruction of RBCs) and resultant low numbers of them (anemia)
152
autoimmune hemolytic anemia is borderline a systemic disease, but it is not because?
blood is considered one tissue
153
there are autoimmune rxns in which antibody & self-antigen pair up into a molecule called?
immune complex
154
the ____ are circulated via bloodstream and instead of damage being done in only one area of body (as in ______), damage is done all over body as _____ gets deposited in ___________ that supply tissues throughout the body.
- immune complex
- tissue-specific type
- immune-complex
- walls of various blood vessels
155
the immune complex ____ the blood vessels and causes inflammation of them (_____), which in turn, causes the ________ to become inflamed.
irritates, vasculitis, surrounding tissue
156
the damage itself and S&S occur in a similar fashion as tissue-specific dzs, but is more _______ since immune complexes can be deposited in the _____.
wide-spread, blood vessels of a variety of tissues
157
examples of systemic autoimmune diseases
lupus and rheumatoid arthritis
158
systemic lupus erythematosus (SLE)
genetic predisposition and mostly seen in women
159
in everyone, there are normally always bits of ___ in the blood on their way to being disposed of in the ____
- degraded cells and nucleic acids like DNA
- spleen, liver
160
due to a not well-understood mechanism, some ____ that happen to be circulating in the blood become _____ when they encounter some of these pits of the person's own _____.
- antibodies
- autoantibodies
- nucleic acids
161
when antibodies attach themselves to DNA, what are they called?
immune complexes
162
immune complexes circulate and are deposited in tiny blood vessels of mostly _______ in variety of areas (which are?) causing vascular inflammation in those tissues. what is that inflammation called?
- connective tissues
- kidneys, lungs, joints, skin
- vasculitis
163
in whichever tissues are involved with immune complexes, process is the same - ______ begins, causing S&Ss related to those tissues
inflammation
164
specific S&S with SLE (list)
- skin rashes in specific patterns
- nonerosive arthritis of at least 2 peripheral joints
- serositis
- proteinuria
- seizures
- fatigue
165
a great ___ of S&S for SLE exists in presentation and degree of the disease. plus, the pattern in one of ______ and _____ - bc of this, SLE is known as one of the ______ - often mistaken for other diseases
- variety
- flare-ups (exacerbations)
- remissions
- great imitators
166
what skin rash patterns does SLE cause?
- classic butterfly malar rash (across cheeks)
* wolf-like facial appearance, hence lupus
167
serositis
inflammation of serous compartments (sacs in body such as pleura and pericardial sac) causes pleurisy, pericarditis
168
SLE diagnosis
- by clinical findings of S&S
- elevated CRP - non-specific inflammatory test
- positive ANA (antinuclear antibody): looks for immune complexes (antibody + nucleic acid/dna) presence
169
serous fluid
- clear gold color
- plasma-type fluid that seeped pathologically outside blood vessel
- found normally in certain spaces/compartments
- fxns as lubricant in normal spaces
170
rheumatoid arthritis (RA) etiology
RA immune complex consists of an autoantibody attached to collagen
171
RA inflammation develops anywhere there is ____, but most commonly in ______ of ____ joints such as?
- collagen
- synovial membranes
- small
- hands
172
synovial refers to?
lining of joints
173
S&S of RA
- fatigue
- joint pain, swelling, deformation
- inflammatory S&S of eyes, heart, lungs, almost any tissue
174
RA diagnosis
- clinical findings of S&S
- elevated CRP
- rheumatoid factor (RF): presence of immune complexes (antibody + collagen)
175
RA differs from?
osteoarthritis
176
osteoarthritis
- age-related and/or overuse-related wear and tear of joints
- NOT due to wide-spread inflammatory process
- no other parts of body involved except joints
- pain in joints tends to get worse as day goes on
177
rheumatoid arthritis
- begins any age and due to inflammation that damages joints
- other areas of body become inflamed and painful
- pain tends to be worse in morn and lessens as day goes on
178
alloimmune hypersensitivity target antigen is>
someone else's cells
179
with alloimmune hypersensitivity, it is not true hypersens. in some respect because?
- body is doing normal fxn of attacking foreign antigens
- but are unwanted + unhelpful since cause problems for person instead of helping with normal antibody/antigen rxn
180
alloimmune concerns in nursing are thought of as?
compatibility issues
181
what does compatibility refer to?
"what treatment might cause an untoward immune rxn" due to introducing foreign antigen and having body attack it
182
types of compatibility issues
- histocompatibility
- ABO/Rh compatibility
183
to be able to distinguish "self" from foreign, almost all body's cell membranes have "_____" composed of protein called?
- self-antigens
- histocompatibility antigens or HLAs (human leukocyte antigens)
184
HLAs are found on the ______ of most _____ cells except _____ and are important in certain patient situations such as _____.
- cell membrane
- body
- RBCs
- transplants
185
_____ testing is done on tissue cells (examples?) of both donors and recipients of transplants to see if?
- histocompatibility
- liver, kidney
- the HLAs on their cells match
186
the _____ the HLAs match, the _____ likely the transplanted tissue will be attacked by ____ that see it as foreign.
- closer
- less
- immunocytes
187
in immunocytes do attack w/ transplants, it is called? what S&S the patient may have in these cases?
- rejection
- pain over the area, fever, etc.
188
to minimize the possibility of rejection during a transplant, patients are usually on what drug? what is the general purpose?
- immunosuppressant drug
- makes immune system lethargic so it won't attack the transplanted tissue
189
RBCs have the ___ blood grp antigens and ____ blood grp antigens on their plasma cell membranes
ABO, Rh
190
the ABO portion of your blood type can be? the Rh portion can be?
- A, B, AB, O
- +/-
191
people w/ certain blood types have ____ antigens and antibodies - nurses need to know which type is ok to give to another type to avoid?
specific, transfusion rxn
192
if you have type B blood...
- born with B antigen on RBC cell membrane
- very quickly after birth, develops "anti-A" immunoglobulin in plasma as part of genetic programming
- "anti-A" primed and ready to engage in 2ndary immune response if meets "A" antigen
193
if person w/ type B blood gets blood from type A person, what happens?
anti-A immunoglobulin attack donor type-A RBCs and hemolyze them
194
what does hemolysis from a transfusion rxn cause?
- problems related to clumping effect
- can block vessels in kidneys (cause kidney failure) and other areas (ischemia to distal tissues)
195
besides hemolytic clumping, a transfusion rxn can also include?
- rash
- fever
- low BP
- body aches
196
a person is either born ___ or ____ the Rh factor on their RBC cell membrane as part of inheritance.
with, without
197
a person is/is not? genetically programmed to immediately develop anti-Rh antibodies.
is NOT
198
a person w/o the Rh factor who is given Rh+ blood will react how?
will be ok the first time they get that blood bc hasn't developed antibodies yet
199
if the person w/o Rh factor gets Rh+ blood the SECOND time, what happens?
may have transfusion rxn
200
normally, mom and fetus blood do/do not? mix during pregnancy. however....
- do NOT
- but during childbirth, some fetal blood may enter mom's system
201
if mom is Rh(-), immunocyte system may see baby's Rh factor as ____ and begin developing _____ if some fetal blood enters her system during childbirth.
foreign, antibodies
202
if fetus of next pregnancy is Rh(+), mom's antibodies ____ cross over and attack the ______ on baby's RBC membrane, resulting in ____. what is this called?
- MAY
- Rh factor
- hemolysis
- erythroblastosis fetalis
203
to prevent hemolytic problems in future pregnancies, mom will get what?
Rhogam shot (med to destroy Rh antibodies) just after birth of Rh(+) child and after every Rh(+) child thereafter
204
A+ blood type characteristics
- A antigens & Rh
- anti-B antibodies
205
A+ can receive
- O +/-
- A +/-
206
A+ can donate to
- A+
- AB+
207
A- blood type characteristics
- A antigens
- Anti-B antibodies
208
A- can receive
- O-
- A-
209
A- can donate to
- A +/-
- AB +/-
210
B+ blood type characteristics
- B antigens & Rh
- anti-A antibodies
211
B+ can receive
- O +/-
- B +/-
212
B+ can donate to
- B+
- AB+
213
B- blood type characteristics
- B antigens
- Anti-A antibodies
214
B- can receive
- O-
- B-
215
B- can donate to
- B +/-
- AB +/-
216
AB+ blood type characteristics
- A/B antigens & Rh
- NO antibodies
217
AB+ can receive
- A +/-
- B +/-
- AB +/-
- O +/-
218
AB+ can donate to
AB+
219
AB- blood type characteristics
- A/B antigens
- NO antibodies
220
AB- can receive
- A-
- B-
- AB-
- O-
221
AB- can donate to
- AB +/-
222
O+ blood type characteristics
- NO antigens & Rh
- Anti-A/B antibodies
223
O+ can receive
- O +/-
224
O+ can donate to
- A+
- B+
- AB+
- O+
225
O- blood type characteristics
- NO antigens or Rh
- Anti-A/B antibodies
226
O- can receive
O-
227
O- can donate to
everyone - universal donor
228
immunodeficiencies generally means?
not enough
229
immunodeficiency
an abnormality in one or more branches of the immune system that renders a person suspectable to diseases normally prevented by an intact immune system
230
no matter the etiology/type, all immunodeficient diseases have what common characteristic?
cause much higher susceptibility to diseases that immunocompetent people get
231
example of high susceptibility with immunodeficient diseases
- everyone gets colds, flus, bacterial infections, etc
- w/ immunocompromised people, get them MORE easily and virulently
232
higher susceptibility greatly increase the chance of immunocompromised person getting?
opportunistic diseases
233
opportunistic diseases
disease caused by an increased susceptibility to diseases that immunocompetent people don't get (ie. microbes that are normally harmless)
234
T/F: immunocompetent people can live with natural flora like yeast, fungi, and certain protozoa
TRUE: immunocompetent people have certain resistance to becoming infected with them
235
in immunocompromised people, the normally harmonious flora....
the normal flora's opportunistic nature takes over and they will invade - opportunistic invader/pathogens
236
immunodeficient disorders categories
- mechanism of action
AND to whether it is
- congenital or acquired
237
subcategories of mechanism of action for immunodeficiency disorders
- humoral/B-cell immunodeficiency
- cell-mediated/T-cell immunodeficiency
- combines B/T cell immunodeficiency
238
congenital/acquired immunodeficiency subcategory of immunodeficiency disorders
- congenital: present at birth
- acquired: develops after birth
239
combined B-cell and T-cell immunodeficiency
diminishment or absence of both humoral and cell-mediated immunity
240
example of congenital B/T cell immunodeficiency
SCIDS: severe combined immunodeficiency syndrome caused by diverse genetic mutations that lead to complete absence of all immune fxn (BUBBLE BOY)
241
examples of acquired combined B/T cell immunodeficiency
- irradiation + cytotoxic drugs for cancer wipe out bone marrow - not enuf T/B lymphocytes
- immunosuppressant drugs post-transplant
- aging
242
humoral/B cell immunodeficiency
most commonly a congenital problem
243
example of humoral/B cell immunodeficiency
X-linked hypogammaglobulinemia
244
X-linked hypogammaglobulinemia
- IgG missing or lessened in amt
- sequela of making fewer/any antibodies, can't fight dz
245
example of congenital cell-mediated/ T cell immunodeficiency
DiGeorge's syndrome
- genetic defect on chromosome 22 that causes failure of thymus development
246
DiGeorge's syndrome - failure to develop thymus causes?
- t-cells will not have full maturation bc they normally mature in thymus
- person will have decreased ability to fight certain infections
247
example of acquired cell-mediated/T cell immunodeficiency
AIDS: acquired immunodeficiency syndrome caused by HIV (human immunodeficiency virus)
248
HIV virus invades ____ cells and begins killing them - decreases ability to _____ immune responses because the ___ cell is most important as an _____ component to development of various immunities.
- CD4
- mount
- CD4
- introductory
249
AIDS is an _____ _____ immunodeficiency that is now worldwide, but originated in Africa as a cross-species jump when chimpanzee meat infected with SIV (_____) was eaten by humans.
- acquired cell-mediated
- simian immunodeficiency virus
250
the virus associated with HIV passes from person to person via (portal of entry)?
- certain infected bodily fluids like semen or vaginal fluids
- breast milk
- direct blood to blood contact such as sharing IV drug implements or receiving tainted blood transfusion (rare)
251
groups of highest risk for HIV infection
- anyone participating in unprotected sex (no latex)
- gay, bi, and other men who have sex with men
- transgender women who have sex with men
- injection drug users
- children born of women who are HIV+ or children who drink breast milk from HIV+ women
252
HIV is what type of virus?
RNA retrovirus
253
a regular RNA virus inserts its ___ into _____ of host cell and takes over _______ protein-building for its own propagation.
RNA, cytoplasm, ribosomal
254
a retrovirus inserts its ___ into a host cell's _____, converts its own _____ to _____ and then back to ____.
- RNA
- cytoplasm
- RNA, DNA, RNA
255
steps in RNA retrovirus (HIV) invasion process
1). HIV introduced into the blood
2). virus finds CD4 cells
3) virus use its capsid (protein coating) to bind to membrane receptors on CD4 cell
4). virus inserts its RNA into CD4 cytoplasm
5). once inside, uses reverse transcriptase enzyme to convert its RNA to DNA
6). viral DNA goes into CD4 nucleus
7). viral DNA uses integrase enzyme to inserts its viral DNA into host cell's DNA
8). in nucleus, it can remain dormant for years
256
T/F: a person has to be HIV+ and have AIDS at the same time
FALSE: minimal destruction of CD4 cells when only HIV+, so AIDS hasn't appeared yet
257
steps to HIV destruction after invasion
1). at some point, HIV wakes up and its DNA is transcribed into new RNA that moves into CD4 cytoplasm
2). new RNA goes to ribosomes
3). new viral proteins built and modified w/ help from proteases enzyme
4). new virus buds from infected cell and ruptures CD4 plasma membrane (destroyed)
5). decrease in number of CD4 cells
6). less CD4 cells - increased susceptibility to infections in gen and opportunistic infections
258
once the HIV wakes up, the CD4 cells get _____ and more likely the patient will have?
destroyed, dx of AIDS
259
diagnosis of HIV
- ELISA lab test (enzyme-linked immunosorbent assay) used FIRST
- if ELISA (+), second/confirmatory test done called Western Blot
260
ELISA test
- test for presence of antibodies to HIV (as soon as virus enters body, immune response triggered and antibodies detectable by 1-2 wks)
261
with the ELISA, ___ of all infected individuals test (+) w/in ___ of initial infection
96%, 2 to 12 weeks
262
if ELISA (-), recommendations for further testing depends on?
factors like patient risk status and timing of testing
263
someone can be HIV+ and live for many years _____ getting AIDS.
without
264
if ELISA (+), what second/confirmatory test is done? what kind of test is it?
Western Blot: more $$$, but more specific and very few false positive
265
a person is usually diagnosed as having AIDS when the CD4 count drops to ____ because it is the approx. point where body cannot fight of ____________.
<200, opportunistic invasion
266
usual criteria for diagnosis for AIDS
- CD4 level < 200
AND
- presence of opportunistic infection
267
examples of most typical opportunistic infection (OI)
- thrush
- pneumocystis jiroveci (formally carinii) pneumonia (PCP)
- cytomegalovirus (CMV) retinitis
- Kaposi's sarcoma
268
thrush and their drug
- yeast infection of mouth and throat
- antifungals
269
pneumocystis jiroveci (formally carinii) pneumonia (PCP) and their drug
- a type of fungus that invades the lungs
- oral and nebulized sulfonamides
270
cytomegalovirus (CMV) retinitis
a virus normally harmless invades eyes
271
Kaposi's sarcoma
a type of malignant skin tumor that invades immunocompromised people
272
S&S of AIDS are due to ____ and _____ of tissue. what are they?
- OIs, atrophy
- weight loss
- anorexia
- general cachexia (weakness + body wasting)
- dementia
273
treatment and prevention of HIV/AIDS
education
- latex condoms for prevention
- understand HIV can effect anyone
- drugs targeted at diff phases of viral invasion/replication + treating OIs
274
all immunodeficient diseases (B, T, or combo B/T)....
- cause much higher susceptibility to diseases that immunocompetent ppl get (flu, colds, etc.)
- greatly increase chance of immunocompromised person getting opportunistic disease (thrush, PCP, CMV, etc.)
